91 results on '"Matteoni, R"'
Search Results
2. Importing genetically altered animals: ensuring quality
- Author
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Birling, M.-C., primary, Fray, M. D., additional, Kasparek, P., additional, Kopkanova, J., additional, Massimi, M., additional, Matteoni, R., additional, Montoliu, L., additional, Nutter, L. M. J., additional, Raspa, M., additional, Rozman, J., additional, Ryder, E. J., additional, Scavizzi, F., additional, Voikar, V., additional, Wells, S., additional, Pavlovic, G., additional, and Teboul, L., additional
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- 2021
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3. Mice lacking the Parkinsonʼs related GPR37/PAEL receptor show non-motor behavioral phenotypes: age and gender effect
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Mandillo, S., Golini, E., Marazziti, D., Di Pietro, C., Matteoni, R., and Tocchini-Valentini, G. P.
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- 2013
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- View/download PDF
4. INFRAFRONTIER-providing mutant mouse resources as research tools for the international scientific community
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Meehan, TF, Chen, CK, Koscielny, G, Relac, M, Wilkinson, P, Flicek, P, Parkinson, H, Castro, A, Fessele, S, Steinkamp, R, Hagn, M, Raess, M, de Angelis, MH, Bottomley, J, Ramirez-Solis, R, Smedley, D, Ball, S, Blake, A, Fray, M, Kenyon, J, Mallon, AM, Brown, S, Massimi, M, Matteoni, R, Tocchini-Valentini, G, Herault, Y, Kollias, G, Ulfhake, B, Demengeot, J, Fremond, C, Bosch, F, Montoliu, L, Soininen, R, Schughart, K, Brakebusch, C, Sedlacek, R, Rulicke, T, McKerlie, C, Malissen, B, Iraqi, F, Jonkers, J, Russig, H, Huylebroeck, Danny, Helmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany., and Cell biology
- Subjects
Internet ,business.industry ,Knowledge Bases ,Mutant ,Biology ,Mice, Mutant Strains ,Biotechnology ,World Wide Web ,Phenotype ,SDG 3 - Good Health and Well-being ,Databases, Genetic ,Models, Animal ,Genetics ,Database Issue ,Animals ,The Internet ,business ,Embryonic Stem Cells - Abstract
This deposit is composed by a publication in which the IGC' authors have had the role of collaboration (it's a collaboration publication). This type of deposit in ARCA is in restrictedAccess (it can't be in open access to the public), and could only be accessed by two ways: either by requesting a legal copy to the author (the email contact present in this deposit) or by visiting the following link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383977/ The laboratory mouse is a key model organism to investigate mechanism and therapeutics of human disease. The number of targeted genetic mouse models of disease is growing rapidly due to high-throughput production strategies employed by the International Mouse Phenotyping Consortium (IMPC) and the development of new, more efficient genome engineering techniques such as CRISPR based systems. We have previously described the European Mouse Mutant Archive (EMMA) resource and how this international infrastructure provides archiving and distribution worldwide for mutant mouse strains. EMMA has since evolved into INFRAFRONTIER (http://www.infrafrontier.eu), the pan-European research infrastructure for the systemic phenotyping, archiving and distribution of mouse disease models. Here we describe new features including improved search for mouse strains, support for new embryonic stem cell resources, access to training materials via a comprehensive knowledgebase and the promotion of innovative analytical and diagnostic techniques. European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI).
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- 2015
- Full Text
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5. INFRAFRONTIER2020 - WP4: Sustainability and Data Management
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Fessele S., Matteoni R., and Roncaglia P.
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disease model ,mutant strain - Abstract
INFRAFRONTIER2020 - WP4: Sustainability and Data Management Task 1 - Reengineering the EMMA database system INFRAFRONTIER, CNR Task 2 - Data annotation and validating mouse models of human disease CNR, INFRAFRONTIER Task 3 - Database sustainability and metrics for INFRAFRONTIER EMBL, INFRAFRONTIER
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- 2017
6. INFRAFRONTIER Informatics and Data Curation
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Wilkinson P. and Matteoni R.
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- 2014
7. Interaction of elements of the golgi apparatus with microtubules
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Kreis, Th. E., Allan, V. J., Matteoni, R., and Ho, W. C.
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- 1988
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- View/download PDF
8. INFRAFRONTIER Informatics and Data Curation
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Meehan T., Koscielny G., and Matteoni R.
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- 2013
9. The orphan GPR37L1 receptor controls postnatal cerebellum development
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Di Pietro C., Marazziti D., Mandillo S., Golini E., La Sala G., Matteoni R., and Tocchini-Valentini G. P.
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- 2012
10. The Orphan Gpr37l1 Receptor Is Involved In Motor Learning In Mice
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Golini E., Mandillo S., Marazziti D., Di Pietro C., La Sala G., Matteoni R., and Tocchini-Valentini G. P.
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- 2012
11. Measurement of the bottom-strange meson mixing phase in the full CDF data set
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Aaltonen, T., Alvarez, González, Amerio, B., Amidei, S., Anastassov, D., Annovi, A., Antos, A., Apollinari, J., Appel, G., J. A., Arisawa, Artikov, T., Asaadi, A., Ashmanskas, J., Auerbach, W., Aurisano, B., Azfar, A., Badgett, F., Bae, W., Barbaro, Galtieri, Barnes, A., V. E., Barnett, B. A., Barria, Bartos, P., Bauce, P., Bedeschi, M., Behari, F., Bellettini, S., Bellinger, G., Benjamin, J., Beretvas, D., Bhatti, A., Bisello, A., Bizjak, D., Bland, I., K. R., Blumenfeld, Bocci, B., Bodek, A., Bortoletto, A., Boudreau, D., Boveia, J., Brigliadori, A., Bromberg, L., Brucken, C., Budagov, E., Budd, J., H. S., Burkett, Busetto, K., Bussey, G., Buzatu, P., Calamba, A., Calancha, A., Camarda, C., Campanelli, S., Campbell, M., Canelli, M., Carls, F., Carlsmith, B., Carosi, D., Carrillo, R., Carron, S., Casal, S., Casarsa, B., Castro, M., Catastini, A., Cauz, P., Cavaliere, D., Cavalli, Sforza, Cerri, M., Cerrito, A., Chen, L., Y. C., Chertok, Chiarelli, M., Chlachidze, G., Chlebana, G., Cho, F., Chokheli, K., Chung, D., W. H., Chung, Y. S., Ciocci, M. A., Clark, Clarke, A., Compostella, C., Convery, G., M. E., Conway, Corbo, J., Cordelli, M., Cox, M., C. A., Cox, D. J., Crescioli, Cuevas, F., Culbertson, J., Dagenhart, R., D'Ascenzo, D., Datta, N., Barbaro, De, Dell'Orso, Mauro, Demortier, M., Deninno, L., Devoto, M., D'Errico, F., Canto, Di, Ruzza, Di, Dittmann, B., J. R., D'Onofrio, Donati, Simone, Dong, P., Dorigo, M., Dorigo, T., Ebina, K., Elagin, A., Eppig, A., Erbacher, R., Errede, S., Ershaidat, N., Eusebi, R., Farrington, S., Feindt, M., Fernandez, J. P., Field, R., Flanagan, G., Forrest, R., Frank, M. J., Franklin, M., Freeman, J. C., Funakoshi, Y., Furic, I., Gallinaro, M., Garcia, J. E., Garfinkel, A. F., Garosi, P., Gerberich, H., Gerchtein, E., Giagu, S., Giakoumopoulou, V., Giannetti, P., Gibson, K., Ginsburg, C. M., Giokaris, N., Giromini, P., Giurgiu, G., Glagolev, V., Glenzinski, D., Gold, M., Goldin, D., Goldschmidt, N., Golossanov, A., Gomez, G., Gomez, Ceballos, Goncharov, G., González, M., Gorelov, O., Goshaw, I., A. T., Goulianos, Grillo, K., Grinstein, L., Grosso, Pilcher, Group, C., R. C., Guimaraes Da Costa, Hahn, J., S. R., Halkiadakis, Hamaguchi, E., Han, A., J. Y., Happacher, Hara, F., Hare, K., Hare, D., Harr, M., R. F., Hatakeyama, Hays, K., Heck, C., Heinrich, M., Herndon, J., Hewamanage, M., Hocker, S., Hopkins, A., Horn, W., Hou, D., Hughes, S., R. E., Hurwitz, Husemann, M., Hussain, U., Hussein, N., Huston, M., Introzzi, J., Iori, G., Ivanov, M., James, A., Jang, E., Jayatilaka, D., Jeon, B., E. J., Jindariani, Jones, S., Joo, M., K. K., Jun, S. Y., Junk, T. R., Kamon, Karchin, T., P. E., Kasmi, Kato, A., Ketchum, Y., Keung, W., Khotilovich, J., Kilminster, V., Kim, B., D. H., Kim, H. S., Kim, J. E., Kim, M. J., Kim, S. B., Kim, S. H., Kim, Y. K., Kim, Y. J., Kimura, Kirby, N., Klimenko, M., Knoepfel, S., Kondo, K., Kong, K., D. J., Konigsberg, Kotwal, J., A. V., Kreps, Kroll, M., Krop, J., Kruse, D., Krutelyov, M., Kuhr, V., Kurata, T., Kwang, M., Laasanen, S., A. T., Lami, Lammel, S., Lancaster, S., Lander, M., R. L., Lannon, Lath, K., Latino, A., Lecompte, G., Lee, T., Lee, E., H. S., Lee, J. S., Lee, S. W., Leo, Leone, S., Lewis, S., J. D., Limosani, Lin, A., C. J., Lindgren, Lipeles, M., Lister, E., Litvintsev, A., D. O., Liu, Liu, C., Liu, H., Liu, Q., Lockwitz, T., Loginov, S., Lucchesi, A., Lueck, D., Lujan, J., Lukens, P., Lungu, P., Lys, G., Lysak, J., Madrak, R., Maeshima, R., Maestro, K., Malik, P., Manca, S., Manousakis, Katsikakis, Margaroli, A., Marino, F., Martínez, C., Mastrandrea, M., Matera, P., Mattson, K., M. E., Mazzacane, Mazzanti, A., Mcfarland, P., K. S., Mcintyre, Mcnulty, P., Mehta, R., Mehtala, A., Mesropian, P., Miao, C., Mietlicki, T., Mitra, D., Miyake, A., Moed, H., Moggi, S., Mondragon, N., M. N., Moon, C. S., Moore, Morello, R., M. J., Morlock, Movilla, Fernandez, Mukherjee, P., Muller, A., Murat, T., Mussini, P., Nachtman, M., Nagai, J., Naganoma, Y., Nakano, J., Napier, I., Nett, A., Neu, J., Neubauer, C., M. S., Nielsen, Nodulman, J., Noh, L., S. Y., Norniella, Oakes, O., Oh, L., S. H., Oh, Y. D., Oksuzian, Okusawa, I., Orava, T., Ortolan, R., Pagan, Griso, Pagliarone, S., Palencia, C., Papadimitriou, E., Paramonov, V., A. A., Patrick, Pauletta, J., Paulini, G., Paus, M., Pellett, C., D. E., Penzo, Phillips, A., T. J., Piacentino, Pianori, G., Pilot, E., Pitts, J., Plager, K., Pondrom, C., Poprocki, L., Potamianos, S., Prokoshin, K., Pranko, F., Ptohos, A., Punzi, Giovanni, Rahaman, G., Ramakrishnan, A., Ranjan, V., Redondo, N., Renton, I., Rescigno, P., Riddick, M., Rimondi, T., Ristori, F., Robson, L., Rodrigo, A., Rodriguez, T., Rogers, T., Rolli, E., Roser, S., Ruffini, R., Ruiz, F., Russ, A., Rusu, J., Safonov, V., Sakumoto, A., W. K., Sakurai, Santi, Y., Sato, L., Saveliev, K., Savoy, Navarro, Schlabach, A., Schmidt, P., Schmidt, A., E. E., Schwarz, Scodellaro, T., Scribano, L., Scuri, A., Seidel, F., Seiya, S., Semenov, Y., Sforza, A., Shalhout, F., S. Z., Shears, Shepard, T., P. F., Shimojima, Shochet, M., Shreyber, Tecker, Simonenko, I., Sinervo, A., Sliwa, P., Smith, K., J. R., Snider, F. D., Soha, Sorin, A., Song, V., Squillacioti, H., Stancari, P., Denis, S. t., Stelzer, R., Stelzer, Chilton, Stentz, O., Strologas, D., Strycker, J., G. L., Sudo, Sukhanov, Y., Suslov, A., Takemasa, I., Takeuchi, K., Tang, Y., Tecchio, J., Teng, M., P. K., Thom, Thome, J., Thompson, J., G. A., Thomson, Toback, E., Tokar, D., Tollefson, S., Tomura, K., Tonelli, T., Torre, D., Torretta, S., Totaro, D., Trovato, P., Ukegawa, M., Uozumi, F., Varganov, S., Vázquez, A., Velev, F., Vellidis, G., Vidal, C., Vila, M., Vilar, I., Vizán, R., Vogel, J., Volpi, M., Wagner, G., Wagner, P., R. L., Wakisaka, Wallny, T., Wang, R., S. M., Warburton, Waters, A., Wester, D., W. C., Whiteson, Wicklund, D., A. B., Wicklund, Wilbur, E., Wick, S., Williams, F., H. H., Wilson, J. S., Wilson, Winer, P., B. L., Wittich, Wolbers, P., Wolfe, S., Wright, H., Wu, T., Wu, X., Yamamoto, Z., Yamato, K., Yang, D., Yang, T., U. K., Yang, Y. C., Yao, W. M., Yeh, G. P., Yi, Yoh, K., Yorita, J., Yoshida, K., Yu, T., G. B., Yu, Yu, I., S. S., Yun, J. C., Zanetti, Zeng, A., Zhou, Y., Zucchelli, C., Jy, S., Koh, Yh, Koike, M, Komatsu, M, Kominami, E, Kong, Hj, Kong, Wj, Korolchuk, Vi, Kotake, Y, Koukourakis, Mi, Kouri Flores JB, Kovács, Al, Kraft, C, Krainc, D, Krämer, H, Kretz Remy, C, Krichevsky, Am, Kroemer, G, Krüger, R, Krut, O, Ktistakis, Nt, Kuan, Cy, Kucharczyk, R, Kumar, A, Kumar, R, Kumar, S, Kundu, M, Kung, Hj, Kurz, T, Kwon, Hj, La Spada AR, Lafont, F, Lamark, T, Landry, J, Lane, Jd, Lapaquette, P, Laporte, Jf, László, L, Lavandero, S, Lavoie, Jn, Layfield, R, Lazo, Pa, Le, W, Le Cam, L, Ledbetter, Dj, Lee, Aj, Lee, Bw, Lee, Gm, Lee, J, Lee, Jh, Lee, M, Lee, Ms, Lee, Sh, Leeuwenburgh, C, Legembre, P, Legouis, R, Lehmann, M, Lei, Hy, Lei, Qy, Leib, Da, Leiro, J, Lemasters, Jj, Lemoine, A, Lesniak, Ms, Lev, D, Levenson, Vv, Levine, B, Levy, E, Li, F, Li, Jl, Li, L, Li, S, Li, W, Li, Xj, Li, Yb, Li, Yp, Liang, C, Liang, Q, Liao, Yf, Liberski, Pp, Lieberman, A, Lim, Hj, Lim, Kl, Lim, K, Lin, Cf, Lin, Fc, Lin, J, Lin, Jd, Lin, K, Lin, Ww, Lin, Wc, Lin, Yl, Linden, R, Lingor, P, Lippincott Schwartz, J, Lisanti, Mp, Liton, Pb, Liu, B, Liu, Cf, Liu, K, Liu, L, Liu, Qa, Liu, W, Liu, Yc, Liu, Y, Lockshin, Ra, Lok, Cn, Lonial, S, Loos, B, Lopez Berestein, G, López Otín, C, Lossi, L, Lotze, Mt, Lőw, P, Lu, B, Lu, Z, Luciano, F, Lukacs, Nw, Lund, Ah, Lynch Day MA, Ma, Y, Macian, F, Mackeigan, Jp, Macleod, Kf, Madeo, F, Maiuri, L, Maiuri, Mc, Malagoli, D, Malicdan, Mc, Malorni, W, Man, N, Mandelkow, Em, Manon, S, Manov, I, Mao, K, Mao, X, Mao, Z, Marambaud, P, Marazziti, D, Marcel, Yl, Marchbank, K, Marchetti, P, Marciniak, Sj, Marcondes, M, Mardi, M, Marfe, G, Mariño, G, Markaki, M, Marten, Mr, Martin, Sj, Martinand Mari, C, Martinet, W, Martinez Vicente, M, Masini, M, Matarrese, P, Matsuo, S, Matteoni, R, Mayer, A, Mazure, Nm, Mcconkey, Dj, Mcconnell, Mj, Mcdermott, C, Mcdonald, C, Mcinerney, Gm, Mckenna, Sl, Mclaughlin, B, Mclean, Pj, Mcmaster, Cr, Mcquibban, Ga, Meijer, Aj, Meisler, Mh, Meléndez, A, Melia, Tj, Melino, G, Mena, Ma, Menendez, Ja, Menna Barreto RF, Menon, Mb, Menzies, Fm, Mercer, Ca, Merighi, A, Merry, De, Meschini, S, Meyer, Cg, Meyer, Tf, Miao, Cy, Miao, Jy, Michels, Pa, Michiels, C, Mijaljica, D, Milojkovic, A, Minucci, S, Miracco, C, Miranti, Ck, Mitroulis, I, Miyazawa, K, Mizushima, N, Mograbi, B, Mohseni, S, Molero, X, Mollereau, B, Mollinedo, F, Momoi, T, Monastyrska, I, Monick, Mm, Monteiro, Mj, Moore, Mn, Mora, R, Moreau, K, Moreira, Pi, Moriyasu, Y, Moscat, J, Mostowy, S, Mottram, Jc, Motyl, T, Moussa, Ce, Müller, S, Muller, S, Münger, K, Münz, C, Murphy, Lo, Murphy, Me, Musarò, A, Mysorekar, I, Nagata, E, Nagata, K, Nahimana, A, Nair, U, Nakagawa, T, Nakahira, K, Nakano, H, Nakatogawa, H, Nanjundan, M, Naqvi, Ni, Narendra, Dp, Narita, M, Navarro, M, Nawrocki, St, Nazarko, Ty, Nemchenko, A, Netea, Mg, Neufeld, Tp, Ney, Pa, Nezis, Ip, Nguyen, Hp, Nie, D, Nishino, I, Nislow, C, Nixon, Ra, Noda, T, Noegel, Aa, Nogalska, A, Noguchi, S, Notterpek, L, Novak, I, Nozaki, T, Nukina, N, Nürnberger, T, Nyfeler, B, Obara, K, Oberley, Td, Oddo, S, Ogawa, M, Ohashi, T, Okamoto, K, Oleinick, Nl, Oliver, Fj, Olsen, Lj, Olsson, S, Opota, O, Osborne, Tf, Ostrander, Gk, Otsu, K, Ou, Jh, Ouimet, M, Overholtzer, M, Ozpolat, B, Paganetti, P, Pagnini, U, Pallet, N, Palmer, Ge, Palumbo, C, Pan, T, Panaretakis, T, Pandey, Ub, Papackova, Z, Papassideri, I, Paris, I, Park, J, Park, Ok, Parys, Jb, Parzych, Kr, Patschan, S, Patterson, C, Pattingre, S, Pawelek, Jm, Peng, J, Perlmutter, Dh, Perrotta, I, Perry, G, Pervaiz, S, Peter, M, Peters, Gj, Petersen, M, Petrovski, G, Phang, Jm, Piacentini, M, Pierre, P, Pierrefite Carle, V, Pierron, G, Pinkas Kramarski, R, Piras, A, Piri, N, Platanias, Lc, Pöggeler, S, Poirot, M, Poletti, A, Poüs, C, Pozuelo Rubio, M, Prætorius Ibba, M, Prasad, A, Prescott, M, Priault, M, Produit Zengaffinen, N, Progulske Fox, A, Proikas Cezanne, T, Przedborski, S, Przyklenk, K, Puertollano, R, Puyal, J, Qian, Sb, Qin, L, Qin, Zh, Quaggin, Se, Raben, N, Rabinowich, H, Rabkin, Sw, Rahman, I, Rami, A, Ramm, G, Randall, G, Randow, F, Rao, Va, Rathmell, Jc, Ravikumar, B, Ray, Sk, Reed, Bh, Reed, Jc, Reggiori, F, Régnier Vigouroux, A, Reichert, As, Reiners JJ Jr, Reiter, Rj, Ren, J, Revuelta, Jl, Rhodes, Cj, Ritis, K, Rizzo, E, Robbins, J, Roberge, M, Roca, H, Roccheri, Mc, Rocchi, S, Rodemann, Hp, Rodríguez de Córdoba, S, Rohrer, B, Roninson, Ib, Rosen, K, Rost Roszkowska MM, Rouis, M, Rouschop, Km, Rovetta, F, Rubin, Bp, Rubinsztein, Dc, Ruckdeschel, K, Rucker EB 3rd, Rudich, A, Rudolf, E, Ruiz Opazo, N, Russo, R, Rusten, Te, Ryan, Km, Ryter, Sw, Sabatini, Dm, Sadoshima, J, Saha, T, Saitoh, T, Sakagami, H, Sakai, Y, Salekdeh, Gh, Salomoni, P, Salvaterra, Pm, Salvesen, G, Salvioli, R, Sanchez, Am, Sánchez Alcázar JA, Sánchez Prieto, R, Sandri, M, Sankar, U, Sansanwal, P, Santambrogio, L, Saran, S, Sarkar, S, Sarwal, M, Sasakawa, C, Sasnauskiene, A, Sass, M, Sato, K, Sato, M, Schapira, Ah, Scharl, M, Schätzl, Hm, Scheper, W, Schiaffino, S, Schneider, C, Schneider, Me, Schneider Stock, R, Schoenlein, Pv, Schorderet, Df, Schüller, C, Schwartz, Gk, Scorrano, L, Sealy, L, Seglen, Po, Segura Aguilar, J, Seiliez, I, Seleverstov, O, Sell, C, Seo, Jb, Separovic, D, Setaluri, V, Setoguchi, T, Settembre, C, Shacka, Jj, Shanmugam, M, Shapiro, Im, Shaulian, E, Shaw, Rj, Shelhamer, Jh, Shen, Hm, Shen, Wc, Sheng, Zh, Shi, Y, Shibuya, K, Shidoji, Y, Shieh, Jj, Shih, Cm, Shimada, Y, Shimizu, S, Shintani, T, Shirihai, Os, Shore, Gc, Sibirny, Aa, Sidhu, Sb, Sikorska, B, Silva Zacarin EC, Simmons, A, Simon, Ak, Simon, Hu, Simone, C, Simonsen, A, Sinclair, Da, Singh, R, Sinha, D, Sinicrope, Fa, Sirko, A, Siu, Pm, Sivridis, E, Skop, V, Skulachev, Vp, Slack, Rs, Smaili, Ss, Smith, Dr, Soengas, Ms, Soldati, T, Song, X, Sood, Ak, Soong, Tw, Sotgia, F, Spector, Sa, Spies, Cd, Springer, W, Srinivasula, Sm, Stefanis, L, Steffan, Js, Stendel, R, Stenmark, H, Stephanou, A, Stern, St, Sternberg, C, Stork, B, Strålfors, P, Subauste, Cs, Sui, X, Sulzer, D, Sun, J, Sun, Sy, Sun, Zj, Sung, Jj, Suzuki, K, Suzuki, T, Swanson, Ms, Swanton, C, Sweeney, St, Sy, Lk, Szabadkai, G, Tabas, I, Taegtmeyer, H, Tafani, M, Takács Vellai, K, Takano, Y, Takegawa, K, Takemura, G, Takeshita, F, Talbot, Nj, Tan, Ks, Tanaka, K, Tang, D, Tanida, I, Tannous, Ba, Tavernarakis, N, Taylor, Gs, Taylor, Ga, Taylor, Jp, Terada, Ls, Terman, A, Tettamanti, G, Thevissen, K, Thompson, Cb, Thorburn, A, Thumm, M, Tian, F, Tian, Y, Tocchini Valentini, G, Tolkovsky, Am, Tomino, Y, Tönges, L, Tooze, Sa, Tournier, C, Tower, J, Towns, R, Trajkovic, V, Travassos, Lh, Tsai, Tf, Tschan, Mp, Tsubata, T, Tsung, A, Turk, B, Turner, Ls, Tyagi, Sc, Uchiyama, Y, Ueno, T, Umekawa, M, Umemiya, Shira, T., Aaltonen, B. A., Gonzalez, S., Amerio, D., Amidei, A., Anastassov, A., Annovi, J., Anto, G., Apollinari, J. A., Appel, T., Arisawa, A., Artikov, J., Asaadi, W., Ashmanska, B., Auerbach, A., Aurisano, F., Azfar, W., Badgett, T., Bae, A., Barbaro Galtieri, V. E., Barne, B. A., Barnett, P., Barria, P., Barto, M., Bauce, F., Bedeschi, S., Behari, G., Bellettini, J., Bellinger, D., Benjamin, A., Beretva, A., Bhatti, D., Bisello, I., Bizjak, K. R., Bland, B., Blumenfeld, A., Bocci, A., Bodek, D., Bortoletto, J., Boudreau, A., Boveia, L., Brigliadori, C., Bromberg, E., Brucken, J., Budagov, H. S., Budd, K., Burkett, G., Busetto, P., Bussey, A., Buzatu, A., Calamba, C., Calancha, S., Camarda, M., Campanelli, M., Campbell, F., Canelli, B., Carl, D., Carlsmith, R., Carosi, S., Carrillo, S., Carron, B., Casal, M., Casarsa, A., Castro, P., Catastini, D., Cauz, V., Cavaliere, M., Cavalli Sforza, A., Cerri, L., Cerrito, Y. C., Chen, M., Chertok, G., Chiarelli, G., Chlachidze, F., Chlebana, K., Cho, D., Chokheli, W. H., Chung, Y. S., Chung, M. A., Ciocci, A., Clark, C., Clarke, G., Compostella, M. E., Convery, J., Conway, M., Corbo, M., Cordelli, C. A., Cox, D. J., Cox, F., Crescioli, J., Cueva, R., Culbertson, D., Dagenhart, N., D'Ascenzo, M., Datta, P. D., Barbaro, M., Dell'Orso, L., Demortier, M., Deninno, F., Devoto, M., D'Errico, A. D., Canto, B. D., Ruzza, J. R., Dittmann, M., D'Onofrio, S., Donati, P., Dong, M., Dorigo, T., Dorigo, K., Ebina, A., Elagin, A., Eppig, R., Erbacher, S., Errede, N., Ershaidat, R., Eusebi, S., Farrington, M., Feindt, J. P., Fernandez, R., Field, G., Flanagan, R., Forrest, M. J., Frank, M., Franklin, J. C., Freeman, Y., Funakoshi, I., Furic, M., Gallinaro, J. E., Garcia, A. F., Garfinkel, P., Garosi, H., Gerberich, E., Gerchtein, S., Giagu, V., Giakoumopoulou, P., Giannetti, K., Gibson, C. M., Ginsburg, N., Giokari, P., Giromini, G., Giurgiu, V., Glagolev, D., Glenzinski, M., Gold, D., Goldin, N., Goldschmidt, A., Golossanov, G., Gomez, G., Gomez Ceballo, M., Goncharov, O., Gonzalez, I., Gorelov, A. T., Goshaw, K., Gouliano, L., Grillo, S., Grinstein, C., Grosso Pilcher, R. C., Group, J. G., Da, S. R., Hahn, E., Halkiadaki, A., Hamaguchi, J. Y., Han, F., Happacher, K., Hara, D., Hare, M., Hare, R. F., Harr, K., Hatakeyama, C., Hay, M., Heck, J., Heinrich, M., Herndon, S., Hewamanage, A., Hocker, W., Hopkin, D., Horn, S., Hou, R. E., Hughe, M., Hurwitz, U., Husemann, N., Hussain, M., Hussein, J., Huston, G., Introzzi, M., Iori, A., Ivanov, E., Jame, D., Jang, B., Jayatilaka, E. J., Jeon, S., Jindariani, M., Jone, K. K., Joo, S. Y., Jun, T. R., Junk, T., Kamon, P. E., Karchin, A., Kasmi, Y., Kato, W., Ketchum, J., Keung, V., Khotilovich, B., Kilminster, D. H., Kim, H. S., Kim, J. E., Kim, M. J., Kim, S. B., Kim, S. H., Kim, Y. K., Kim, Y. J., Kim, N., Kimura, M., Kirby, S., Klimenko, K., Knoepfel, K., Kondo, D. J., Kong, J., Konigsberg, A. V., Kotwal, M., Krep, J., Kroll, D., Krop, M., Kruse, V., Krutelyov, T., Kuhr, M., Kurata, S., Kwang, A. T., Laasanen, S., Lami, S., Lammel, M., Lancaster, R. L., Lander, K., Lannon, A., Lath, G., Latino, T., Lecompte, E., Lee, H. S., Lee, J. S., Lee, S. W., Lee, S., Leo, S., Leone, J. D., Lewi, A., Limosani, C. J., Lin, M., Lindgren, E., Lipele, A., Lister, D. O., Litvintsev, C., Liu, H., Liu, Q., Liu, T., Liu, S., Lockwitz, A., Loginov, D., Lucchesi, J., Lueck, P., Lujan, P., Luken, G., Lungu, J., Ly, R., Lysak, R., Madrak, K., Maeshima, P., Maestro, S., Malik, G., Manca, A., Manousakis Katsikaki, F., Margaroli, C., Marino, M., Martinez, P., Mastrandrea, K., Matera, M. E., Mattson, A., Mazzacane, P., Mazzanti, K. S., Mcfarland, P., Mcintyre, R., Mcnulty, A., Mehta, P., Mehtala, C., Mesropian, T., Miao, D., Mietlicki, A., Mitra, H., Miyake, S., Moed, N., Moggi, M. N., Mondragon, C. S., Moon, R., Moore, Morello, MICHAEL JOSEPH, J., Morlock, P. M., Fernandez, A., Mukherjee, T., Muller, P., Murat, M., Mussini, J., Nachtman, Y., Nagai, J., Naganoma, I., Nakano, A., Napier, J., Nett, C., Neu, M. S., Neubauer, J., Nielsen, L., Nodulman, S. Y., Noh, O., Norniella, L., Oake, S. H., Oh, Y. D., Oh, I., Oksuzian, T., Okusawa, R., Orava, L., Ortolan, S. P., Griso, C., Pagliarone, E., Palencia, V., Papadimitriou, A. A., Paramonov, J., Patrick, G., Pauletta, M., Paulini, C., Pau, D. E., Pellett, A., Penzo, T. J., Phillip, G., Piacentino, E., Pianori, J., Pilot, K., Pitt, C., Plager, L., Pondrom, S., Poprocki, K., Potamiano, F., Prokoshin, A., Pranko, F., Ptoho, G., Punzi, A., Rahaman, V., Ramakrishnan, N., Ranjan, I., Redondo, P., Renton, M., Rescigno, T., Riddick, F., Rimondi, L., Ristori, A., Robson, T., Rodrigo, T., Rodriguez, E., Roger, S., Rolli, R., Roser, F., Ruffini, A., Ruiz, J., Ru, V., Rusu, A., Safonov, W. K., Sakumoto, Y., Sakurai, L., Santi, K., Sato, V., Saveliev, A., Savoy Navarro, P., Schlabach, A., Schmidt, E. E., Schmidt, T., Schwarz, L., Scodellaro, A., Scribano, F., Scuri, S., Seidel, Y., Seiya, A., Semenov, F., Sforza, S. Z., Shalhout, T., Shear, P. F., Shepard, M., Shimojima, M., Shochet, I., Shreyber Tecker, A., Simonenko, P., Sinervo, K., Sliwa, J. R., Smith, F. D., Snider, A., Soha, V., Sorin, H., Song, P., Squillacioti, M., Stancari, R. S., Deni, B., Stelzer, O., Stelzer Chilton, D., Stentz, J., Strologa, G. L., Strycker, Y., Sudo, A., Sukhanov, I., Suslov, K., Takemasa, Y., Takeuchi, J., Tang, M., Tecchio, P. K., Teng, J., Thom, J., Thome, G. A., Thompson, E., Thomson, D., Toback, S., Tokar, K., Tollefson, T., Tomura, D., Tonelli, S., Torre, D., Torretta, P., Totaro, M., Trovato, F., Ukegawa, S., Uozumi, A., Varganov, F., Vazquez, G., Velev, C., Vellidi, M., Vidal, I., Vila, R., Vilar, J., Vizan, M., Vogel, G., Volpi, P., Wagner, R. L., Wagner, T., Wakisaka, R., Wallny, S. M., Wang, A., Warburton, D., Water, W. C., Wester, D., Whiteson, A. B., Wicklund, E., Wicklund, S., Wilbur, F., Wick, H. H., William, J. S., Wilson, P., Wilson, B. L., Winer, P., Wittich, S., Wolber, H., Wolfe, T., Wright, X., Wu, Z., Wu, K., Yamamoto, D., Yamato, T., Yang, U. K., Yang, Y. C., Yang, W. M., Yao, G. P., Yeh, K., Yi, J., Yoh, K., Yorita, T., Yoshida, G. B., Yu, I., Yu, S. S., Yu, J. C., Yun, A., Zanetti, Y., Zeng, C., Zhou, S., Zucchelli, B. c., Alvarez, A. c., Anastassov, J. c., Anto, J., Appel, T. c., Ct, V., Barne, B., Barnett, P. a., Barria, P. c., Barto, M. a., Bauce, G. a., Bellettini, D. a., Bisello, K., Bland, L. g., Brigliadori, H., Budd, G. a., Busetto, A. b., Cx, F. p., Canelli, S. b., Carrillo, B. b., Casal, A. g., Castro, A. b., Cerri, L. c., Cerrito, Y., Chen, K. c., Ct, W., Chung, Y., Chung, M. a., Ciocci, G. a., Compostella, M., Convery, C., Cox, D., Cox, F. a., Crescioli, J. c., Cueva, N. c., D'Ascenzo, M. a., Dell'Orso, M. a., D'Errico, A. a., Di, J., Dittmann, S. a., Donati, Dorigo, Mirco, N. c., Ershaidat, J., Fernandez, G. c., Flanagan, M., Frank, J., Freeman, J., Garcia, A., Garfinkel, P. a., Garosi, C., Ginsburg, O., González, A., Goshaw, R. b., Group, S., Hahn, J., Han, R., Harr, W. b., Hopkin, R., Hughe, N. b., Cx, M. b., Iori, A. c., Ivanov, E. c., Ct, S., Jun, T., Junk, T. b., C, P., Karchin, Y. c., Kato, D. c., Ct, H. c., Ct, J. c., Ct, M., Kim, S. c., Ct, S., Kim, Y., Kim, Y. c., Ct, A., Kotwal, V. b., Krutelyov, A., Laasanen, R., Lander, K. c., Lannon, G. a., Latino, H. c., Lee, S. c., Lee, S. a., Leo, J., Lewi, A. c., Limosani, C., Lin, D., Litvintsev, D. a., Lucchesi, R. b., Cr, P. a., Maestro, G. b., Manca, M., Martínez, M., Mattson, K., Mcfarland, R. b., Mcnulty, M. b., Mondragon, C. c., Ct, M. a., Morello, M. g., Mussini, J. c., Nachtman, M., Neubauer, J. b., Nielsen, S., Oh, S. a., Pagan, E. b., Palencia, A., Paramonov, G. b., Pauletta, D., Pellett, T., Phillip, S. b., Poprocki, F. c., Prokoshin, F. b., Ptoho, G. a., Punzi, F. g., Rimondi, L. a., Ristori, S. b., Rolli, F. a., Ruffini, W., Sakumoto, L. b., Santi, V. c., Saveliev, A. c., Savoy Navarro, E., Schmidt, A. a., Scribano, F. a., Sforza, S., Shalhout, P., Shepard, M. c., Shimojima, P. b., Cx, J., Smith, F., Snider, P. a., Squillacioti, B. b., Cx, O. b., Cx, D. c., Stentz, G., Strycker, P., Teng, J. b., Thom, G., Thompson, S. c., Tokar, M. a., Trovato, F. b., Vázquez, J., Vizán, R., Wagner, S., Wang, W., Wester, D. b., Whiteson, A., Wicklund, H., William, J., Wilson, B., Winer, P. b., Wittich, U. c., Yang, W., Yao, G., Yeh, K. c., Yi, T. b., Yoshida, G., Yu, I. c., Ct, S., Yu, J., Yun, S. g., Zucchelli, T. Aaltonen, B. Álvarez González, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Anto, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanska, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro-Galtieri, V. Barne, B. Barnett, P. Barria, P. Barto, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretva, A. Bhatti, D. Bisello, I. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, L. Brigliadori, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, A. Buzatu, A. Calamba, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. Canelli, B. Carl, D. Carlsmith, R. Carosi, S. Carrillo, S. Carron, B. Casal, M. Casarsa, A. Castro, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli-Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. Cho, D. Chokheli, W. Chung, Y. Chung, M. Ciocci, A. Clark, C. Clarke, G. Compostella, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, F. Crescioli, J. Cueva, R. Culbertson, D. Dagenhart, N. d’Ascenzo, M. Datta, P. de Barbaro, M. Dell’Orso, L. Demortier, M. Deninno, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, P. Dong, M. Dorigo, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, S. Errede, N. Ershaidat, R. Eusebi, S. Farrington, M. Feindt, J. Fernandez, R. Field, G. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Garcia, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokari, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez-Ceballo, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Gouliano, L. Grillo, S. Grinstein, C. Grosso-Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, E. Halkiadaki, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hay, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, A. Hocker, W. Hopkin, D. Horn, S. Hou, R. Hughe, M. Hurwitz, U. Husemann, N. Hussain, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. Jame, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jone, K. Joo, S. Jun, T. Junk, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, S. Klimenko, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Krep, J. Kroll, D. Krop, M. Kruse, V. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. Lannon, A. Lath, G. Latino, T. LeCompte, E. Lee, H. Lee, J. Lee, S. Lee, S. Leo, S. Leone, J. Lewi, A. Limosani, C.-J. Lin, M. Lindgren, E. Lipele, A. Lister, D. Litvintsev, C. Liu, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Luken, G. Lungu, J. Ly, R. Lysak, R. Madrak, K. Maeshima, P. Maestro, S. Malik, G. Manca, A. Manousakis-Katsikaki, F. Margaroli, C. Marino, M. Martínez, P. Mastrandrea, K. Matera, M. Mattson, A. Mazzacane, P. Mazzanti, K. McFarland, P. McIntyre, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, M. Mondragon, C. Moon, R. Moore, M. Morello, J. Morlock, P. Movilla Fernandez, A. Mukherjee, Th. Muller, P. Murat, M. Mussini, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. Nielsen, L. Nodulman, S. Noh, O. Norniella, L. Oake, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. Pagan Griso, C. Pagliarone, E. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. Pauletta, M. Paulini, C. Pau, D. Pellett, A. Penzo, T. Phillip, G. Piacentino, E. Pianori, J. Pilot, K. Pitt, C. Plager, L. Pondrom, S. Poprocki, K. Potamiano, F. Prokoshin, A. Pranko, F. Ptoho, G. Punzi, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, T. Riddick, F. Rimondi, L. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Roger, S. Rolli, R. Roser, F. Ruffini, A. Ruiz, J. Ru, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy-Navarro, P. Schlabach, A. Schmidt, E. Schmidt, T. Schwarz, L. Scodellaro, A. Scribano, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shear, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber-Tecker, A. Simonenko, P. Sinervo, K. Sliwa, J. Smith, F. Snider, A. Soha, V. Sorin, H. Song, P. Squillacioti, M. Stancari, R. St. Deni, B. Stelzer, O. Stelzer-Chilton, D. Stentz, J. Strologa, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, J. Thome, G. Thompson, E. Thomson, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, F. Ukegawa, S. Uozumi, A. Varganov, F. Vázquez, G. Velev, C. Vellidi, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, C. Zhou, S. Zucchelli, and Universidad de Cantabria
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FERMILAB TEVATRON COLLIDER ,Particle physics ,CP-violating asymmetries ,Meson ,B physic ,General Physics and Astronomy ,FOS: Physical sciences ,B physics ,Angle distribution, Branching ratio, CDF experiments, CP violations, CP-violating asymmetries, Data sample, Fermilab Tevatron collider, Integrated luminosity, Longitudinal polarization, Vector meson ,Longitudinal polarization ,7. Clean energy ,01 natural sciences ,High Energy Physics - Experiment ,Vector meson ,Physics and Astronomy (all) ,High Energy Physics - Experiment (hep-ex) ,High Energy Physics - Phenomenology (hep-ph) ,Mixing (mathematics) ,Strange b mesons ,Phase (matter) ,0103 physical sciences ,STRANGE QUARK ,mixing ,Bottom-Strange Meson Mixing Phase ,proton antiproton collisions ,010306 general physics ,TEVATRON ,Nuclear Experiment ,BOTTOM QUARK ,Physics ,Integrated luminosity ,010308 nuclear & particles physics ,Branching ratio ,High Energy Physics - Phenomenology ,CDF experiments ,CP violations ,Full data ,Content (measure theory) ,Angle distribution ,CDF ,Production (computer science) ,High Energy Physics::Experiment ,Data sample - Abstract
We report a measurement of the bottom-strange meson mixing phase βs using the time evolution of Bs0→J/ψ(→μ+μ-)ϕ(→K+K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at s=1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of βs and the Bs0 decay-width difference ΔΓs and measure βs∈[-π/2,-1.51]∪[-0.06,0.30]∪[1.26,π/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of βs, we also determine ΔΓs=0.068±0.026(stat)±0.009(syst) ps-1 and the mean Bs0 lifetime τs=1.528±0.019(stat)±0.009(syst) ps, which are consistent and competitive with determinations by other experiments., This work was supported by the U.S. Department of Energy and National Science Foundation; the Italian Istituto Nazionale di Fisica Nucleare; the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Natural Sciences and Engineering Research Council of Canada; the National Science Council of the Republic of China; the Swiss National Science Foundation; the A. P. Sloan Foundation; the Bundesministerium für Bildung und Forschung, Germany; the Korean World Class University Program, the National Research Foundation of Korea; the Science and Technology Facilities Council and the Royal Society, UK; the Russian Foundation for Basic Research; the Ministerio de Ciencia e Innovación, and Programa Consolider-Ingenio 2010, Spain; the Slovak R&D Agency; the Academy of Finland; and the Australian Research Council (ARC).
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- 2012
12. EMMAService Data Curation
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Matteoni R.
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- 2012
13. Altered dopamine receptor-mediated signalling in GR37/PAEL-R knockout mice
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Di Pietro C., Marazziti D., Golini E., Mandillo S., Matteoni R., and Tocchini-Valentini G. P.
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Disease model ,Parkinson's disease - Published
- 2011
14. Non-motor behavioral phenotypes depend on age and gender in mice lacking the Parkinsons disease related GPR37/Pael receptor
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Mandillo S., Golini E., Marazziti D., Di Pietro C., Matteoni R., and Tocchini-Valentini G. P.
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Disease model ,Parkinson's disease - Published
- 2011
15. The Parkinsons disease associated Gpr37 receptor has a role during mouse testis development
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La Sala G., Marazziti D., Golini E., Di Pietro C., Mandillo S., Matteoni R., and Tocchini-Valentini G. P.
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Disease model ,Parkinson's disease - Published
- 2011
16. Strain Nomenclature Overview
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Matteoni R.
- Published
- 2011
17. Absence of the GPR37/PAEL receptor impairs striatal Akt and ERK2 phosphorylation, DeltaFosB expression, and conditioned place preference to amphetamine and cocaine
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Marazziti D., Di Pietro C., Mandillo S., Golini E., Matteoni R., and Tocchini-Valentini G.P.
- Abstract
The orphan G-protein-coupled receptor 37 (GPR37) colocalizes with the dopamine (DA) transporter (DAT) in mouse nigrostriatal presynaptic membranes, and its genetic ablation in homozygous null-mutant (GPR37-KO) mice provokes the marked increase of plasma membrane expression of DAT, alteration of psychostimulant-induced locomotor activity, and reduction of catalepsy induced by DA-receptor antagonists. We report that extracts from GPR37-KO mice displayed biochemical alterations of the nigrostriatal signaling pathways mediated by D1 and D2 dopaminergic receptors. Null-mutant mice showed an increase of the basal phosphorylation level of the D2-regulated Akt kinase. The basal phosphorylation of the D1-activated ERK2 kinase was not altered, but acute treatments with amphetamine or cocaine failed to produce its specific increase, as detected in samples from wild-type littermates. Furthermore, the chronic administration of cocaine to GPR37-KO mice did not increase the expression of the FosB transcription factor isoforms. Consistently, behavioral analysis showed that null-mutant animals did not respond to the incentive properties of amphetamine or cocaine, in conditioned place preference tests. Thus, the lack of GPR37 affects both ERK2- and Akt-mediated striatal signaling pathways, impairing the biochemical and behavioral responses typically induced by acute and chronic administration of psychostimulant drugs.
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- 2011
18. Non-motor behavioral impairments depend on age and gender in mice lacking the Parkinson's disease related GPR37/Pael receptor
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Mandillo, S., Golini, E., Marazziti, D., Di Pietro, C., Matteoni, R., and Tocchini-Valentini, G. P.
- Subjects
Disease model ,Depression ,Parkinson's disease ,Anxiety ,Olfactory - Abstract
Non-motor symptoms in Parkinson's disease (PD) have been often described at different stages of the disease and seem to be influenced by gender. We observed specific phenotypes resembling these symptoms in mice lacking the PD associated GPR37/Pael receptor. GPR37 is an orphan G-protein coupled receptor highly expressed in the mammalian central nervous system. It has been shown to be a substrate of parkin and to be involved in the pathogenesis of PD. In previous reports GPR37 knock-out (KO) mice were reported to exhibit several motor behavioral abnormalities related to altered dopaminergic system function. We have shown that GPR37 interacts with the dopamine transporter (DAT), modulating its presynaptic functional expression, striatal Akt and ERK2 phosphorylation, DeltaFosB expression, and conditioned place preference to amphetamine and cocaine. To evaluate other non-motor behavioral domains (autonomic and sensory functions, anxiety and depression, cognitive functions) adult and aged, male and female GPR37 KO mice and their wild-type (WT) littermates were used in a series of crosssectional studies. Mild deficits were observed in olfactory function of mutant mice tested in the block and habituation to non-social odors tests as well as in their colonic motility function. Anxiety and depression-like behaviors appeared to be significantly increased in aged GPR37 KO female mice, in the elevated plus maze and forced swimming tests. While no differences were detected in fear conditioned freezing and pre-pulse inhibition, a significant reduction of the startle response to acoustic stimuli was observed in adult GPR37 KO mice of both genders. Furthermore, HPLC analysis of major neurotransmitter levels revealed significant gender differences in the striatum and olfactory bulbs of mutant mice. The study of non-motor behavioral impairments in GPR37 mutant mice could elucidate the possible role of this receptor in modulating various symptoms observed in PD and also extend the understanding of gender and age influences on these type of distressing symptoms.
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- 2011
19. AUTOPHAGIC CLEARANCE OF THE PARKINSON'S DISEASE-ASSOCIATED GPR37 RECEPTOR
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Di Pietro C, Marazziti D, Golini E, Mandillo S, Matteoni R, and Tocchini-Valentini GP
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- 2009
20. INFRAFRONTIER
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Matteoni R. and Tocchini-Valentini G. P.
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- 2009
21. EMMA Cre-driver line archiving
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Hagn M. and Matteoni R.
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- 2007
22. Data repository of archived mutant strains of mice
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Matteoni R.
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- 2007
23. The Parkinson's disease associated GPR37 receptor interacts with DAT to modulate dopamine uptake and behavioural responses to dopaminergic drugs
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Di Pietro C., Golini E., Mandillo S., Matteoni R., Marazziti D., and Tocchini-Valentini G.P.
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- 2007
24. The European Mouse Mutant Archive and Resource DataBase
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Matteoni R.
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- 2006
25. Archivi di geni mutanti e risorse bio-informatiche
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Matteoni R. and Tocchini-Valentini G.
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- 2005
26. The Parkinsons disease associated GPR37 receptor is involved in the nigro-striatal dopaminergic signaling pathway
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Di Pietro C., Marazziti D., Golini E., Mandillo S., Matteoni R., and Tocchini-Valentini G.
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- 2005
27. EUMORPHIA Final report, 2003-2005, EU FP5 contract n. QLRT-2001-00930
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Tocchini Valentini G.P., Mandillo S., Golini E., Marazziti D., Deidda G., Rossi N., Raspa M., Scavizzi F., and Matteoni R.
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- 2005
28. Involvement of the Parkinsons disease-associated GPR37 receptor in the nigro-striatal dopaminergic signaling pathway
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Marazziti D., Mandillo S., Golini E., Di Pietro C., Matteoni R., and Tocchini-Valentini G.
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- 2005
29. GPR37/PAEL-R knock-out mice show abnormalities in nigro-striatal dopaminergic function
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Mandillo S., Marazziti D., Golini E., Matteoni R., and Tocchini-Valentini G.
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- 2004
30. The European Mouse Mutant Archive
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Raspa M, Scavizzi F, Matteoni R, Blanquet, Soulat G, Ziadi A, Fray M, Pickard AR, Greenaway S, Fartoo M, Karlsson H, Bonaparte D, Marschall S, Zeretzke S, Sengerova J, Tocchini-Valentini G, Herault Y, Brown S, Ahrlund-Richter L, Mallo M, Cameron G, and Hrabe de Angelis M.
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- 2004
31. Gpr37/Pael-R knockout mice are resistant to acute MPTP treatment
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Marazziti D., Golini E., Magrelli A., Mandillo S., Matteoni R., and Tocchini-Valentini G
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- 2003
32. Guidelines for the use and interpretation of assays for monitoring autophagy.
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Weiss, Wa, Welford, Sm, Wen, Lp, Whitehouse, Ca, Whitton, Jl, Whitworth, Aj, Wileman, T, Wiley, Jw, Wilkinson, S, Willbold, D, Williams, Rl, Williamson, Pr, Wouters, Bg, Wu, C, Wu, Dc, Wu, Wk, Wyttenbach, A, Xavier, Rj, Xi, Z, Xia, P, Xiao, G, Xie, Z, Xu, Dz, Xu, J, Xu, L, Xu, X, Yamamoto, A, Yamashina, S, Yamashita, M, Yan, X, Yanagida, M, Yang, D, Yang, E, Yang, Jm, Yang, Sy, Yang, W, Yang, Wy, Yang, Z, Yao, Mc, Yao, Tp, Yeganeh, B, Yen, Wl, Yin, Jj, Yin, Xm, Yoo, Oj, Yoon, G, Yoon, Sy, Yorimitsu, T, Yoshikawa, Y, Yoshimori, T, Yoshimoto, K, You, Hj, Youle, Rj, Younes, A, Yu, L, Yu, Sw, Yu, Wh, Yuan, Zm, Yue, Z, Yun, Ch, Yuzaki, M, Zabirnyk, O, Silva-Zacarin, E, Zacks, D, Zacksenhaus, E, Zaffaroni, N, Zakeri, Z, Zeh HJ, 3rd, Zeitlin, So, Zhang, H, Zhang, Hl, Zhang, J, Zhang, Jp, Zhang, L, Zhang, My, Zhang, Xd, Zhao, M, Zhao, Yf, Zhao, Y, Zhao, Zj, Zheng, X, Zhivotovsky, B, Zhong, Q, Zhou, Cz, Zhu, C, Zhu, Wg, Zhu, Xf, Zhu, X, Zhu, Y, Zoladek, T, Zong, Wx, Zorzano, A, Zschocke, J, Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o
- Published
- 2012
33. EMMA--mouse mutant resources for the international scientific community
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Wilkinson, P., primary, Sengerova, J., additional, Matteoni, R., additional, Chen, C.-K., additional, Soulat, G., additional, Ureta-Vidal, A., additional, Fessele, S., additional, Hagn, M., additional, Massimi, M., additional, Pickford, K., additional, Butler, R. H., additional, Marschall, S., additional, Mallon, A.-M., additional, Pickard, A., additional, Raspa, M., additional, Scavizzi, F., additional, Fray, M., additional, Larrigaldie, V., additional, Leyritz, J., additional, Birney, E., additional, Tocchini-Valentini, G. P., additional, Brown, S., additional, Herault, Y., additional, Montoliu, L., additional, de Angelis, M. H., additional, and Smedley, D., additional
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- 2009
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34. P41 ALTERED DOPAMINERGIC FUNCTION IN GPR37/PAEL-R KNOCKOUT MICE
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Mandillo, S., primary, Golini, E., additional, Marazziti, D., additional, Santini, E., additional, Matteoni, R., additional, and Tocchini-Valentini, G., additional
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- 2004
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35. Genomic Analysis of GPR37 and Related Orphan G-Protein Coupled Receptor Genes Highly Expressed in the Mammalian Brain
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Marazziti, D., primary, Golini, E., additional, Magrelli, A., additional, Matteoni, R., additional, and Tocchini-Valentini, G., additional
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- 2001
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36. Mice lacking the Parkinson's related GPR37/ PAEL receptor show non-motor behavioral phenotypes: age and gender effect.
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Mandillo, S., Golini, E., Marazziti, D., Di Pietro, C., Matteoni, R., and Tocchini‐Valentini, G. P.
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PARKINSON'S disease ,PHENOTYPES ,LABORATORY mice ,G protein coupled receptors ,KNOCKOUT mice ,AMPHETAMINES ,COCAINE - Abstract
Non-motor symptoms in Parkinson's disease ( PD) have been often described at different stages of the disease but they are poorly understood. We observed specific phenotypes related to these symptoms in mice lacking the PD-associated GPR37/ PAEL receptor. GPR37 is an orphan G-protein-coupled receptor highly expressed in the mammalian central nervous system. It is a substrate of parkin and it is involved in the pathogenesis of PD. GPR37 interacts with the dopamine transporter ( DAT), modulating nigro-striatal dopaminergic signaling and behavioral responses to amphetamine and cocaine. GPR37 knockout ( KO) mice are resistant to MPTP and exhibit several motor behavioral abnormalities related to altered dopaminergic system function. To evaluate non-motor behavioral domains, adult and aged, male and female GPR37 KO mice and their wild-type ( WT) littermates were analyzed in a series of cross-sectional studies. Aged GPR37 KO female mice showed mild improvements in olfactory function, while anxiety and depression-like behaviors appeared to be significantly increased. A reduction of the startle response to acoustic stimuli was observed only in adult GPR37 KO mice of both genders. Furthermore, HPLC analysis of major neurotransmitter levels revealed gender differences in the striatum, hippocampus and olfactory bulb of mutant mice. The absence of GPR37 receptor could have a neuroprotective effect in an age and gender-dependent manner, and the study of this receptor could be valuable in the search for novel therapeutic targets. [ABSTRACT FROM AUTHOR]
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- 2013
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37. Microtubule depolymerization inhibits transport of cathepsin D from the Golgi apparatus to lysosomes
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Scheel, J., primary, Matteoni, R., additional, Ludwig, T., additional, Hoflack, B., additional, and Kreis, T.E., additional
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- 1990
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38. Characterization of the cation-independent mannose 6-phosphate receptor-enriched prelysosomal compartment in NRK cells
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Griffiths, G., primary, Matteoni, R., additional, Back, R., additional, and Hoflack, B., additional
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- 1990
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39. Translocation and clustering of endosomes and lysosomes depends on microtubules.
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Matteoni, R and Kreis, T E
- Abstract
Indirect immunofluorescence labeling of normal rat kidney (NRK) cells with antibodies recognizing a lysosomal glycoprotein (LGP 120; Lewis, V., S.A. Green, M. Marsh, P. Vihko, A. Helenius, and I. Mellman, 1985, J. Cell Biol., 100:1839-1847) reveals that lysosomes accumulate in the region around the microtubule-organizing center (MTOC). This clustering of lysosomes depends on microtubules. When the interphase microtubules are depolymerized by treatment of the cells with nocodazole or during mitosis, the lysosomes disperse throughout the cytoplasm. Lysosomes recluster rapidly (within 30-60 min) in the region of the centrosomes either upon removal of the drug, or, in telophase, when repolymerization of interphase microtubules has occurred. During this translocation process the lysosomes can be found aligned along centrosomal microtubules. Endosomes and lysosomes can be visualized by incubating living cells with acridine orange. We have analyzed the movement of these labeled endocytic organelles in vivo by video-enhanced fluorescence microscopy. Translocation of endosomes and lysosomes occurs along linear tracks (up to 10 microns long) by discontinuous saltations (with velocities of up to 2.5 microns/s). Organelles move bidirectionally with respect to the MTOC. This movement ceases when microtubules are depolymerized by treatment of the cells with nocodazole. After nocodazole washout and microtubule repolymerization, the translocation and reclustering of fluorescent organelles predominantly occurs in a unidirectional manner towards the area of the MTOC. Organelle movement remains unaffected when cells are treated with cytochalasin D, or when the collapse of intermediate filaments is induced by microinjected monoclonal antivimentin antibodies. It can be concluded that translocation of endosomes and lysosomes occurs along microtubules and is independent of the intermediate filament and microfilament networks.
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- 1987
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40. Approccio interattivo alle Scienze della Terra. L’esperienza del GEOLAB a Pisa
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Cristian Biagioni, Giovanni Bianucci, Elena Bonaccorsi, Andrea Ciampalini, Consoloni, I., Donatio, D., D Orazio, Ma, Frassi, C., Gasperini, D., Gini, C., Anna Gioncada, Guelfi, F., Landi, S., Marco Lezzerini, Matteoni, R., Marco Pasero, Perinelli, C., Sergio Rocchi, Roni, E., Roverato, M., and Vezzoni, S.
41. Hands-on and minds-on in learning Earth sciences: the experience of the small Geolab in Pisa
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Cristian Biagioni, Giovanni Bianucci, Elena Bonaccorsi, Andrea Ciampalini, Consoloni, I., Donatio, D., Orazio, Massimo D., Frassi, C., Gasperini, D., Gini, C., Anna Gioncada, Guelfi, F., Landi, S., Marco Lezzerini, Matteoni, R., Marco Pasero, Perinelli, C., Sergio Rocchi, Roni, E., Roverato, M., and VEZZONI S.
42. "Be sustainable": EOSC-Life recommendations for implementation of FAIR principles in life science data handling.
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David R, Rybina A, Burel JM, Heriche JK, Audergon P, Boiten JW, Coppens F, Crockett S, Exter K, Fahrner S, Fratelli M, Goble C, Gormanns P, Grantner T, Grüning B, Gurwitz KT, Hancock JM, Harmse H, Holub P, Juty N, Karnbach G, Karoune E, Keppler A, Klemeier J, Lancelotti C, Legras JL, Lister AL, Longo DL, Ludwig R, Madon B, Massimi M, Matser V, Matteoni R, Mayrhofer MT, Ohmann C, Panagiotopoulou M, Parkinson H, Perseil I, Pfander C, Pieruschka R, Raess M, Rauber A, Richard AS, Romano P, Rosato A, Sánchez-Pla A, Sansone SA, Sarkans U, Serrano-Solano B, Tang J, Tanoli Z, Tedds J, Wagener H, Weise M, Westerhoff HV, Wittner R, Ewbank J, Blomberg N, and Gribbon P
- Subjects
- Software, Workflow, Biomedical Research, Biological Science Disciplines
- Abstract
The main goals and challenges for the life science communities in the Open Science framework are to increase reuse and sustainability of data resources, software tools, and workflows, especially in large-scale data-driven research and computational analyses. Here, we present key findings, procedures, effective measures and recommendations for generating and establishing sustainable life science resources based on the collaborative, cross-disciplinary work done within the EOSC-Life (European Open Science Cloud for Life Sciences) consortium. Bringing together 13 European life science research infrastructures, it has laid the foundation for an open, digital space to support biological and medical research. Using lessons learned from 27 selected projects, we describe the organisational, technical, financial and legal/ethical challenges that represent the main barriers to sustainability in the life sciences. We show how EOSC-Life provides a model for sustainable data management according to FAIR (findability, accessibility, interoperability, and reusability) principles, including solutions for sensitive- and industry-related resources, by means of cross-disciplinary training and best practices sharing. Finally, we illustrate how data harmonisation and collaborative work facilitate interoperability of tools, data, solutions and lead to a better understanding of concepts, semantics and functionalities in the life sciences., (© 2023 The Authors. Published under the terms of the CC BY 4.0 license.)
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- 2023
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43. INFRAFRONTIER: mouse model resources for modelling human diseases.
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Ali Khan A, Valera Vazquez G, Gustems M, Matteoni R, Song F, Gormanns P, Fessele S, Raess M, and Hrabĕ de Angelis M
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- Mice, Animals, Humans, Disease Models, Animal, Europe, Biomedical Research
- Abstract
Over the last decade, INFRAFRONTIER has positioned itself as a world-class Research Infrastructure for the generation, phenotyping, archiving, and distribution of mouse models in Europe. The INFRAFRONTIER network consists of 22 partners from 15 countries, and is continuously enhancing and broadening its portfolio of resources and services that are offered to the research community on a non-profit basis. By bringing together European rodent model expertise and providing valuable disease model services to the biomedical research community, INFRAFRONTIER strives to push the accessibility of cutting-edge human disease modelling technologies across the European research landscape. This article highlights the latest INFRAFRONTIER developments and informs the research community about its extensively utilised services, resources, and technical developments, specifically the intricacies of the INFRAFRONTIER database, use of Curated Disease Models, overview of the INFRAFRONTIER Cancer and Rare Disease resources, and information about its main state-of-the-art services., (© 2023. The Author(s).)
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- 2023
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44. Mouse Mutants of Gpr37 and Gpr37l1 Receptor Genes: Disease Modeling Applications.
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Massimi M, Di Pietro C, La Sala G, and Matteoni R
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- Animals, Astrocytes metabolism, Brain metabolism, Humans, Mice, Neurons metabolism, Parkinsonian Disorders metabolism, Receptors, G-Protein-Coupled metabolism
- Abstract
The vertebrate G protein-coupled receptor 37 and G protein-coupled receptor 37-like 1 (GPR37 and GPR37L1) proteins have amino acid sequence homology to endothelin and bombesin-specific receptors. The prosaposin glycoprotein, its derived peptides, and analogues have been reported to interact with and activate both putative receptors. The GPR37 and GPR37L1 genes are highly expressed in human and rodent brains. GPR37 transcripts are most abundant in oligodendrocytes and in the neurons of the substantia nigra and hippocampus, while the GPR37L1 gene is markedly expressed in cerebellar Bergmann glia astrocytes. The human GPR37 protein is a substrate of parkin, and its insoluble form accumulates in brain samples from patients of inherited juvenile Parkinson's disease. Several Gpr37 and Gpr37l1 mouse mutant strains have been produced and applied to extensive in vivo and ex vivo analyses of respective receptor functions and involvement in brain and other organ pathologies. The genotypic and phenotypic characteristics of the different mouse strains so far published are reported and discussed, and their current and proposed applications to human disease modeling are highlighted.
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- 2022
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45. Gpr37l1/prosaposin receptor regulates Ptch1 trafficking, Shh production, and cell proliferation in cerebellar primary astrocytes.
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La Sala G, Di Pietro C, Matteoni R, Bolasco G, Marazziti D, and Tocchini-Valentini GP
- Abstract
Mammalian cerebellar astrocytes critically regulate the differentiation and maturation of neuronal Purkinje cells and granule precursors. The G protein-coupled receptor 37-like 1 (Gpr37l1) is expressed by Bergmann astrocytes and interacts with patched 1 (Ptch1) at peri-ciliary membranes. Cerebellar primary astrocyte cultures from wild-type and Gpr37l1 null mutant mouse pups were established and studied. Primary cilia were produced by cultures of both genotypes, as well as Ptch1 and smoothened (Smo) components of the sonic hedgehog (Shh) mitogenic pathway. Compared to wild-type cells, Gpr37l1
-/- astrocytes displayed striking increases in proliferative activity, Ptch1 protein expression and internalization, intracellular cholesterol content, ciliary localization of Smo, as well as a marked production of active Shh. Similar effects were reproduced by treating wild-type astrocytes with a putative prosaptide ligand of Gpr37l1. These findings indicate that Gpr37l1-Ptch1 interactions specifically regulate Ptch1 internalization and trafficking, with consequent stimulation of Shh production and activation of proliferative signaling., (© 2020 Wiley Periodicals LLC.)- Published
- 2020
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46. Genetic ablation of Gpr37l1 delays tumor occurrence in Ptch1 +/- mouse models of medulloblastoma.
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Di Pietro C, La Sala G, Matteoni R, Marazziti D, and Tocchini-Valentini GP
- Subjects
- Animals, Carcinogenesis genetics, Cell Proliferation physiology, Cerebellar Neoplasms genetics, Cerebellar Neoplasms pathology, Female, Male, Medulloblastoma genetics, Medulloblastoma pathology, Mice, Mice, Inbred C57BL, Mice, Transgenic, Patched-1 Receptor genetics, Receptors, G-Protein-Coupled genetics, Carcinogenesis metabolism, Cerebellar Neoplasms metabolism, Medulloblastoma metabolism, Patched-1 Receptor metabolism, Receptors, G-Protein-Coupled deficiency
- Abstract
The G-protein coupled receptor 37-like 1 (Gpr37l1) is specifically expressed in most astrocytic glial cells, including cerebellar Bergmann astrocytes and interacts with patched 1 (Ptch1), a co-receptor of the sonic hedgehog (Shh)-smoothened (Smo) signaling complex. Gpr37l1 null mutant mice exhibit precocious post-natal cerebellar development, with altered Shh-Smo mitogenic cascade and premature down-regulation of granule cell precursor (GCP) proliferation. Gpr37l1 expression is downregulated in medulloblastoma (MB) and upregulated in glioma and glioblastoma tumors. Shh-associated MBs originate postnatally, from dysregulated hyperproliferation of GCPs in developing cerebellum's external granular layer (EGL), as shown in heterozygous Ptch1
+/- knock-out mouse strains that model human MB occurrence and progression. This study investigates cerebellar MB phenotypes in newly produced Gpr37l1, Ptch1 double mutant mice. Natural history analysis shows that Gpr37l1 genetic ablation, in Ptch1+/- model animals, results in marked deferment of post-natal tumor occurrence and decreased incidence of more aggressive tumor types. It is also associated with the delayed and diminished presence of more severe types of hyperplastic lesions in Ptch1+/- mice. Consistently, during early post-natal development Gpr37l1-/- ;Ptch1+/- pups exhibit reduction in cerebellar GCP proliferation and EGL thickness and a precocious, sustained expression of wingless-type MMTV integration site member 3 (Wnt3), a specific inhibitor of Shh-induced neuronal mitogenesis, in comparison with Ptch1+/- heterozygous single mutants. These findings highlight the specific involvement of Gpr37l1 in modulating postnatal cerebellar Shh-Ptch1-Smo mitogenic signaling in both normal and pathological conditions. The novel Gpr37l1-/- ;Ptch1+/- mouse models may thus be instrumental in the detailed characterization of the initial phases of Shh-associated MB insurgence and development., (Copyright © 2018 Elsevier Inc. All rights reserved.)- Published
- 2019
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47. Primary Cilia in the Murine Cerebellum and in Mutant Models of Medulloblastoma.
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Di Pietro C, Marazziti D, La Sala G, Abbaszadeh Z, Golini E, Matteoni R, and Tocchini-Valentini GP
- Subjects
- Animals, Animals, Newborn, Cerebellum pathology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mutation genetics, Cerebellar Neoplasms genetics, Cerebellar Neoplasms pathology, Cilia genetics, Cilia pathology, Medulloblastoma genetics, Medulloblastoma pathology
- Abstract
Cellular primary cilia crucially sense and transduce extracellular physicochemical stimuli. Cilium-mediated developmental signaling is tissue and cell type specific. Primary cilia are required for cerebellar differentiation and sonic hedgehog (Shh)-dependent proliferation of neuronal granule precursors. The mammalian G-protein-coupled receptor 37-like 1 is specifically expressed in cerebellar Bergmann glia astrocytes and participates in regulating postnatal cerebellar granule neuron proliferation/differentiation and Bergmann glia and Purkinje neuron maturation. The mouse receptor protein interacts with the patched 1 component of the cilium-associated Shh receptor complex. Mice heterozygous for patched homolog 1 mutations, like heterozygous patched 1 humans, have a higher incidence of Shh subgroup medulloblastoma (MB) and other tumors. Cerebellar cells bearing primary cilia were identified during postnatal development and in adulthood in two mouse strains with altered Shh signaling: a G-protein-coupled receptor 37-like 1 null mutant and an MB-susceptible, heterozygous patched homolog 1 mutant. In addition to granule and Purkinje neurons, primary cilia were also expressed by Bergmann glia astrocytes in both wild-type and mutant animals, from birth to adulthood. Variations in ciliary number and length were related to the different levels of neuronal and glial cell proliferation and maturation, during postnatal cerebellar development. Primary cilia were also detected in pre-neoplastic MB lesions in heterozygous patched homolog 1 mutant mice and they could represent specific markers for the development and analysis of novel cerebellar oncogenic models.
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- 2017
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48. Modulation of Dhh signaling and altered Sertoli cell function in mice lacking the GPR37-prosaposin receptor.
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La Sala G, Marazziti D, Di Pietro C, Golini E, Matteoni R, and Tocchini-Valentini GP
- Subjects
- Animals, Apoptosis, Blotting, Western, Cell Differentiation, Cell Proliferation, Cells, Cultured, Hedgehog Proteins genetics, Immunoenzyme Techniques, Immunoprecipitation, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Patched Receptors, Patched-1 Receptor, RNA, Messenger genetics, Real-Time Polymerase Chain Reaction, Receptors, Cell Surface genetics, Receptors, Cell Surface metabolism, Reverse Transcriptase Polymerase Chain Reaction, Sertoli Cells cytology, Signal Transduction, Testis cytology, Gene Expression Regulation, Hedgehog Proteins metabolism, Receptors, G-Protein-Coupled physiology, Saposins metabolism, Sertoli Cells metabolism, Spermatogenesis physiology, Testis metabolism
- Abstract
The mammalian G-protein-coupled receptor 37 (GPR37) is expressed in brain, in adult testis, and during the early phase of gonad differentiation. Somatic Sertoli cells (SCs) are located within the seminiferous tubules where they support the germinal epithelium. An adequate number of SCs is required for the complete prepubertal differentiation of germ cells and adult fertility. This study shows that Gpr37 and its ligand prosaposin are both postnatally expressed by SCs, whose proliferation and maturation are affected in Gpr37-null mutant mice during postnatal testicular development. Mutant pups show a delayed timing in sperm cell development, with a partial arrest of spermatocytes at the meiotic pachytene (e.g., 1.5-fold increase in Gpr37(-/-) P21 pups) and their increased apoptosis (e.g., 1.8-fold and 3.5-fold increase in Gpr37(-/-) P21 and adult mice, respectively). Mutant adults have reduced testis weight (wild type, 299 ± 5 mg; knockout, 258 ± 16 mg; P < 0.05) and epididymal sperm count and motility (e.g., 1.5-fold and 1.45-fold decrease in Gpr37(-/-) mice, respectively). Lack of Gpr37 results in the reduction in androgen receptor levels during prepubertal testis development, alongside the altered expression of SC maturation markers. It also affects the prepubertal testis expression of desert hedgehog (Dhh) mitogenic cascade components (Dhh, 1.3-fold increase in Gpr37(-/-) P10 and P21 pups; Gli2, 1.4-fold and 1.6-fold increase in Gpr37(-/-) P10 and P21 pups, respectively) including patched homolog 1 (1.3-fold increase in Gpr37(-/-) P10 and P21 pups), which is found localized in prepubertal SCs and is associated with Gpr37 in cultured primary SC samples. These results indicate that Gpr37 is a specific modulator of murine testis Dhh mitogenic signaling and SC proliferation and maturation., (© FASEB.)
- Published
- 2015
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49. Precocious cerebellum development and improved motor functions in mice lacking the astrocyte cilium-, patched 1-associated Gpr37l1 receptor.
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Marazziti D, Di Pietro C, Golini E, Mandillo S, La Sala G, Matteoni R, and Tocchini-Valentini GP
- Subjects
- Animals, Blotting, Western, Cell Proliferation, Cerebellum cytology, DNA Primers genetics, Fluorescent Antibody Technique, Gene Deletion, Genetic Vectors genetics, Hedgehog Proteins metabolism, Immunoprecipitation, In Situ Hybridization, Mice, Mice, Knockout, Mitogens metabolism, Patched Receptors, Patched-1 Receptor, Receptors, Cell Surface metabolism, Cerebellum growth & development, Neuroglia physiology, Psychomotor Performance physiology, Purkinje Cells physiology, Receptors, G-Protein-Coupled genetics
- Abstract
In the developing cerebellum, the proliferation and differentiation of glial and neuronal cell types depend on the modulation of the sonic hedgehog (Shh) signaling pathway. The vertebrate G-protein-coupled receptor 37-like 1 (GPR37L1) gene encodes a putative G-protein-coupled receptor that is expressed in newborn and adult cerebellar Bergmann glia astrocytes. This study shows that the ablation of the murine Gpr37l1 gene results in premature down-regulation of proliferation of granule neuron precursors and precocious maturation of Bergmann glia and Purkinje neurons. These alterations are accompanied by improved adult motor learning and coordination. Gpr37l1(-/-) mice also exhibit specific modifications of the Shh signaling cascade. Specific assays show that in Bergmann glia cells Gpr37l1 is associated with primary cilium membranes and it specifically interacts and colocalizes with the Shh primary receptor, patched 1. These findings indicate that the patched 1-associated Gpr37l1 receptor participates in the regulation of postnatal cerebellum development by modulating the Shh pathway.
- Published
- 2013
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50. Guidelines for the use and interpretation of assays for monitoring autophagy.
- Author
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Klionsky DJ, Abdalla FC, Abeliovich H, Abraham RT, Acevedo-Arozena A, Adeli K, Agholme L, Agnello M, Agostinis P, Aguirre-Ghiso JA, Ahn HJ, Ait-Mohamed O, Ait-Si-Ali S, Akematsu T, Akira S, Al-Younes HM, Al-Zeer MA, Albert ML, Albin RL, Alegre-Abarrategui J, Aleo MF, Alirezaei M, Almasan A, Almonte-Becerril M, Amano A, Amaravadi R, Amarnath S, Amer AO, Andrieu-Abadie N, Anantharam V, Ann DK, Anoopkumar-Dukie S, Aoki H, Apostolova N, Arancia G, Aris JP, Asanuma K, Asare NY, Ashida H, Askanas V, Askew DS, Auberger P, Baba M, Backues SK, Baehrecke EH, Bahr BA, Bai XY, Bailly Y, Baiocchi R, Baldini G, Balduini W, Ballabio A, Bamber BA, Bampton ET, Bánhegyi G, Bartholomew CR, Bassham DC, Bast RC Jr, Batoko H, Bay BH, Beau I, Béchet DM, Begley TJ, Behl C, Behrends C, Bekri S, Bellaire B, Bendall LJ, Benetti L, Berliocchi L, Bernardi H, Bernassola F, Besteiro S, Bhatia-Kissova I, Bi X, Biard-Piechaczyk M, Blum JS, Boise LH, Bonaldo P, Boone DL, Bornhauser BC, Bortoluci KR, Bossis I, Bost F, Bourquin JP, Boya P, Boyer-Guittaut M, Bozhkov PV, Brady NR, Brancolini C, Brech A, Brenman JE, Brennand A, Bresnick EH, Brest P, Bridges D, Bristol ML, Brookes PS, Brown EJ, Brumell JH, Brunetti-Pierri N, Brunk UT, Bulman DE, Bultman SJ, Bultynck G, Burbulla LF, Bursch W, Butchar JP, Buzgariu W, Bydlowski SP, Cadwell K, Cahová M, Cai D, Cai J, Cai Q, Calabretta B, Calvo-Garrido J, Camougrand N, Campanella M, Campos-Salinas J, Candi E, Cao L, Caplan AB, Carding SR, Cardoso SM, Carew JS, Carlin CR, Carmignac V, Carneiro LA, Carra S, Caruso RA, Casari G, Casas C, Castino R, Cebollero E, Cecconi F, Celli J, Chaachouay H, Chae HJ, Chai CY, Chan DC, Chan EY, Chang RC, Che CM, Chen CC, Chen GC, Chen GQ, Chen M, Chen Q, Chen SS, Chen W, Chen X, Chen X, Chen X, Chen YG, Chen Y, Chen Y, Chen YJ, Chen Z, Cheng A, Cheng CH, Cheng Y, Cheong H, Cheong JH, Cherry S, Chess-Williams R, Cheung ZH, Chevet E, Chiang HL, Chiarelli R, Chiba T, Chin LS, Chiou SH, Chisari FV, Cho CH, Cho DH, Choi AM, Choi D, Choi KS, Choi ME, Chouaib S, Choubey D, Choubey V, Chu CT, Chuang TH, Chueh SH, Chun T, Chwae YJ, Chye ML, Ciarcia R, Ciriolo MR, Clague MJ, Clark RS, Clarke PG, Clarke R, Codogno P, Coller HA, Colombo MI, Comincini S, Condello M, Condorelli F, Cookson MR, Coombs GH, Coppens I, Corbalan R, Cossart P, Costelli P, Costes S, Coto-Montes A, Couve E, Coxon FP, Cregg JM, Crespo JL, Cronjé MJ, Cuervo AM, Cullen JJ, Czaja MJ, D'Amelio M, Darfeuille-Michaud A, Davids LM, Davies FE, De Felici M, de Groot JF, de Haan CA, De Martino L, De Milito A, De Tata V, Debnath J, Degterev A, Dehay B, Delbridge LM, Demarchi F, Deng YZ, Dengjel J, Dent P, Denton D, Deretic V, Desai SD, Devenish RJ, Di Gioacchino M, Di Paolo G, Di Pietro C, Díaz-Araya G, Díaz-Laviada I, Diaz-Meco MT, Diaz-Nido J, Dikic I, Dinesh-Kumar SP, Ding WX, Distelhorst CW, Diwan A, Djavaheri-Mergny M, Dokudovskaya S, Dong Z, Dorsey FC, Dosenko V, Dowling JJ, Doxsey S, Dreux M, Drew ME, Duan Q, Duchosal MA, Duff K, Dugail I, Durbeej M, Duszenko M, Edelstein CL, Edinger AL, Egea G, Eichinger L, Eissa NT, Ekmekcioglu S, El-Deiry WS, Elazar Z, Elgendy M, Ellerby LM, Eng KE, Engelbrecht AM, Engelender S, Erenpreisa J, Escalante R, Esclatine A, Eskelinen EL, Espert L, Espina V, Fan H, Fan J, Fan QW, Fan Z, Fang S, Fang Y, Fanto M, Fanzani A, Farkas T, Farré JC, Faure M, Fechheimer M, Feng CG, Feng J, Feng Q, Feng Y, Fésüs L, Feuer R, Figueiredo-Pereira ME, Fimia GM, Fingar DC, Finkbeiner S, Finkel T, Finley KD, Fiorito F, Fisher EA, Fisher PB, Flajolet M, Florez-McClure ML, Florio S, Fon EA, Fornai F, Fortunato F, Fotedar R, Fowler DH, Fox HS, Franco R, Frankel LB, Fransen M, Fuentes JM, Fueyo J, Fujii J, Fujisaki K, Fujita E, Fukuda M, Furukawa RH, Gaestel M, Gailly P, Gajewska M, Galliot B, Galy V, Ganesh S, Ganetzky B, Ganley IG, Gao FB, Gao GF, Gao J, Garcia L, Garcia-Manero G, Garcia-Marcos M, Garmyn M, Gartel AL, Gatti E, Gautel M, Gawriluk TR, Gegg ME, Geng J, Germain M, Gestwicki JE, Gewirtz DA, Ghavami S, Ghosh P, Giammarioli AM, Giatromanolaki AN, Gibson SB, Gilkerson RW, Ginger ML, Ginsberg HN, Golab J, Goligorsky MS, Golstein P, Gomez-Manzano C, Goncu E, Gongora C, Gonzalez CD, Gonzalez R, González-Estévez C, González-Polo RA, Gonzalez-Rey E, Gorbunov NV, Gorski S, Goruppi S, Gottlieb RA, Gozuacik D, Granato GE, Grant GD, Green KN, Gregorc A, Gros F, Grose C, Grunt TW, Gual P, Guan JL, Guan KL, Guichard SM, Gukovskaya AS, Gukovsky I, Gunst J, Gustafsson AB, Halayko AJ, Hale AN, Halonen SK, Hamasaki M, Han F, Han T, Hancock MK, Hansen M, Harada H, Harada M, Hardt SE, Harper JW, Harris AL, Harris J, Harris SD, Hashimoto M, Haspel JA, Hayashi S, Hazelhurst LA, He C, He YW, Hébert MJ, Heidenreich KA, Helfrich MH, Helgason GV, Henske EP, Herman B, Herman PK, Hetz C, Hilfiker S, Hill JA, Hocking LJ, Hofman P, Hofmann TG, Höhfeld J, Holyoake TL, Hong MH, Hood DA, Hotamisligil GS, Houwerzijl EJ, Høyer-Hansen M, Hu B, Hu CA, Hu HM, Hua Y, Huang C, Huang J, Huang S, Huang WP, Huber TB, Huh WK, Hung TH, Hupp TR, Hur GM, Hurley JB, Hussain SN, Hussey PJ, Hwang JJ, Hwang S, Ichihara A, Ilkhanizadeh S, Inoki K, Into T, Iovane V, Iovanna JL, Ip NY, Isaka Y, Ishida H, Isidoro C, Isobe K, Iwasaki A, Izquierdo M, Izumi Y, Jaakkola PM, Jäättelä M, Jackson GR, Jackson WT, Janji B, Jendrach M, Jeon JH, Jeung EB, Jiang H, Jiang H, Jiang JX, Jiang M, Jiang Q, Jiang X, Jiang X, Jiménez A, Jin M, Jin S, Joe CO, Johansen T, Johnson DE, Johnson GV, Jones NL, Joseph B, Joseph SK, Joubert AM, Juhász G, Juillerat-Jeanneret L, Jung CH, Jung YK, Kaarniranta K, Kaasik A, Kabuta T, Kadowaki M, Kagedal K, Kamada Y, Kaminskyy VO, Kampinga HH, Kanamori H, Kang C, Kang KB, Kang KI, Kang R, Kang YA, Kanki T, Kanneganti TD, Kanno H, Kanthasamy AG, Kanthasamy A, Karantza V, Kaushal GP, Kaushik S, Kawazoe Y, Ke PY, Kehrl JH, Kelekar A, Kerkhoff C, Kessel DH, Khalil H, Kiel JA, Kiger AA, Kihara A, Kim DR, Kim DH, Kim DH, Kim EK, Kim HR, Kim JS, Kim JH, Kim JC, Kim JK, Kim PK, Kim SW, Kim YS, Kim Y, Kimchi A, Kimmelman AC, King JS, Kinsella TJ, Kirkin V, Kirshenbaum LA, Kitamoto K, Kitazato K, Klein L, Klimecki WT, Klucken J, Knecht E, Ko BC, Koch JC, Koga H, Koh JY, Koh YH, Koike M, Komatsu M, Kominami E, Kong HJ, Kong WJ, Korolchuk VI, Kotake Y, Koukourakis MI, Kouri Flores JB, Kovács AL, Kraft C, Krainc D, Krämer H, Kretz-Remy C, Krichevsky AM, Kroemer G, Krüger R, Krut O, Ktistakis NT, Kuan CY, Kucharczyk R, Kumar A, Kumar R, Kumar S, Kundu M, Kung HJ, Kurz T, Kwon HJ, La Spada AR, Lafont F, Lamark T, Landry J, Lane JD, Lapaquette P, Laporte JF, László L, Lavandero S, Lavoie JN, Layfield R, Lazo PA, Le W, Le Cam L, Ledbetter DJ, Lee AJ, Lee BW, Lee GM, Lee J, Lee JH, Lee M, Lee MS, Lee SH, Leeuwenburgh C, Legembre P, Legouis R, Lehmann M, Lei HY, Lei QY, Leib DA, Leiro J, Lemasters JJ, Lemoine A, Lesniak MS, Lev D, Levenson VV, Levine B, Levy E, Li F, Li JL, Li L, Li S, Li W, Li XJ, Li YB, Li YP, Liang C, Liang Q, Liao YF, Liberski PP, Lieberman A, Lim HJ, Lim KL, Lim K, Lin CF, Lin FC, Lin J, Lin JD, Lin K, Lin WW, Lin WC, Lin YL, Linden R, Lingor P, Lippincott-Schwartz J, Lisanti MP, Liton PB, Liu B, Liu CF, Liu K, Liu L, Liu QA, Liu W, Liu YC, Liu Y, Lockshin RA, Lok CN, Lonial S, Loos B, Lopez-Berestein G, López-Otín C, Lossi L, Lotze MT, Lőw P, Lu B, Lu B, Lu B, Lu Z, Luciano F, Lukacs NW, Lund AH, Lynch-Day MA, Ma Y, Macian F, MacKeigan JP, Macleod KF, Madeo F, Maiuri L, Maiuri MC, Malagoli D, Malicdan MC, Malorni W, Man N, Mandelkow EM, Manon S, Manov I, Mao K, Mao X, Mao Z, Marambaud P, Marazziti D, Marcel YL, Marchbank K, Marchetti P, Marciniak SJ, Marcondes M, Mardi M, Marfe G, Mariño G, Markaki M, Marten MR, Martin SJ, Martinand-Mari C, Martinet W, Martinez-Vicente M, Masini M, Matarrese P, Matsuo S, Matteoni R, Mayer A, Mazure NM, McConkey DJ, McConnell MJ, McDermott C, McDonald C, McInerney GM, McKenna SL, McLaughlin B, McLean PJ, McMaster CR, McQuibban GA, Meijer AJ, Meisler MH, Meléndez A, Melia TJ, Melino G, Mena MA, Menendez JA, Menna-Barreto RF, Menon MB, Menzies FM, Mercer CA, Merighi A, Merry DE, Meschini S, Meyer CG, Meyer TF, Miao CY, Miao JY, Michels PA, Michiels C, Mijaljica D, Milojkovic A, Minucci S, Miracco C, Miranti CK, Mitroulis I, Miyazawa K, Mizushima N, Mograbi B, Mohseni S, Molero X, Mollereau B, Mollinedo F, Momoi T, Monastyrska I, Monick MM, Monteiro MJ, Moore MN, Mora R, Moreau K, Moreira PI, Moriyasu Y, Moscat J, Mostowy S, Mottram JC, Motyl T, Moussa CE, Müller S, Muller S, Münger K, Münz C, Murphy LO, Murphy ME, Musarò A, Mysorekar I, Nagata E, Nagata K, Nahimana A, Nair U, Nakagawa T, Nakahira K, Nakano H, Nakatogawa H, Nanjundan M, Naqvi NI, Narendra DP, Narita M, Navarro M, Nawrocki ST, Nazarko TY, Nemchenko A, Netea MG, Neufeld TP, Ney PA, Nezis IP, Nguyen HP, Nie D, Nishino I, Nislow C, Nixon RA, Noda T, Noegel AA, Nogalska A, Noguchi S, Notterpek L, Novak I, Nozaki T, Nukina N, Nürnberger T, Nyfeler B, Obara K, Oberley TD, Oddo S, Ogawa M, Ohashi T, Okamoto K, Oleinick NL, Oliver FJ, Olsen LJ, Olsson S, Opota O, Osborne TF, Ostrander GK, Otsu K, Ou JH, Ouimet M, Overholtzer M, Ozpolat B, Paganetti P, Pagnini U, Pallet N, Palmer GE, Palumbo C, Pan T, Panaretakis T, Pandey UB, Papackova Z, Papassideri I, Paris I, Park J, Park OK, Parys JB, Parzych KR, Patschan S, Patterson C, Pattingre S, Pawelek JM, Peng J, Perlmutter DH, Perrotta I, Perry G, Pervaiz S, Peter M, Peters GJ, Petersen M, Petrovski G, Phang JM, Piacentini M, Pierre P, Pierrefite-Carle V, Pierron G, Pinkas-Kramarski R, Piras A, Piri N, Platanias LC, Pöggeler S, Poirot M, Poletti A, Poüs C, Pozuelo-Rubio M, Prætorius-Ibba M, Prasad A, Prescott M, Priault M, Produit-Zengaffinen N, Progulske-Fox A, Proikas-Cezanne T, Przedborski S, Przyklenk K, Puertollano R, Puyal J, Qian SB, Qin L, Qin ZH, Quaggin SE, Raben N, Rabinowich H, Rabkin SW, Rahman I, Rami A, Ramm G, Randall G, Randow F, Rao VA, Rathmell JC, Ravikumar B, Ray SK, Reed BH, Reed JC, Reggiori F, Régnier-Vigouroux A, Reichert AS, Reiners JJ Jr, Reiter RJ, Ren J, Revuelta JL, Rhodes CJ, Ritis K, Rizzo E, Robbins J, Roberge M, Roca H, Roccheri MC, Rocchi S, Rodemann HP, Rodríguez de Córdoba S, Rohrer B, Roninson IB, Rosen K, Rost-Roszkowska MM, Rouis M, Rouschop KM, Rovetta F, Rubin BP, Rubinsztein DC, Ruckdeschel K, Rucker EB 3rd, Rudich A, Rudolf E, Ruiz-Opazo N, Russo R, Rusten TE, Ryan KM, Ryter SW, Sabatini DM, Sadoshima J, Saha T, Saitoh T, Sakagami H, Sakai Y, Salekdeh GH, Salomoni P, Salvaterra PM, Salvesen G, Salvioli R, Sanchez AM, Sánchez-Alcázar JA, Sánchez-Prieto R, Sandri M, Sankar U, Sansanwal P, Santambrogio L, Saran S, Sarkar S, Sarwal M, Sasakawa C, Sasnauskiene A, Sass M, Sato K, Sato M, Schapira AH, Scharl M, Schätzl HM, Scheper W, Schiaffino S, Schneider C, Schneider ME, Schneider-Stock R, Schoenlein PV, Schorderet DF, Schüller C, Schwartz GK, Scorrano L, Sealy L, Seglen PO, Segura-Aguilar J, Seiliez I, Seleverstov O, Sell C, Seo JB, Separovic D, Setaluri V, Setoguchi T, Settembre C, Shacka JJ, Shanmugam M, Shapiro IM, 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AJ, Wileman T, Wiley JW, Wilkinson S, Willbold D, Williams RL, Williamson PR, Wouters BG, Wu C, Wu DC, Wu WK, Wyttenbach A, Xavier RJ, Xi Z, Xia P, Xiao G, Xie Z, Xie Z, Xu DZ, Xu J, Xu L, Xu X, Yamamoto A, Yamamoto A, Yamashina S, Yamashita M, Yan X, Yanagida M, Yang DS, Yang E, Yang JM, Yang SY, Yang W, Yang WY, Yang Z, Yao MC, Yao TP, Yeganeh B, Yen WL, Yin JJ, Yin XM, Yoo OJ, Yoon G, Yoon SY, Yorimitsu T, Yoshikawa Y, Yoshimori T, Yoshimoto K, You HJ, Youle RJ, Younes A, Yu L, Yu L, Yu SW, Yu WH, Yuan ZM, Yue Z, Yun CH, Yuzaki M, Zabirnyk O, Silva-Zacarin E, Zacks D, Zacksenhaus E, Zaffaroni N, Zakeri Z, Zeh HJ 3rd, Zeitlin SO, Zhang H, Zhang HL, Zhang J, Zhang JP, Zhang L, Zhang L, Zhang MY, Zhang XD, Zhao M, Zhao YF, Zhao Y, Zhao ZJ, Zheng X, Zhivotovsky B, Zhong Q, Zhou CZ, Zhu C, Zhu WG, Zhu XF, Zhu X, Zhu Y, Zoladek T, Zong WX, Zorzano A, Zschocke J, and Zuckerbraun B
- Subjects
- Animals, Humans, Models, Biological, Autophagy genetics, Biological Assay methods
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
- Published
- 2012
- Full Text
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