Search

Your search keyword '"Greenberg, Michael E."' showing total 844 results
Start Over Author "Greenberg, Michael E."
844 results on '"Greenberg, Michael E."'

103. EphA receptors regulate growth cone dynamics through the novel guanine nucleotide exchange factor ephexin

Author

Shamah, Steven M., Lin, Michael Z., Goldberg, Jeffrey L., Estrach, Soline, Sahin, Mustafa, Hu, Linda, Bazalakova, Mihaela, Neve, Rachel L., Corfas, Gabriel, Debant, Anne, and Greenberg, Michael E.

Subjects
Cell research -- Analysis, Nucleotides -- Physiological aspects, Guanine -- Physiological aspects, Proteins -- Genetic aspects, Cloning -- Genetic aspects, Actin -- Physiological aspects, Biological sciences
Abstract

Research has been conducted on the Eph receptors transducing repulsive short-range signals for axon guidance via actin dynamics modulation within growth cones. The cloning and characterization of the Eph receptor-interacting protein ephexin have been carried out and the results indicate the creation of the molecular link between Eph receptors and the actin cytoskeleton providing a localized regulation of the growth cone motility.

Published
2001

104. Neurogenin promotes neurogenesis and inhibits glial differentiation by independent mechanisms

Author

Sun, Yi, Nadal-Vicens, Mireya, Misono, Stephanie, Lin, Michael Z., Zubiaga, Ana, Hua, Xianxing, Fan, Guoping, and Greenberg, Michael E.

Subjects
Cell research -- Analysis, Developmental neurology -- Genetic aspects, Genetic transcription -- Physiological aspects, Stem cells -- Genetic aspects, Astrocytes -- Genetic aspects, Biological sciences
Abstract

Research has been conducted on the bHLH transcription factor neurogenin (Ngn1) inhibiting neural stem cell differentiation into astrocytes. Results indicate that Ngn1 effectively inhibits astrocyte differentiation, and the Ngn1 glial-specific gene-transcription repression mechanisms have been identified.

Published
2001

106. Proteomic analysis identifies the E3 ubiquitin ligase Pdzrn3 as a regulatory target of Wnt5a-Ror signaling

Author

Konopelski Snavely, Sara E., primary, Susman, Michael W., additional, Kunz, Ryan C., additional, Tan, Jia, additional, Srinivasan, Srisathya, additional, Cohen, Michael D., additional, Okada, Kyoko, additional, Lamb, Helen, additional, Choi, Shannon S., additional, Karuna, Edith P., additional, Scales, Michael K., additional, Gygi, Steven P., additional, Greenberg, Michael E., additional, and Ho, Hsin-Yi Henry, additional

Published
2020
Full Text
View/download PDF

109. EphB receptors interact with NMDA receptors and regulate excitatory synapse formation

Author

Dalva, Matthew B., Takasu, Mari A., Lin, Michael Z., Shamah, Steven M., Hu, Linda, Gale, Nicholas W., and Greenberg, Michael E.

Subjects
Neural transmission -- Regulation, Neurotransmitter receptors -- Physiological aspects, Synapses -- Physiological aspects, Protein tyrosine kinase -- Physiological aspects, Biological sciences
Abstract

Research demonstrates that EphrinB activation leads to the recruitment of N-methyl-D-aspartate receptors to EphB receptor complexes, which influences the synapse development and/or function. Data indicate that unusually the extracellular domains of the EphB and the receptors mediate their interaction.

Published
2000

110. Orchestral maneuvers in the axon: trio and the control of axon guidance

Author

Lin, Michael Z. and Greenberg, Michael E.

Subjects
Cytochemistry -- Research, Axons -- Genetic aspects, Cellular signal transduction -- Research, Biological sciences
Abstract

Orchestral actions in the axon involving trio and the control of axon guidance are discussed in this minireview article. The ways in which a group of independent genetic studies comes together on the very versatile growth cone molecule, a dynamic and mobile structure at the axon's distal end, are the focus.

Published
2000

113. CREB: a stimulus-induced transcription factor activated by a diverse array of extracellular signals

Author

Shaywitz, Adam J. and Greenberg, Michael E.

Subjects
Phosphorylation -- Research, Cytochemistry -- Research, Biological sciences
Abstract

CRE-binding protein (CREB) are phosphorylated, in turn activating target gene transcription by several protein kinases. The mechanism by which CREB activates transcription depends on the stimulus, with different signaling pathways giving specificity at the level of activation.

Published
1999

115. Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions

Author

Saudou, Frederic, Finkbeiner, Steven, Devys, Didier, and Greenberg, Michael E.

Subjects
Huntington's chorea -- Research, Nervous system -- Degeneration, Cell death -- Research, Biological sciences
Abstract

The mechanisms involved in neurogeneration induced by the huntingtin gene in Hungtington disease (HD) were investigated. A murine cellular model of HD was conceived through the incorporation of huntingtin into cultured striatal neurons by transfection. It was revealed that neurodegeneration was prompted by huntingtin through apoptosis since it was involved in the translocation of the nucleus that triggered the nuclear apoptosis. Also, the induced neurogeneration relied on the presence of the mutant polyglutamine tract within the huntingtin.

Published
1998

118. Contributors

Author

Abrams, John M., primary, Adelman, John P., additional, Alcorn, Joseph L., additional, Alessi, Dario R., additional, Alexov, Emil, additional, Alford, Simon, additional, Alitalo, Kari, additional, Allison, James P., additional, Almo, Steven C., additional, Alory, Christelle, additional, Al-Shamkhani, Aymen, additional, Amundson, Sally A., additional, Anderson, Carl W., additional, Andersen, Jannik N., additional, Angel, Peter, additional, Appella, Ettore, additional, Arendshorst, William J., additional, Arkinstall, Steve, additional, Audhya, Anjon, additional, Avruch, Joseph, additional, Bader, Gary D., additional, Bagala, Cinzia, additional, Balch, William E., additional, Balsinde, Jesus, additional, Banerjee, Utpal, additional, Barford, David, additional, Bar-Sagi, Dafna, additional, Bartlett, Perry F., additional, Bastiaens, Philippe I.H., additional, Battelli, Chiara, additional, Baudhuin, Linnea M., additional, Beavil, Andrew J., additional, Beavil, Rebecca L., additional, Beavo, Joseph A., additional, Bello-Reuss, Elsa, additional, Bellum, Stephen, additional, Belmonte, Juan Carlos Izpisúa, additional, Bennett, Craig B., additional, Benovic, Jeffrey L., additional, Berridge, Michael J., additional, Beuning, Penny J., additional, Bhandari, Rashna, additional, Bhattacharya, Ananya, additional, Biel, Martin, additional, Bielinski, Vincent A., additional, Bilak, Hana, additional, Birnbaumer, Lutz, additional, Birrell, Geoff, additional, Bishop, Gail A., additional, Blackmer, Trillium, additional, Blackshear, Perry J., additional, Blattner, Christine, additional, Blaustein, Mordecai P., additional, Bokoch, Gary M., additional, Bonewald, Lynda F., additional, Bonomi, Marco, additional, Booden, Michelle A., additional, Boone, Charles, additional, Bootman, Martin D., additional, Bos, Johannes L., additional, Bradbury, Jane M., additional, Bradshaw, Ralph A., additional, Bresnick, Anne R., additional, Brevnova, Lena, additional, Brinkworth, Ross I., additional, Brown, Michael S., additional, Brown, Steven A., additional, Brunet, Anne, additional, Bucki, Robert, additional, Burgoyne, Robert D., additional, Buss, Janice E., additional, Butow, Ronald A., additional, Capdevila, Javier, additional, Carafoli, Ernesto, additional, Carlson, Cathrine R., additional, Carpenter, Graham, additional, Carrillo, Juan J., additional, Casey, Patrick J., additional, Catterall, William A., additional, Cerione, Richard A., additional, Cesareni, Gianni, additional, Chan, Andrew C., additional, Chang, Geoffrey, additional, Chao, Moses V., additional, Charbonneau, Harry, additional, Chen, Philip, additional, Cheng, Alan, additional, Chiu, Chris, additional, Chow, Dar-chone, additional, Chrisman, Ted D., additional, Christensen, Anne Elisabeth, additional, Chung, Jee Y., additional, Churchill, Grant C., additional, Ciechanover, Aaron, additional, Cingolani, Gino, additional, Claeysen, Sylvie, additional, Closset, Jean, additional, Cockcroft, Shamshad, additional, Cohen, Patricia T.W., additional, Cohen, Philip, additional, Colbran, Roger J., additional, Comstock, Clay E.S., additional, Conti, Marco, additional, Corbin, Jackie D., additional, Corda, Daniela, additional, Costagliola, Sabine, additional, Cote, Rick H., additional, Coughlin, Shaun R., additional, Cowart, L. Ashley, additional, Cox, Adrienne D., additional, Cragg, Mark S., additional, Crespo, José L., additional, Crosio, Claudia, additional, Daly, Christopher, additional, Damak, Sami, additional, Dasso, Mary, additional, David, Michael, additional, Davis, Anthony J., additional, Davis, Roger J., additional, Day, Richard N., additional, Degerman, Eva, additional, DeLano, Warren L., additional, Dell'Acqua, Mark L., additional, Délot, Emmanuèle, additional, Demple, Bruce, additional, Dennis, Edward A., additional, Denu, John M., additional, DePaoli-Roach, Anna A., additional, Der, Channing J., additional, de Rooij, Johan, additional, de Sauvage, Frederic, additional, Devreotes, Peter N., additional, Dewaste, Valérie, additional, Dickson, Robert B., additional, Diebold, Becky A., additional, Fiori, Pier Paolo Di, additional, Girolamo, Maria Di, additional, Diplexcito, Julie, additional, Dixon, Jack E., additional, Doms, Robert W., additional, Donoghue, Daniel J., additional, Doolittle, Russell F., additional, Døskeland, Stein Ove, additional, Dostmann, Wolfgang R.G., additional, Dreyer, Matthias K., additional, Du, Guo Guang, additional, Du, Keyong, additional, Duchen, Michael R., additional, Dunphy, William G., additional, Durgan, Joanne, additional, Dustin, Michael L., additional, Edwards, Peter A., additional, Egen, Jackson G., additional, Eiden, Lee E., additional, Elion, Elaine A., additional, Emr, Scott, additional, Engelhardt, Othmar G., additional, Erneux, Christophe, additional, Espenshade, Peter J., additional, Esplin, Edward D., additional, Evers, B. Mark, additional, Eyles, Joanne L., additional, Fame, Sheelagh, additional, Farquhar, Marilyn, additional, Feil, Robert, additional, Feng, Gui-Jie, additional, Fields, Stanley, additional, Fiordalisi, James J., additional, Firtel, Richard A., additional, Fitzgerald, Garret A., additional, Flint, Andrew, additional, Foiani, Marco, additional, Forman, Barry Marc, additional, Fornace, Albert J., additional, Francis, Sharron H., additional, Fritz, Günter, additional, Fruman, David A., additional, Galione, Antony, additional, Gandhi, Chris S., additional, Garbers, David L., additional, Garcia, K. Christopher, additional, Geiger, Benjamin, additional, Gerace, Larry, additional, Gerstner, Andrea, additional, Giaccia, Amato J., additional, Giannattasio, Michele, additional, Giguère, Vincent, additional, Glass, Christopher K., additional, Glennie, Martin J., additional, Glick, Jennifer L., additional, Goldstein, Joseph L., additional, Gopal, Venkatesh, additional, Gorospe, Myriam, additional, Govaerts, Cedric, additional, Graves, Paul R., additional, Gray, Patrick W., additional, Graziani, Irene, additional, Green, Douglas R., additional, Greenberg, Michael E., additional, Greenwald, Iva, additional, Gu, Haihua, additional, Gueven, Nuri, additional, Gutkind, J. Silvio, additional, Haeggström, Jesper Z., additional, Hall, Alan, additional, Hall, Michael N., additional, Haller, Otto, additional, Hamm, Heidi E., additional, Hannun, Yusef A., additional, Hansen, Carl A., additional, Harden, T. Kendall, additional, Hardie, D. Grahame, additional, Hasegawa, Kiminori, additional, Hawkins, Phillip T., additional, Haystead, Timothy A.J., additional, He, Xiao-lin, additional, Heizmann, Claus W., additional, Heldin, Carl-Henrik, additional, Hermiston, Michelle L., additional, Herrlich, Peter, additional, Hewat, Elizabeth A., additional, Hille, Bertil, additional, Hilton, Douglas J., additional, Hinchliffe, K.A., additional, Ho, Steffan N., additional, Ho, Su-Chin, additional, Hochstrasser, Mark, additional, Hofmann, Franz, additional, Hogue, Christopher W., additional, Hol, Wim G.J., additional, Holash, Jocelyn, additional, Holmgren, Robert A., additional, Honig, Barry, additional, Hostager, Bruce S., additional, Hubbard, Stevan R., additional, Huber, Michael, additional, Hunter, Tony, additional, Huttenlocher, Anna, additional, Hymowitz, Sarah G., additional, Ihle, James N., additional, Imler, Jean-Luc, additional, Irvine, R.F., additional, Isacoff, Ehud Y., additional, Iturrioz, Xavier, additional, Iversen, Lars F., additional, Iyengar, Ravi, additional, Jackson, Stephen P., additional, Jan, Lily Yeh, additional, Janiak-Spens, Fabiola, additional, Janmey, Paul A., additional, Jansen, Peter Gildsig, additional, Jarriault, Sophie, additional, Javitch, Jonathan A., additional, Jensen, Elwood V., additional, Jepsen, Kristen, additional, Jones, E. Yvonne, additional, Jones, Katherine A., additional, Jordan, J. Dedrick, additional, Joseph, Jomon, additional, Justement, Louis B., additional, Kafri, Yariv, additional, Kahn, Richard A., additional, Kang, Shin W., additional, Karlin, Arthur, additional, Kast-Woelbern, Heidi R., additional, Kaufman, Randal J., additional, Kazlauskas, Andrius, additional, Keen, James H., additional, Kemler, Rolf, additional, Kemp, Bruce E., additional, Kennedy, Mary B., additional, Kennedy, Matthew A., additional, Kikkawa, Ushio, additional, Kim, Albert H., additional, Kim, Soo-A, additional, Kim, Sung-Hou, additional, Kim, Youngjoo, additional, King-Jones, Kirst, additional, Kintner, Chris, additional, Kivimäe, Saul, additional, Klee, Claude B., additional, Klein, Rüdiger, additional, Kleppisch, Thomas, additional, Kliewer, Steven A., additional, Klinghoffer, Richard A., additional, Knoblich, Juergen A., additional, Kobe, Bostjan, additional, Kochs, George, additional, Kong-Beltran, Monica, additional, König, Rolf, additional, Koong, Albert C., additional, Korc, Murray, additional, Kornitzer, Daniel, additional, Kossiakoff, Anthony A., additional, Kotera, Jun, additional, Kovalenko, M.V., additional, Kozasa, Tohru, additional, Kozlov, Sergei, additional, Kozminski, Keith G., additional, Krugmann, Sonja, additional, Kuriyan, John, additional, Kurokawa, Riki, additional, Kwong, Peter D., additional, Lai, Wi S., additional, Lamar, Elise, additional, Lambert, Millard H., additional, Lambright, David G., additional, Lancet, Doron, additional, Landry, Reiko, additional, Langdon, Wallace Y., additional, Langeberg, Lorene K., additional, Lasko, Paul, additional, Latham, Vaughn, additional, Lavin, Martin F., additional, Lease, Kevin A., additional, Leffler, Hakon, additional, Lemmon, Mark A., additional, Leonard, Ann E., additional, Levitzki, Alexander, additional, Liao, Hong-Jun, additional, Liaw, Lucy, additional, Liberi, Giordano, additional, Lickert, Heiko, additional, Liddington, Robert C., additional, Lincoln, Thomas M., additional, Linder, Jürgen U., additional, Linder, Maurine E., additional, Liu, Hui, additional, Liu, Zhengchang, additional, Lohela, Marja K., additional, Louie, Sarah H., additional, Luttrell, Deirdre K., additional, Luttrell, Louis M., additional, Lyons, Karen M., additional, Macaulay, S. Lance, additional, Maceyka, Michael, additional, Maciag, Thomas, additional, Macian, Fernando, additional, MacKintosh, Carol, additional, MacLennan, David H., additional, Mahmood, Nadir A., additional, Malbon, Craig C., additional, Malik, Sohail, additional, Man, Orna, additional, Manahan, Carol L., additional, Mandinova, Anna, additional, Manganiello, Vincent C., additional, Manley, James L., additional, Mann, Matthias, additional, Manning, Gerald, additional, Manser, Ed, additional, Margeta-Mitrovic, Marta, additional, Margolskee, Robert F., additional, Marinissen, Julia, additional, Mariuzza, Roy A., additional, Marmor, Mina D., additional, Martin, G. Steven, additional, Martin, Karen H., additional, Martinez, Sergio E., additional, Mathews, Michael B., additional, Mayer, Bruce J., additional, Mayer, Mark L., additional, Mazzoni, Maria R., additional, McCormick, Frank, additional, McGowan, Clare H., additional, McKay, Melissa M., additional, McKeehan, Wallace L., additional, McLean, Alison J., additional, Means, Anthony R., additional, Meili, Ruedi, additional, Meng, Jingwei, additional, Merchant, Mark, additional, Mercurio, Frank, additional, Milligan, Graeme, additional, Ming, Guo-Li, additional, Minor, Daniel L., additional, Moghal, Nadeem, additional, Møller, Neils Peter H., additional, Mongillo, Marco, additional, Montminy, Marc, additional, Moon, Randall T., additional, Morimoto, Richard I., additional, Moss, Stephen E., additional, Mott, Helen R., additional, Mouta, Carla, additional, Muda, Marco, additional, Mumby, Marc C., additional, Murphy, Gretchen A., additional, Muzi-Falconi, Marco, additional, Nagaraj, Raghavendra, additional, Nahorski, Stefan R., additional, Nairn, Angus C., additional, Nash, Piers, additional, Neel, Benjamin G., additional, Newton, Alexandra C., additional, Nishizuka, Yasutomi, additional, Noel, Joseph P., additional, Nollen, Ellen A.A., additional, Nooren, Irene M.A., additional, O'Connor, Rodney, additional, Offermanns, Stefan, additional, Olender, Tsviya, additional, Ong, Shao-En, additional, Owen, Darerca, additional, Pagliari, Lisa J., additional, Pao, Lily, additional, Papaconstantinou, John, additional, Pardo, Leonardo, additional, Park, Hay-Oak, additional, Park, Young Chul, additional, Parker, Peter J., additional, Parsons, J. Thomas, additional, Passner, J.M., additional, Pawson, Tony, additional, Pelliccioli, Achille, additional, Perez-Polo, J. Regino, additional, Perrimon, Norbert, additional, Petite, Fabrice G., additional, Petroulakis, Emmanuel, additional, Pfaff, Samuel L., additional, Piehler, Jacob, additional, Pike, Linda J., additional, Pinkoski, Michael J., additional, Pixley, Fiona J., additional, Plevani, Paolo, additional, Poo, Mu-ming, additional, Pozzan, Tullioi, additional, Prescott, Stephen M., additional, Prudovsky, Igor, additional, Putney, James W., additional, Radimerski, Thomas, additional, Radzio-Andzelm, Elzbieta, additional, Ram, Prahlad T., additional, Rameh, Lucia, additional, Ramljak, Danica, additional, Ranscht, Barbara, additional, Rao, Anjana, additional, Raport, Carol J., additional, Reeves, Jacqueline D., additional, Rehman, Holger, additional, Reichman, Trevor W., additional, Reiter, Eric, additional, Resnick, Michael A., additional, Reth, Michael, additional, Rhee, Sue Goo, additional, Richter, Joel D., additional, Rietze, Rodney L., additional, Rini, James M., additional, Ripperger, Jürgen A., additional, Rizo, Josep, additional, Robishaw, Janet D., additional, Roderick, H. Llewelyn, additional, Roeder, Robert G., additional, Rohrschneider, Larry R., additional, Ron, David, additional, Rosenfeld, Michael G., additional, Rosenfeldt, Hans, additional, Rossman, Kent L., additional, Roth, Christopher B., additional, Rudolph, Markus G., additional, Ruppelt, Anja, additional, Saez, Lino, additional, Sakmar, Thomas P., additional, Salvesen, Guy S., additional, Sassone-Corsi, Paolo, additional, Saxe, Charles L., additional, Schäfer, Beat W., additional, Schibler, Ueli, additional, Schindler, Christian W., additional, Schmelzle, Tobias, additional, Schmid, Sandra L., additional, Schmidt, Anja, additional, Schmidt, Eric F., additional, Schreiber, Gideon, additional, Schultz, Joachim E., additional, Schwaller, Beat, additional, Schwamborn, Klaus, additional, Schwartz, Thue, additional, Schwindinger, William F., additional, Scita, Giorgio, additional, Scott, John D., additional, Scott, Shaun, additional, Seebeck, Thomas, additional, Serhan, Charles N., additional, Shabb, John B., additional, Shaw, Andrey S., additional, Shears, Stephen B., additional, Shenolikar, Shirish, additional, Shi, Lei, additional, Shin, Chanseok, additional, Shiozaki, Kazuhiro, additional, Shokat, Kevan M., additional, Shuttleworth, Trevor J., additional, Siderovski, David P., additional, Siegelbaum, Steven A., additional, Silverstein, Adam M., additional, Singer, Robert H., additional, Skinner, Michael K., additional, Slack-Davis, Jill K., additional, Smerdon, Stephen J., additional, Smith, Graeme C.M., additional, Smits, Guillaume, additional, Smolik, Sarah M., additional, Smotrys, Jessica E., additional, Smyth, Emer M., additional, Snyder, Jason T., additional, Sogame, Naoko, additional, Soldi, Raffaella, additional, Sondek, John, additional, Sonenberg, Nahum, additional, Sonneberg, Erica Dutil, additional, Sparrow, Lindsay G., additional, Spiegel, Sarah, additional, Sprang, Stephen R., additional, Srivastava, Deepak, additional, Stanfield, Robyn L., additional, Stanley, E. Richard, additional, Stauber, Deborah J., additional, Stefan, Christopher, additional, Stenson-Holst, Lena, additional, Stephens, Len, additional, Sternberg, Paul W., additional, Sternweis, Paul C., additional, Steward, Ruth, additional, Stickney, John T., additional, Stoker, Andrew W., additional, Strittmatter, Stephen M., additional, Stronach, Beth E., additional, Strong, Roland K., additional, Stroud, Robert M., additional, Südhof, Thomas C., additional, Sunahara, Roger K., additional, Sutton, Brian J., additional, Szabolcs, Sipeki, additional, Tang, Xiao-Bo, additional, Taskén, Kjetil, additional, Tatebe, Hisashi, additional, Tauszig-Delamasure, Servane, additional, Taylor, Colin W., additional, Taylor, Garry L., additional, Taylor, Laura J., additional, Taylor, Susan S., additional, Thomas, George, additional, Thomas, Robert P., additional, Thompson, E. Brad, additional, Thompson, Michael J., additional, Thornton, Janet M., additional, Thummel, Carl S., additional, Togashi, Hideaki, additional, Tong, Amy Hin Yan, additional, Tonks, Nicholas K., additional, Tontonoz, Peter, additional, Topham, M.K., additional, Torgersen, Knut Martin, additional, Tran, Hien, additional, Tremblay, Michel L., additional, Tsai, Ming-Jer, additional, Tsai, Sophia Y., additional, Tsunoda, Susan, additional, Turley, Stewart, additional, Tyson, Darren, additional, Van Etten, Robert L., additional, Vassart, Gilbert, additional, Verveer, Peter J., additional, Vlaeminck, Virginie, additional, de Vos, Abraham M., additional, Voss, Ty C., additional, Walczak, Robert, additional, Walker, Graham C., additional, Walker, John C., additional, Walter, Gernot, additional, Walter, Mark R., additional, Wang, Fen, additional, Wang, Jean Y.J., additional, Wang, Weiru, additional, Ward, Richard J., additional, Wedegaertner, Philip, additional, Wehrle, Christian, additional, Weiss, Arthur, additional, Weiss, Jamie L., additional, Wells, Alan, additional, Werner, Claudia, additional, West, Ann H., additional, Weston, Marie C., additional, Westwick, John K., additional, Wetterholm, Anders, additional, White, Morris F., additional, Whitman, Malcolm, additional, Whorton, Matt R., additional, Wiesmann, Christian, additional, Williams, Roger L., additional, Willis, William D., additional, Willson, Timothy M., additional, Wilson, Ian A., additional, Wiser, Ofer, additional, Wishart, Matthew J., additional, Wittinghofer, Alfred, additional, Woodgett, James R., additional, Worthylake, David K., additional, Wrana, Jeffrey L., additional, Wu, Hao, additional, Xiao, Yijin, additional, Xu, H. Eric, additional, Xu, Yan, additional, Xu, Zheng, additional, Yaffe, Michael B., additional, Yamada, Kenneth M., additional, Yang, Seun-Ah, additional, Yang, Wannian, additional, Yarden, Yosef, additional, Ye, Hong, additional, Ye, Weilan, additional, Yeates, Todd O., additional, Yin, Helen L., additional, York, John D., additional, Young, Edgar C., additional, Young, Kenneth W., additional, Young, Matthew A., additional, Young, Michael W., additional, Yu, Minmin, additional, Zaccai, Nathan R., additional, Zaccolo, Manuela, additional, Zamir, Eli, additional, von Zastrow, Mark, additional, Zhang, Chao, additional, Zhang, Xuewu, additional, Zhang, Zhong-Yin, additional, Zhou, Wenhong, additional, and Zoraghi, Roya, additional

Published
2003
Full Text
View/download PDF

120. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery

Author

Datta, Sandeep Robert, Dudek, Henryk, Tao, Xu, Masters, Shane, Fu, Haian, Gotoh, Yukiko, and Greenberg, Michael E.

Subjects
Recombinant proteins -- Research, Protein kinases -- Research, Cell death -- Research, Growth factors -- Research, Biological sciences
Abstract

Experiment was conducted to examine the hypothesis that the Pl3'K/Akt pathway may result in BAD phosphorylation and may, thus, suppress cell death and promote cell survival. Growth factors can promote cell survival by activating the phosphatidylinositide-3'-OH kinase and its downstream target, the serine-threonine kinase Akt but the mechanism by which Akt functions need to be examined. Akt phosphorylates BAD in vitro and in vivo, and blocks the BAD-induced death of primary neurons. Results suggest a mechanism by which growth factors inactivate a vital component of cell-death machinery.

Published
1997

121. Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway

Author

Bonnie, Azad, Nadal-Vicens, Mireya, Bhatt, Ami, Frank, David A., Rozovsky, Irina, Stahl, Neil, Yancopoulos, George D., and Greenberg, Michael E.

Subjects
Cytokines -- Research, Ligands (Biochemistry) -- Research, Cilia and ciliary motion -- Research, Science and technology, Research
Abstract

A mechanism by which members of the ciliary neurotrophic factor (CNTF)--leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized. Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage. Although CNTF stimulated both the Janus kinase--signal transducer and activator of transcription (JAK-STAT) and Ras--mitogen-activated protein kinase signaling pathways in cortical precursor cells. the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage. These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development., The cells of the central nervous system (CNS) are thought to arise from multipotential precursor cells whose developmental potential becomes progressively restricted (1-8). Environmental cues may have a critical role [...]

Published
1997

123. Influenza-Associated Deaths among Children in the United States, 2003-2004

Author

Bhat, Niranjan, Wright, Jennifer G., Broder, Karen R., Murray, Erin L., Greenberg, Michael E., Glover, Maleeka J., Likos, Anna M., Posey, Drew L., Klimov, Alexander, Lindstrom, Stephen E., Balish, Amanda, Medina, Marie-jo, Wallis, Teresa R., Guarner, Jeannette, Paddock, Christopher D., Shieh, Wun-Ju, Zaki, Sherif R., Sejvar, James J., Shay, David K., Harper, Scott A., Cox, Nancy J., Fukuda, Keiji, and Uyeki, Timothy M.

Published
2005
Full Text
View/download PDF

124. A defect in nurturing in mice lacking the immediate early gene fos

Author

Brown, Jennifer R., Ye, Hong, Bronson, Roderick T., Dikkes, Pieter, and Greenberg, Michael E.

Subjects
Genetic transcription -- Research, Genetically modified mice -- Research, Nurturing behavior -- Genetic aspects, Biological sciences
Abstract

Previous research has shown that environmental stimuli that trigger adaptive neuronal responses induce the expression of the Fos family of transcription factors. However, whether Fos family members mediate these responses remains unknown. To resolve this problem, mice with an inactivating mutation in the fosB gene are generated. Results show that complex behavior in mice is controlled by a transcription factor that regulates a specific neuronal circuit. These indicate a genetic component behind nurturing in mammals.

Published
1996

125. E2F-1 functions in mice to promote apoptosis and suppress proliferation

Author

Field, Seth J., Tsai, Fong-Ying, Kuo, Frank, Zubiaga, Ana M., Kaelin, William G., Jr., Livingston, David M., Orkin, Stuart H., and Greenberg, Michael E.

Subjects
Genetic transcription -- Regulation, T cells -- Genetic aspects, Cell proliferation -- Genetic aspects, Cell death -- Genetic aspects, Biological sciences
Abstract

The E2F transcription factors promote entry into the S-phase of DNA transcription to induce cell proliferation and cellular apoptosis. The disruption of E2F-1 gene in mice did not affect embryonic and reproductive development. Enlargement of the thymus and lymphoid nodes were detected one month after birth. This is caused by the accumulation of mature CD4/CD8 single-positive thymocytes and peripheral T-cells due to a defective pathway of apoptosis. The hyperproliferation of immature thymocytes indicates the importance of E2F-1 as a suppressor of aberrant cell proliferation.

Published
1996

128. Calcium activation of Ras mediated by neuronal exchange factor Ras-GRF

Author

Farnsworth, Charles L., Freshney, Norman W., Rosen, Laura B., Ghosh, Anirvan, Greenberg, Michael E., and Feig, Larry A.

Subjects
Ras genes -- Research, Developmental neurology -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Ras in vivo appears to activate in response to neuronal exchange factor Ras-GRF's exposure to Ca2+ as well as activating through the accepted tyrosine kinase receptor pathway. The activation link to Ca2+ indicates that Ras-GRF may be involved in the regulation of Ca2+ influenced neuronal functions. Calmodulin appears responsible for mediating Ras activation through binding to an IQ motif.

Published
1995

129. CREB: a mediator of long-term memory from mollusks to mammals

Author

Frank, David A. and Greenberg, Michael E.

Subjects
Memory -- Genetic aspects, Biological sciences
Abstract

A single transcription factor, the cAMP response element-binding protein (CREB), is involved in the process of memory retention in humans. The ability to remember past events is a characteristic feature of all living organisms. The ability requires the encoding of long-term memories, which is performed by the CREB protein.

Published
1994

130. Nerve growth factor activates a Ras-dependent protein kinase that stimulates c-fos transcription via phosphorylation of CRE

Author

Ginty, David D., Bonni, Azad, and Greenberg, Michael E.

Subjects
Nerve growth factor -- Research, Protein kinases -- Research, Genetic transcription -- Analysis, Biological sciences
Abstract

Nerve growth factor (NGF) signal is transmitted to the nucleus to induce c-fos transcription through a has-dependent protein kinase that phosphorylates the cyclic AMP response element-binding protein (CREB) at SRE-133. Phosphorylation of S-133 is important for CREB to stimulate C-fos transcription. CREB plays an important role in influencing growth factor responses.

Published
1994

134. A scalable platform for the development of cell-type-specific viral drivers

Author

Hrvatin, Sinisa, primary, Tzeng, Christopher P, additional, Nagy, M Aurel, additional, Stroud, Hume, additional, Koutsioumpa, Charalampia, additional, Wilcox, Oren F, additional, Assad, Elena G, additional, Green, Jonathan, additional, Harvey, Christopher D, additional, Griffith, Eric C, additional, and Greenberg, Michael E, additional

Published
2019
Full Text
View/download PDF

136. Correction: Mapping the genomic landscape of inherited retinal disease genes prioritizes genes prone to coding and noncoding copy-number variations

Author

Van Schil, Kristof, primary, Naessens, Sarah, additional, Van de Sompele, Stijn, additional, Carron, Marjolein, additional, Aslanidis, Alexander, additional, Van Cauwenbergh, Caroline, additional, Mayer, Anja K., additional, Van Heetvelde, Mattias, additional, Bauwens, Miriam, additional, Verdin, Hannah, additional, Coppieters, Frauke, additional, Greenberg, Michael E., additional, Yang, Marty G., additional, Karlstetter, Marcus, additional, Langmann, Thomas, additional, De Preter, Katleen, additional, Kohl, Susanne, additional, Cherry, Timothy J., additional, Leroy, Bart P., additional, De Baere, Elfride, additional, Lupski, James R, additional, Carvalho, Claudia, additional, van Min, Max, additional, Klous, Petra, additional, De Jaegere, Sarah, additional, and Hooghe, Sally, additional

Published
2019
Full Text
View/download PDF

137. Loss of Adaptive Myelination Contributes to Methotrexate Chemotherapy-Related Cognitive Impairment

Author

Geraghty, Anna C., primary, Gibson, Erin M., additional, Ghanem, Reem A., additional, Greene, Jacob J., additional, Ocampo, Alfonso, additional, Goldstein, Andrea K., additional, Ni, Lijun, additional, Yang, Tao, additional, Marton, Rebecca M., additional, Paşca, Sergiu P., additional, Greenberg, Michael E., additional, Longo, Frank M., additional, and Monje, Michelle, additional

Published
2019
Full Text
View/download PDF

140. Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

Author

Gunner, Georgia, primary, Cheadle, Lucas, additional, Johnson, Kasey M., additional, Ayata, Pinar, additional, Badimon, Ana, additional, Mondo, Erica, additional, Nagy, Aurel, additional, Liu, Liwang, additional, Bemiller, Shane M., additional, Kim, Ki-Wook, additional, Lira, Sergio A., additional, Lamb, Bruce T., additional, Tapper, Andrew R., additional, Ransohoff, Richard M., additional, Greenberg, Michael E., additional, Schaefer, Anne, additional, and Schafer, Dorothy P., additional

Published
2019
Full Text
View/download PDF

143. Contributors

Author

Baker, Ellen J., primary, Bechhofer, David, additional, Belasco, Joel G., additional, Binder, Roberta, additional, Brawerman, George, additional, Causton, Helen C., additional, Cleveland, Don W., additional, Court, Donald, additional, Dance, Geoffrey S.C., additional, Greenberg, Michael E., additional, Gruissem, Wilhelm, additional, Hanson, Roberta J., additional, Harford, Joe B., additional, Higgins, Christopher F., additional, Jacobson, Allan, additional, Lundberg, Urban, additional, Marzluff, William F., additional, McTigue, Monica, additional, Melefors, Öjar, additional, Mudd, Elisabeth A., additional, Peltz, Stuart W., additional, Petersen, Carsten, additional, Ross, Jeff, additional, Schuster, Gadi, additional, Sensel, Martha, additional, Stevens, Audrey, additional, Theodorakis, Nicholas G., additional, von Gabain, Alexander, additional, and Williams, David L., additional

Published
1993
Full Text
View/download PDF

147. The Drosophila Forkhead transcription factor FOXO mediates the reduction in cell number associated with reduced insulin signaling

Author

Végh Mátyás, Stocker Hugo, Wasserman Jonathan D, Rintelen Felix, Jünger Martin A, Radimerski Thomas, Greenberg Michael E, and Hafen Ernst

Subjects
Biology (General), QH301-705.5
Abstract

Abstract Background Forkhead transcription factors belonging to the FOXO subfamily are negatively regulated by protein kinase B (PKB) in response to signaling by insulin and insulin-like growth factor in Caenorhabditis elegans and mammals. In Drosophila, the insulin-signaling pathway regulates the size of cells, organs, and the entire body in response to nutrient availability, by controlling both cell size and cell number. In this study, we present a genetic characterization of dFOXO, the only Drosophila FOXO ortholog. Results Ectopic expression of dFOXO and human FOXO3a induced organ-size reduction and cell death in a manner dependent on phosphoinositide (PI) 3-kinase and nutrient levels. Surprisingly, flies homozygous for dFOXO null alleles are viable and of normal size. They are, however, more sensitive to oxidative stress. Furthermore, dFOXO function is required for growth inhibition associated with reduced insulin signaling. Loss of dFOXO suppresses the reduction in cell number but not the cell-size reduction elicited by mutations in the insulin-signaling pathway. By microarray analysis and subsequent genetic validation, we have identified d4E-BP, which encodes a translation inhibitor, as a relevant dFOXO target gene. Conclusion Our results show that dFOXO is a crucial mediator of insulin signaling in Drosophila, mediating the reduction in cell number in insulin-signaling mutants. We propose that in response to cellular stresses, such as nutrient deprivation or increased levels of reactive oxygen species, dFOXO is activated and inhibits growth through the action of target genes such as d4E-BP.

Published
2003
Full Text
View/download PDF

148. Neurons that regulate mouse torpor.

Author

Hrvatin, Sinisa, Sun, Senmiao, Wilcox, Oren F., Yao, Hanqi, Lavin-Peter, Aurora J., Cicconet, Marcelo, Assad, Elena G., Palmer, Michaela E., Aronson, Sage, Banks, Alexander S., Griffith, Eric C., and Greenberg, Michael E.

Abstract

The advent of endothermy, which is achieved through the continuous homeostatic regulation of body temperature and metabolism1,2, is a defining feature of mammalian and avian evolution. However, when challenged by food deprivation or harsh environmental conditions, many mammalian species initiate adaptive energy-conserving survival strategies—including torpor and hibernation—during which their body temperature decreases far below its homeostatic set-point3–5. How homeothermic mammals initiate and regulate these hypothermic states remains largely unknown. Here we show that entry into mouse torpor, a fasting-induced state with a greatly decreased metabolic rate and a body temperature as low as 20 °C6, is regulated by neurons in the medial and lateral preoptic area of the hypothalamus. We show that restimulation of neurons that were activated during a previous bout of torpor is sufficient to initiate the key features of torpor, even in mice that are not calorically restricted. Among these neurons we identify a population of glutamatergic Adcyap1-positive cells, the activity of which accurately determines when mice naturally initiate and exit torpor, and the inhibition of which disrupts the natural process of torpor entry, maintenance and arousal. Taken together, our results reveal a specific neuronal population in the mouse hypothalamus that serves as a core regulator of torpor. This work forms a basis for the future exploration of mechanisms and circuitry that regulate extreme hypothermic and hypometabolic states, and enables genetic access to monitor, initiate, manipulate and study these ancient adaptations of homeotherm biology. A specific neuronal population in the medial and lateral preoptic area of the hypothalamus regulates entry into torpor in mice. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

149. Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes.

Author

Kalish, Brian T., Barkat, Tania R., Diel, Erin E., Zhang, Elizabeth J., Greenberg, Michael E., and Hensch, Takao K.

Subjects
AUDITORY cortex, RNA sequencing, NEURAL circuitry, GENETIC regulation, GENE expression
Abstract

Auditory experience drives neural circuit refinement during windows of heightened brain plasticity, but little is known about the genetic regulation of this developmental process. The primary auditory cortex (A1) of mice exhibits a critical period for thalamocortical connectivity between postnatal days P12 and P15, during which tone exposure alters the tonotopic topography of A1. We hypothesized that a coordinated, multicellular transcriptional program governs this window for patterning of the auditory cortex. To generate a robust multicellular map of gene expression, we performed droplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points (P10, P15, and P20) spanning the tonotopic critical period. We also tonereared mice (7 kHz pips) during the 3-d critical period and collected A1 at P15 and P20. We identified and profiled both neuronal (glutamatergic and GABAergic) and nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types. By comparing normal- and tone-reared mice, we found hundreds of genes across cell types showing altered expression as a result of sensory manipulation during the critical period. Functional voltage-sensitive dye imaging confirmed GABA circuit function determines critical period onset, while Nogo receptor signaling is required for its closure. We further uncovered previously unknown effects of developmental tone exposure on trajectories of gene expression in interneurons, as well as candidate genes that might execute tonotopic plasticity. Our single-nucleus transcriptomic resource of developing auditory cortex is thus a powerful discovery platform with which to identify mediators of tonotopic plasticity. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

150. Mapping the cis-regulatory architecture of the human retina reveals noncoding genetic variation in disease.

Author

Cherry, Timothy J., Yang, Marty G., Harmin, David A., Tao, Peter, Timms, Andrew E., Bauwens, Miriam, Allikmets, Rando, Jones, Evan M., Rui Chen, De Baere, Elfride, and Greenberg, Michael E.

Subjects
RETINA, GENETIC disorders, RHODOPSIN, EYE, VISION disorders
Abstract

The interplay of transcription factors and cis-regulatory elements (CREs) orchestrates the dynamic and diverse genetic programs that assemble the human central nervous system (CNS) during development and maintain its function throughout life. Genetic variation within CREs plays a central role in phenotypic variation in complex traits including the risk of developing disease. We took advantage of the retina, a well-characterized region of the CNS known to be affected by pathogenic variants in CREs, to establish a roadmap for characterizing regulatory variation in the human CNS. This comprehensive analysis of tissue-specific regulatory elements, transcription factor binding, and gene expression programs in three regions of the human visual system (retina, macula, and retinal pigment epithelium/choroid) reveals features of regulatory element evolution that shape tissue-specific gene expression programs and defines regulatory elements with the potential to contribute to Mendelian and complex disorders of human vision. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results