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2. microRNA signature of hypoxia

Author

KULSHRESHTHA R, WOJCIK S. E, GARZON R, ALDER H, AGOSTO PEREZ F. J, DAVULURI R, LIU C. G, CROCE C. M, M. NEGRINI, CALIN G. A, IVAN M. A., FERRACIN, MANUELA, KULSHRESHTHA R, FERRACIN M, WOJCIK S. E, GARZON R, ALDER H, AGOSTO-PEREZ F. J, DAVULURI R, LIU C. G, CROCE C. M, M. NEGRINI, CALIN G. A, and IVAN M. A

Subjects
Chromatin Immunoprecipitation, Colonic Neoplasm, Oligonucleotide Array Sequence Analysi, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Apoptosi, MicroRNA, Transfection, Plasmid, Cell Hypoxia, HT29 Cell, Genes, Reporter, Cell Line, Tumor, HCT116 Cell, Female, Luciferase, Breast Neoplasm, Human
Abstract

Recent research has identified critical roles for microRNAs in a large number of cellular processes, including tumorigenic transformation. While significant progress has been made towards understanding the mechanisms of gene regulation by microRNAs, much less is known about factors affecting the expression of these noncoding transcripts. Here, we demonstrate for the first time a functional link between hypoxia, a well-documented tumor microenvironment factor, and microRNA expression. Microarray-based expression profiles revealed that a specific spectrum of microRNAs (including miR-23, -24, -26, -27, -103, -107, -181, -210, and -213) is induced in response to low oxygen, at least some via a hypoxia-inducible-factor-dependent mechanism. Select members of this group (miR-26, -107, and -210) decrease proapoptotic signaling in a hypoxic environment, suggesting an impact of these transcripts on tumor formation. Interestingly, the vast majority of hypoxia-induced microRNAs are also overexpressed in a variety of human tumors.

Published
2007

8. CTCF binding site sequence differences are associated with unique regulatory and functional trends during embryonic stem cell differentiation

Author

Plasschaert, R. N., primary, Vigneau, S., additional, Tempera, I., additional, Gupta, R., additional, Maksimoska, J., additional, Everett, L., additional, Davuluri, R., additional, Marmorstein, R., additional, Lieberman, P. M., additional, Schultz, D., additional, Hannenhalli, S., additional, and Bartolomei, M. S., additional

Published
2014
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9. Nonlinear partial differential equations and applications: Gene expression profiling of isogenic cells with different TP53 gene dosage reveals numerous genes that are affected by TP53 dosage and identifies CSPG2 as a direct target of p53

Author

de la Chapelle, A., Lockman, J. C., Yoon, H., Liyanarachchi, S., Wright, F. A., Davuluri, R., and Pellegata, N. S.

Abstract

TP53 does not fully comply with the Knudson model [Knudson, A. G., Jr. (1971) Proc. Natl. Acad. Sci. USA 68, 820–823] in that a reduction of constitutional expression of p53 may be sufficient for tumor predisposition . This finding suggests a gene-dosage effect for p53 function. To determine whether TP53 gene dosage affects the transcriptional regulation of target genes, we performed oligonucleotide-array gene expression analysis by using human cells with wild-type p53 (p53 +/+), or with one (p53 +/−), or both (p53 −/−) TP53 alleles disrupted by homologous recombination. We identified 35 genes whose expression is significantly correlated to the dosage of TP53. These genes are involved in a variety of cellular processes including signal transduction, cell adhesion, and transcription regulation. Several of them are involved in neurogenesis and neural crest migration, developmental processes in which p53 is known to play a role. Motif search analysis revealed that of the genes highly expressed in p53 +/+ and +/− cells, several contain a putative p53 consensus binding site (bs), suggesting that they could be directly regulated by p53. Among those genes, we chose CSPG2 (which encodes versican) for further study because it contains a bona fide p53 bs in its first intron and its expression highly correlates with TP53 dosage. By using in vitro and in vivo assays, we showed CSPG2 to be directly transactivated by p53. In conclusion, we developed a strategy to demonstrate that many genes are affected by TP53 gene dosage for their expression. We report several candidate genes as potential downstream targets of p53 in nonstressed cells. Among them, CSPG2 is validated as being directly transactivated by p53. Our method provides a useful tool to elucidate additional mechanisms by which p53 exerts its functions.

Published
2002
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10. CTCF binding site sequence differences are associated with unique regulatory and functional trends during embryonic stem cell differentiation

Author

Plasschaert, R. N., primary, Vigneau, S., additional, Tempera, I., additional, Gupta, R., additional, Maksimoska, J., additional, Everett, L., additional, Davuluri, R., additional, Mamorstein, R., additional, Lieberman, P. M., additional, Schultz, D., additional, Hannenhalli, S., additional, and Bartolomei, M. S., additional

Published
2013
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11. HINCUTs in cancer: hypoxia-induced noncoding ultraconserved transcripts

Author

Ferdin, J, primary, Nishida, N, additional, Wu, X, additional, Nicoloso, M S, additional, Shah, M Y, additional, Devlin, C, additional, Ling, H, additional, Shimizu, M, additional, Kumar, K, additional, Cortez, M A, additional, Ferracin, M, additional, Bi, Y, additional, Yang, D, additional, Czerniak, B, additional, Zhang, W, additional, Schmittgen, T D, additional, Voorhoeve, M P, additional, Reginato, M J, additional, Negrini, M, additional, Davuluri, R V, additional, Kunej, T, additional, Ivan, M, additional, and Calin, G A, additional

Published
2013
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12. LAB-CELL BIOLOGY AND SIGNALING

Author

Kijima, N., primary, Hosen, N., additional, Kagawa, N., additional, Hashimoto, N., additional, Chiba, Y., additional, Kinoshita, M., additional, Sugiyama, H., additional, Yoshimine, T., additional, Kim, Y. Z., additional, Kim, K. H., additional, Lee, E. H., additional, Hu, B., additional, Sim, H., additional, Mohan, N., additional, Agudelo-Garcia, P., additional, Nuovo, G., additional, Cole, S., additional, Viapiano, M. S., additional, McFarland, B. C., additional, Hong, S. W., additional, Rajbhandari, R., additional, Twitty, G. B., additional, Kenneth Gray, G., additional, Yu, H., additional, Langford, C. P., additional, Yancey Gillespie, G., additional, Benveniste, E. N., additional, Nozell, S. E., additional, Nitta, R., additional, Mitra, S., additional, Bui, T., additional, Li, G., additional, Munoz, J. L., additional, Rodriguez-Cruz, V., additional, Rameshwar, P., additional, See, W. L., additional, Mukherjee, J., additional, Shannon, K. M., additional, Pieper, R. O., additional, Floyd, D. H., additional, Xiao, A., additional, Purow, B. W., additional, Lavon, I., additional, Zrihan, D., additional, Refael, M., additional, Bier, A., additional, Canello, T., additional, Siegal, T., additional, Granit, A., additional, Xie, Q., additional, Wang, X., additional, Gong, Y., additional, Mao, Y., additional, Chen, X., additional, Zhou, L., additional, Lee, S. X., additional, Tunkyi, A., additional, Wong, E. T., additional, Swanson, K. D., additional, Zhang, K., additional, Chen, L., additional, Zhang, J., additional, Shi, Z., additional, Han, L., additional, Pu, P., additional, Kang, C., additional, Cho, W. H., additional, Ogawa, D., additional, Godlewski, J., additional, Bronisz, A., additional, Antonio Chiocca, E., additional, Mustafa, D. A. M., additional, Sieuwerts, A. M., additional, Smid, M., additional, de Weerd, V., additional, Martens, J. W., additional, Foekens, J. A., additional, Kros, J. M., additional, McCulloch, C., additional, Graff, J., additional, Sui, Y., additional, Dinn, S., additional, Huang, Y., additional, Li, Q., additional, Fiona, G., additional, Nakashima, H., additional, Leiss, L., additional, Manini, I., additional, Enger, P. O., additional, Yang, C., additional, Iyer, R., additional, Yu, A. C. H., additional, Li, S., additional, Ikejiri, B. L., additional, Zhuang, Z., additional, Lonser, R., additional, Massoud, T. F., additional, Paulmurugan, R., additional, Gambhir, S. S., additional, Merrill, M. J., additional, Sun, M., additional, Chen, M., additional, Edwards, N. A., additional, Shively, S. B., additional, Lonser, R. R., additional, Baia, G. S., additional, Caballero, O. L., additional, Orr, B. A., additional, Lal, A., additional, Ho, J. S., additional, Cowdrey, C., additional, Tihan, T., additional, Mawrin, C., additional, Riggins, G. J., additional, Lu, D., additional, Leo, C., additional, Wheeler, H., additional, McDonald, K., additional, Schulte, A., additional, Zapf, S., additional, Stoupiec, M., additional, Kolbe, K., additional, Riethdorf, S., additional, Westphal, M., additional, Lamszus, K., additional, Timmer, M., additional, Rohn, G., additional, Koch, A., additional, Goldbrunner, R., additional, Ruggieri, R., additional, Vanan, I., additional, Dong, Z., additional, Sarkaria, J. N., additional, Tran, N. L., additional, Berens, M. E., additional, Symons, M., additional, Rowther, F. B., additional, Dawson, T., additional, Ashton, K., additional, Darling, J., additional, Warr, T., additional, Okamoto, M., additional, Palanichamy, K., additional, Gordon, N., additional, Patel, D., additional, Walston, S., additional, Krishanan, T., additional, Chakravarti, A., additional, Kalinina, J., additional, Carroll, A., additional, Wang, L., additional, Yu, Q., additional, Mancheno, D. E., additional, Wu, S., additional, Liu, F., additional, Ahn, J., additional, He, M., additional, Mao, H., additional, Van Meir, E. G., additional, Debinski, W., additional, Gonzales, O., additional, Beauchamp, A., additional, Gibo, D. M., additional, Seals, D. F., additional, Speranza, M. C., additional, Frattini, V., additional, Kapetis, D., additional, Pisati, F., additional, Eoli, M., additional, Pellegatta, S., additional, Finocchiaro, G., additional, Maherally, Z., additional, Smith, J. R., additional, Pilkington, G. J., additional, Zhu, W., additional, Wang, Q., additional, Clark, P. A., additional, Yang, S.-S., additional, Lin, S.-H., additional, Kahle, K. T., additional, Kuo, J. S., additional, Sun, D., additional, Hossain, M. B., additional, Cortes-Santiago, N., additional, Gururaj, A., additional, Thomas, J., additional, Gabrusiewicz, K., additional, Gumin, J., additional, Xipell, E., additional, Lang, F., additional, Fueyo, J., additional, Yung, W. K. A., additional, Gomez-Manzano, C., additional, Cook, N. J., additional, Lawrence, J. E., additional, Rovin, R. A., additional, Belton, R. J., additional, Winn, R. J., additional, Ferluga, S., additional, Lee, S.-H., additional, Khwaja, F. W., additional, Zerrouqi, A., additional, Devi, N. S., additional, Drucker, K. L., additional, Lee, H. K., additional, Finniss, S., additional, Cazacu, S., additional, Poisson, L., additional, Xiang, C., additional, Rempel, S. A., additional, Mikkelsen, T., additional, Brodie, C., additional, Shen, J., additional, Kenchappa, R. S., additional, Valadez, J. G., additional, Cooper, M. K., additional, Carter, B. D., additional, Forsyth, P. A., additional, Lee, J. S., additional, Erdreich-Epstein, A., additional, Song, H.-R., additional, Lawn, S., additional, Kenchappa, R., additional, Forsyth, P., additional, Lim, K. J., additional, Bar, E. E., additional, Eberhart, C. G., additional, Blough, M., additional, Alnajjar, M., additional, Chesnelong, C., additional, Weiss, S., additional, Chan, J., additional, Cairncross, G., additional, Wykosky, J., additional, Cavenee, W., additional, Furnari, F., additional, Brown, K. E., additional, Keir, S. T., additional, Sampson, J. H., additional, Bigner, D. D., additional, Kwatra, M. M., additional, Kotipatruni, R. P., additional, Thotala, D. K., additional, Jaboin, J., additional, Taylor, T. E., additional, Schinzel, A. C., additional, Hahn, W. C., additional, Cavenee, W. K., additional, Furnari, F. B., additional, Kapoor, G. S., additional, Macyszyn, L., additional, Bi, Y., additional, Fetting, H., additional, Poptani, H., additional, Ittyerah, R., additional, Davuluri, R. V., additional, O'Rourke, D., additional, Pitter, K. L., additional, Hosni-Ahmed, A., additional, Colevas, K., additional, Holland, E. C., additional, Jones, T. S., additional, Malhotra, A., additional, Potts, C., additional, Fernandez-Lopez, A., additional, Kenney, A. M., additional, Cheng, S., additional, Feng, H., additional, Jarzynka, M. J., additional, Li, Y., additional, Keezer, S., additional, Johns, T. G., additional, Hamilton, R. L., additional, Vuori, K., additional, Nishikawa, R., additional, Fenton, T., additional, Cheng, T., additional, Mikheev, A. M., additional, Mikheeva, S. A., additional, Silber, J. R., additional, Horner, P. J., additional, Rostomily, R., additional, Henson, E. S., additional, Brown, M., additional, Eisenstat, D. D., additional, Gibson, S. B., additional, Price, R. L., additional, Song, J., additional, Bingmer, K., additional, Oglesbee, M., additional, Cook, C., additional, Kwon, C.-H., additional, Nguyen, T. T., additional, Chiocca, E. A., additional, Lukiw, W. J., additional, Culicchia, F., additional, Jones, B. M., additional, Zhao, Y., additional, and Bhattacharjee, S., additional

Published
2012
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13. LAB-OMICS AND PROGNOSTIC MARKERS

Author

Jensen, R. L., primary, Abraham, S., additional, Hu, N., additional, Jensen, R. L., additional, Boulay, J.-L., additional, Leu, S., additional, Frank, S., additional, Vassella, E., additional, Vajtai, I., additional, von Felten, S., additional, Taylor, E., additional, Schulz, M., additional, Hutter, G., additional, Sailer, M., additional, Hench, J., additional, Mariani, L., additional, van Thuijl, H. F., additional, Scheinin, I., additional, van Essen, D. F., additional, Heimans, J. J., additional, Wesseling, P., additional, Ylstra, B., additional, Reijneveld, J. C., additional, Borges, A. R., additional, Larrubia, P. L., additional, Marques, J. M. B., additional, Cerdan, S. G., additional, Brastianos, P., additional, Horowitz, P., additional, Santagata, S., additional, Jones, R. T., additional, McKenna, A., additional, Getz, G., additional, Ligon, K., additional, Palescandolo, E., additional, Van Hummelen, P., additional, Stemmer-Rachamimov, A., additional, Louis, D., additional, Hahn, W. C., additional, Dunn, I., additional, Beroukhim, R., additional, Guan, X., additional, Vengoechea, J., additional, Zheng, S., additional, Sloan, A., additional, Chen, Y., additional, Brat, D., additional, O'Neill, B. P., additional, Cohen, M., additional, Aldape, K., additional, Rosenfeld, S., additional, Noushmehr, H., additional, Verhaak, R. G., additional, Barnholtz-Sloan, J., additional, Bahassi, E. M., additional, Li, Y.-Q., additional, Cross, E., additional, Li, W., additional, Vijg, J., additional, McPherson, C., additional, Warnick, R., additional, Stambrook, P., additional, Rixe, O., additional, Manterola, L., additional, Tejada-Solis, S., additional, Diez-Valle, R., additional, Gonzalez, M., additional, Jauregui, P., additional, Sampron, N., additional, Barrena, C., additional, Ruiz, I., additional, Gallego, J., additional, Delattre, J.-Y., additional, de Munain, A. L., additional, Mlonso, M. M., additional, Saito, K., additional, Mukasa, A., additional, Nagae, G., additional, Aihara, K., additional, Takayanagi, S., additional, Aburatani, H., additional, Saito, N., additional, Kong, X.-T., additional, Fu, B. D., additional, Du, S., additional, Hasso, A. N., additional, Linskey, M. E., additional, Bota, D., additional, Li, C., additional, Chen, Y.-S., additional, Chen, Z.-p., additional, Kim, C. H., additional, Cheong, J. H., additional, Kim, J. M., additional, Yelon, N. P., additional, Jacoby, E., additional, Cohen, Z. R., additional, Ishida, J., additional, Kurozumi, K., additional, Ichikawa, T., additional, Onishi, M., additional, Fujii, K., additional, Shimazu, Y., additional, Date, I., additional, Narayanan, R., additional, Ho, Q. H., additional, Levin, B. S., additional, Maeder, M. L., additional, Joung, J. K., additional, Nutt, C. L., additional, Louis, D. N., additional, Thorsteinsdottir, J., additional, Fu, P., additional, Gehrmann, M., additional, Multhoff, G., additional, Tonn, J.-C., additional, Schichor, C., additional, Thirumoorthy, K., additional, Gordon, N., additional, Walston, S., additional, Patel, D., additional, Okamoto, M., additional, Chakravarti, A., additional, Palanichamy, K., additional, French, P., additional, Erdem, L., additional, Gravendeel, L., additional, de Rooi, J., additional, Eilers, P., additional, Idbaih, A., additional, Spliet, W., additional, den Dunnen, W., additional, Teepen, J., additional, Smitt, P. S., additional, Kros, J. M., additional, Gorlia, T., additional, van den Bent, M., additional, McCarthy, D., additional, Cook, R. W., additional, Oelschlager, K., additional, Maetzold, D., additional, Hanna, M., additional, Wick, W., additional, Meisner, C., additional, Hentschel, B., additional, Platten, M., additional, Sabel, M. C., additional, Koeppen, S., additional, Ketter, R., additional, Weiler, M., additional, Tabatabai, G., additional, Schilling, A., additional, von Deimling, A., additional, Gramatzki, D., additional, Westphal, M., additional, Schackert, G., additional, Loeffler, M., additional, Simon, M., additional, Reifenberger, G., additional, Weller, M., additional, Moren, L., additional, Johansson, M., additional, Bergenheim, T., additional, Antti, H., additional, Sulman, E. P., additional, Goodman, L. D., additional, Wani, K. M., additional, DeMonte, F., additional, Aldape, K. D., additional, Krischek, B., additional, Gugel, I., additional, Aref, D., additional, Marshall, C., additional, Croul, S., additional, Zadeh, G., additional, Nilsson, C. L., additional, Sulman, E., additional, Liu, H., additional, Wild, C., additional, Lichti, C. F., additional, Emmett, M. R., additional, Lang, F. F., additional, Conrad, C., additional, Alentorn, A., additional, Marie, Y., additional, Boisselier, B., additional, Carpetier, C., additional, Mokhtari, K., additional, Hoang-Xuan, K., additional, Capelle, L., additional, Lautenschlaeger, T., additional, Huebner, A., additional, McIntyre, J. B., additional, Magliocco, T., additional, Hamilton, M., additional, Easaw, J., additional, Pollo, B., additional, Calatozzolo, C., additional, Vuono, R., additional, Guzzetti, S., additional, Eoli, M., additional, Silvani, A., additional, Di Meco, F., additional, Filippini, G., additional, Finocchiaro, G., additional, Joy, A., additional, Ramesh, A., additional, Smirnov, I., additional, Reiser, M., additional, Shapiro, W., additional, Mills, G., additional, Kim, S., additional, Feuerstein, B., additional, Gonda, D. D., additional, Li, J., additional, McCabe, N., additional, Walker, S., additional, Goffard, N., additional, Wikstrom, K., additional, McLean, E., additional, Greenan, C., additional, Delaney, T., additional, McCarthy, M., additional, McDyer, F., additional, Keating, K. E., additional, James, I. F., additional, Harrison, T., additional, Mullan, P., additional, Harkin, D. P., additional, Carter, B. S., additional, Kennedy, R. D., additional, Chen, C. C., additional, Patel, A. S., additional, Allen, J. E., additional, Dicker, D. T., additional, Rizzo, K., additional, Sheehan, J. M., additional, Glantz, M. J., additional, El-Deiry, W. S., additional, Salhia, B., additional, Ross, J. T., additional, Kiefer, J., additional, Van Cott, C., additional, Metpally, R., additional, Baker, A., additional, Sibenaller, Z., additional, Nasser, S., additional, Ryken, T., additional, Ramanathan, R., additional, Berens, M. E., additional, Carpten, J., additional, Tran, N. L., additional, Bi, Y., additional, Pal, S., additional, Zhang, Z., additional, Gupta, R., additional, Macyszyn, L., additional, Fetting, H., additional, O'Rourke, D., additional, Davuluri, R. V., additional, Ezrin, A. M., additional, Moore, K., additional, Stummer, W., additional, Hadjipanayis, C. G., additional, Cahill, D. P., additional, Beiko, J., additional, Suki, D., additional, Prabhu, S., additional, Weinberg, J., additional, Lang, F., additional, Sawaya, R., additional, Rao, G., additional, McCutcheon, I., additional, Barker, F. G., additional, Trister, A. D., additional, Bot, B., additional, Fontes, K., additional, Bridge, C., additional, Baldock, A. L., additional, Rockhill, J. K., additional, Mrugala, M. M., additional, Rockne, R. R., additional, Huang, E., additional, Swanson, K. R., additional, Underhill, H. R., additional, Zhang, J., additional, Shi, M., additional, Lin, X., additional, Mikheev, A., additional, Rostomily, R. C., additional, Scheck, A. C., additional, Stafford, P., additional, Hughes, A., additional, Cichacz, Z., additional, Coons, S. W., additional, Johnston, S. A., additional, Mainwaring, L., additional, Craig, J., additional, Garcia, D., additional, Bergthold, G., additional, Burns, M., additional, Rich, B., additional, Ramkissoon, S., additional, Eberhart, C., additional, Ligon, A., additional, Goumnerova, L., additional, Stiles, C., additional, Kieran, M., additional, Hahn, W., additional, Olausson, K. H., additional, Correia, J., additional, Gafni, E., additional, Theisen, M., additional, Hayashi, M., additional, Haidar, S., additional, Maire, C., additional, Mainwaring, L. A., additional, Norden, A., additional, Wen, P., additional, Kung, A., additional, Alexander, B., additional, Tonellato, P., additional, and Ligon, K. L., additional

Published
2012
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17. CELL BIOLOGY AND SIGNALING

Author

Furnari, F., primary, Fenton, T., additional, Nathanson, D., additional, de Alberquerque, C. P., additional, Kuga, D., additional, Wanami, A., additional, Dang, J., additional, Yang, H., additional, Tanaka, K., additional, Gao, L., additional, Oba-Shinjo, S., additional, Uno, M., additional, Inda, M.-d.-M., additional, Bachoo, R., additional, James, C. D., additional, DePinho, R., additional, Vandenberg, S., additional, Zhou, H., additional, Marie, S., additional, Mischel, P., additional, Cavenee, W., additional, Szerlip, N., additional, Pedraza, A., additional, Huse, J., additional, Mikkelsen, T., additional, Brennan, C., additional, Castellani, R. J., additional, Ivanova, S., additional, Gerzanich, V. V., additional, Simard, J. M., additional, Ito, M., additional, See, W., additional, Mukherjee, J., additional, Ohba, S., additional, Tan, I.-L., additional, Pieper, R. O., additional, Lukiw, W. J., additional, Culicchia, F., additional, Pogue, A., additional, Bhattacharjee, S., additional, Zhao, Y., additional, Proescholdt, M. A., additional, Merrill, M., additional, Storr, E. M., additional, Lohmeier, A., additional, Brawanski, A., additional, Abraham, S., additional, Jensen, R., additional, Khatua, S., additional, Gopal, U., additional, Du, J., additional, He, F., additional, Golub, T., additional, Isaacs, J. S., additional, Dietrich, J., additional, Kalogirou-Valtis, Y., additional, Ly, I., additional, Scadden, D., additional, Proschel, C., additional, Mayer-Proschel, M., additional, Rempel, S. A., additional, Schultz, C. R., additional, Golembieski, W., additional, Brodie, C., additional, Mathew, L. K., additional, Skuli, N., additional, Mucaj, V., additional, Imtiyaz, H. Z., additional, Venneti, S., additional, Lal, P., additional, Zhang, Z., additional, Davuluri, R. V., additional, Koch, C., additional, Evans, S., additional, Simon, M. C., additional, Ranganathan, P., additional, Clark, P., additional, Salamat, S., additional, Kuo, J. S., additional, Kalejta, R. F., additional, Bhattacharjee, B., additional, Renzette, N., additional, Moser, R. P., additional, Kowalik, T. F., additional, McFarland, B. C., additional, Ma, J.-Y., additional, Langford, C. P., additional, Gillespie, G. Y., additional, Yu, H., additional, Zheng, Y., additional, Nozell, S. E., additional, Huszar, D., additional, Benveniste, E. N., additional, Lawrence, J. E., additional, Cook, N. J., additional, Rovin, R. A., additional, Winn, R. J., additional, Godlewski, J. A., additional, Ogawa, D., additional, Bronisz, A., additional, Lawler, S., additional, Chiocca, E. A., additional, Lee, S. X., additional, Wong, E. T., additional, Swanson, K. D., additional, Liu, K.-w., additional, Feng, H., additional, Kazlauskas, A., additional, Smith, E. M., additional, Symes, K., additional, Hamilton, R. L., additional, Nagane, M., additional, Nishikawa, R., additional, Hu, B., additional, Cheng, S.-Y., additional, Silber, J., additional, Jacobsen, A., additional, Ozawa, T., additional, Harinath, G., additional, Brennan, C. W., additional, Holland, E. C., additional, Sander, C., additional, Huse, J. T., additional, Sengupta, R., additional, Dubuc, A., additional, Ward, S., additional, Yang, L., additional, Northcott, P., additional, Kroll, K., additional, Taylor, M., additional, Wechsler-Reya, R., additional, Rubin, J., additional, Chu, W.-T., additional, Lee, H.-T., additional, Huang, F.-J., additional, Aldape, K., additional, Yao, J., additional, Steeg, P. S., additional, Lu, Z., additional, Xie, K., additional, Huang, S., additional, Sim, H., additional, Agudelo-Garcia, P. A., additional, Viapiano, M. S., additional, Saldivar, J., additional, Dolan, C., additional, Mora, M., additional, Nuovo, G., additional, Cole, S., additional, Stegh, A. H., additional, Ryu, M.-J., additional, Liu, Y., additional, Zhong, X., additional, Marwaha, S., additional, Li, H., additional, Wang, J., additional, Chang, Q., additional, Zhang, J., additional, Ng, H.-K., additional, Poon, W. S., additional, Zhou, L., additional, Pang, J. C., additional, Chan, A., additional, Didier, S., additional, Kwiatkowska, A., additional, Ennis, M., additional, Fortin, S., additional, Rushing, E., additional, Eschbacher, J., additional, Tran, N., additional, Symons, M., additional, Roldan, G., additional, McIntyre, J. B., additional, Easaw, J., additional, Magliocco, A., additional, Wykosky, J., additional, Furnari, F., additional, Lu, D., additional, Mreich, E., additional, Chung, S., additional, Teo, C., additional, Wheeler, H., additional, McDonald, K. L., additional, Lawn, S., additional, Forsyth, P., additional, Sonabend, A. M., additional, Lei, L., additional, Kennedy, B., additional, Soderquist, C., additional, Guarnieri, P., additional, Leung, R., additional, Yun, J., additional, Sisti, J., additional, Castelli, M., additional, Bruce, S., additional, Bruce, R., additional, Ludwig, T., additional, Rosenfeld, S., additional, Bruce, J. N., additional, Canoll, P., additional, Lamszus, K., additional, Schulte, A., additional, Gunther, H. S., additional, Riethdorf, S., additional, Phillips, H. S., additional, Westphal, M., additional, Siegal, T., additional, Zrihan, D., additional, Granit, A., additional, Lavon, I., additional, Singh, M., additional, Chandra, J., additional, Nakashima, H., additional, Godlewski, J., additional, Chiocca, A. E., additional, Kapoor, G. S., additional, Poptani, H., additional, Ittyerah, R., additional, O'Rourke, D. M., additional, Sadraei, N. H., additional, Burgett, M., additional, Ahluwalia, M., additional, Tipps, R., additional, Khosla, D., additional, Weil, R., additional, Nowacki, A., additional, Prayson, R., additional, Shi, T., additional, Gladson, C., additional, Moeckel, S., additional, Meyer, K., additional, Bosserhoff, A., additional, Spang, R., additional, Leukel, P., additional, Vollmann, A., additional, Jachnick, B., additional, Stangl, C., additional, Proescholdt, M., additional, Bogdahn, U., additional, Hau, P., additional, Kaur, G., additional, Sun, M., additional, Kaur, R., additional, Bloch, O., additional, Jian, B., additional, Parsa, A. T., additional, Hossain, A., additional, Shinojima, N., additional, Gumin, J., additional, Feng, G., additional, Lang, F. 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A., additional, and Petritsch, C., additional

Published
2011
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18. miR-145 participates with TP53 in a death-promoting regulatory loop and targets estrogen receptor-α in human breast cancer cells

Author

Spizzo, R, primary, Nicoloso, M S, additional, Lupini, L, additional, Lu, Y, additional, Fogarty, J, additional, Rossi, S, additional, Zagatti, B, additional, Fabbri, M, additional, Veronese, A, additional, Liu, X, additional, Davuluri, R, additional, Croce, C M, additional, Mills, G, additional, Negrini, M, additional, and Calin, G A, additional

Published
2009
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26. RP58/ZNF238 directly modulates proneurogenic gene levels and is required for neuronal differentiation and brain expansion.

Author

Xiang, C, Baubet, V, Pal, S, Holderbaum, L, Tatard, V, Jiang, P, Davuluri, R V, and Dahmane, N

Subjects
NEOCORTEX, TUMOR growth, BRAIN tumors, CEREBRAL cortex, NEURONS
Abstract

Although neurogenic pathways have been described in the developing neocortex, less is known about mechanisms ensuring correct neuronal differentiation thus also preventing tumor growth. We have shown that RP58 (aka zfp238 or znf238) is highly expressed in differentiating neurons, that its expression is lost or diminished in brain tumors, and that its reintroduction blocks their proliferation. Mice with loss of RP58 die at birth with neocortical defects. Using a novel conditional RP58 allele here we show that its CNS-specific loss yields a novel postnatal phenotype: microencephaly, agenesis of the corpus callosum and cerebellar hypoplasia that resembles the chr1qter deletion microcephaly syndrome in human. RP58 mutant brains maintain precursor pools but have reduced neuronal and increased glial differentiation. Well-timed downregulation of pax6, ngn2 and neuroD1 depends on RP58 mediated transcriptional repression, ngn2 and neuroD1 being direct targets. Thus, RP58 may act to favor neuronal differentiation and brain growth by coherently repressing multiple proneurogenic genes in a timely manner. [ABSTRACT FROM AUTHOR]

Published
2012
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27. miR-145 participates with TP53 in a death-promoting regulatory loop and targets estrogen receptor-α in human breast cancer cells.

Author

Spizzo, R., Nicoloso, M. S., Lupini, L., Lu, Y., Fogarty, J., Rossi, S., Zagatti, B., Fabbri, M., Veronese, A., Liu, X., Davuluri, R., Croce, C. M., Mills, G., Negrini, M., and Calin, G. A.

Subjects
RNA, P53 protein, BREAST cancer, CANCER cells, APOPTOSIS
Abstract

Understanding the consequences of miR-145 reintroduction in human breast cancer (BC) could reveal its tumor-suppressive functions and may disclose new aspects of BC biology. Therefore, we characterized the effects of miR-145 re-expression in BC cell lines by using proliferation and apoptosis assays. As a result, we found that miR-145 exhibited a pro-apoptotic effect, which is dependent on TP53 activation, and that TP53 activation can, in turn, stimulate miR-145 expression, thus establishing a death-promoting loop between miR-145 and TP53. We also found that miR-145 can downregulate estrogen receptor-α (ER-α) protein expression through direct interaction with two complementary sites within its coding sequence. In conclusion, we described a tumor suppression function of miR-145 in BC cell lines, and we linked miR-145 to TP53 and ER-α. Moreover, our findings support a view that miR-145 re-expression therapy could be mainly envisioned in the specific group of patients with ER-α-positive and/or TP53 wild-type tumors. [ABSTRACT FROM AUTHOR]

Published
2010
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28. Identifying the 3'-terminal exon in human DNA.

Author

Tabaska, J E, Davuluri, R V, and Zhang, M Q

Abstract

We present JTEF, a new program for finding 3' terminal exons in human DNA sequences. This program is based on quadratic discriminant analysis, a standard non-linear statistical pattern recognition method. The quadratic discriminant functions used for building the algorithm were trained on a set of 3' terminal exons of type 3tuexon (those containing the true STOP codon).

Published
2001
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29. Dehydrohalogenation of glycosyl halides with 1,5-diazabicyclo[5.4.0]undec-s-ene

Author

Davuluri R. Rao and Leon M. Lerner

Subjects
Chemistry, Organic Chemistry, Halide, General Medicine, Cellobiose, Biochemistry, Analytical Chemistry, chemistry.chemical_compound, Galactose, Reagent, Dehydrohalogenation, Organic chemistry, Glycosyl, Lactose, Ene reaction
Abstract

The 2-hydroxyglycals derived from D -glucose, D -galactose, cellobiose and lactose, as well as 2,3,4-tri-O-benzoyl-2-hydroxy- D -xylal and 2,3,5-tri-O-benzoyl-2-hydroxy- D -ribal were prepared by the use of 1,5-diazabicyclo[5.4.0]undec-5-ene (2) in N,N-dimethylformamide. The reagent, 1,5-diazabicyclo[4.3.0]non-5-ene, was found to be a suitable substitute for 2.

Published
1972
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33. A new synthesis of 2-hydroxyglycals

Author

Leon M. Lerner and Davuluri R. Rao

Subjects
Bridged-Ring Compounds, Aza Compounds, Chemistry, business.industry, Organic Chemistry, Carbohydrates, Galactose, Stereoisomerism, General Medicine, Bromine, Biochemistry, Data science, Analytical Chemistry, Text mining, Heterocyclic Compounds, Glycosides, Crystallization, business, Pyrans
Published
1971
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34. Sequencing and analysis of a South Asian-Indian personal genome

Author

Gupta Ravi, Ratan Aakrosh, Rajesh Changanamkandath, Chen Rong, Kim Hie Lim, Burhans Richard, Miller Webb, Santhosh Sam, Davuluri Ramana V, Butte Atul J, Schuster Stephan C, Seshagiri Somasekar, and Thomas George

Subjects
Indian genome, Personal genomics, Whole genome sequencing, Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background With over 1.3 billion people, India is estimated to contain three times more genetic diversity than does Europe. Next-generation sequencing technologies have facilitated the understanding of diversity by enabling whole genome sequencing at greater speed and lower cost. While genomes from people of European and Asian descent have been sequenced, only recently has a single male genome from the Indian subcontinent been published at sufficient depth and coverage. In this study we have sequenced and analyzed the genome of a South Asian Indian female (SAIF) from the Indian state of Kerala. Results We identified over 3.4 million SNPs in this genome including over 89,873 private variations. Comparison of the SAIF genome with several published personal genomes revealed that this individual shared ~50% of the SNPs with each of these genomes. Analysis of the SAIF mitochondrial genome showed that it was closely related to the U1 haplogroup which has been previously observed in Kerala. We assessed the SAIF genome for SNPs with health and disease consequences and found that the individual was at a higher risk for multiple sclerosis and a few other diseases. In analyzing SNPs that modulate drug response, we found a variation that predicts a favorable response to metformin, a drug used to treat diabetes. SNPs predictive of adverse reaction to warfarin indicated that the SAIF individual is not at risk for bleeding if treated with typical doses of warfarin. In addition, we report the presence of several additional SNPs of medical relevance. Conclusions This is the first study to report the complete whole genome sequence of a female from the state of Kerala in India. The availability of this complete genome and variants will further aid studies aimed at understanding genetic diversity, identifying clinically relevant changes and assessing disease burden in the Indian population.

Published
2012
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35. IsoformEx: isoform level gene expression estimation using weighted non-negative least squares from mRNA-Seq data

Author

Gupta Ravi, Pal Sharmistha, Bi Yingtao, Kim Hyunsoo, and Davuluri Ramana V

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Biology (General), QH301-705.5
Abstract

Abstract Background mRNA-Seq technology has revolutionized the field of transcriptomics for identification and quantification of gene transcripts not only at gene level but also at isoform level. Estimating the expression levels of transcript isoforms from mRNA-Seq data is a challenging problem due to the presence of constitutive exons. Results We propose a novel algorithm (IsoformEx) that employs weighted non-negative least squares estimation method to estimate the expression levels of transcript isoforms. Validations based on in silico simulation of mRNA-Seq and qRT-PCR experiments with real mRNA-Seq data showed that IsoformEx could accurately estimate transcript expression levels. In comparisons with published methods, the transcript expression levels estimated by IsoformEx showed higher correlation with known transcript expression levels from simulated mRNA-Seq data, and higher agreement with qRT-PCR measurements of specific transcripts for real mRNA-Seq data. Conclusions IsoformEx is a fast and accurate algorithm to estimate transcript expression levels and gene expression levels, which takes into account short exons and alternative exons with a weighting scheme. The software is available at http://bioinformatics.wistar.upenn.edu/isoformex.

Published
2011
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36. Genome-wide analysis of host-chromosome binding sites for Epstein-Barr Virus Nuclear Antigen 1 (EBNA1)

Author

Wang Pu, Tsai Kevin, Norseen Julie, Wikramasinghe Priyankara, Lu Fang, Showe Louise, Davuluri Ramana V, and Lieberman Paul M

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Abstract The Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1) protein is required for the establishment of EBV latent infection in proliferating B-lymphocytes. EBNA1 is a multifunctional DNA-binding protein that stimulates DNA replication at the viral origin of plasmid replication (OriP), regulates transcription of viral and cellular genes, and tethers the viral episome to the cellular chromosome. EBNA1 also provides a survival function to B-lymphocytes, potentially through its ability to alter cellular gene expression. To better understand these various functions of EBNA1, we performed a genome-wide analysis of the viral and cellular DNA sites associated with EBNA1 protein in a latently infected Burkitt lymphoma B-cell line. Chromatin-immunoprecipitation (ChIP) combined with massively parallel deep-sequencing (ChIP-Seq) was used to identify cellular sites bound by EBNA1. Sites identified by ChIP-Seq were validated by conventional real-time PCR, and ChIP-Seq provided quantitative, high-resolution detection of the known EBNA1 binding sites on the EBV genome at OriP and Qp. We identified at least one cluster of unusually high-affinity EBNA1 binding sites on chromosome 11, between the divergent FAM55 D and FAM55B genes. A consensus for all cellular EBNA1 binding sites is distinct from those derived from the known viral binding sites, suggesting that some of these sites are indirectly bound by EBNA1. EBNA1 also bound close to the transcriptional start sites of a large number of cellular genes, including HDAC3, CDC7, and MAP3K1, which we show are positively regulated by EBNA1. EBNA1 binding sites were enriched in some repetitive elements, especially LINE 1 retrotransposons, and had weak correlations with histone modifications and ORC binding. We conclude that EBNA1 can interact with a large number of cellular genes and chromosomal loci in latently infected cells, but that these sites are likely to represent a complex ensemble of direct and indirect EBNA1 binding sites.

Published
2010
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37. Genome-wide analysis of alternative promoters of human genes using a custom promoter tiling array

Author

Plass Christoph, Yan Pearlly, Wu Jiejun, Singer Gregory AC, Huang Tim HM, and Davuluri Ramana V

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background Independent lines of evidence suggested that a large fraction of human genes possess multiple promoters driving gene expression from distinct transcription start sites. Understanding which promoter is employed in which cellular context is required to unravel gene regulatory networks within the cell. Results We have developed a custom microarray platform that tiles roughly 35,000 alternative putative promoters from nearly 7,000 genes in the human genome. To demonstrate the utility of this array platform, we have analyzed the patterns of promoter usage in 17β-estradiol (E2)-treated and untreated MCF7 cells and show widespread usage of alternative promoters. Most intriguingly, we show that the downstream promoter in E2-sensitive multiple promoter genes tends to be very close to the 3'-terminus of the gene, suggesting exotic mechanisms of expression regulation in these genes. Conclusion The usage of alternative promoters greatly multiplies the transcriptional complexity available within the human genome. The fact that many of these promoters are incapable of driving the synthesis of a meaningful protein-encoding transcript further complicates the story.

Published
2008
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38. Genome-wide analysis of core promoter elements from conserved human and mouse orthologous pairs

Author

Liyanarachchi Sandya, Agosto-Pérez Francisco J, Singer Gregory AC, Jin Victor X, and Davuluri Ramana V

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Biology (General), QH301-705.5
Abstract

Abstract Background The canonical core promoter elements consist of the TATA box, initiator (Inr), downstream core promoter element (DPE), TFIIB recognition element (BRE) and the newly-discovered motif 10 element (MTE). The motifs for these core promoter elements are highly degenerate, which tends to lead to a high false discovery rate when attempting to detect them in promoter sequences. Results In this study, we have performed the first analysis of these core promoter elements in orthologous mouse and human promoters with experimentally-supported transcription start sites. We have identified these various elements using a combination of positional weight matrices (PWMs) and the degree of conservation of orthologous mouse and human sequences – a procedure that significantly reduces the false positive rate of motif discovery. Our analysis of 9,010 orthologous mouse-human promoter pairs revealed two combinations of three-way synergistic effects, TATA-Inr-MTE and BRE-Inr-MTE. The former has previously been putatively identified in human, but the latter represents a novel synergistic relationship. Conclusion Our results demonstrate that DNA sequence conservation can greatly improve the identification of functional core promoter elements in the human genome. The data also underscores the importance of synergistic occurrence of two or more core promoter elements. Furthermore, the sequence data and results presented here can help build better computational models for predicting the transcription start sites in the promoter regions, which remains one of the most challenging problems.

Published
2006
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39. Genomic structure and alternative splicing of murine R2B receptor protein tyrosine phosphatases (PTPκ, μ, ρ and PCP-2)

Author

Frostholm Adrienne, Davuluri Ramana V, Popesco Magdalena C, Besco Julie, and Rotter Andrej

Subjects
central nervous system, dephosphorylation, alternative splicing, adhesion molecules, Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background Four genes designated as PTPRK (PTPκ), PTPRL/U (PCP-2), PTPRM (PTPμ) and PTPRT (PTPρ) code for a subfamily (type R2B) of receptor protein tyrosine phosphatases (RPTPs) uniquely characterized by the presence of an N-terminal MAM domain. These transmembrane molecules have been implicated in homophilic cell adhesion. In the human, the PTPRK gene is located on chromosome 6, PTPRL/U on 1, PTPRM on 18 and PTPRT on 20. In the mouse, the four genes ptprk, ptprl, ptprm and ptprt are located in syntenic regions of chromosomes 10, 4, 17 and 2, respectively. Results The genomic organization of murine R2B RPTP genes is described. The four genes varied greatly in size ranging from ~64 kb to ~1 Mb, primarily due to proportional differences in intron lengths. Although there were also minor variations in exon length, the number of exons and the phases of exon/intron junctions were highly conserved. In situ hybridization with digoxigenin-labeled cRNA probes was used to localize each of the four R2B transcripts to specific cell types within the murine central nervous system. Phylogenetic analysis of complete sequences indicated that PTPρ and PTPμ were most closely related, followed by PTPκ. The most distant family member was PCP-2. Alignment of RPTP polypeptide sequences predicted putative alternatively spliced exons. PCR experiments revealed that five of these exons were alternatively spliced, and that each of the four phosphatases incorporated them differently. The greatest variability in genomic organization and the majority of alternatively spliced exons were observed in the juxtamembrane domain, a region critical for the regulation of signal transduction. Conclusions Comparison of the four R2B RPTP genes revealed virtually identical principles of genomic organization, despite great disparities in gene size due to variations in intron length. Although subtle differences in exon length were also observed, it is likely that functional differences among these genes arise from the specific combinations of exons generated by alternative splicing.

Published
2004
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40. AGRIS: Arabidopsis Gene Regulatory Information Server, an information resource of Arabidopsis cis-regulatory elements and transcription factors

Author

Molina Carlos, Kurtz Mike, Matthews Nicole, Palaniswamy Saranyan K, Sun Hao, Davuluri Ramana V, and Grotewold Erich

Subjects
Computer applications to medicine. Medical informatics, R858-859.7, Biology (General), QH301-705.5
Abstract

Abstract Background The gene regulatory information is hardwired in the promoter regions formed by cis-regulatory elements that bind specific transcription factors (TFs). Hence, establishing the architecture of plant promoters is fundamental to understanding gene expression. The determination of the regulatory circuits controlled by each TF and the identification of the cis-regulatory sequences for all genes have been identified as two of the goals of the Multinational Coordinated Arabidopsis thaliana Functional Genomics Project by the Multinational Arabidopsis Steering Committee (June 2002). Results AGRIS is an information resource of Arabidopsis promoter sequences, transcription factors and their target genes. AGRIS currently contains two databases, AtTFDB (Arabidopsis thaliana transcription factor database) and AtcisDB (Arabidopsis thaliana cis-regulatory database). AtTFDB contains information on approximately 1,400 transcription factors identified through motif searches and grouped into 34 families. AtTFDB links the sequence of the transcription factors with available mutants and, when known, with the possible genes they may regulate. AtcisDB consists of the 5' regulatory sequences of all 29,388 annotated genes with a description of the corresponding cis-regulatory elements. Users can search the databases for (i) promoter sequences, (ii) a transcription factor, (iii) a direct target genes for a specific transcription factor, or (vi) a regulatory network that consists of transcription factors and their target genes. Conclusion AGRIS provides the necessary software tools on Arabidopsis transcription factors and their putative binding sites on all genes to initiate the identification of transcriptional regulatory networks in the model dicotyledoneous plant Arabidopsis thaliana. AGRIS can be accessed from http://arabidopsis.med.ohio-state.edu.

Published
2003
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42. Regulation of microRNA expression: The hypoxic component

Author

Manuela Ferracin, Ramana V. Davuluri, Mircea Ivan, Ritu Kulshreshtha, Massimo Negrini, George A. Calin, KULSHRESHTHA R, FERRACIN M, M. NEGRINI, CALIN G. A, DAVULURI R. V, and IVAN M

Subjects
Apoptosis, Biology, medicine.disease_cause, Neoplasms, microRNA, medicine, cancer, Molecular Biology, Gene, Tumor microenvironment, hypoxia, Computational Biology, Cancer, regulation, Cell Biology, Hypoxia (medical), medicine.disease, target genes, Cell Hypoxia, Cell biology, expression profile, MicroRNAs, Gene Expression Regulation, Expression (architecture), Hypoxia-Inducible Factor 1, medicine.symptom, Carcinogenesis, Signal Transduction, Developmental Biology
Abstract

microRNAs are involved in a wide variety of normal and pathological cellular processes, including tumorigenic transformation. Despite significant progress made towards understanding their mechanisms of action, much less is known about the regulation of expression of specific microRNAs. Recent reports have established a link between hypoxia, a key feature of the tumor microenvironment, and a group of microRNAs. Select members of this group seem to affect apoptotic signaling in a hypoxic environment and are also predicted to target genes of critical importance for tumor biology. Interestingly, most hypoxia-induced microRNAs are also overexpressed in human cancers, suggesting a role in tumorigenesis. We hereby discuss the known and predicted regulators of microRNA expression and approaches for expanding this fledgling research area.

43. Immunoglobulin superfamily 3 (Igsf3) function is dispensable for brain development.

Author

Cocito C, Xiang C, Huang M, Gongora T, Surana P, Davuluri R, Dahmane N, and Greenfield JP

Subjects
Animals, Mice, Neurons metabolism, Membrane Proteins metabolism, Membrane Proteins genetics, Neurogenesis genetics, Immunoglobulins genetics, Immunoglobulins metabolism, Gene Expression Regulation, Developmental, Mice, Knockout, Brain metabolism, Brain growth & development, Cell Movement genetics
Abstract

The Immunoglobulin superfamily (IgSF) is a heterogeneous and conserved family of adhesion proteins crucial during the development of the central nervous system including neuronal migration and synaptogenesis. The Immunoglobulin superfamily member 3 (IGSF3) is expressed in the developing brain and has been suggested to play a role during morphological development of the granule cells neurites in the cerebellum. In addition, a role for IGSF3 in supporting glioma progression has been recently demonstrated. Remaining unexplored is the physiological role of IGSF3 in regulating brain development, including neocortical development. We generated an Igsf3 knockout (KO) mouse using a CRISPR/Cas9-based approach and explored the function of Igsf3 in regulating cortical development. We found that Igsf3 largely co-localizes with other IgSF proteins during cortical development and despite its expression being developmentally regulated in neuronal progenitors and in postmitotic neurons, Igsf3 is not essential for brain development, neuronal migration, or neuronal maturation., Competing Interests: Declarations. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Published
2025
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44. Designing a Time-Dependent Therapeutic Strategy using CDK4/6 Inhibitors in an Intracranial ATRT Model.

Author

Martin B, Guadix SW, Sathian R, Laramee M, Pandey A, Ray I, Wang A, Davuluri R, Thomas CJ, Dahmane N, and Souweidane M

Abstract

Background: Inhibitors targeting cyclin-dependent kinases 4 and 6 (CDK4/6), crucial for cell cycle regulation, have shown promise in early-stage studies for treating central nervous system (CNS) tumors. However, challenges such as limited CNS penetration, optimal treatment duration, and systemic side effects have impeded their clinical translation for pediatric brain tumors (PBTs)., Methods: We evaluated the potency of CDK4/6 inhibitors across various PBTs cell lines, focusing particularly on palbociclib against atypical teratoid rhabdoid tumor (ATRT) with cell viability assays and gene expression analysis. Additionally, we assessed the efficacy and safety of intrathecal (IT) delivery of palbociclib through neurotoxicity and pharmacokinetic studies, along with survival assessments in murine leptomeningeal ATRT models., Results: Palbociclib showed the highest potency across various PBT cells, with extended treatments reducing growth inhibition 50 (GI50) values from the micromolar to nanomolar range. It suppressed critical cell cycle genes (CCNB1, CCNA2, CDK1) in BT-16 ATRT cells. Neurotoxicity (GFAP, CD45, NeuN, Iba1) and pharmacokinetic assays confirmed IT route as a feasible and effective method for delivering palbociclib to the cerebrospinal fluid (CSF), avoiding systemic toxicity and enhancing drug concentration to the brain. Finally, metronomic IT delivery using an osmotic pump (48mg/kg) increased survival in two murine leptomeningeal ATRT models, showcasing its potential as a novel therapy for leptomeningeal tumors., Conclusions: Metronomic IT delivery of palbociclib enhances drug efficacy and safety, improves survival, and offers a promising treatment strategy for PBTs with CSF dissemination., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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45. Epithelial-mesenchymal transition: an organizing principle of mammalian regeneration.

Author

Bedelbaeva K, Cameron B, Latella J, Aslanukov A, Gourevitch D, Davuluri R, and Heber-Katz E

Abstract

Introduction: The MRL mouse strain is one of the few examples of a mammal capable of healing appendage wounds by regeneration, a process that begins with the formation of a blastema, a structure containing de-differentiating mesenchymal cells. HIF-1α expression in the nascent MRL wound site blastema is one of the earliest identified events and is sufficient to initiate the complete regenerative program. However, HIF-1α regulates many cellular processes modulating the expression of hundreds of genes. A later signal event is the absence of a functional G1 checkpoint, leading to G2 cell cycle arrest with increased cellular DNA but little cell division observed in the blastema. This lack of mitosis in MRL blastema cells is also a hallmark of regeneration in classical invertebrate and vertebrate regenerators such as planaria, hydra, and newt. Results and discussion: Here, we explore the cellular events occurring between HIF-1α upregulation and its regulation of the genes involved in G2 arrest ( EVI-5 , γH3 , Wnt5a , and ROR2 ), and identify epithelial-mesenchymal transition (EMT) (Twist and Slug) and chromatin remodeling (EZH-2 and H3K27me3) as key intermediary processes. The locus of these cellular events is highly regionalized within the blastema, occurring in the same cells as determined by double staining by immunohistochemistry and FACS analysis, and appears as EMT and chromatin remodeling, followed by G2 arrest determined by kinetic expression studies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Bedelbaeva, Cameron, Latella, Aslanukov, Gourevitch, Davuluri and Heber-Katz.)

Published
2023
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46. Integrated Multi-Omic Analysis Reveals Immunosuppressive Phenotype Associated with Poor Outcomes in High-Grade Serous Ovarian Cancer.

Author

Keathley R, Kocherginsky M, Davuluri R, and Matei D

Abstract

High-grade serous ovarian cancer (HGSOC) is characterized by a complex genomic landscape, with both genetic and epigenetic diversity contributing to its pathogenesis, disease course, and response to treatment. To better understand the association between genomic features and response to treatment among 370 patients with newly diagnosed HGSOC, we utilized multi-omic data and semi-biased clustering of HGSOC specimens profiled by TCGA. A Cox regression model was deployed to select model input features based on the influence on disease recurrence. Among the features most significantly correlated with recurrence were the promotor-associated probes for the NFRKB and DPT genes and the TREML1 gene. Using 1467 transcriptomic and methylomic features as input to consensus clustering, we identified four distinct tumor clusters-three of which had noteworthy differences in treatment response and time to disease recurrence. Each cluster had unique divergence in differential analyses and distinctly enriched pathways therein. Differences in predicted stromal and immune cell-type composition were also observed, with an immune-suppressive phenotype specific to one cluster, which associated with short time to disease recurrence. Our model features were additionally used as a neural network input layer to validate the previously defined clusters with high prediction accuracy (91.3%). Overall, our approach highlights an integrated data utilization workflow from tumor-derived samples, which can be used to uncover novel drivers of clinical outcomes.

Published
2023
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47. Deep multi-omics integration by learning correlation-maximizing representation identifies prognostically stratified cancer subtypes.

Author

Ji Y, Dutta P, and Davuluri R

Abstract

Motivation: Molecular subtyping by integrative modeling of multi-omics and clinical data can help the identification of robust and clinically actionable disease subgroups; an essential step in developing precision medicine approaches., Results: We developed a novel outcome-guided molecular subgrouping framework, called Deep Multi-Omics Integrative Subtyping by Maximizing Correlation (DeepMOIS-MC), for integrative learning from multi-omics data by maximizing correlation between all input -omics views. DeepMOIS-MC consists of two parts: clustering and classification. In the clustering part, the preprocessed high-dimensional multi-omics views are input into two-layer fully connected neural networks. The outputs of individual networks are subjected to Generalized Canonical Correlation Analysis loss to learn the shared representation. Next, the learned representation is filtered by a regression model to select features that are related to a covariate clinical variable, for example, a survival/outcome. The filtered features are used for clustering to determine the optimal cluster assignments. In the classification stage, the original feature matrix of one of the -omics view is scaled and discretized based on equal frequency binning, and then subjected to feature selection using RandomForest. Using these selected features, classification models (for example, XGBoost model) are built to predict the molecular subgroups that were identified at clustering stage. We applied DeepMOIS-MC on lung and liver cancers, using TCGA datasets. In comparative analysis, we found that DeepMOIS-MC outperformed traditional approaches in patient stratification. Finally, we validated the robustness and generalizability of the classification models on independent datasets. We anticipate that the DeepMOIS-MC can be adopted to many multi-omics integrative analyses tasks., Availability and Implementation: Source codes for PyTorch implementation of DGCCA and other DeepMOIS-MC modules are available at GitHub (https://github.com/duttaprat/DeepMOIS-MC)., Supplementary Information: Supplementary data are available at Bioinformatics Advances online., Competing Interests: None declared., (© The Author(s) 2023. Published by Oxford University Press.)

Published
2023
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49. Personizing the prediction of future susceptibility to a specific disease.

Author

Taha K, Davuluri R, Yoo P, and Spencer J

Subjects
Biomarkers metabolism, Chemokines, CXC metabolism, Diabetes Mellitus, Type 2 pathology, Humans, Information Storage and Retrieval, Logic, Risk, Algorithms, Disease Susceptibility
Abstract

A traceable biomarker is a member of a disease's molecular pathway. A disease may be associated with several molecular pathways. Each different combination of these molecular pathways, to which detected traceable biomarkers belong, may serve as an indicative of the elicitation of the disease at a different time frame in the future. Based on this notion, we introduce a novel methodology for personalizing an individual's degree of future susceptibility to a specific disease. We implemented the methodology in a working system called Susceptibility Degree to a Disease Predictor (SDDP). For a specific disease d, let S be the set of molecular pathways, to which traceable biomarkers detected from most patients of d belong. For the same disease d, let S' be the set of molecular pathways, to which traceable biomarkers detected from a certain individual belong. SDDP is able to infer the subset S'' ⊆{S-S'} of undetected molecular pathways for the individual. Thus, SDDP can infer undetected molecular pathways of a disease for an individual based on few molecular pathways detected from the individual. SDDP can also help in inferring the combination of molecular pathways in the set {S'+S''}, whose traceable biomarkers collectively is an indicative of the disease. SDDP is composed of the following four components: information extractor, interrelationship between molecular pathways modeler, logic inferencer, and risk indicator. The information extractor takes advantage of the exponential increase of biomedical literature to automatically extract the common traceable biomarkers for a specific disease. The interrelationship between molecular pathways modeler models the hierarchical interrelationships between the molecular pathways of the traceable biomarkers. The logic inferencer transforms the hierarchical interrelationships between the molecular pathways into rule-based specifications. It employs the specification rules and the inference rules for predicate logic to infer as many as possible undetected molecular pathways of a disease for an individual. The risk indicator outputs a risk indicator value that reflects the individual's degree of future susceptibility to the disease. We evaluated SDDP by comparing it experimentally with other methods. Results revealed marked improvement., Competing Interests: The author has declared that no competing interests exist.

Published
2021
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50. Prospective Study of Use of Edmonton Symptom Assessment Scale Versus Routine Symptom Management During Weekly Radiation Treatment Visits.

Author

Goyal UD, Riegert K, Davuluri R, Ong S, Yi SK, Dougherty ST, and Hsu CC

Subjects
Humans, Pain, Prospective Studies, Symptom Assessment, Anxiety diagnosis, Palliative Care
Abstract

Purpose: During radiotherapy (RT), patient symptoms are evaluated and managed weekly during physician on-treatment visits (OTVs). The Edmonton Symptom Assessment Scale (ESAS) is a 9-symptom validated self-assessment tool for reporting common symptoms in patients with cancer. We hypothesized that implementation and physician review of ESAS during weekly OTVs may result in betterment of symptom severity during RT for certain modifiable domains., Methods: As an institutional quality improvement project, patients were partitioned into 2 groups: (1) 85 patients completing weekly ESAS (preintervention) but blinded to their providers who gave routine symptom management and (2) 170 completing weekly ESAS (postintervention group) reviewed by providers during weekly OTVs with possible intervention. To determine the independent association with symptom severity of the intervention, multivariate logistic regression was performed. At study conclusion, provider assessments of ESAS utility were also collected., Results: Compared with the preintervention group, stable or improved symptom severity was seen in the postintervention group for pain (70.7% v 85.6%; P = .005) and anxiety (79.3% v 92.9%; P = .002). The postintervention group had decreased association (on multivariate analysis) with worsening severity of pain (OR, 0.13; P < .001), nausea (OR, 0.25; P = .023), loss of appetite (OR, 0.30; P = .024), and anxiety (OR, 0.19; P = .005). Most physicians (87.5%) and nurses (75%) found ESAS review useful in symptom management., Conclusion: Incorporation of ESAS for OTVs was associated with stable or improved symptom severity where therapeutic intervention is more readily available, such as counseling, pain medication, anti-emetics, appetite stimulants, and anti-anxiolytics. The incorporation of validated patient-reported symptom-scoring tools may improve provider management.

Published
2020
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