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204 results on '"Rice, Judd C"'

3. Bent bone dysplasia syndrome reveals nucleolar activity for FGFR2 in ribosomal DNA transcription

Author

Neben, Cynthia L, Idoni, Brian, Salva, Joanna E, Tuzon, Creighton T, Rice, Judd C, Krakow, Deborah, and Merrill, Amy E

Subjects
Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Dental/Oral and Craniofacial Disease, Biotechnology, Genetics, Underpinning research, 1.1 Normal biological development and functioning, Acrocephalosyndactylia, Animals, Binding Sites, Cell Differentiation, Cell Line, Cell Nucleus, Core Binding Factor Alpha 1 Subunit, DNA, Ribosomal, Fibroblast Growth Factor 2, Gene Expression Regulation, Humans, MAP Kinase Signaling System, Mice, Mutation, Osteoblasts, Pol1 Transcription Initiation Complex Proteins, Protein Binding, Protein Transport, Receptor, Fibroblast Growth Factor, Type 2, Repetitive Sequences, Nucleic Acid, Transcription, Genetic, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Fibroblast growth factor receptor 2 (FGFR2) promotes osteoprogenitor proliferation and differentiation during bone development, yet how the receptor elicits these distinct cellular responses remains unclear. Analysis of the FGFR2-skeletal disorder bent bone dysplasia syndrome (BBDS) demonstrates that FGFR2, in addition to its canonical signaling activities at the plasma membrane, regulates bone formation from within the nucleolus. Previously, we showed that the unique FGFR2 mutations that cause BBDS reduce receptor levels at the plasma membrane and diminish responsiveness to extracellular FGF2. In this study, we find that these mutations, despite reducing canonical signaling, enhance nucleolar occupancy of FGFR2 at the ribosomal DNA (rDNA) promoter. Nucleolar FGFR2 activates rDNA transcription via interactions with FGF2 and UBF1 by de-repressing RUNX2. An increase in the nucleolar activity of FGFR2 in BBDS elevates levels of ribosomal RNA in the developing bone, consequently promoting osteoprogenitor cell proliferation and decreasing differentiation. Identifying FGFR2 as a transcriptional regulator of rDNA in bone unexpectedly reveals a nucleolar route for FGF signaling that allows for independent regulation of osteoprogenitor cell proliferation and differentiation.

Published
2014

4. Concerted activities of distinct H4K20 methyltransferases at DNA double-strand breaks regulate 53BP1 nucleation and NHEJ-directed repair.

Author

Tuzon, Creighton T, Spektor, Tanya, Kong, Xiaodong, Congdon, Lauren M, Wu, Shumin, Schotta, Gunnar, Yokomori, Kyoko, and Rice, Judd C

Subjects
Hela Cells, Cell Nucleus, Humans, Histone-Lysine N-Methyltransferase, Intracellular Signaling Peptides and Proteins, Protein Binding, Active Transport, Cell Nucleus, DNA Breaks, Double-Stranded, HEK293 Cells, DNA End-Joining Repair, Tumor Suppressor p53-Binding Protein 1, HeLa Cells, Active Transport, DNA Breaks, Double-Stranded, Biochemistry and Cell Biology, Medical Physiology
Abstract

Although selective binding of 53BP1 to dimethylated histone H4 lysine 20 (H4K20me2) at DNA double-strand breaks (DSBs) is a necessary and pivotal determinant of nonhomologous end joining (NHEJ)-directed repair, the enzymes that generate H4K20me2 at DSBs were unclear. Here, we determined that the PR-Set7 monomethyltransferase (H4K20me1) regulates de novo H4K20 methylation at DSBs. Rapid recruitment of PR-Set7 to DSBs was dependent on the NHEJ Ku70 protein and necessary for NHEJ-directed repair. PR-Set7 monomethyltransferase activity was required, but insufficient, for H4K20me2 and 53BP1 nucleation at DSBs. We determined that PR-Set7-mediated H4K20me1 facilitates Suv4-20 methyltransferase recruitment and catalysis to generate H4K20me2 necessary for 53BP1 binding. The orchestrated and concerted activities of PR-Set7 and Suv4-20 were required for proficient 53BP1 nucleation and DSB repair. This report identifies PR-Set7 as an essential component of NHEJ and implicates PR-Set7 as a central determinant of NHEJ-directed repair early in mammalian DSB repair pathway choice.

Published
2014

10. Exercise does not influence myostatin and follustatin messenger RNA expression in young women

Author

Jensky, Nicole E., Sims, Jennifer K., Dieli-Conwright, Christina M., Sattler, Fred R., Rice, Judd C., and Schroeder, E. Todd

Subjects
Exercise -- Physiological aspects, Young women -- Genetic aspects, Young women -- Physiological aspects, Messenger RNA -- Research, Health, Sports and fitness
Abstract

We evaluated changes in myostatin, follistatin, and MyoD messenger RNA (mRNA) gene expression using eccentric exercise (EE) and concentric exercise (CE) as probes to better understand the mechanisms of muscle hypertrophy in young women. Twelve women performed single-leg maximal eccentric (n = 6, 25 [+ or -] 1 years, 59 [+ or -] 7 kg) or concentric (n = 6, 24 [+ or -] 1 years, 65 [+ or -] 7 kg) isokinetic knee extension exercise for 7 sessions. Muscle biopsies were taken from the vastus lateralis at baseline, 8 hours after the first exercise session, and 8 hours after the seventh exercise session. In the EE group, there were no changes in myostatin and follistatin (p [greater than or equal to] 0.17); however, MyoD expression increased after 1 exercise bout (p = 0.02). In the CE group, there were no changes in myostatin, follistatin, or MyoD mRNA gene expression (p [greater than or equal to] 0.07). Differences between the EE and CE groups were not significant (p [greater than or equal to] 0.05). These data suggest that a single bout or multiple bouts of maximal EE or CE may not significantly alter myostatin or follistatin mRNA gene expression in young women. However, MyoD mRNA expression seems to increase only after EE. KEY WORDS eccentric, concentric, MyoD, resistance training, hypertrophy

Published
2010

11. Identification and characterization of functional risk variants for colorectal cancer mapping to chromosome 11q23.1

Author

Biancolella, Michela, Fortini, Barbara K., Tring, Stephanie, Plummer, Sarah J., Mendoza-Fandino, Gustavo A., Hartiala, Jaana, Hitchler, Michael J., Yan, Chunli, Schumacher, Fredrick R., Conti, David V., Edlund, Christopher K., Noushmehr, Houtan, Coetzee, Simon G., Bresalier, Robert S., Ahnen, Dennis J., Barry, Elizabeth L., Berman, Benjamin P., Rice, Judd C., Coetzee, Gerhard A., and Casey, Graham

Published
2014
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18. Mitotic-specific methylation of histone H4 Lys 20 follows increased PR-Set7 expression and its localization to mitotic chromosomes

Author

Rice, Judd C., Nishioka, Kenichi, Sarma, Kavitha, Steward, Ruth, Reinberg, Danny, and Allis, C. David

Subjects
Genetic research -- Analysis, Chromosomes -- Genetic aspects, Mitosis -- Genetic aspects, Gene expression -- Physiological aspects, Methylation -- Physiological aspects, Histones -- Genetic aspects, Cell cycle -- Genetic aspects, Methyltransferases -- Genetic aspects, Biological sciences
Abstract

Research has been conducted on histone methylation. The patterns of this methylation studied during human cell cycle progression are discussed and the results indicate that histone H4 methyltransferase activity is cell cycle-regulated.

Published
2002

19. Gene regulation: Code of silence

Author

Rice, Judd C. and Allis, C. David

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Judd C. Rice [1]; C. David Allis (corresponding author) [1] Every cell in your body contains the same genetic material. Yet your cells are not physically identical, in part [...]

Published
2001
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33. The SUV4-20 inhibitor A-196 verifies a role for epigenetics in genomic integrity

Author

Bromberg, Kenneth D, primary, Mitchell, Taylor R H, additional, Upadhyay, Anup K, additional, Jakob, Clarissa G, additional, Jhala, Manisha A, additional, Comess, Kenneth M, additional, Lasko, Loren M, additional, Li, Conglei, additional, Tuzon, Creighton T, additional, Dai, Yujia, additional, Li, Fengling, additional, Eram, Mohammad S, additional, Nuber, Alexander, additional, Soni, Niru B, additional, Manaves, Vlasios, additional, Algire, Mikkel A, additional, Sweis, Ramzi F, additional, Torrent, Maricel, additional, Schotta, Gunnar, additional, Sun, Chaohong, additional, Michaelides, Michael R, additional, Shoemaker, Alex R, additional, Arrowsmith, Cheryl H, additional, Brown, Peter J, additional, Santhakumar, Vijayaratnam, additional, Martin, Alberto, additional, Rice, Judd C, additional, Chiang, Gary G, additional, Vedadi, Masoud, additional, Barsyte-Lovejoy, Dalia, additional, and Pappano, William N, additional

Published
2017
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41. Identification and characterization of functional risk variants for colorectal cancer mapping to chromosome 11q23.1

Author

Biancolella, Michela, primary, Fortini, Barbara K., additional, Tring, Stephanie, additional, Plummer, Sarah J., additional, Mendoza-Fandino, Gustavo A., additional, Hartiala, Jaana, additional, Hitchler, Michael J., additional, Yan, Chunli, additional, Schumacher, Fredrick R., additional, Conti, David V., additional, Edlund, Christopher K., additional, Noushmehr, Houtan, additional, Coetzee, Simon G., additional, Bresalier, Robert S., additional, Ahnen, Dennis J., additional, Barry, Elizabeth L., additional, Berman, Benjamin P., additional, Rice, Judd C., additional, Coetzee, Gerhard A., additional, and Casey, Graham, additional

Published
2013
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