Zobrazeno 1 - 10
of 56
pro vyhledávání: '"Transcription-Coupled DNA Repair"'
Publikováno v:
Frontiers in Cellular Neuroscience, Vol 16 (2022)
Emerging evidence suggests that DNA repair deficiency and genome instability may be the impending signs of many neurological diseases. Genome-wide association (GWAS) studies have established a strong correlation between genes that play a role in DNA
Externí odkaz:
https://doaj.org/article/44b9d8f5c1bd43acbc71f2daeabc54e7
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 3, p 2295 (2023)
Transcription through nucleosomes by RNA polymerases (RNAP) is accompanied by formation of small intranucleosomal DNA loops (i-loops). The i-loops form more efficiently in the presence of single-strand breaks or gaps in a non-template DNA strand (NT-
Externí odkaz:
https://doaj.org/article/1f16f7674e384ceaa67d37c4f6b2d11b
Autor:
Hanawalt, Philip C.
Publikováno v:
Environmental Health Perspectives, 1996 May 01. 104, 547-551.
Externí odkaz:
https://www.jstor.org/stable/3432821
Autor:
Rui Gao, Anirban Chakraborty, Charlene Geater, Subrata Pradhan, Kara L Gordon, Jeffrey Snowden, Subo Yuan, Audrey S Dickey, Sanjeev Choudhary, Tetsuo Ashizawa, Lisa M Ellerby, Albert R La Spada, Leslie M Thompson, Tapas K Hazra, Partha S Sarkar
Publikováno v:
eLife, Vol 8 (2019)
How huntingtin (HTT) triggers neurotoxicity in Huntington’s disease (HD) remains unclear. We report that HTT forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase II subunit A (POLR2A), ataxin-3, the DNA repair enzyme polynucle
Externí odkaz:
https://doaj.org/article/868605a660db461085d000609c271e4b
Akademický článek
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Publikováno v:
Trends in genetics: TIG
Trends in genetics: TIG, 2020, ⟨10.1016/j.tig.2020.08.015⟩
Trends in genetics: TIG, 2020, ⟨10.1016/j.tig.2020.08.015⟩
Dysfunctions of nuclear processes including transcription and DNA repair lead to severe human diseases. Gaining an understanding of how these processes operate in the crowded context of chromatin can be particularly challenging. Mediator is a large m
Autor:
Audrey S. Dickey, Subrata Pradhan, Jeffrey Snowden, Anirban Chakraborty, Kara L Gordon, Subo Yuan, Albert R. La Spada, Tapas K. Hazra, Lisa M. Ellerby, Partha S. Sarkar, Rui Gao, Leslie M. Thompson, Charlene Geater, Sanjeev Choudhary, Tetsuo Ashizawa
Publikováno v:
Gao, Rui; Chakraborty, Anirban; Geater, Charlene; Pradhan, Subrata; Gordon, Kara L; Snowden, Jeffrey; et al.(2019). Mutant huntingtin impairs PNKP and ATXN3, disrupting DNA repair and transcription.. eLife, 8. doi: 10.7554/eLife.42988. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/6qw59090
eLife
eLife, Vol 8 (2019)
eLife
eLife, Vol 8 (2019)
How huntingtin (HTT) triggers neurotoxicity in Huntington’s disease (HD) remains unclear. We report that HTT forms a transcription-coupled DNA repair (TCR) complex with RNA polymerase II subunit A (POLR2A), ataxin-3, the DNA repair enzyme polynucle
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3dbf531576d4518bc76c36a8e79d74df
http://www.escholarship.org/uc/item/6qw59090
http://www.escholarship.org/uc/item/6qw59090
Autor:
Annelieke S. de Wit, Sander Barnhoorn, Mirjam M.C. Wamelink, Renata M. C. Brandt, César Payán-Gómez, Akos Gyenis, Jan H.J. Hoeijmakers, Wilbert P. Vermeij, Pier G. Mastroberardino, André B.P. van Kuilenburg, Donatella Caruso, Sara Sepe, Matteo Audano, René Leen, Roel C. Janssens, Nico Mitro, Cíntia R. Bombardieri, Chiara Milanese, Silvia Pedretti
Publikováno v:
Nature Communications, 10:4887. Nature Publishing Group
Nature Communications
Repositorio EdocUR-U. Rosario
Universidad del Rosario
instacron:Universidad del Rosario
Nature Communications, Vol 10, Iss 1, Pp 1-16 (2019)
Nature communications, 10(1):4887. Nature Publishing Group
Nature Communications, 10(1):4887. Nature Publishing Group
Milanese, C, Bombardieri, C N R, Sepe, S, Barnhoorn, S, Payán-Goméz, C S, Caruso, D, Audano, M, Pedretti, S, Vermeij, W P, Brandt, R M C, Gyenis, A, Wamelink, M M, de Wit, A S, Janssens, R C, Leen, R, van Kuilenburg, A B P, Mitro, N, Hoeijmakers, J H J & Mastroberardino, P G 2019, ' DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering ', Nature Communications, vol. 10, no. 1, 4887 . https://doi.org/10.1038/s41467-019-12640-5
Nature Communications
Repositorio EdocUR-U. Rosario
Universidad del Rosario
instacron:Universidad del Rosario
Nature Communications, Vol 10, Iss 1, Pp 1-16 (2019)
Nature communications, 10(1):4887. Nature Publishing Group
Nature Communications, 10(1):4887. Nature Publishing Group
Milanese, C, Bombardieri, C N R, Sepe, S, Barnhoorn, S, Payán-Goméz, C S, Caruso, D, Audano, M, Pedretti, S, Vermeij, W P, Brandt, R M C, Gyenis, A, Wamelink, M M, de Wit, A S, Janssens, R C, Leen, R, van Kuilenburg, A B P, Mitro, N, Hoeijmakers, J H J & Mastroberardino, P G 2019, ' DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering ', Nature Communications, vol. 10, no. 1, 4887 . https://doi.org/10.1038/s41467-019-12640-5
Accumulation of DNA lesions causing transcription stress is associated with natural and accelerated aging and culminates with profound metabolic alterations. Our understanding of the mechanisms governing metabolic redesign upon genomic instability, h
Akademický článek
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Publikováno v:
Molecular Biology and Evolution
Molecular Biology and Evolution, Oxford University Press (OUP), 2017, 34 (7), pp.1770-1779. ⟨10.1093/molbev/msx119⟩
Molecular Biology and Evolution, 2017, 34 (7), pp.1770-1779. ⟨10.1093/molbev/msx119⟩
Molecular Biology and Evolution, Oxford University Press (OUP), 2017, 34 (7), pp.1770-1779. ⟨10.1093/molbev/msx119⟩
Molecular Biology and Evolution, 2017, 34 (7), pp.1770-1779. ⟨10.1093/molbev/msx119⟩
International audience; Mutation is the ultimate source of genetic variation, and knowledge of mutation rates is fundamental for our understanding of all evolutionary processes. High throughput sequencing of mutation accumulation lines has provided g
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::8bd5d1233906654fce3fb74c64c06662
https://hal.sorbonne-universite.fr/hal-01546014
https://hal.sorbonne-universite.fr/hal-01546014