ArticleMolecular and cellular biology2004
BRCA1 can modulate RNA polymerase II carboxy-terminal domain phosphorylation levels.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- BRCA1 mutations in high-grade serous ovarian cancer are associated with proteomic changes in DNA repair, splicing, transcription regulation and signaling.Scientific reports · 2022Article
- Trans-activation-based risk assessment of BRCA1 BRCT variants with unknown clinical significance.Human genomics · 2018Article
- Genome-wide analysis reveals a role for BRCA1 and PALB2 in transcriptional co-activation.The EMBO journal · 2014Article
- BRCA1 and Oxidative Stress.Cancers · 2014Article
- Rrd1 isomerizes RNA polymerase II in response to rapamycin.BMC molecular biology · 2010Article
- The ubiquitin-proteasome system in cancer, a major player in DNA repair. Part 2: transcriptional regulation.Journal of cellular and molecular medicine · 2009Review
- Human U2 snRNA genes exhibit a persistently open transcriptional state and promoter disassembly at metaphase.Molecular and cellular biology · 2008Article
- Corepressor CtBP and nuclear speckle protein Pnn/DRS differentially modulate transcription and splicing of the E-cadherin gene.Molecular and cellular biology · 2008Article
- Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.PloS one · 2008Article
- Review
- Cellular splicing and transcription regulatory protein p32 represses adenovirus major late transcription and causes hyperphosphorylation of RNA polymerase II.Journal of virology · 2006Article
- Tax interacts with P-TEFb in a novel manner to stimulate human T-lymphotropic virus type 1 transcription.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A high incidence of breast and ovarian cancers has been linked to mutations in the BRCA1 gene. BRCA1 has been shown to be involved in both positive and negative regulation of gene activity as well as in numerous other processes such as DNA repair and cell cycle regulation. Since modulation of the RNA polymerase II carboxy-terminal domain (CTD) phosphorylation levels could constitute an interface to all these functions, we wanted to directly test the possibility that BRCA1 might regulate the phosphorylation state of the CTD. We have shown that the BRCA1 C-terminal region can negatively modulate phosphorylation levels of the RNA polymerase II CTD by the Cdk-activating kinase (CAK) in vitro. Interestingly, the BRCA1 C-terminal region can directly interact with CAK and inhibit CAK activity by competing with ATP. Finally, we demonstrated that full-length BRCA1 can inhibit CTD phosphorylation when introduced in the BRCA1(-/-) HCC1937 cell line. Our results suggest that BRCA1 could play its ascribed roles, at least in part, by modulating CTD kinase components.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.