ArticleGenes & development2005
BRCA1/BARD1 inhibition of mRNA 3' processing involves targeted degradation of RNA polymerase II.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 151 citations in OpenAlex.
- K63-linked ubiquitylation of S2P-RNAPII regulates transcription in a DNAPK inter-dependent manner in response to double-strand breaks.Nucleic acids research · 2026Article
- Review
- Distinct mechanisms of recognition of phosphorylated RNAPII C-terminal domain by BRCT repeats of the BRCA1-BARD1 complex.The Journal of biological chemistry · 2026Article
- Regulation of RNA Polymerase I Stability and Function.Cancers · 2022Review
- DNA damage-induced transcription stress triggers the genome-wide degradation of promoter-bound Pol II.Nature communications · 2022Article
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- The Bidirectional Link Between RNA Cleavage and Polyadenylation and Genome Stability: Recent Insights From a Systematic Screen.Frontiers in genetics · 2022Review
- The BRCA1/BARD1 ubiquitin ligase and its substrates.The Biochemical journal · 2021Review
- Timely upstream events regulating nucleotide excision repair by ubiquitin-proteasome system: ubiquitin guides the way.DNA repair · 2021Review
- Article
- BRCA1-BARD1 regulates transcription through BRD4 in Xenopus nucleoplasmic extract.Nucleic acids research · 2021Article
- BRCA1-BARD1 Regulates Axon Regeneration in Concert with the Gqα-DAG Signaling Network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Review
- Review
- The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication.Nature reviews. Molecular cell biology · 2020Review
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- ISOGO: Functional annotation of protein-coding splice variants.Scientific reports · 2020Article
- XAB2 depletion induces intron retention in POLR2A to impair global transcription and promote cellular senescence.Nucleic acids research · 2019Article
- Regulating BRCA1 protein stability by cathepsin S-mediated ubiquitin degradation.Cell death and differentiation · 2019Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Mammalian cells exhibit a complex response to DNA damage. The tumor suppressor BRCA1 and associated protein BARD1 are thought to play an important role in this response, and our previous work demonstrated that this includes transient inhibition of the pre-mRNA 3' processing machinery. Here we provide evidence that this inhibition involves proteasomal degradation of a component necessary for processing, RNA polymerase II (RNAP II). We further show that RNAP IIO, the elongating form of the enzyme, is a specific in vitro target of the BRCA1/BARD1 ubiquitin ligase activity. Significantly, siRNA-mediated knockdown of BRCA1 and BARD1 resulted in stabilization of RNAP II after DNA damage. In addition, inhibition of 3' cleavage induced by DNA damage was reverted in extracts of BRCA1-, BARD1-, or BRCA1/BARD1-depleted cells. We also describe corresponding changes in the nuclear localization and/or accumulation of these factors following DNA damage. Our results support a model in which a BRCA1/BARD1-containing complex functions to initiate degradation of stalled RNAP IIO, inhibiting the coupled transcription-RNA processing machinery and facilitating repair.
Indexed as
Identifiers
What OpenQuestion holds
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.