ArticleNature communications2022
Unveiling RCOR1 as a rheostat at transcriptionally permissive chromatin.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- CoREST complex inhibition alters RNA splicing to promote neoantigen expression and enhance tumor immunity.JCI insight · 2026Article
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- Uncoupling histone modification crosstalk by engineering lysine demethylase LSD1.Nature chemical biology · 2025Article
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- An autoinhibitory switch of the LSD1 disordered region controls enhancer silencing.Molecular cell · 2024Article
- Targeting intracellular proteins with cell type-specific functions for cancer immunotherapy.Life medicine · 2023Review
- Establishing a prediction model of severe acute mountain sickness using machine learning of support vector machine recursive feature elimination.Scientific reports · 2023Article
- The H2A.Z and NuRD associated protein HMG20A controls early head and heart developmental transcription programs.Nature communications · 2023Article
- Nuclear Coregulatory Complexes in Tregs as Targets to Promote Anticancer Immune Responses.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
RCOR1 is a known transcription repressor that recruits and positions LSD1 and HDAC1/2 on chromatin to erase histone methylation and acetylation. However, there is currently an incomplete understanding of RCOR1's range of localization and function. Here, we probe RCOR1's distribution on a genome-wide scale and unexpectedly find that RCOR1 is predominantly associated with transcriptionally active genes. Biochemical analysis reveals that RCOR1 associates with RNA Polymerase II (POL-II) during transcription and deacetylates its carboxy-terminal domain (CTD) at lysine 7. We provide evidence that this non-canonical RCOR1 activity is linked to dampening of POL-II productive elongation at actively transcribing genes. Thus, RCOR1 represses transcription in two ways-first, via a canonical mechanism by erasing transcriptionally permissive histone modifications through associating with HDACs and, second, via a non-canonical mechanism that deacetylates RNA POL-II's CTD to inhibit productive elongation. We conclude that RCOR1 is a transcription rheostat.
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Registered trials
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