ArticleCell discovery2015
The PRC2-associated factor C17orf96 is a novel CpG island regulator in mouse ES cells.
Article in Cell discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Convergence of aging- and rejuvenation-related epigenetic alterations on PRC2 targets.Molecular systems biology · 2026Article
- EPOP and MTF2 activate PRC2 activity through DNA-sequence specificity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization.Nature communications · 2026Article
- Auto-inhibition of PRC2 by the broadly expressed long isoform of AEBP2.The EMBO journal · 2025Article
- Crosstalk within and beyond the Polycomb repressive system.The Journal of cell biology · 2024Review
- The role of histone post-translational modifications in cancer and cancer immunity: functions, mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- PALI1 promotes tumor growth through competitive recruitment of PRC2 to G9A-target chromatin for dual epigenetic silencing.Molecular cell · 2022Article
- Review
- Evolutionary adaptation of the Polycomb repressive complex 2.Epigenetics & chromatin · 2022Review
- Polycomb Gene Silencing Mechanisms: PRC2 Chromatin Targeting, H3K27me3 'Readout', and Phase Separation-Based Compaction.Trends in genetics : TIG · 2021Review
- A Structural Perspective on Gene Repression by Polycomb Repressive Complex 2.Sub-cellular biochemistry · 2021Review
- No Easy Way Out for EZH2: Its Pleiotropic, Noncanonical Effects on Gene Regulation and Cellular Function.International journal of molecular sciences · 2020Review
- Post-translational modifications of PRC2: signals directing its activity.Epigenetics & chromatin · 2020Review
- Dynamic Competition of Polycomb and Trithorax in Transcriptional Programming.Annual review of biochemistry · 2020Review
- A Dimeric Structural Scaffold for PRC2-PCL Targeting to CpG Island Chromatin.Molecular cell · 2020Article
- Non-core Subunits of the PRC2 Complex Are Collectively Required for Its Target-Site Specificity.Molecular cell · 2019Article
- PRC2 is high maintenance.Genes & development · 2019Review
- Molecular Mechanisms Directing PRC2 Recruitment and H3K27 Methylation.Molecular cell · 2019Review
- Unique Structural Platforms of Suz12 Dictate Distinct Classes of PRC2 for Chromatin Binding.Molecular cell · 2018Article
- Polycomb Repressive Complex 2 Methylates Elongin A to Regulate Transcription.Molecular cell · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CpG islands (CGIs) are key DNA regulatory elements in the vertebrate genome and are often found at gene promoters. In mammalian embryonic stem (ES) cells, CGIs are decorated by either the active or repressive histone marks, H3K4me3 and H3K27me3, respectively, or by both modifications ('bivalent domains'), but their precise regulation is incompletely understood. Remarkably, we find that the polycomb repressive complex 2 (PRC2)-associated protein C17orf96 (a.k.a. esPRC2p48 and E130012A19Rik) is present at most CGIs in mouse ES cells. At PRC2-rich CGIs, loss of C17orf96 results in an increased chromatin binding of Suz12 and elevated H3K27me3 levels concomitant with gene repression. In contrast, at PRC2-poor CGIs, located at actively transcribed genes, C17orf96 colocalizes with RNA polymerase II and its depletion leads to a focusing of H3K4me3 in the core of CGIs. Our findings thus identify C17orf96 as a novel context-dependent CGI regulator.
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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.