ArticleGenomics, proteomics & bioinformatics2022
Npac Is A Co-factor of Histone H3K36me3 and Regulates Transcriptional Elongation in Mouse Embryonic Stem Cells.
Article in Genomics, proteomics & bioinformatics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Metabolic oxidoreductases: central regulators of the epigenetic landscapes in stemness.Experimental & molecular medicine · 2026Review
- The TDG protein environment connects active DNA demethylation with chromatin and RNA biology.Cellular and molecular life sciences : CMLS · 2025Article
- Nucleosome context regulates chromatin reader preference.Nucleic acids research · 2025Article
- CD320 expression is increased in breast cancer stem cells but does not promote their expansion or alter key histone methylation marks.microPublication biology · 2025Article
- CHD6 eviction of promoter nucleosomes maintains housekeeping transcriptional program in prostate cancer.Molecular therapy. Nucleic acids · 2024Article
- Npac Regulates Pre-mRNA Splicing in Mouse Embryonic Stem Cells.International journal of molecular sciences · 2024Article
- Histone methyltransferase activity affects metabolism in human cells independently of transcriptional regulation.PLoS biology · 2023Article
- Article
- H3K36 trimethylation-mediated biological functions in cancer.Clinical epigenetics · 2021Review
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromatin modification contributes to pluripotency maintenance in embryonic stem cells (ESCs). However, the related mechanisms remain obscure. Here, we show that Npac, a "reader" of histone H3 lysine 36 trimethylation (H3K36me3), is required to maintain mouse ESC (mESC) pluripotency since knockdown of Npac causes mESC differentiation. Depletion of Npac in mouse embryonic fibroblasts (MEFs) inhibits reprogramming efficiency. Furthermore, our chromatin immunoprecipitation followed by sequencing (ChIP-seq) results of Npac reveal that Npac co-localizes with histone H3K36me3 in gene bodies of actively transcribed genes in mESCs. Interestingly, we find that Npac interacts with positive transcription elongation factor b (p-TEFb), Ser2-phosphorylated RNA Pol II (RNA Pol II Ser2P), and Ser5-phosphorylated RNA Pol II (RNA Pol II Ser5P). Furthermore, depletion of Npac disrupts transcriptional elongation of the pluripotency genes Nanog and Rif1. Taken together, we propose that Npac is essential for the transcriptional elongation of pluripotency genes by recruiting p-TEFb and interacting with RNA Pol II Ser2P and Ser5P.
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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 Socratic graph.