ArticleInternational journal of molecular sciences2025
NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Protocol for generating endogenous degron tags in essential transcription factors in human iPSCs via CRISPR-Cas9.STAR protocols · 2026Article
- GLYR1-mediated downregulation of lncRNA HSD11B1-AS1 promotes proliferation, migration, and invasion of breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Phase-separated NDF-FACT condensates facilitate transcription elongation on chromatin.Nature cell biology · 2025Article
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Authors and funding
2 authors.
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Abstract
The Nucleosome Destabilizing Factor (NDF) facilitates transcription through chromatin, but its precise mechanism remains incompletely understood. Here, we identify a critical region (amino acids 140-160) within NDF that specifically interacts with phosphorylated RPB1, the largest subunit of elongating RNA Polymerase II (Pol II). Mutations in this region disrupt Pol II interaction and impair Pol II elongation both in vitro and in cells, yet do not affect NDF's ability to destabilize nucleosomes, establishing a functional separation between these two activities. Cellular studies reveal that NDF knockout cells display faster Pol II elongation rates but produce fewer nascent transcripts, demonstrating NDF's primary role in maintaining transcriptional processivity throughout gene bodies. Our findings demonstrate that NDF uses distinct mechanisms to ensure productive transcription elongation rather than simply enhancing elongation speed, offering new insights into how transcription efficiency is maintained in chromatin.
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