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TFIIH kinase CDK7 drives cell proliferation through a common core transcription factor network

GSE262536 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/12/19 Platform GPL16791
Summary
We combined cryo-EM, transcriptomics, and a clinically relevant inhibitor to define how the TFIIH-associated CDK7 kinase coordinately controls the cell cycle and RNA polymerase II (RNAPII) transcription. CDK7 inhibition rapidly blocked expression of constitutively active genes, whereas inducible genes were unaffected. Distinct sets of sequence-specific, DNA-binding transcription factors (TFs) regulate constitutive vs. inducible genes; accordingly, inducible TFs (e.g. HSF1) were refractory to CDK7 inhibition. By contrast, CDK7 was required to maintain activity of a core set of promoter-associated TFs that drive proliferative gene expression programs; these core TFs (n=78) are constitutively active in proliferating cells. Thus, a major biological function for CDK7 is regulation of TFs that drive cell proliferation, revealing an apparent universal mechanism by which CDK7 coordinates RNAPII transcription with cell cycle regulation.
Published in
Multi-omics and biochemical reconstitution reveal CDK7-dependent mechanisms controlling RNA polymerase II function at gene 5'- and 3'-ends
Luyties O, Sanford L, Rodino J et al. · bioRxiv : the preprint server for biology 2025 · PMID 39829884 · doi:10.1101/2025.01.08.632016
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Also filed as BioProject PRJNA1092248 and SRA study SRP497979. Searching any of these in the dataset finder brings you back here.

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