EMBO RepJClub
CDK4 maintains cytoskeletal homeostasis by restraining actomyosin contractility.
EMBO Reports · · Journal Article · Open access
Parashar, Geller + more
Abstract ↗AI summary
The abstract is read at the publisher; the summary is JClub's.
CDK4 maintains cytoskeletal mechanical homeostasis in triple-negative breast cancer cells by phosphorylating Myo9b at serine 1935 to restrain actomyosin contractility.
- Why it matters: How CDK4 activity intersects with cellular architecture is unclear, despite evidence that cytoskeletal mechanics shape tumor cell structure and stability.
- What they did: CDK4 phosphorylates Myo9b at serine 1935, boosting its GAP activity to limit the RhoA–ROCK–pMLC pathway; CDK4 loss or inhibition disrupts actin organization and increases contractility.
- The result: Increased contractility in CDK4-deficient TNBC cells collapses the intermediate filament network, with Vimentin reorganization and mitochondrial redistribution, and CDK4 expression negatively correlates with pMLC in mouse tumors and human breast cancer samples.
The findingWhy it mattersWhat they didThe result
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- 1 cites