Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms
By A. Satyanarayana, Philipp Kaldis. Oncogene, 2009
802 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/156d0c3eb5ac13e613bc0cc27f58050987f852eb
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Citations in the corpus
- Estrogen receptor β causes a G2 cell cycle arrest by inhibiting CDK1 activity through the regulation of cyclin B1, GADD45A, and BTG2 (2011, background): “The major activator of CDK1 is cyclin B1 [16].”
- WHSC1L1 drives cell cycle progression through transcriptional regulation of CDC6 and CDK2 in squamous cell carcinoma of the head and neck (2016, neutral): “CDK2 is critical for the transition from the G1 to the S phase by binding to cyclin E and promoting the E2F transcriptional program and the initiation of DNA synthesis [12].”
- Partial inhibition of Cdk1 in G2 phase overrides the SAC and decouples mitotic events (2014, background): “During G 2 phase, the levels of cyclin B1 rise rapidly, allowing the formation of cyclin B1/Cdk1 complexes.(1,2) These complexes are held in an inactive state until mitotic entry by 2 inhibitory phosphorylations on Cdk1 (T14 and Y15).”