Targeting CDK4 and CDK6: From Discovery to Therapy.
London, United Kingdom. In Cancer Discov, Jan 2016
UNASSIGNED: Biochemical and genetic characterization of D-type cyclins, their cyclin D-dependent kinases (CDK4 and CDK6), and the polypeptide CDK4/6 inhibitor p16(INK4) over two decades ago revealed how mammalian cells regulate entry into the DNA synthetic (S) phase of the cell-division cycle in a retinoblastoma protein-dependent manner.
Roscovitine in cancer and other diseases.
Genève, Switzerland. In Ann Transl Med, Jun 2015
It is a broad-range purine inhibitor, which inhibits CDK1, CDK2, CDK5 and CDK7, but is a poor inhibitor for CDK4 and CDK6.
The history and future of targeting cyclin-dependent kinases in cancer therapy.
Dallas, United States. In Nat Rev Drug Discov, Feb 2015
In particular, cyclin-dependent kinases (CDKs) that promote transition through the cell cycle were expected to be key therapeutic targets because many tumorigenic events ultimately drive proliferation by impinging on CDK4 or CDK6 complexes in the G1 phase of the cell cycle.
Genetic screens in human cells using the CRISPR-Cas9 system.
Cambridge, United States. In Science, 2014
A screen for resistance to the nucleotide analog 6-thioguanine identified all expected members of the DNA mismatch repair pathway, whereas another for the DNA topoisomerase II (TOP2A) poison etoposide identified TOP2A, as expected, and also cyclin-dependent kinase 6, CDK6.