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Article

CDK4 and CDK6 delay senescence by kinase-dependent and p16INK4a-independent mechanisms.

Molecular and cellular biology - 1 Jun 2007

Ruas Margarida, Gregory Fiona, Jones Rebecca, Poolman Robert, Starborg Maria, Rowe Janice, Brookes Sharon, Peters Gordon

Abstract excerpt

Replicative senescence of human diploid fibroblasts (HDFs) is largely implemented by the cyclin-dependent kinase (CDK) inhibitors p16(INK4a) and p21(CIP1). Their accumulation results in a loss of CDK2 activity, and cells arrest with the retinoblastoma protein (pRb) in its hypophosphorylated state. It has become standard practice to bypass the effects of p16(INK4a) by overexpressing CDK4 or a variant form that is...

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Identifiers

PMID: 17420273
DOI: 10.1128/MCB.02286-06
PMCID: PMC1900050

Genes

CDK4
CDK6
CDK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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