Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4

Stable Identifier
R-HSA-9632697
Type
Pathway
Species
Homo sapiens
ReviewStatus
5/5
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Missense mutations and small indels in the CDKN2A gene, which result in amino acid changes in p16INK4A that impair its ability to bind to CDK4, interfere with p16INK4A-mediated, oxidative stress-induced, cellular senescence (Chen 2000, Vurusaner et al. 2012).
Loss-of-function mutations in p16INK4A can also contribute to cancer by interfering with p16INK4A-mediated inhibition of NFKB signaling (Becker et al. 2005).
Literature References
PubMed ID Title Journal Year
10911952 Replicative senescence and oxidant-induced premature senescence. Beyond the control of cell cycle checkpoints

Chen, QM

Ann. N. Y. Acad. Sci. 2000
22019631 Tumor suppressor genes and ROS: complex networks of interactions

Poli, G, Vurusaner, B, Basaga, H

Free Radic. Biol. Med. 2012
Participants
Participates
Disease
Name Identifier Synonyms
cancer DOID:162 malignant tumor, malignant neoplasm, primary cancer
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