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

Stable Identifier
R-HSA-9632697
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Pathway
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Homo sapiens
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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
22019631 Tumor suppressor genes and ROS: complex networks of interactions

Vurusaner, B, Poli, G, Basaga, H

Free Radic. Biol. Med. 2012
10911952 Replicative senescence and oxidant-induced premature senescence. Beyond the control of cell cycle checkpoints

Chen, QM

Ann. N. Y. Acad. Sci. 2000
Participants
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Disease
Name Identifier Synonyms
cancer 162 malignant tumor, malignant neoplasm, primary cancer
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