Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4 and CDK6

Stable Identifier
R-HSA-9632700
Type
Pathway
Species
Homo sapiens
Locations in the PathwayBrowser
General
SVG |   | PPTX  | SBGN
Click the image above or here to open this pathway in the Pathway Browser

Missense and nonsense mutations in the CDKN2A gene that result in amino acid substitutions in p16INK4A or p16INK4A truncations, respectively, impairing its ability to bind to CDK4 and CDK6, interfere with p16INK4A-mediated induction of cellular senescence in response to oxidative stress (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
Participant Of
Disease
Name Identifier Synonyms
cancer 162 malignant tumor, malignant neoplasm, primary cancer
Authored
Reviewed
Created
Cite Us!