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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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Diseases of cellular response to stress (Homo sapiens)
Diseases of Cellular Senescence (Homo sapiens)
Evasion of Oxidative Stress Induced Senescence Due to p16INK4A Defects (Homo sapiens)
Evasion of Oxidative Stress Induced Senescence Due to Defective p16INK4A binding to CDK4 (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
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
Events
p16INK4A mutants do not bind CDK4
(Homo sapiens)
Participates
as an event of
Evasion of Oxidative Stress Induced Senescence Due to p16INK4A Defects (Homo sapiens)
Disease
Name
Identifier
Synonyms
cancer
DOID:162
malignant tumor, malignant neoplasm, primary cancer
Cross References
BioModels Database
BIOMD0000000939
Authored
Orlic-Milacic, M (2018-12-24)
Reviewed
Bennett, DC (2019-04-23)
Hayward, NK (2019-06-03)
Nathan, V (2019-06-03)
Created
Orlic-Milacic, M (2018-12-21)
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