Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling
Article Abstract:
Oncogenic Ras puts immortal rodent cells into a tumorigenic state. It does so partly by transmitting mitogenic signals constitutively through the mitogen-activated protein kinase (MAPK) cascade. MEK is a component of the MAPK cascade. Premature senescence related to p16 and p53 is brought on as a response to constitutive mitogenic signaling of MEK/MAPK. Constitutive MAPK signaling activates p16 and p53 as tumor suppressors. It seems premature senescence acts as a fail-safe to limit transforming potential of too much Ras mitogenic signaling. Activated MEK stops primary murine fibroblasts permanently, but bring uncontrolled mitogenesis and transformation to cells without either p53 (ital) of INK4a (ital).
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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p63 deficiency activates a program of cellular senescence and leads to accelerated aging
Article Abstract:
A study is conducted on two mouse models in which p63 protein is compromised to demonstrate that cellular senescence and organismal aging are intimately linked. The results show that p63 deficiency induces cellular senescence and causes accelerated aging phenotypes in the adults.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2005
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The p400 E1A-associated protein is a novel component of the p53 --> p21 senescence pathway
Article Abstract:
Adenovirus E1A-associated p400 belongs to the SW12/SNF2 family of chromatin remodeling proteins. It is reported that p400 is a component of the p53-p21(super WAF1/CIP1/sid1) pathway, regulating the p21 transcription and senescence induction program.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2005
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