Journal ArticleDOI
Regulation of p53 downstream genes.
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TLDR
The p53 tumor suppressor is the most commonly mutated gene in human cancer and its activation of expression of a number of target genes including p21WAFI, GADD45, 14-3-3 sigma, bax, Fas/APO1, KILLER/DR5, PIG3, Tsp1, IGF-BP3 and others are reviewed.About:
This article is published in Seminars in Cancer Biology.The article was published on 1998-01-01. It has received 821 citations till now. The article focuses on the topics: Tumor suppressor gene & Regulation of gene expression.read more
Citations
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Surfing the p53 network
TL;DR: The p53 tumour-suppressor gene integrates numerous signals that control cell life and death, and the disruption of p53 has severe consequences when a highly connected node in the Internet breaks down.
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Blinded by the Light: The Growing Complexity of p53
Karen H. Vousden,Carol Prives +1 more
TL;DR: Control of p53's transcriptional activity is crucial for determining which p53 response is activated, a decision that must be understood if the next generation of drugs that selectively activate or inhibit p53 are to be exploited efficiently.
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PUMA, a novel proapoptotic gene, is induced by p53.
TL;DR: A novel gene named PUMA (p53 upregulated modulator of apoptosis) is identified as a target for activation by p53, and PUMA is likely to play a role in mediating p53-induced cell death through the cytochrome c/Apaf-1-dependent pathway.
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PUMA induces the rapid apoptosis of colorectal cancer cells.
TL;DR: Through global profiling of genes that were expressed soon after p53 expression, a novel gene termed PUMA (p53 upregulated modulator of apoptosis) was identified and it was found to be exclusively mitochondrial and to bind to Bcl-2 and Bcl(L) through a BH3 domain.
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Post-translational modifications and activation of p53 by genotoxic stresses
Ettore Appella,Carl W. Anderson +1 more
TL;DR: It is suggested that N-terminal phosphorylations are important for stabilizing p53 and are crucial for acetylation of C- terminal sites, which in combination lead to the full p53-mediated response to genotoxic stresses.
References
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Journal ArticleDOI
WAF1, a potential mediator of p53 tumor suppression
Wafik S. El-Deiry,Takashi Tokino,Victor E. Velculescu,Daniel B. Levy,Ramon Parsons,Jeffrey M. Trent,D Lin,W. Edward Mercer,Kenneth W. Kinzler,Bert Vogelstein +9 more
TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
TL;DR: Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line and counters the death repressor activity of B cl-2, suggesting a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.
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Death receptors: signaling and modulation
Avi Ashkenazi,Vishva M. Dixit +1 more
TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
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Apoptosis by death factor.
TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
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Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
Jie Yang,Xuesong Liu,Xuesong Liu,Kapil N. Bhalla,Caryn Naekyung Kim,Ana Maria Ibrado,Jiyang Cai,Tsung I. Peng,Dean P. Jones,Xiaodong Wang,Xiaodong Wang +10 more
TL;DR: One possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria, which is normally located in the mitochondrial intermembrane space.