Mutant p53 gain of function: repression of CD95(Fas/APO-1) gene expression by tumor-associated p53 mutants (Q73876727)

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7 November 2019

title

Mutant p53 gain of function: repression of CD95(Fas/APO-1) gene expression by tumor-associated p53 mutants (English)

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7 November 2019

8

Varda Rotter

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7 November 2019

author name string

Amir Zalcenstein

1

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7 November 2019

Perry Stambolsky

2

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7 November 2019

Lilach Weisz

3

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7 November 2019

Martina Müller

4

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7 November 2019

David Wallach

5

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7 November 2019

Tanya M Goncharov

6

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7 November 2019

Peter H Krammer

7

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7 November 2019

Moshe Oren

9

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7 November 2019

language of work or name

English

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publication date

1 August 2003

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7 November 2019

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7 November 2019

volume

22

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7 November 2019

page(s)

5667-5676

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7 November 2019

issue

36

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1206724

7 November 2019

exact match

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Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy

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Alterations of Fas (APO-1/CD 95) gene and its relationship with p53 in non small cell lung cancer

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p73 function is inhibited by tumor-derived p53 mutants in mammalian cells.

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Fas is involved in the p53-dependent apoptotic response to ionizing radiation in mouse testis

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Activation of c-myc gene expression by tumor-derived p53 mutants requires a discrete C-terminal domain

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Involvement of the CD95 (APO–1/Fas) receptor/ligand system in drug–induced apoptosis in leukemia cells

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A subset of tumor-derived mutant forms of p53 down-regulate p63 and p73 through a direct interaction with the p53 core domain

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7 January 2021

An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control

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Different tumor-derived p53 mutants exhibit distinct biological activities

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The Rb/E2F pathway: expanding roles and emerging paradigms

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Role for the p53 homologue p73 in E2F-1-induced apoptosis

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Mutant p53 protein expression interferes with p53-independent apoptotic pathways.

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Several hydrophobic amino acids in the p53 amino-terminal domain are required for transcriptional activation, binding to mdm-2 and the adenovirus 5 E1B 55-kD protein

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High metastatic potential in mice inheriting a targeted p53 missense mutation

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A mutant p53 antagonizes the deregulated c-myc-mediated enhancement of apoptosis and decrease in leukemogenicity

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A common polymorphism acts as an intragenic modifier of mutant p53 behaviour

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Integrity of the N-terminal transcription domain of p53 is required for mutant p53 interference with drug-induced apoptosis

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The p53 and Mdm2 families in cancer.

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p53 mutations: gains or losses?

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Drug-induced apoptosis in hepatoma cells is mediated by the CD95 (APO-1/Fas) receptor/ligand system and involves activation of wild-type p53.

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7 January 2021

p53 activates the CD95 (APO-1/Fas) gene in response to DNA damage by anticancer drugs

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Human and mouse Fas (APO-1/CD95) death receptor genes each contain a p53-responsive element that is activated by p53 mutants unable to induce apoptosis

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7 January 2021

A gain of function p53 mutant promotes both genomic instability and cell survival in a novel p53-null mammary epithelial cell model

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Mutant p53 cooperates with ETS and selectively up-regulates human MDR1 not MRP1.

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Activation of the Fas pathway independently of Fas ligand during apoptosis induced by camptothecin in p53 mutant human colon carcinoma cells

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7 January 2021

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