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2016 ; 138
(7
): 1577-85
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Transcription factors that interact with p53 and Mdm2
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Inoue K
; Fry EA
; Frazier DP
Int J Cancer
2016[Apr]; 138
(7
): 1577-85
PMID26132471
show ga
The tumor suppressor p53 is activated upon cellular stresses such as DNA damage,
oncogene activation, hypoxia, which transactivates sets of genes that induce DNA
repair, cell cycle arrest, apoptosis, or autophagy, playing crucial roles in the
prevention of tumor formation. The central regulator of the p53 pathway is Mdm2
which inhibits transcriptional activity, nuclear localization and protein
stability. More than 30 cellular p53-binding proteins have been isolated and
characterized including Mdm2, Mdm4, p300, BRCA1/2, ATM, ABL and 53BP-1/2. Most of
them are nuclear proteins; however, not much is known about p53-binding
transcription factors. In this review, we focus on transcription factors that
directly interact with p53/Mdm2 through direct binding including Dmp1, E2F1, YB-1
and YY1. Dmp1 and YB-1 bind only to p53 while E2F1 and YY1 bind to both p53 and
Mdm2. Dmp1 has been shown to bind to p53 and block all the known functions for
Mdm2 on p53 inhibition, providing a secondary mechanism for tumor suppression in
Arf-null cells. Although E2F1-p53 binding provides a checkpoint mechanism to
silence hyperactive E2F1, YB-1 or YY1 interaction with p53 subverts the activity
of p53, contributing to cell cycle progression and tumorigenesis. Thus, the modes
and consequences for each protein-protein interaction vary from the viewpoint of
tumor development and suppression.
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