The WRAP53α gene undergoes p53 tumor suppressor-dependent transcriptional regulation in response to DNA Damage

Gene Reports ◽  
2021 ◽  
pp. 101431
Author(s):  
Anne Hucks Moxley ◽  
David Reisman
Keyword(s):  
Dna Damage ◽  
Transcriptional Regulation ◽  
Tumor Suppressor ◽  
P53 Tumor Suppressor

scholarly journals The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis

2001 ◽  
Vol 11 (21) ◽  
pp. 1722-1727 ◽  
Author(s):  
Björn Schumacher ◽  
Kay Hofmann ◽  
Simon Boulton ◽  
Anton Gartner
Keyword(s):  
Dna Damage ◽  
Tumor Suppressor ◽  
P53 Tumor Suppressor ◽  
C Elegans ◽  
Induced Apoptosis

scholarly journals MDM4 Isoform Expression in Melanoma Supports an Oncogenic Role for MDM4-A

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Abdullah Alatawi ◽  
SoonJye Kho ◽  
Michael P. Markey
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
P53 Gene ◽  
Genomic Databases ◽  
P53 Tumor Suppressor ◽  
Cycle Arrest ◽  
Biopsy Specimens ◽  
Direct Mutation

The p53 tumor suppressor integrates upstream signals such as DNA damage and active oncogenes to initiate cell cycle arrest or apoptosis. This response is critical to halting inappropriate growth signals. As such, p53 activity is lost in cancer. In melanoma, however, the p53 gene is intact in a reported 94% of human cases. Rather than direct mutation, p53 is held inactive through interaction with inhibitory proteins. Here, we examine the expression of the two primary inhibitors of p53, MDM2 and MDM4, in genomic databases and biopsy specimens. We find that MDM4 is frequently overexpressed. Moreover, changes in splicing of MDM4 occur frequently and early in melanomagenesis. These changes in splicing must be considered in the design of therapeutic inhibitors of the MDM2/4 proteins for melanoma.

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