Work

PRMT5-dependent p53 escape in tumorigenesis

Year: 2015

Type: article

Abstract: Extensive studies have characterized mutational disruption of p53 signaling in human cancers. However, the mechanism for bypass of p53 function in tumors retaining wild-type p53 has remained ambiguous. Recent studies suggest that PRMT5, which is frequently elevated in human cancers, cooperates with oncogenic cyclin D1 and leaves marks on p53 by way of arginine methylation, promoting the bypass of wild-type p53, and in doing so, evade apoptosis.

Source: Oncoscience

DOI: 10.18632/oncoscience.222

Authors: Yan Li, J. Alan Diehl

Institution: Medical University of South Carolina

Language: English

Topic: Cancer-related gene regulation

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: diamond

Funder: National Cancer Institute