PRMT5-dependent p53 escape in tumorigenesis
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...
| Main Authors: | , |
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| Format: | Online |
| Language: | English |
| Published: |
Impact Journals LLC
2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580063/ |