Mutant p53 elicits context-dependent pro-tumorigenic phenotypes
收藏NIAID Data Ecosystem2026-03-13 收录
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2022-02-02
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Altered mRNA splicing by mutant p53 activates oncogenic RAS in pancreatic cancer. Altered mRNA splicing by mutant p53 activates oncogenic RAS in pancreatic cancer
Integrating transcriptomic analyses of both clinical PDAC and PDAC models, we identified that the most common neomorphic TP53 mutation (p53R175H) rewires RNA splicing promoting transcriptome-wide rete
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Proteasome machinery is instrumental in a common gain-of-function program of the p53 missense mutants in cancer.
Mutant p53 proteins, resulting from the missense mutations of the TP53 tumor suppressor gene, possess gain-of-function activities and are among the most robust oncoproteins in human tumors. They are p
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LFPM Inhibition of RING1-Mediated p53R175H Degradation Drives Oncogenesis in p53R175H-Mutant Cancers
The p53R175H mutant, a prevalent hotspot mutation in the p53 tumor suppressor gene, is associated with poor clinical outcomes due to its gain-of-function activities in cancer. Despite high expression
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Mouse oral tumors induced by activation of Ras and p53 mutations. Mus musculus
The p53 gain of function p53R172H promotes accelerated tumor growth and progression to carcinoma. To identify gene expression changes associated with the oncogenic function of mutant p53 we compared t
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LFPM Inhibition of RING1-Mediated p53R175H Degradation Drives Oncogenesis in p53R175H-Mutant Cancers
The p53R175H mutant, a prevalent hotspot mutation in the p53 tumor suppressor gene, is linked to adverse clinical outcomes due to its gain-of-function properties in malignancies. Despite high expressi
NIAID Data Ecosystem10
