Mutant p53: an oncogenic transcription factor
نویسندگان
چکیده
منابع مشابه
The activating transcription factor 3 protein suppresses the oncogenic function of mutant p53 proteins.
Mutant p53 proteins (mutp53) often acquire oncogenic activities, conferring drug resistance and/or promoting cancer cell migration and invasion. Although it has been well established that such a gain of function is mainly achieved through interaction with transcriptional regulators, thereby modulating cancer-associated gene expression, how the mutp53 function is regulated remains elusive. Here ...
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Among genetic alterations in human cancers, mutations in the tumor suppressor p53 gene are the most common, occurring in over 50% of human cancers. The majority of p53 mutations are missense mutations and result in the accumulation of dysfunctional p53 protein in tumors. These mutants frequently have oncogenic gain-of-function activities and exacerbate malignant properties of cancer cells, such...
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Mutations of p53 are remarkably rare in acute promyelocytic leukemias (APLs). Here, we demonstrate that the APL-associated fusion proteins PML-RAR and PLZF-RAR directly inhibit p53, allowing leukemic blasts to evade p53-dependent cancer surveillance pathways. PML-RAR causes deacetylation and degradation of p53, resulting in repression of p53 transcriptional activity, and protection from p53-dep...
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At least some mutant p53 proteins not s imply have los t the wild-type p53 specific tumor suppressor function, but exhibit oncogenic functions on their own. Recently we showed that binding of mutant p53 to MAR/SAR elements is an act ivity specif ic for mutant p53 and clearly distinguishable from the previously reported DNA-binding activities of p53. Since MAR/SAR elements are considered to be i...
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Despite the wealth of information on the regulation of wild-type p53 function by phosphorylation, nothing is known about the biological effect of phosphorylation on mutant p53. Here we show that p53H175 is phosphorylated like wild-type p53 in cells of the same background. Ser nonphosphorylatable p53 mutants p53H175A392 and p53W248A392 more potently transformed rat embryo fibroblasts in cooperat...
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ژورنال
عنوان ژورنال: Oncogene
سال: 2007
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1210296