p73 is transcriptionally regulated by DNA damage, p53, and p73
نویسندگان
چکیده
منابع مشابه
p63 and p73 Transcriptionally Regulate Genes Involved in DNA Repair
The p53 family activates many of the same genes in response to DNA damage. Because p63 and p73 have structural differences from p53 and play distinct biological functions in development and metastasis, it is likely that they activate a unique transcriptional network. Therefore, we performed a genome-wide analysis using cells lacking the p53 family members after treatment with DNA damage. We ide...
متن کاملThe p53/p63/p73 family
The p53 gene is a tumor suppressor gene and the most frequent site of genetic alterations found in human cancers (Hollstein et al., 1991, 1996). Transgenic mice expressing mutant p53 or p53−/− mice are very prone to both spontaneous and induced tumors (Donehower et al., 1992). The p53 protein is a sequencespecific transcription factor that regulates the expression of genes involved in cell cycl...
متن کاملStructure of p73 DNA-binding domain tetramer modulates p73 transactivation.
The transcription factor p73 triggers developmental pathways and overlaps stress-induced p53 transcriptional pathways. How p53-family response elements determine and regulate transcriptional specificity remains an unsolved problem. In this work, we have determined the first crystal structures of p73 DNA-binding domain tetramer bound to response elements with spacers of different length. The str...
متن کاملSubcellular distribution of p53 and p73 are differentially regulated by MDM2.
The binding of MDM2 targets p53, but not p73, for degradation, whereas it suppresses the transactivation function of both proteins. MDM2 also mediates p53 nuclear export, but its role in the regulation of p73 distribution is unknown at the present time. We show here that, in sharp contrast to p53, MDM2 induces p73 to form nuclear aggregates that colocalize with MDM2 but are distinct from the pr...
متن کاملComparative Analysis of P73 and P53 Regulation and Effector Functions
p53 is mutated in approximately 50% of human cancers, whereas mutations of the related p73 gene are rare. p73 can activate p53-responsive promoters and induce apoptosis when overexpressed in certain p53-deficient tumor cells. We show that p73 isoforms, p73alpha and p73beta, can each induce permanent growth arrest with markers of replicative senescence when overexpressed in a tetracycline-regula...
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ژورنال
عنوان ژورنال: Oncogene
سال: 2001
ISSN: 0950-9232,1476-5594
DOI: 10.1038/sj.onc.1204149