p53 Induction: Phosphorylation Sites Cooperate in Regulating Interatction
نویسندگان
چکیده
منابع مشابه
Cell type- and promoter-specific roles of Ser18 phosphorylation in regulating p53 responses.
Phosphorylation of mouse p53 at Ser18 occurs after DNA damage. To determine the physiological roles of this phosphorylation event in p53-dependent DNA damage responses, a Ser18 to Ala missense mutation was introduced into the germline of mice. Thymocytes and fibroblasts from the knock-in mice show reduced transactivation of many p53 target genes following DNA damage. p53 protein stabilization a...
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Recognition of the molecular mechanisms of cAMP action against DNA damage-induced apoptosis can be useful to improve the efficacy of DNA damaging therapeutic agents. Considering the critical role of bcl-2-associated death promoter (BAD) and p53 proteins in DNA damage -induced apoptosis, the aim of this study was to assess the effect of cAMP-elevating agents on these proteins in doxorubicin-trea...
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DNA damage can cause mutations that contribute to cellular transformation and tumorigenesis. The p53 tumor suppressor acts to protect the organism from DNA damage by inducing either G1 arrest to facilitate DNA repair or by activating physiological cell death (apoptosis). Consistent with this critical function of p53, mice lacking p53 are predisposed to developing tumors, particularly lymphoma. ...
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The combined impact of mutations in p16 and p53 was examined in cellular growth, transformation, and tumor formation. In cultured cells, p16 loss enhanced growth at high density and conferred susceptibility to oncogene-induced transformation. In vivo, mice doubly deficient for p16 and p53 showed an increased rate of tumor formation with particular susceptibility to aggressive angiosarcomas. Fur...
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Skeletal muscle postnatal growth and repair depend on satellite cells and are regulated by molecular signals within the satellite cell niche. We investigated the molecular and cellular events that lead to altered myogenesis upon genetic ablation of Syndecan-3, a component of the satellite cell niche. In the absence of Syndecan-3, satellite cells stall in S phase, leading to reduced proliferatio...
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ژورنال
عنوان ژورنال: Cancer Biology & Therapy
سال: 2002
ISSN: 1538-4047,1555-8576
DOI: 10.4161/cbt.82