p53 biological network: at the crossroads of the cellular-stress response pathway and molecular carcinogenesis.

p53 biological network: at the crossroads of the cellular-stress response pathway and molecular carcinogenesis.
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DOI:
10.1272/jnms.73.54
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发表时间:
2006-04
期刊:
Journal of Nippon Medical School = Nippon Ika Daigaku zasshi
影响因子:
--
通讯作者:
S. Hussain;C. C. Harris-C.
S. Hussain;C. C. Harris-C.
中科院分区:
其他
文献类型:
--
作者:
S. Hussain;C. C. Harris-C.

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P53是包括炎症在内的应激反应通路中的关键分子节点。P53参与了细胞周期停滞、细胞凋亡、DNA修复和细胞衰老等几个关键途径,这些途径对于正常的细胞内稳态和维持基因组的完整性是必不可少的。TP53基因的改变或P53蛋白的翻译后修饰可以改变其对细胞应激的反应。TP53突变谱的分子考古学产生了关于人类癌症的病因和分子发病机制的假说。TP53基因的体细胞突变谱与环境致癌物以及人类癌症的内源性因素和过程有关。
p53 as a key molecular node in the stress response pathway, including inflammation. p53 is involved in several critical pathways including cell cycle arrest, apoptosis, DNA repair, and cellular senescence, which are essential for normal cellular homeostasis and maintaining genome integrity. The alteration of the TP53 gene or posttranslational modification in the p53 protein can alter its response to cellular stress. The molecular archaeology of the TP53 mutation spectrum generates hypotheses concerning the etiology and molecular pathogenesis of human cancer. The spectrum of somatic mutations in the TP53 gene implicates environmental carcinogens, and both endogenous agents and processes in the etiology of human cancer.