p53 Signaling Pathway

The p53 gene is an important tumor suppressor gene, and its encoded p53 protein plays a key role in cell cycle regulation, DNA repair, and induction of apoptosis. Mutation of the p53 gene is one of the important factors in tumorigenesis. The p53 gene is mutated in more than 50% of cancer types, which causes the p53 signaling pathway to lose the function of cell growth "brakes". The wild-type p53 protein is located at the intersection of the cell signaling and death signaling networks and plays a decisive role in cell growth, differentiation, senescence, stress, and apoptosis. At the same time, it has intricate relationships with other intracellular signaling pathways. The p53-related target genes verified by a large number of studies mainly include p21, MDM2, CD95/fas, Bax, WT1, p53AIP1, PAG608, HER2, PCNA, cyclin G, and the like. These target genes regulated by the p53 gene directly perform various functions of p53.

Upstream signaling of p53

Under normal conditions, the intracellular concentration of wild-type p53 protein in cells is finely regulated by transcriptional level, translation level, post-translational modification level, and intracellular subcellular localization level. Its level is maintained at a very low level and the p53 signal network is off. When cells are stressed or damaged, p53 is stabilized and accumulated, exerting its "brake" function of damaging cell growth, clearing damaged DNA and mutant cells, and preventing cancer. Upstream signals that activate the p53 signaling network include ultraviolet damage caused by ultraviolet (UV) and ionizing radiation, abnormal activation of proto-oncogenes, and hypoxia.

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