The p53 protein is critical to regulation of normal cell growth and is a suppressor of tumor cell proliferation. Inactivation of p53 by a number of mechanisms, such as missense mutations or interaction with oncogenic viral or cellular proteins, can result in tumor progression. Mutations and/or allelic loss of the p53 gene are associated with a wide variety of human tumors. Known to have a role in transcriptional regulation, p53 suppresses various promoters containing TATA elements in an apparently sequence-independent fashion. p53 also binds to DNA in a sequence-specific manner via recognition of a 20-bp consensus-binding site. This interaction stimulates the expression of genes downstream of the p53 binding site. A number of genes that contain p53-binding sites have been identified, including MDM2, GADD45, and muscle creatine kinase. MDM2 mediates feedback inhibition of p53, which is prevented by phosphorylations of p53 amino-terminal serines and threonines. UV radiation-induced phosphorylation of Serine 46 (S46) is mediated by homeodomain-interacting protein kinase-2 (HIPK2) and is involved in the promotion of apoptosis. Other stress stimuli mediate S46 phosphorylation in p53 via as yet unidentified kinase(s).
原厂资料：
注意事项：
1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before
discarding to avoid accumulation of potentially explosive deposits in plumbing.
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