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. In
addition, Bcl2 and p53 are involved in apoptosis in an antagonistic fashion such that overexpressed Bcl2 inhibits p53-induced apoptosis.
53BP1 and 53BP2 were identified in a yeast two-hybrid screen of proteins that bind p53. Both 53BP1 and 53BP2 bind wild type p53, but not
mutant p53 found in tumor cells. p53BP1 is localized to the cytoplasm and nucleus, while p53BP2 is found only in the cytoplasm. 53BP1 has
BRCT motifs found in proteins involved in cell cycle control and DNA repair. DNA damage leads to 53BP1 hyperphosphorylation, which
may be mediated by ATM. 53BP2 has four ankyrin repeats and a SH3 domain that are required for interactions with Bcl2 and p53.
Overexpression of 53BP2 in 293 cells inhibits progression of the cell cycle in G2/M phase, while co-transfection of 53BP2 with p53 in H358
cells enhances p53-mediated transcriptional activation. The interaction between 53BP2 and p53 may be regulated by Bcl2, since competition
experiments demonstrate that Bcl2 prevents p53 binding to 53BP2. In addition, 53BP2 can also bind the apoptotic-related p65 subunit of
NFκB and this subunit can inhibit 53BP2-induced cell death.
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.
3.This antibody has been developed and certified for the bioimaging application. However, a routine bioimaging test is not performed on every lot. Researchers are encouraged to titrate the reagent for optimal performance.