Identification of Acetylated-TP53 Lys120 monoclonal antibody, clone 10E5 (Cat # MAB0661) by Western blotting with 10E5 monoclonal antibody. Samples are crude lysates of HCT116 cells. Left lanes are control. Right lanes are cells treated with siRNA to knockdown the expression of a Tip60 interacting protein. Total p53 was immunoprecipitated with omnipotent anti-p53 monoclonal antibody from the crude extracts and analyzed by western blotting with anti-p53 antibody (upper panel) or anti-p53 acetyl-K120 monoclonal antibody (10E5) (middle panel) . The lower panel shows total p53.
Crude cell extracts were prepared from H-129 cells (TP53 negative cell line) expressing only Myc-TP53 (first lane), and both Myc-TP53 and His-Tip60. In the upper panel, the whole cell extracts were immuno-blotted with anti-Myc, anti-His-tag or anti-alphatublin antibodies. In the lower panel, the extracts were immunoprecipitated with Acetylated-TP53 Lys120 monoclonal antibody, clone 10E5 (Cat # MAB0661) and the precipitates were immuno-blotted with anti-Myc antibody. Acetylation of TP53 at K120 is dependent on Tip60 and promoted by over-expression of His-Tip60.
This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity. [provided by RefSeq
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