Clone: HR231.
Background: p53 is a 53 kDa transcription factor that can inhibit cell cycle progression or induce apoptosis in response to stress or DNA damage. Disruption of the p53 signalling pathway through various mechanisms is the most common alteration in human cancer occuring in over half of all tumors. The p53 protein is short lived and expressed at low levels in normal cells but accumulates and/or is activated in cells that have undergone genotoxic damage or oncogene activation. Many tumor derived and transformed cell lines express elevated levels of mutant p53 protein. Other genes also implicated in the downstream effects as a result of p53 activation are: p21WAF1, GADD45, 14-3-3, bax, Fas/APO1, KILLER/ DR5, Tsp1, IGF-BP3 and others.
Positive Control: Breast or colon carcinoma cells.
Purification Method: Protein A/G Chromatography.
Source: Hybridoma produced by the fusion of splenocytes from immunized with full length human p53 protein and mouse myeloma cells.
Formulation: Provided as solution in phosphate buffered saline with 0.08% sodium azide.
References: 1. Zeng, X., et al. UV but not gamma irradiation accelerates p53-induced apoptosis of teratocarcinoma cells by repressing MDM2 transcription. Cancer Res. 2000, 60, 6184-6188
2. Hussain, S.P., et al. p53 tumor suppressor gene: at the crossroads of molecular carcinogenesis, molecular epidemiology and human risk assessment. Ann. N.Y. Acad. Sci. 2000, 919, 79-85
3. Hellin, A.C., et al. Roles of Nuclear Factor-kappaB, p53 and p21/WAF1 in Daunomycin-induced cell cycle arrest and apoptosis. J. Pharmacol. Exp. Ther. 2000, 295, 870-878.
UniProt: Q9BRQ8.
Caution: This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving humans or animals.
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