|Specificity:||The antibody BP53-12 recognizes defined epitope (aa 16-25) on human p53, a 50 kDa tumour suppressor found in increased amounts in a wide variety of transformed cells; it is frequently mutated or inactivated in many types of cancer.|
|Immunogen:||Bacterially expressed full-length wild-type p53|
|Species Reactivity:||Human, Non-Human Primates|
|Preparation:||The purified antibody is conjugated with Fluorescein isothiocyanate (FITC) under optimum conditions. The reagent is free of unconjugated FITC.|
|Storage Buffer:||Phosphate buffered saline (PBS) with 15 mM sodium azide, approx. pH 7.4|
|Storage / Stability:||Store in the dark at 2-8°C. Do not freeze. Avoid prolonged exposure to light.
Do not use after expiration date stamped on vial label.
Short-term exposure to room temperature should not affect the quality of the reagent. However, if reagent is stored under any conditions other than those specified, the conditions must be verified by the user.
|Usage:||The reagent is designed for direct immunofluorescence analysis.
Note: This conjugate is routinely tested by flow cytometry analysis using permeabilized transient wild-type p53-tranfectants.
|Expiration:||See vial label|
|Lot Number:||See vial label|
|Background:||The tumour suppressor protein p53 is a key element of intracellular anticancer protection. It mediates cell cycle arrest or apoptosis in response to DNA damage or to starvation for pyrimidine nukleotides. It is up-regulated in response to these stress signals and stimulated to activate transcription of specific genes, resulting in expression of p21waf1 and other proteins involved in G1 or G2/M arrest, or proteins that trigger apoptosis, such as Bcl-2. The structure of p53 comprises N-terminal transactivation domain, central DNA-binding domain, oligomerisation domain, and C-terminal regulatory domain. There are various phosphorylation sites on p53, of which the phosphorylation at Ser15 is important for p53 activation and stabilization.|
*Agarwal ML, Agarwal A, Taylor WR, Stark GR: p53 controls both the G2/M and the G1 cell cycle checkpoints and mediates reversible growth arrest in human fibroblasts. Proc Natl Acad Sci U S A. 1995 Aug 29;92(18):8493-7.
*Agarwal ML, Agarwal A, Taylor WR, Chernova O, Sharma Y, Stark GR: A p53-dependent S-phase checkpoint helps to protect cells from DNA damage in response to starvation for pyrimidine nucleotides. Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14775-80.
*Taylor WR, DePrimo SE, Agarwal A, Agarwal ML, Schönthal AH, Katula KS, Stark GR: Mechanisms of G2 arrest in response to overexpression of p53. Mol Biol Cell. 1999 Nov;10(11):3607-22.
*Taylor WR, Agarwal ML, Agarwal A, Stacey DW, Stark GR: p53 inhibits entry into mitosis when DNA synthesis is blocked. Oncogene. 1999 Jan 14;18(2):283-95.
*Tanigawa S, Fujii M, Hou DX: Stabilization of p53 is involved in quercetin-induced cell cycle arrest and apoptosis in HepG2 cells. Biosci Biotechnol Biochem. 2008 Mar;72(3):797-804.
*Bartek J, Bartkova J, Vojtesek B, Staskova Z, Lukas J, Rejthar A, Kovarik J, Midgley CA, Gannon JV, Lane DP: Aberrant expression of the p53 oncoprotein is a common feature of a wide spectrum of human malignancies. Oncogene. 1991 Sep;6(9):1699-703.
*Bartkova J, Bartek J, Lukas J, Vojtesek B, Staskova Z, Rejthar A, Kovarik J, Midgley CA, Lane DP: p53 protein alterations in human testicular cancer including pre-invasive intratubular germ-cell neoplasia. Int J Cancer. 1991 Sep 9;49(2):196-202.
*Dolezalova H, Vojtesek B, Kovarik J: Epitope analysis of the human p53 tumour suppressor protein. Folia Biol (Praha). 1997;43(1):49-51.
For laboratory research only, not for drug, diagnostic or other use.
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