|Application ||WB, IHC|
|Calculated MW||43653 Da|
|Positive Control||WB: NIH3T3, IHC: human brain tissue|
|Application & Usage||WB; 1:500 – 1:2000, IHC; 1:50 – 1:200|
|Other Names||P53, Cellular tumor antigen p53, Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53|
|Formulation||In 0.42% Potassium phosphate; 0.87% Sodium chloride; pH 7.3; 30% glycerol and 0.01% sodium azide|
|Reconstitution & Storage||-20 °C|
|Precautions||Phospho-p53 (Ser376) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA- Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1- mediated transcriptional activation of PER2 (PubMed:24051492).|
|Cellular Location||Cytoplasm. Nucleus. Nucleus, PML body. Endoplasmic reticulum. Mitochondrion matrix. Note=Interaction with BANP promotes nuclear localization. Recruited into PML bodies together with CHEK2. Translocates to mitochondria upon oxidative stress. Translocates to mitochondria in response to mitomycin C treatment (PubMed:27323408). Isoform 2: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm Isoform 4: Nucleus. Cytoplasm. Note=Predominantly nuclear but translocates to the cytoplasm following cell stress Isoform 8: Nucleus. Cytoplasm. Note=Localized in both nucleus and cytoplasm in most cells. In some cells, forms foci in the nucleus that are different from nucleoli|
|Tissue Location||Ubiquitous. Isoforms are expressed in a wide range of normal tissues but in a tissue-dependent manner. Isoform 2 is expressed in most normal tissues but is not detected in brain, lung, prostate, muscle, fetal brain, spinal cord and fetal liver. Isoform 3 is expressed in most normal tissues but is not detected in lung, spleen, testis, fetal brain, spinal cord and fetal liver. Isoform 7 is expressed in most normal tissues but is not detected in prostate, uterus, skeletal muscle and breast Isoform 8 is detected only in colon, bone marrow, testis, fetal brain and intestine. Isoform 9 is expressed in most normal tissues but is not detected in brain, heart, lung, fetal liver, salivary gland, breast or intestine.|
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p53, a 53 kDa protein, binds to a DNA consensus sequence, the p53 response element, and regulates normal cell cycle events by activating transcription of genes involved either in progression through the cell cycle, or causing arrest in G1 when the genome is damaged. In most transformed and tumor cells the concentration of p53 is increased 5-1000 fold over the concentration in normal cells, principally due to the increased half-life (4 hrs) compared to that of wild-type (20 min). p53 localizes in the nucleus, but is detectable at the plasma membrane during mitosis and certain mutations also modulate cytoplasmic/nuclear distribution. p53 downregulates Bcl-2 expression and upregulates Bax expression, but may not always be necessary for apoptosis.
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