|Application ||WB, IHC|
|Calculated MW||43653 Da|
|Other Names||Cellular tumor antigen p53, Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, TP53, P53|
|Target/Specificity||A synthetic peptide corresponding to N-terminal residues human p53 was used as immunogen. The antibody should recognize human wild-type and mutant p53.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||p53 Antibody (N-term) 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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Provided below are standard protocols that you may find useful for product applications.
p53 acts as both a tumor-suppressor and transcription factor that, upon activation by DNA damage and other cellular stress signals, leads to the transcription of genes triggering cell-cycle arrest, apoptosis, and DNA repair (1,2). The gene for the nuclear phosphoprotein p53 is the most commonly mutated gene yet identified in human cancers (3). p53 is frequently mutated or inactivated in about 60% of cancers (4,5).
1. Levine, A.J., et al. Cell 88: 323-331 (1997)
2. Lakin, N.D. and S.P. Jackson. Oncogene 18: 7644-7655 (1999)
3. Vogelstein, B., et al. Nature 348: 681-2 (1990)
4. Hoolstein, M., et al. Science 253: 49-53 (1991)
5. Harris C.C., et al. Science 262: 1980-1981 (1993)
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