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p53 Tumor Suppressor Protein Antibody - With BSA and Azide
Mouse Monoclonal Antibody [Clone TRP/816 ]
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC, IF, FC |
|---|---|
| Primary Accession | P04637 |
| Other Accession | 7157, 654481 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Isotype | Mouse / IgG2a |
| Clone Names | TRP/816 |
| Calculated MW | 53kDa |
| Gene ID | 7157 |
|---|---|
| Other Names | Cellular tumor antigen p53, Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53, TP53, P53 |
| Storage | Store at 2 to 8°C.Antibody is stable for 24 months. |
| Precautions | p53 Tumor Suppressor Protein Antibody - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | TP53 |
|---|---|
| Synonyms | P53 |
| Function | Multifunctional transcription factor that induces cell cycle arrest, DNA repair or apoptosis upon binding to its target DNA sequence (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:35618207, PubMed:36634798, PubMed:38653238, PubMed:9840937). Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17189187, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:38653238, PubMed:9840937). Negatively regulates cell division by controlling expression of a set of genes required for this process (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:9840937). 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 (PubMed:12524540, PubMed:17189187). Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 (PubMed:12524540). However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP (PubMed:12524540). 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 seems to have an 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-BMAL1-mediated transcriptional activation of PER2 (PubMed:24051492). |
| Cellular Location | Cytoplasm. Nucleus. Nucleus, PML body. Endoplasmic reticulum. Mitochondrion matrix. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome Note=Recruited into PML bodies together with CHEK2 (PubMed:12810724) Translocates to mitochondria upon oxidative stress (PubMed:22726440) Translocates to mitochondria in response to mitomycin C treatment (PubMed:27323408). Competitive inhibition of TP53 interaction with HSPA9/MOT-2 by UBXN2A results in increased protein abundance and subsequent translocation of TP53 to the nucleus (PubMed:24625977) [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.
Background
Recognizes a 53kDa protein, which is identified as p53 suppressor gene product. It reacts with the mutant as well as the wild form of p53 under denaturing and non-denaturing conditions. p53 is a tumor suppressor gene expressed in a wide variety of tissue types and is involved in regulating cell growth, replication, and apoptosis. It binds to MDM2, SV40 T antigen and human papilloma virus E6 protein. Positive nuclear staining with p53 antibody has been reported to be a negative prognostic factor in breast carcinoma, lung carcinoma, colorectal, and urothelial carcinoma. Anti-p53 positivity has also been used to differentiate uterine serous carcinoma from endometrioid carcinoma as well as to detect intratubular germ cell neoplasia. Mutations involving p53 are found in a wide variety of malignant tumors, including breast, ovarian, bladder, colon, lung, and melanoma.
References
Soussi, T., et al. 2000. p53 website and analysis of p53 gene mutations in human cancer: forging a link between epidemiology and carcinogenesis. Hum. Mutat. 15: 105-113
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