Antigen NY-CO-13; BCC7; Cellular tumor antigen p53; FLJ92943; LFS1; Mutant tumor protein 53; p53; p53 tumor suppressor; P53_HUMAN; Phosphoprotein p53; Tp53; Transformation related protein 53; TRP53; Tumor protein 53; Tumor protein p53; Tumor suppressor p53;
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
Human, Mouse, Rat
Pig(100%), Bovine(88%), Sheep(88%), Rabbit(100%)
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
p53 Antibody detects endogenous levels of p53.
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt.
A synthesized peptide derived from human p53, corresponding to a region within N-terminal amino acids.
Observed Mol.Wt.: 53kDa.
Predicted Mol.Wt.: 44kDa.
Cytoplasm; Cytoplasm. Nucleus. Nucleus > PML body. Endoplasmic reticulum. Interaction with BANP promotes nuclear localization. Recruited into PML bodies together with CHEK2; Nucleus. Cytoplasm. Localized in both nucleus and cytoplasm in most cells. In some cells, forms foci in the nucleus that are different from nucleoli; Nucleus. Cytoplasm. Localized in the nucleus in most cells but found in the cytoplasm in some cells; Nucleus. Cytoplasm. Localized mainly in the nucleus with minor staining in the cytoplasm; Nucleus. Cytoplasm. Predominantly nuclear but localizes to the cytoplasm when expressed with isoform 4 and Nucleus. Cytoplasm. Predominantly nuclear but translocates to the cytoplasm following cell stress.
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.
Tumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome.
10 20 30 40 50
MEEPQSDPSV EPPLSQETFS DLWKLLPENN VLSPLPSQAM DDLMLSPDDI
60 70 80 90 100
EQWFTEDPGP DEAPRMPEAA PPVAPAPAAP TPAAPAPAPS WPLSSSVPSQ
110 120 130 140 150
KTYQGSYGFR LGFLHSGTAK SVTCTYSPAL NKMFCQLAKT CPVQLWVDST
160 170 180 190 200
PPPGTRVRAM AIYKQSQHMT EVVRRCPHHE RCSDSDGLAP PQHLIRVEGN
210 220 230 240 250
LRVEYLDDRN TFRHSVVVPY EPPEVGSDCT TIHYNYMCNS SCMGGMNRRP
260 270 280 290 300
ILTIITLEDS SGNLLGRNSF EVRVCACPGR DRRTEEENLR KKGEPHHELP
310 320 330 340 350
PGSTKRALPN NTSSSPQPKK KPLDGEYFTL QIRGRERFEM FRELNEALEL
360 370 380 390
KDAQAGKEPG GSRAHSSHLK SKKGQSTSRH KKLMFKTEGP DSD
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).
Acetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence. Deacetylation by SIRT2 impairs its ability to induce transcription activation in a AKT-dependent manner.Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1 (By similarity). Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. Phosphorylated on Thr-18 by VRK1. Phosphorylated on Ser-20 by CHEK2 in response to DNA damage, which prevents ubiquitination by MDM2. Phosphorylated on Ser-20 by PLK3 in response to reactive oxygen species (ROS), promoting p53/TP53-mediated apoptosis. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-33 by CDK7 in a CAK complex in response to DNA damage. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. Phosphorylated by NUAK1 at Ser-15 and Ser-392; was initially thought to be mediated by STK11/LKB1 but it was later shown that it is indirect and that STK11/LKB1-dependent phosphorylation is probably mediated by downstream NUAK1 (PubMed:21317932). It is unclear whether AMP directly mediates phosphorylation at Ser-15. Phosphorylated on Thr-18 by isoform 1 and isoform 2 of VRK2. Phosphorylation on Thr-18 by isoform 2 of VRK2 results in a reduction in ubiquitination by MDM2 and an increase in acetylation by EP300. Stabilized by CDK5-mediated phosphorylation in response to genotoxic and oxidative stresses at Ser-15, Ser-33 and Ser-46, leading to accumulation of p53/TP53, particularly in the nucleus, thus inducing the transactivation of p53/TP53 target genes. Phosphorylated by DYRK2 at Ser-46 in response to genotoxic stress. Phosphorylated at Ser-315 and Ser-392 by CDK2 in response to DNA-damage.Dephosphorylated by PP2A-PPP2R5C holoenzyme at Thr-55. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A.May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line.Ubiquitinated by MDM2 and SYVN1, which leads to proteasomal degradation (PubMed:10722742, PubMed:12810724, PubMed:15340061, PubMed:17170702, PubMed:19880522). Ubiquitinated by RFWD3, which works in cooperation with MDM2 and may catalyze the formation of short polyubiquitin chains on p53/TP53 that are not targeted to the proteasome (PubMed:10722742, PubMed:12810724, PubMed:20173098). Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation (PubMed:19536131). Deubiquitinated by USP10, leading to its stabilization (PubMed:20096447). Ubiquitinated by TRIM24, RFFL, RNF34 and RNF125, which leads to proteasomal degradation (PubMed:19556538). Ubiquitination by TOPORS induces degradation (PubMed:19473992). Deubiquitination by USP7, leading to stabilization (PubMed:15053880). Isoform 4 is monoubiquitinated in an MDM2-independent manner (PubMed:15340061). Ubiquitinated by COP1, which leads to proteasomal degradation (PubMed:19837670). Ubiquitination and subsequent proteasomal degradation is negatively regulated by CCAR2 (PubMed:25732823).Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370. Dimethylated at Lys-373 by EHMT1 and EHMT2. Monomethylated at Lys-382 by KMT5A, promoting interaction with L3MBTL1 and leading to repress transcriptional activity. Dimethylation at Lys-370 and Lys-382 diminishes p53 ubiquitination, through stabilizing association with the methyl reader PHF20. Demethylation of dimethylated Lys-370 by KDM1A prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.Sumoylated with SUMO1. Sumoylated at Lys-386 by UBC9.
Interacts with AXIN1. Probably part of a complex consisting of TP53, HIPK2 and AXIN1 (By similarity). Binds DNA as a homotetramer. Interacts with histone acetyltransferases EP300 and methyltransferases HRMT1L2 and CARM1, and recruits them to promoters. In vitro, the interaction of TP53 with cancer-associated/HPV (E6) viral proteins leads to ubiquitination and degradation of TP53 giving a possible model for cell growth regulation. This complex formation requires an additional factor, E6-AP, which stably associates with TP53 in the presence of E6. Interacts (via C-terminus) with TAF1; when TAF1 is part of the TFIID complex. Interacts with ING4; this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and TP53INP1. Interacts with WWOX. May interact with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1. Interacts with CHD8; leading to recruit histone H1 and prevent transactivation activity (By similarity). Interacts with ARMC10, BANP, CDKN2AIP, NUAK1, STK11/LKB1, UHRF2 and E4F1. Interacts with YWHAZ; the interaction enhances TP53 transcriptional activity. Phosphorylation of YWHAZ on 'Ser-58' inhibits this interaction. Interacts (via DNA-binding domain) with MAML1 (via N-terminus). Interacts with MKRN1. Interacts with PML (via C-terminus). Interacts with MDM2; leading to ubiquitination and proteasomal degradation of TP53. Directly interacts with FBXO42; leading to ubiquitination and degradation of TP53. Interacts (phosphorylated at Ser-15 by ATM) with the phosphatase PP2A-PPP2R5C holoenzyme; regulates stress-induced TP53-dependent inhibition of cell proliferation. Interacts with PPP2R2A. Interacts with AURKA, DAXX, BRD7 and TRIM24. Interacts (when monomethylated at Lys-382) with L3MBTL1. Isoform 1 interacts with isoform 2 and with isoform 4. Interacts with GRK5. Binds to the CAK complex (CDK7, cyclin H and MAT1) in response to DNA damage. Interacts with CDK5 in neurons. Interacts with AURKB, SETD2, UHRF2 and NOC2L. Interacts (via N-terminus) with PTK2/FAK1; this promotes ubiquitination by MDM2. Interacts with PTK2B/PYK2; this promotes ubiquitination by MDM2. Interacts with PRKCG. Interacts with PPIF; the association implicates preferentially tetrameric TP53, is induced by oxidative stress and is impaired by cyclosporin A (CsA). Interacts with human cytomegalovirus/HHV-5 protein UL123. Interacts with SNAI1; the interaction induces SNAI1 degradation via MDM2-mediated ubiquitination and inhibits SNAI1-induced cell invasion. Interacts with KAT6A. Interacts with UBC9. Interacts with ZNF385B; the interaction is direct. Interacts (via DNA-binding domain) with ZNF385A; the interaction is direct and enhances p53/TP53 transactivation functions on cell-cycle arrest target genes, resulting in growth arrest. Interacts with ANKRD2. Interacts with RFFL and RNF34; involved in p53/TP53 ubiquitination. Interacts with MTA1 and COP1. Interacts with CCAR2 (via N-terminus). Interacts (via N-terminus) with human adenovirus 5 E1B-55K protein; this interaction leads to the inhibition of TP53 function and/or its degradation (PubMed:25772236). Interacts with MORC3 (PubMed:17332504). Interacts (via C-terminus) with POU4F2 isoform 1 (via C-terminus) (PubMed:17145718). Interacts (via oligomerization region) with NOP53; the interaction is direct and may prevent the MDM2-mediated proteasomal degradation of TP53 (PubMed:22522597). Interacts with AFG1L; mediates mitochondrial translocation of TP53 (PubMed:27323408). Interacts with UBD (PubMed:25422469).
The nuclear export signal acts as a transcriptional repression domain. The TADI and TADII motifs (residues 17 to 25 and 48 to 56) correspond both to 9aaTAD motifs which are transactivation domains present in a large number of yeast and animal transcription factors.Belongs to the p53 family.
· Cellular Processes > Cell growth and death > Cell cycle.(View pathway)
· Cellular Processes > Cell growth and death > Ferroptosis.(View pathway)
· Cellular Processes > Cell growth and death > p53 signaling pathway.(View pathway)
· Cellular Processes > Cell growth and death > Apoptosis.(View pathway)
· Cellular Processes > Cell growth and death > Cellular senescence.(View pathway)
· Environmental Information Processing > Signal transduction > MAPK signaling pathway.(View pathway)
· Environmental Information Processing > Signal transduction > Wnt signaling pathway.(View pathway)
· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.(View pathway)
· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.(View pathway)
· Human Diseases > Cancers: Specific types > Pancreatic cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Basal cell carcinoma.(View pathway)
· Human Diseases > Cancers: Specific types > Thyroid cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Bladder cancer.(View pathway)
· Human Diseases > Cancers: Overview > Pathways in cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Gastric cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Non-small cell lung cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Glioma.(View pathway)
· Human Diseases > Cancers: Specific types > Colorectal cancer.(View pathway)
· Human Diseases > Cancers: Overview > Proteoglycans in cancer.
· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.(View pathway)
· Human Diseases > Cancers: Overview > MicroRNAs in cancer.
· Human Diseases > Cancers: Specific types > Endometrial cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Breast cancer.(View pathway)
· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.(View pathway)
· Human Diseases > Cancers: Specific types > Small cell lung cancer.(View pathway)
· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).
· Human Diseases > Cancers: Overview > Central carbon metabolism in cancer.(View pathway)
· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.
· Human Diseases > Infectious diseases: Viral > Hepatitis C.
· Human Diseases > Cancers: Overview > Viral carcinogenesis.
· Human Diseases > Infectious diseases: Viral > Measles.
· Human Diseases > Infectious diseases: Viral > Hepatitis B.
· Human Diseases > Cancers: Specific types > Melanoma.(View pathway)
· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.
· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.
· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.
· Human Diseases > Neurodegenerative diseases > Huntington's disease.
· Human Diseases > Infectious diseases: Viral > HTLV-I infection.
· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.
· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.
· Human Diseases > Cancers: Specific types > Prostate cancer.(View pathway)
· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.(View pathway)
· Organismal Systems > Nervous system > Neurotrophin signaling pathway.(View pathway)
· Organismal Systems > Aging > Longevity regulating pathway.(View pathway)
Application: WB Species:mouse; Sample:Not available
Fig. 4. Effects of PM2.5, SO2 and NO2 co-exposure on apoptosis-related gene protein expression in the mouse cortex. (A) Protein bands; (B) Protein expression of p53; (C) Protein expression of bax; (D) Protein expression of bcl-2; (E) Ratio of bax to bcl-2. Data were expressed as the means ± SE (n ¼ 6 mice/group), *P < 0.05 vs. control. C ¼ control; L ¼ low concentration air pollutants PM2.5þSO2þNO2 (L); H ¼ high concentration air pollutants PM2.5þSO2þNO2 (H).
Application: WB Species:human; Sample:Not available
Figure 2. Crocetin induces cell cycle arrest and influences PCNA, p21, and p53 expression in RPE cells. (A) Cells were harvested after treatment with or without 50 and 100 μM crocetin for 24 h. DNA was stained with PI for flow cytometric analysis. The number of cells in G1 phase was significantly increased in the crocetin-treated group compared with that in the untreated group. (B) Cells were treated or without with 50, 100 and 200 μM crocetin for 48 h. Western blot analysis was used to evaluated the expression of PCNA, p21, p53 and the housekeeping protein β-actin. *P< 0.05 vs 0 μM crocetin, **P< 0.01 vs 0 μM crocetin. The data are presented as the mean ± S.D. (n = 3/group).
Application: IF/ICC Species:rat; Sample:Not available
Figure 2. Effects of ALD on the distribution of p53 (magnification, x400). The level of p53 expression was markedly higher in renal cortical sections from ALD-infused rats, as compared with those from the control group rats, as determined by immunohistochemical analyses. Furthermore, the p53 protein was predominantly expressed in the renal cortex, whereas negligible p53 protein expression was observed in the normal tissue samples. ALD, aldosterone.
Tips: For phospho antibody, we provide phospho peptide（0.5mg) and non-phospho peptide(0.5mg).
Blocking peptides are peptides that bind specifically to the target antibody and block antibody binding. These peptide usually contains the epitope recognized by the antibody. Antibodies bound to the blocking peptide no longer bind to the epitope on the target protein. This mechanism is useful when non-specific binding is an issue, for example, in Western blotting (immunoblot) and immunohistochemistry (IHC). By comparing the staining from the blocked antibody versus the antibody alone, one can see which staining is specific; Specific binding will be absent from the western blot or immunostaining performed with the neutralized antibody.
Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 10 mg/ml.The purity is >90%,tested by HPLC and MS.Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.
This product is for research use only. Not for use in diagnostic or therapeutic procedures.
|S9||Phosphorylation||P78527 (PRKDC) , Q13315 (ATM) , P48730 (CSNK1D)||Uniprot|
|S15||Phosphorylation||Q16539 (MAPK14) , O60285 (NUAK1) , Q15831 (STK11) , Q13315 (ATM) , P78527 (PRKDC) , Q05655 (PRKCD) , Q13464 (ROCK1) , P57059 (SIK1) , Q96Q15 (SMG1) , P27361 (MAPK3) , P28482 (MAPK1) , Q14680 (MELK) , O14757 (CHEK1) , O96017 (CHEK2) , Q96S44 (TP53RK) , Q13535 (ATR) , Q00535 (CDK5) , Q13131 (PRKAA1) , P51812 (RPS6KA3) , Q13627 (DYRK1A)||Uniprot|
|T18||Phosphorylation||P53355 (DAPK1) , P48730 (CSNK1D) , Q99986 (VRK1) , O96017 (CHEK2) , Q86Y07-2 (VRK2) , P33981 (TTK) , P78527 (PRKDC) , P48729 (CSNK1A1) , Q13131 (PRKAA1) , O14757 (CHEK1)||Uniprot|
|S20||Phosphorylation||P78527 (PRKDC) , Q13131 (PRKAA1) , Q13315 (ATM) , O96017 (CHEK2) , Q9H4B4 (PLK3) , Q9UEE5 (STK17A) , P45983 (MAPK8) , P48729 (CSNK1A1) , P49137 (MAPKAPK2) , Q00535 (CDK5) , O14757 (CHEK1) , O43293 (DAPK3) , P53355 (DAPK1) , P48730 (CSNK1D) , Q683Z8 (CHK2) , P45984 (MAPK9)||Uniprot|
|S33||Phosphorylation||P50750 (CDK9) , O15264 (MAPK13) , Q00535 (CDK5) , P50613 (CDK7) , Q16539 (MAPK14) , P49841 (GSK3B) , P45985 (MAP2K4)||Uniprot|
|S37||Phosphorylation||O96017 (CHEK2) , Q8IW41 (MAPKAPK5) , O14757 (CHEK1) , P78527 (PRKDC) , Q13535 (ATR) , P53779 (MAPK10) , P45984 (MAPK9) , P45983 (MAPK8)||Uniprot|
|S46||Phosphorylation||Q92630 (DYRK2) , Q00535 (CDK5) , Q13315 (ATM) , Q05655 (PRKCD) , Q16539 (MAPK14) , P78527 (PRKDC) , Q9H2X6 (HIPK2) , O15264 (MAPK13)||Uniprot|
|T55||Phosphorylation||P28482 (MAPK1) , P21675 (TAF1) , P34947 (GRK5)||Uniprot|
|T81||Phosphorylation||P45984 (MAPK9) , P45983 (MAPK8)||Uniprot|
|S215||Phosphorylation||O14965 (AURKA) , Q96GD4 (AURKB) , O96013 (PAK4)||Uniprot|
|S269||Phosphorylation||P53355 (DAPK1) , Q96GD4 (AURKB)||Uniprot|
|S315||Phosphorylation||P24941 (CDK2) , P06493 (CDK1) , O14965 (AURKA) , P50750 (CDK9)||Uniprot|
|S366||Phosphorylation||O14757 (CHEK1) , O14920 (IKBKB) , O96017 (CHEK2)||Uniprot|
|S371||Phosphorylation||P17252 (PRKCA) , P50613 (CDK7)||Uniprot|
|S376||Phosphorylation||P50613 (CDK7) , P17252 (PRKCA) , P49841 (GSK3B)||Uniprot|
|T377||Phosphorylation||P17252 (PRKCA) , Q5S007 (LRRK2)||Uniprot|
|S378||Phosphorylation||O96017 (CHEK2) , P50613 (CDK7) , P17612 (PRKACA) , P17252 (PRKCA) , O14757 (CHEK1)||Uniprot|
|S392||Phosphorylation||P19525 (EIF2AK2) , O60285 (NUAK1) , P23443 (RPS6KB1) , Q15831 (STK11) , P50750 (CDK9) , P27361 (MAPK3) , P50613 (CDK7) , P68400 (CSNK2A1)||Uniprot|
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