Recombinant Human Cellular Tumor Antigen P53 (TP53) Protein (His)

Beta LifeScience SKU/CAT #: BLC-00988P
Greater than 85% as determined by SDS-PAGE.
Greater than 85% as determined by SDS-PAGE.

Recombinant Human Cellular Tumor Antigen P53 (TP53) Protein (His)

Beta LifeScience SKU/CAT #: BLC-00988P
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Product Overview

Description Recombinant Human Cellular Tumor Antigen P53 (TP53) Protein (His) is produced by our Baculovirus expression system. This is a full length protein.
Purity Greater than 85% as determined by SDS-PAGE.
Uniprotkb P04637
Target Symbol TP53
Synonyms (Antigen NY-CO-13)(Phosphoprotein p53)(Tumor suppressor p53)
Species Homo sapiens (Human)
Expression System Baculovirus
Tag C-6His
Target Protein Sequence MEEPQSDPSVEPPLSQETFSDLWKLLPENNVLSPLPSQAMDDLMLSPDDIEQWFTEDPGPDEAPRMPEAAPPVAPAPAAPTPAAPAPAPSWPLSSSVPSQKTYQGSYGFRLGFLHSGTAKSVTCTYSPALNKMFCQLAKTCPVQLWVDSTPPPGTRVRAMAIYKQSQHMTEVVRHCPHHERCSDSDGLAPPQHLIRVEGNLRVEYLDDRNTFRHSVVVPYEPPEVGSDCTTIHYNYMCNSSCMGGMNRRPILTIITLEDSSGNLLGRNSFEVRVCACPGRDRRTEEENLRKKGEPHHELPPGSTKRALPNNTSSSPQPKKKPLDGEYFTLQIRGRERFEMFRELNEALELKDAQAGKEPGGSRAHSSHLKSKKGQSTSRHKKLMFKTEGPDSD
Expression Range 1-393aa(R175H)
Protein Length Full Length
Mol. Weight 49.3 kDa
Research Area Apoptosis
Form Liquid or Lyophilized powder
Buffer Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage 1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target 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. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. 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-ARNTL/BMAL1-mediated transcriptional activation of PER2.
Subcellular Location Cytoplasm. Nucleus. Nucleus, PML body. Endoplasmic reticulum. Mitochondrion matrix. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome.; [Isoform 1]: Nucleus. Cytoplasm. Note=Predominantly nuclear but localizes to the cytoplasm when expressed with isoform 4.; [Isoform 2]: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.; [Isoform 3]: Nucleus. Cytoplasm. Note=Localized in the nucleus in most cells but found in the cytoplasm in some cells.; [Isoform 4]: Nucleus. Cytoplasm. Note=Predominantly nuclear but translocates to the cytoplasm following cell stress.; [Isoform 7]: Nucleus. Cytoplasm. Note=Localized mainly in the nucleus with minor staining in the cytoplasm.; [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.; [Isoform 9]: Cytoplasm.
Protein Families P53 family
Database References
Associated Diseases Esophageal cancer (ESCR); Li-Fraumeni syndrome (LFS); Squamous cell carcinoma of the head and neck (HNSCC); Lung cancer (LNCR); Papilloma of choroid plexus (CPP); Adrenocortical carcinoma (ADCC); Basal cell carcinoma 7 (BCC7)
Tissue Specificity 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

Gene Functions References

  1. Study summarizes the different functions of p53 in adipocyte development and in adipose tissue homeostasis. Furthermore, It explores the manipulation of p53 levels in adipose tissue depots and the impact on systemic energy metabolism in the context of insulin resistance and obesity. [review] PMID: 30181511
  2. a USP15-dependent lysosomal pathway controls p53-R175H turnover in ovarian cancer cells PMID: 29593334
  3. Results indicate that the underlying mechanisms whereby etoposide and ellipticine regulate CYP1A1 expression must be different and may not be linked to p53 activation alone. PMID: 29471073
  4. Studied association of tumor protein p53 and drug metabolizing enzyme polymorphisms with clinical outcome in patients with advanced nonsmall cell lung cancer. PMID: 28425245
  5. POH1 knockdown induced cell apoptosis through increased expression of p53 and Bim. PMID: 29573636
  6. a heretofore unappreciated effect of chronic high fat diet on beta-cells, wherein continued DNA damage owing to persistent oxidative stress results in p53 activation and a resultant inhibition of mRNA translation. PMID: 28630491
  7. diffuse large B cell lymphoma lacking CD19 or PAX5 expression were more likely to have mutant TP53. PMID: 28484276
  8. that proliferation potential-related protein promotes esophageal cancer cell proliferation and migration, and suppresses apoptosis by mediating the expression of p53 and IL-17 PMID: 30223275
  9. Infection of HIV-1 and subsequent HIV-1 reverse transcription are inhibited in HCT116 p53(+/+) cells in comparison to HCT116 p53(-/-) cells. Tumor suppressor gene p53 expression is upregulated in non-cycling cells. The restrictions of HIV by p53 is associated with the suppression of ribonucleotide reductase R2 subunit expression and phosphorylation of SAMHD1 protein. PMID: 29587790
  10. It has been shown that MDM2 and MDMX are targetable vulnerabilities within TP53-wild-type T-cell lymphomas. PMID: 29789628
  11. A significant increase in the expression of p53 and Bax was observed in cells treated with alpha-spinasterol, while cdk4/6 were significantly down-regulated upon exposure to alpha-spinasterol. PMID: 29143969
  12. There was a significant correlation between telomere dysfunction indices, p53, oxidative stress indices, and malignant stages of GI cancer patients PMID: 29730783
  13. PGEA-AN modulates P53 system which further leads to the death of the neuroblastoma cells with no effect on renal system in vivo owing it to be a future prospect for development of anticancer moiety against neuroblastoma. PMID: 29644528
  14. these data indicate that activation of autophagy reduces expression of STMN1 and p53, and the migration and invasion of cancer cells contributes to the anti-cancer effects of the Halofuginone. These findings may provide new insight into breast cancer prevention and therapy. PMID: 29231257
  15. miR-150 suppresses cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis, which is causally linked to repression of p53 expression and NF-kappaB activity. PMID: 29205062
  16. tumors harboring TP53 mutations, which can impair epithelial function, have a unique bacterial consortium that is higher in relative abundance in smoking-associated tumors. PMID: 30143034
  17. crosstalk among p53, lipid metabolism, insulin resistance, inflammation and oxidative stress has roles in Non-alcoholic fatty liver disease [review] PMID: 30473026
  18. Ubiquitin-conjugating enzyme E2S (UBE2S) enhanced the ubiquitination of p53 protein to facilitate its degradation in hepatocellular carcinoma (HCC) cells. PMID: 29928880
  19. p53 knockout compensates osteopenia in murine Mysm1 deficiency. PMID: 29203593
  20. SIRT1 had a pivotally protective role in the regulation of ADSCs aging and apoptosis induced by H2O2 PMID: 29803744
  21. 133p53 promotes tumour invasion via IL-6 by activation of the JAK-STAT and RhoA-ROCK pathways. PMID: 29343721
  22. mutant TP53 G245C and R273H can lead to more aggressive phenotypes and enhance cancer cell malignancy. PMID: 30126368
  23. PD-L1, Ki-67, and p53 staining individually had significant prognostic value for patients with stage II and III colorectal cancer PMID: 28782638
  24. This study of patients with ccRCC, pooled analysis and multivariable modeling demonstrated that three recurrently mutated genes, BAP1, SETD2, and TP53, have statistically significant associations with poor clinical outcomes. Important clinical confounders, mutations of TP53 and SETD2 were associated with decreased CSS and RFS, respectively. PMID: 28753773
  25. Study revealed that the Wnt/beta-catenin signaling pathway and its major downstream target, c-Myc increased the miR552 levels and miR552 directly targets p53 tumor suppressor. miR552 may serve as an important link between functional loss of APC, leading to abnormal Wnt signals, and the absence of p53 protein in colorectal cancer. PMID: 30066856
  26. High levels of glucose leads to endothelial dysfunction via TAF1-mediated p53 Thr55 phosphorylation and subsequent GPX1 inactivation. PMID: 28673515
  27. Although tumor protein p53 (p53) does not directly control the luminal fate, its loss facilitates acquisition of mammary stem cell (MaSC)-like properties by luminal cells and predisposes them to development of mammary tumors with loss of luminal identity. PMID: 28194015
  28. Fifty-two percent of patients diagnosed with glioma/glioblastoma with a positive TP53 mutation. PMID: 29454261
  29. the expression of Ser216pCdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway. PMID: 30085332
  30. In the former, p53 binds to the CDH1 (encoding E-cadherin) locus to antagonize EZH2-mediated H3K27 trimethylation (H3K27me3) to maintain high levels of acetylation of H3K27 (H3K27ac). PMID: 29371630
  31. Among the hits, miR-596 was identified as a regulator of p53. The overexpression of miR-596 significantly increased p53 at the protein level, thereby inducing apoptosis. PMID: 28732184
  32. Apoptosis pathways are impaired in fibroblasts from patients with SSc, leading to chronic fibrosis. Nonetheless, PUMA/p53 pathway may not be involved in dysfunction of apoptosis mechanisms in fibroblasts of patients with SSc. PMID: 28905491
  33. Low TP53 expression is associated with drug resistance in colorectal cancer. PMID: 30106452
  34. The activation of p38 in response to low doses of ultraviolet radiation was postulated to be protective for p53-inactive cells. Therefore, MCPIP1 may favor the survival of p53-defective HaCaT cells by sustaining the activation of p38. PMID: 29103983
  35. TP53 missense mutations are associated with castration-resistant prostate cancer. PMID: 29302046
  36. P53 degradation is mediated by COP1 in the breast cancer. PMID: 29516369
  37. Combined inactivation of the XRCC4 non-homologous end-joining (NHEJ) DNA repair gene and p53 efficiently induces brain tumours with hallmark characteristics of human glioblastoma. PMID: 28094268
  38. A direct link between Y14 and p53 expression and suggests a function for Y14 in DNA damage signaling. PMID: 28361991
  39. TP53 Mutation is associated with Mouth Neoplasms. PMID: 30049200
  40. Cryo-Electron Microscopy studies on p53-bound RNA Polymerase II (Pol II) reveal that p53 structurally regulates Pol II to affect its DNA binding and elongation, providing new insights into p53-mediated transcriptional regulation. PMID: 28795863
  41. Increased nuclear p53 phosphorylation and PGC-1alpha protein content immediately following SIE but not CE suggests these may represent important early molecular events in the exercise-induced response to exercise PMID: 28281651
  42. E6/E7-p53-POU2F1-CTHRC1 axis promotes cervical cancer cell invasion and metastasis PMID: 28303973
  43. accumulated mutant-p53 protein suppresses the expression of SLC7A11, a component of the cystine/glutamate antiporter, system xC(-), through binding to the master antioxidant transcription factor NRF2. PMID: 28348409
  44. Consistently, forced expression of p53 significantly stimulated ACER2 transcription. Notably, p53-mediated autophagy and apoptosis were markedly enhanced by ACER2. Depletion of the essential autophagy gene ATG5 revealed that ACER2-induced autophagy facilitates its effect on apoptosis. PMID: 28294157
  45. results indicate that LGASC of the breast is a low-grade triple-negative breast cancer that harbours a basal-like phenotype with no androgen receptor expression, and shows a high rate of PIK3CA mutations but no TP53 mutations PMID: 29537649
  46. this study shows an inhibitory effect of wild-type P53 gene transfer on graft coronary artery disease in rat model PMID: 29425775
  47. Our results suggest that TP53 c.215G>C, p. (Arg72Pro) polymorphism may be considered as a genetic marker for predisposition to breast cancer in Moroccan population PMID: 29949804
  48. higher level of the p53 isoform, p53beta, predict better prognosis in patients with renal cell carcinoma through enhancing apoptosis in tumors. PMID: 29346503
  49. TP53 mutations are associated with colorectal liver metastases. PMID: 29937183
  50. High expression of TP53 is associated with oral epithelial dysplasia and oral squamous cell carcinoma. PMID: 29893337

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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