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p53 Human ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
  • Other names:Tumor suppressor p53, TP53, Li-Fraumeni syndrome
  • Species:Human
Cat. No. Size Price


RAF082R 96 wells (1 kit) $721,83
PubMed Product Details
Technical Data

Type

Sandwich ELISA, Biotin-labelled antibody

Applications

Serum, Cell culture supernatant

Sample Requirements

50 µl/well

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

0.78–50 U/ml

Limit of Detection

0.33 U/ml

Intra-assay (Within-Run)

CV = 5.5%

Inter-assay (Run-to-Run)

CV = 8.9%

Spiking Recovery

95,00%

Dilution Linearity

102,00%

Summary

Research topic

Oncology

Summary

p53 is the most commonly mutated gene in human cancer. Mutations and allele loss in the gene located on chromosome 17p are the most frequent alterations yet identified in human malignancies. The p53 protein is highly conserved the evolution and expressed in most normal tissues. Wild-type p53 has been shown to be a sequence-specific transcription factor, directly interacting with various cellular and viral proteins.
p53 is considered a stress response gene, the p53 protein acts to induce cell cycle arrest or apoptosis in response to DNA damage, thereby maintaining genetic stability in the organism. These functions are executed by a complex and incompletely understood series of steps known as the p53 pathway.
Initially described as an oncogene, p53 was shown to be capable of suppressing the proliferation of transformed cells. Studies furthermore demonstrated that intact p53 function is essential for the maintenance of the non-tumorgenic phenotype of cells Thus p53 plays a vital role is suppressing the development of cancer.
p53 is a tumor suppressor gene which induces apoptosis. An inverse relationship in some neoplasms has been shown between p53 and Bcl-2, a proto-oncogene inhibiting apoptosis. The Bcl-2 homologue BAX gene has also been characterized to be regulated by p53; BAX acts to accelerate the rate at which apoptosis proceeds. p53 was further shown to mediated apoptosis through cell surface trafficking of APO-1/Fas.
p53 as a transcription factor induces the expression of p21WAF1/CIP1/Sdi1 leading to G1 arrest of the cell. p53 is known to be regulated by phosphorylation by a number of specific protein kinases. Activation by autoproteolysis has been shown. In addition to proliferation control, a role for p53 is cell senescence has been describe. More than 500 mutations in the p53 gene have been described. These mutations were found
in various types of malignancies, hematologic as well as solid tumors. However, all the mutants are not necessarily equivalent in terms of biological activity.
The mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver brain, skin, and hemopoietic tissues. The chemotherapy-supported p53 gene therapy is under clinical investigation.

Product References (2)

References

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Summary References (21)

References to p53

  • Bennett M, Macdonald K, Chan SW, Luzio JP, Simari R, Weissberg P. Cell surface trafficking of Fas: a rapid mechanism of p53-mediated apoptosis. Science. 1998 Oct 9;282 (5387):290-3
  • Engel P, Francis D, Graem N. Expression of bcl-2 in fetal thymus, thymomas and thymic carcinomas. Association with p53 expression and review of the literature. APMIS. 1998 Apr;106 (4):449-55
  • Hansen R, Oren M. p53; from inductive signal to cellular effect. Curr Opin Genet Dev. 1997 Feb;7 (1):46-51
  • Harris CC. p53: at the crossroads of molecular carcinogenesis and molecular epidemiology. J Investig Dermatol Symp Proc. 1996 Apr;1 (2):115-8
  • Hollstein M, Sidransky D, Vogelstein B, Harris CC. p53 mutations in human cancers. Science. 1991 Jul 5;253 (5015):49-53
  • Hung J, Anderson R. p53: functions, mutations and sarcomas. Acta Orthop Scand Suppl. 1997 Feb;273:68-73
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  • Khan S, Do KA, Kuhnert P, Pillay SP, Papadimos D, Conrad R, Jass JR. Diagnostic value of p53 immunohistochemistry in Barrett's esophagus: an endoscopic study. Pathology. 1998 May;30 (2):136-40
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  • Scherer SJ, Maier SM, Seifert M, Hanselmann RG, Zang KD, Muller-Hermelink HK, Angel P, Welter C, Schartl M. p53 and c-Jun functionally synergize in the regulation of the DNA repair gene hMSH2 in response to UV. J Biol Chem. 2000 Dec 1;275 (48):37469-73
  • Shaw PH. The role of p53 in cell cycle regulation. Pathol Res Pract. 1996 Jul;192 (7):669-75
  • Soddu S, Sacchi A. p53: prospects for cancer gene therapy. Cytokines Cell Mol Ther. 1998 Sep;4 (3):177-85
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  • Tominaga O, Hamelin R, Remvikos Y, Salmon RJ, Thomas G. p53 from basic research to clinical applications. Crit Rev Oncog. 1992;3 (3):257-82
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  • Wynford-Thomas D, Blaydes J. The influence of cell context on the selection pressure for p53 mutation in human cancer. Carcinogenesis. 1998 Jan;19 (1):29-36
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