p53 antibody | GeneTex GTX102965 product information

This webpage contains legacy information. The product is either no longer available from the supplier or has been delisted at Labome.

product summary

company name :

GeneTex

product type :

antibody

product name :

p53 antibody

catalog :

GTX102965

clonality :

polyclonal

host :

domestic rabbit

conjugate :

nonconjugated

reactivity :

human

citations: 3

Reference
Chen R, Lin C, Liang S, Villalobos O, Villaflores O, Lou B, et al. UVB Irradiation Induced Cell Damage and Early Onset of Junbb Expression in Zebrafish. Animals (Basel). 2020;10: pubmed publisher
Weng J, Yu C, Lee Y, Lin C, Chang W, Kuo Y. miR-494-3p Induces Cellular Senescence and Enhances Radiosensitivity in Human Oral Squamous Carcinoma Cells. Int J Mol Sci. 2016;17: pubmed publisher
Hsieh Y, Huang T, Lo H, Jhan J, Chen S, Yang P. Systematic discovery of drug action mechanisms by an integrated chemical genomics approach: identification of functional disparities between azacytidine and decitabine. Oncotarget. 2016;7:27363-78 pubmed publisher

product information

Catalog Number :

GTX102965

Product Name :

p53 antibody

Host Species :

Rabbit

Clonality :

Polyclonal

Product Type :

Primary Antibody

list of Pubmed id :

22837195,21454715,23583370,27036028,27399693

Background :

This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind 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 this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity. [provided by RefSeq]