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||p53 was identified as a tumor suppressor by showing that this protein has the ability to block transformation and to inhibit tumor cell growth. In addition, p53 is a transcription factor capable of regulating the expression of a subset of downstream genes. Mutation of two specific N-terminal residues in p53 (residues Leu22 and Trp23) impairs the ability of p53 to transactivate and has been correlated with its ability to bind TAFII40 and TAFII60 (or TAFII31 and TAFII70) suggesting that one or both of these interactions is important for activation. Mutation of residues 22 and 23 to Ala does not affect binding to TBP, although mutation of these residues to charged amino acids has been reported to disrupt the p53-TBP interaction. Different mutations in p53 gene have been characterized in a variety of human cancers. Loss or mutation of p53 function is highly correlated with tumorigenesis. GST-p53 is isolated from a strain ofE. colithat contains the coding sequence of wild type human p53 (amino acids 1-81) under the control of T7 promoter. The fusion protein is immunoreactive with the human p53 specific monoclonal antibody.
||Liquid. Supplied in 20mM Tris-HCl pH8.0, 20% glycerol, 100mM KCl, 0.2mM EDTA and 1mM DTT.
||1ng are sufficient for a protein-protein interaction assay.
||GST-p53 can be used forprotein-protein interaction assay.
||>95% by SDS-PAGE.
||For in vitro use only.
||Quality guaranteed for 12 months. Store at -80℃. Avoid freeze / thaw cycles.