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|Tested species reactivity||Human , Mouse , Rat|
|Published species reactivity||Mouse|
|Host / Isotype||Mouse / IgG1, kappa|
|Immunogen||Recombinant p53 peptide.|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|Immunohistochemistry (Frozen) (IHC (F))||Assay Dependent|
|Immunoprecipitation (IP)||Assay Dependent|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
UV-induced ablation of the epidermal basal layer including p53-mutant clones resets UV carcinogenesis showing squamous cell carcinomas to originate from interfollicular epidermis.
13-4100 was used in immunohistochemistry to investigate the origin of UV-induced squamous cell carcinomas.
|Rebel HG,Bodmann CA,van de Glind GC,de Gruijl FR||Carcinogenesis (33:714)||2012|
Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways.
13-4100 was used in western blot to test if p53 and MMR mediate X-ray cytotoxicity via the same pathway.
|Zeng M,Narayanan L,Xu XS,Prolla TA,Liskay RM,Glazer PM||Cancer research (60:4889)||2000|
bbl, TRP53, p44, bfy, Tp53, bhy, p53, BCC7, P53, Trp53, LFS1
antigen NY-CO-13, cellular tumor antigen p53, p53 tumor suppressor, phosphoprotein p53, transformation-related protein 53, transformation related protein 53, tumor protein p53 (Li-Fraumeni syndrome), tumor suppressor p53, mutant p53, p53 cellular tumor antigen, tumor supressor p53, TP53