|Tested species reactivity||Human|
|Host / Isotype||Mouse / IgG1|
|Immunogen||Phosphopeptide containing the human p53 S15 site|
|Storage buffer||Buffered saline solution with BSA|
|Contains||0.1% sodium azide|
|Storage Conditions||4° C, store in dark|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||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.
In Western blots, no cross-reactivity with human p53 that is unphosphorylated at S15 is detected.
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.