Human Tumor suppressor p53,p53;TP53 ELI
3,140.00 ₪
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.
Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 (PubMed:12524540).
However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP (PubMed:12524540).
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 seems to have an 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.
Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1-mediated transcriptional activation of PER2 (PubMed:24051492).
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