Anti-TP53INP1

TP53INP1 (tumor protein p53-inducible nuclear protein 1), also known as p53DINP1, SIP or Teap, is a 240 amino acid protein that localizes to nuclear bodies and exists as two alternatively spliced isoforms, designated p53DINP1a and p53DINP1b. Expressed ubiquitously with higher expression in testis, pancreas and spleen tissue, TP53INP1 functions in response to double-stranded DNA breaks and regulates p53-mediated apoptosis, specifically by phosphorylating human p53 at Ser 46, an event that leads to cell death. Additionally, TP53INP1 is thought to interact with p73 and may be involved in the regulation of p73-controlled cell cycle progression. TP53INP1 expression is downregulated in pancreatic ductal adenocarcinomas, suggesting that, via its ability to induce cell death, TP53INP1 plays a role in tumor suppression. Protein function: Antiproliferative and proapoptotic protein involved in cell stress response which acts as a dual regulator of transcription and autophagy. Acts as a positive regulator of autophagy. In response to cellular stress or activation of autophagy, relocates to autophagosomes where it interacts with autophagosome-associated proteins GABARAP, GABARAPL1/L2, MAP1LC3A/B/C and regulates autophagy. Acts as an antioxidant and plays a major role in p53/TP53-driven oxidative stress response. Possesses both a p53/TP53-independent intracellular reactive oxygen species (ROS) regulatory function and a p53/TP53-dependent transcription regulatory function. Positively regulates p53/TP53 and p73/TP73 and stimulates their capacity to induce apoptosis and regulate cell cycle. In response to double-strand DNA breaks, promotes p53/TP53 phosphorylation on 'Ser-46' and subsequent apoptosis. Acts as a tumor suppressor by inducing cell death by an autophagy and caspase-dependent mechanism. Can reduce cell migration by regulating the expression of SPARC. [The UniProt Consortium]