Anti-SESTRIN2 SESN2 Antibody

SESTRIN2, also known as Hi95, is a member of the sestrin family of PA26-related proteins and is induced following DNA damage or oxidative stress (1) . SESTRIN2 and the related protein SESTRIN1 interact with the NRF2 suppressor KEAP1, the autophagy substrate p62 and the ubiquitin ligase RBX1 to protect cells against oxidative stress by activating NRF2 and promoting the p62-dependent autophagic degradation of KEAP1 (2) . SESTRIN2 also negatively regulates TOR signaling by activating AMP-activated protein kinase (AMPK) and TSC2 phosphorylation (3), thereby protecting cells against energetic stress-induced death (4) .

SESTRIN2 antibody is human, mouse and rat reactive. At least two isoforms of SESTRIN2 are known to exist; this antibody will detect both isoforms. SESTRIN2 antibody is predicted to not cross-react with SESTRIN1.

SESTRIN2 antibody was raised against a 19 amino acid peptide near the center of human SESTRIN2. The immunogen is located within amino acids 220 - 270 of SESTRIN2.

Functions as an intracellular leucine sensor that negatively regulates the TORC1 signaling pathway through the GATOR complex. In absence of leucine, binds the GATOR subcomplex GATOR2 and prevents TORC1 signaling (PubMed:18692468, PubMed:25263562, PubMed:25457612, PubMed:26449471, PubMed:26612684, PubMed:26586190) . Binding of leucine to SESN2 disrupts its interaction with GATOR2 thereby activating the TORC1 signaling pathway (PubMed:26449471, PubMed:26586190) . This stress-inducible metabolic regulator also plays a role in protection against oxidative and genotoxic stresses. May negatively regulate protein translation in response to endoplasmic reticulum stress, via TORC1 (PubMed:24947615) . May positively regulate the transcription by NFE2L2 of genes involved in the response to oxidative stress by facilitating the SQSTM1-mediated autophagic degradation of KEAP1 (PubMed:23274085) . May also mediate TP53 inhibition of TORC1 signaling upon genotoxic stress (PubMed:18692468) . Has an alkylhydroperoxide reductase activity born by the N-terminal domain of the protein (PubMed:26612684) . Was originally reported to contribute to oxidative stress resistance by reducing PRDX1 (PubMed:15105503) . However, this could not be confirmed (PubMed:19113821) .