Anti-SARM antibody

Target data

NAD(+) hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD(+) metabolism (PubMed : 25908823, PubMed : 27671644, PubMed : 28334607). Acts as a negative regulator of MYD88- and TRIF-dependent toll-like receptor signaling pathway by promoting Wallerian degeneration, an injury-induced form of programmed subcellular death which involves degeneration of an axon distal to the injury site (PubMed : 15123841, PubMed : 16964262, PubMed : 20306472, PubMed : 25908823). Wallerian degeneration is triggered by NAD(+) depletion : in response to injury, SARM1 is activated and catalyzes cleavage of NAD(+) into ADP-D-ribose (ADPR), cyclic ADPR (cADPR) and nicotinamide; NAD(+) cleavage promoting cytoskeletal degradation and axon destruction (PubMed : 25908823, PubMed : 28334607, PubMed : 30333228, PubMed : 31128467, PubMed : 31439792, PubMed : 31439793, PubMed : 32049506, PubMed : 32828421, PubMed : 33053563). Also able to hydrolyze NADP(+), but not other NAD(+)-related molecules (PubMed : 29395922). Can activate neuronal cell death in response to stress (PubMed : 20306472). Regulates dendritic arborization through the MAPK4-JNK pathway (By similarity). Involved in innate immune response : inhibits both TICAM1/TRIF- and MYD88-dependent activation of JUN/AP-1, TRIF-dependent activation of NF-kappa-B and IRF3, and the phosphorylation of MAPK14/p38 (PubMed : 16964262).