SARM1 Polyclonal Antibody

NAD (+ hydrolase, which plays a key role in axonal degeneration following injury by regulating NAD (+ metabolism. 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. 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. Also able to hydrolyze NADP (+, but not other NAD (+-related molecules. Can activate neuronal cell death in response to stress. 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.