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Overview
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Calculated MW: 50kDa
Observed MW: 58KDaPlease contact us at for specific academic pricing.
Background
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.
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