Anti-SARM1

Make to order. Production time: 70-80 business days. Deliverables: 1. 200 µg antigen (used as positive control), 2. 1 ml pre-immune serum (used as negative control) , 3. Rabbit polyclonal antibody, antigen affinity purified. Quality Guarantee: 1. Antibody purity > 90% confirmed by SDS-PAGE, 2. Antibody titer > 1: 64,000 confirmed by ELISA, 3. WB positive with the immunogen protein (not applicable for synthetic peptide). Applications: ELISA, WB (positive for the recombinant immunogen protein/peptide). Buffer: Preservative: 0.03% Proclin 300, Constituents: 50% Glycerol, 0.01M PBS, pH 7.4. Protein function: 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:31439793, PubMed:32049506, PubMed:32828421, PubMed:31439792, 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. 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). [The UniProt Consortium]