
Thermo Fisher Scientific Human SARM Synthetic Peptide
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Applications
Tested Dilution
Publications
Control (Ctrl)
Assay-dependent
Blocking Assay (BLOCK)
Assay-dependent
Product Specifications
Species Reactivity
Human
Class
Synthetic
Type
Peptide
Conjugate
Unconjugated Unconjugated Unconjugated
Form
Liquid
Concentration
200 µg/mL
Purification
purified
Storage buffer
PBS, pH 7.2, with 0.1% BSA
Contains
0.02% sodium azide
Storage conditions
-20°C
Product Specific Information
This peptide corresponds to 16 amino acid peptide near the amino terminus of human SARM.
PEP-1444 can be used as a blocking peptide with polyclonal antibody PA5-34402.
Target Information
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:31439792). 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). [UniProt]
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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