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SARM1 / SARM Antibody (clone Sarmy-1)
Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, IP |
|---|---|
| Primary Accession | Q6SZW1 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | Sarmy-1 |
| Calculated MW | 79kDa |
| Dilution | IHC-P (10 µg/ml), IP (1:200), |
| Gene ID | 23098 |
|---|---|
| Other Names | Sterile alpha and TIR motif-containing protein 1, Sterile alpha and Armadillo repeat protein, Sterile alpha motif domain-containing protein 2, MyD88-5, SAM domain-containing protein 2, Tir-1 homolog, SARM1, KIAA0524, SAMD2, SARM |
| Target/Specificity | Recognizes human SARM. |
| Reconstitution & Storage | Long term: -70°C; Short term: +4°C |
| Precautions | SARM1 / SARM Antibody (clone Sarmy-1) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | SARM1 |
|---|---|
| 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: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). |
| Cellular Location | Cytoplasm. Cell projection, axon {ECO:0000250|UniProtKB:Q6PDS3}. Cell projection, dendrite {ECO:0000250|UniProtKB:Q6PDS3}. Synapse {ECO:0000250|UniProtKB:Q6PDS3}. Mitochondrion Note=Associated with microtubules. {ECO:0000250|UniProtKB:Q6PDS3} |
| Tissue Location | Predominantly expressed in brain, kidney and liver. Expressed at lower level in placenta. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Negative regulator of MYD88- and TRIF-dependent toll- like receptor signaling pathway which plays a pivotal role in activating axonal degeneration following injury. Promotes Wallerian degeneration an injury-induced axonal death pathway which involves degeneration of an axon distal to the injury site. Can activate neuronal death in response to stress. 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.
References
Mink M.,et al.Genomics 74:234-244(2001).
Bousson J.-C.,et al.Submitted (OCT-2003) to the EMBL/GenBank/DDBJ databases.
Nagase T.,et al.DNA Res. 5:31-39(1998).
Liberati N.T.,et al.Proc. Natl. Acad. Sci. U.S.A. 101:6593-6598(2004).
Carty M.,et al.Nat. Immunol. 7:1074-1081(2006).
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