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Hence, pro-degenerative MAPK (show MAPK1 Proteins) signaling functions upstream of SARM1 by limiting the levels of the essential axonal survival factor NMNAT2 (show NMNAT2 Proteins) to promote injury-dependent SARM1 activation.
we identify a physical interaction between the autoinhibitory N terminus and the TIR domain of SARM1, revealing a previously unrecognized direct connection between these domains that we propose mediates autoinhibition and activation upon injury.
Using steady-state and flux analysis of NAD(+) metabolites in healthy and injured mouse dorsal root ganglion axons, we find that rather than altering NAD(+) synthesis, NMNAT1 (show NMNAT1 Proteins) instead blocks the injury-induced, SARM1-dependent NAD(+) consumption that is central to axon degeneration.
demonstrate that the NADase activity of full-length SARM1 is required in axons to promote axonal NAD+ depletion and axonal degeneration after injury.
Genetic deletion of SARM1 decreases axonal degeneration in a mouse model of neuropathy.
SARM is a potential regulator of sepsis-induced splenocyte apoptosis.
Sarm1(-/-)mice developed fewer Beta-amyloid precursor protein aggregates in axons of corpus callosum after traumatic brain injury.
MMP-12 (show MMP12 Proteins) up-regulation mediated by SARM-TRIF (show RNF138 Proteins) signaling pathway contributes to IFN-gamma (show IFNG Proteins)-independent airway inflammation and AHR (show AHR Proteins) post RSV infection in nude mice.
SARM1, Not MyD88 (show MYD88 Proteins), Mediates TLR7 (show TLR7 Proteins)/TLR9 (show TLR9 Proteins)-Induced Apoptosis in Neurons
nicotinamide mononucleotide adenylyltransferase 2 (show NMNAT2 Proteins)-depletion-dependent degeneration of established axons and restricted extension of developing axons are thus both SARM1 dependent
Active nerve degeneration requires SARM1 and MAP kinases, including DLK (show DAPK3 Proteins), while the NAD+ synthetic enzyme NMNAT2 (show NMNAT2 Proteins) prevents degeneration.
Data show that sterile alpha- and armadillo-motif-containing protein (SARM) modulates MyD88 protein-mediated Toll-like receptors (TLRs) activation through BB-loop dependent interleukin-1 receptor (TIR) TIR-TIR interactions.
These results indicate that association of PINK1 (show PINK1 Proteins) with SARM1 and TRAF6 (show TRAF6 Proteins) is an important step for mitophagy.
The innate immunity adaptor SARM translocates to the nucleus to stabilize lamins and prevent DNA fragmentation in response to pro-apoptotic signaling.
Rapid Wallerian degeneration requires the pro-degenerative molecules SARM1.
Data found that the UXT (show UXT Proteins) isoforms elicit dual opposing regulatory effects on SARM-induced apoptosis.
SARM overexpression caused mitochondrial clustering which has also been observed in several cell death phenomenon.
The N-terminal 27 amino acids (S27 (show RPS27 Proteins)) of SARM, which is hydrophobic and polybasic, acts as a mitochondria-targeting signal sequence, associating SARM to the mitochondria. The S27 (show RPS27 Proteins) peptide has an inherent ability to bind to lipids and mitochondria.
SARM-mediated inhibition may not be exclusively directed at TRIF (show TRIM69 Proteins) or MyD88 (show MYD88 Proteins), but that SARM may also directly inhibit MAPK (show MAPK1 Proteins) phosphorylation
Involved in innate immnune response. Acts as a negative regulator of TICAM1/TRIF-dependent Toll-like receptor signaling by inhibiting induction of TLR3- and TLR4-dependent genes. Specifically blocks TICAM1/TRIF-dependent transcription-factor activation and gene induction, without affecting the MYD88- dependent pathway or non-TLR signaling. Negative regulator of NF- kappa-B and IRF activation (By similarity).
sterile alpha and TIR motif-containing protein 1
, sterile alpha and TIR motif containing 1
, Tir-1 homolog
, SAM domain-containing protein 2
, sterile alpha and Armadillo repeat protein
, sterile alpha and HEAT/Armadillo motif protein, ortholog of Drosophila
, sterile alpha motif domain-containing protein 2
, tir-1 homolog