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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
SARM1-induced depletion of NAD(+) may explain the potent axon protection in Wallerian degeneration slow (Wld(s)) mutant mice.
The findings suggest that Sarm1 regulates social behaviors and cognition.
Therefore, Sarm1 functions downstream of ROS (show ROS1 Proteins) to induce neuronal cell death and axon degeneration during oxidative stress.
SARM expression was reduced and TRIF (show RNF138 Proteins) expression was increased after respiratory syncytial virus infection.
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
TIR adaptor SARM is a negative regulator of Toll (show TLR4 Proteins)-like receptor signaling.
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