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• W3186605328 abstract "SUMMARY SARM1 is an inducible TIR-domain NAD + hydrolase that mediates pathological axon degeneration. SARM1 is activated by an increased ratio of NMN to NAD + , which competes for binding to an allosteric activating site. When NMN binds, the TIR domain is released from autoinhibition, activating its NAD + hydrolase activity. The discovery of this allosteric activating site led us to hypothesize that other NAD + -related metabolites might also activate SARM1. Here we show that the nicotinamide analogue 3-acetylpyridine (3-AP), first identified as a neurotoxin in the 1940s, is converted to 3-APMN which activates SARM1 and induces SARM1-dependent NAD + depletion, axon degeneration and neuronal death. Systemic treatment with 3-AP causes rapid SARM1-dependent death, while local application to peripheral nerve induces SARM1-dependent axon degeneration. We also identify a related pyridine derivative, 2-aminopyridine, as another SARM1-dependent neurotoxin. These findings identify SARM1 as a candidate mediator of environmental neurotoxicity, and furthermore, suggest that SARM1 agonists could be developed into selective agents for neurolytic therapy." @default.
• W3186605328 created "2021-08-02" @default.
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• W3186605328 date "2021-07-16" @default.
• W3186605328 modified "2023-10-15" @default.
• W3186605328 title "Neurotoxins subvert the allosteric activation mechanism of SARM1 to induce neuronal loss" @default.
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• W3186605328 doi "https://doi.org/10.1101/2021.07.16.452689" @default.
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