Title : Vincristine and bortezomib use distinct upstream mechanisms to activate a common SARM1-dependent axon degeneration program.

Pub. Date : 2019 Sep 5

PMID : 31484833






6 Functional Relationships(s)
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1 Vincristine and bortezomib use distinct upstream mechanisms to activate a common SARM1-dependent axon degeneration program. Vincristine sterile alpha and TIR motif containing 1 Homo sapiens
2 Vincristine and bortezomib use distinct upstream mechanisms to activate a common SARM1-dependent axon degeneration program. Bortezomib sterile alpha and TIR motif containing 1 Homo sapiens
3 We showed previously that genetic deletion of SARM1 blocks vincristine-induced neuropathy and demonstrate here that it also prevents axon destruction following administration of bortezomib in vitro and in vivo. Vincristine sterile alpha and TIR motif containing 1 Homo sapiens
4 We showed previously that genetic deletion of SARM1 blocks vincristine-induced neuropathy and demonstrate here that it also prevents axon destruction following administration of bortezomib in vitro and in vivo. Bortezomib sterile alpha and TIR motif containing 1 Homo sapiens
5 Using cultured neurons, we found that vincristine and bortezomib converge on a core axon degeneration program consisting of nicotinamide mononucleotide NMNAT2, SARM1, and loss of NAD+ but engage different upstream mechanisms that closely resemble Wallerian degeneration after vincristine and apoptosis after bortezomib. Vincristine sterile alpha and TIR motif containing 1 Homo sapiens
6 Using cultured neurons, we found that vincristine and bortezomib converge on a core axon degeneration program consisting of nicotinamide mononucleotide NMNAT2, SARM1, and loss of NAD+ but engage different upstream mechanisms that closely resemble Wallerian degeneration after vincristine and apoptosis after bortezomib. Bortezomib sterile alpha and TIR motif containing 1 Homo sapiens