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• W3020408885 endingPage "2827" @default.
• W3020408885 startingPage "2810" @default.
• W3020408885 abstract "Abstract Axonal degeneration is a key and early pathological feature in traumatic and neurodegenerative disorders of the CNS. Following a focal lesion to axons, extended axonal disintegration by acute axonal degeneration (AAD) occurs within several hours. During AAD, the accumulation of autophagic proteins including Unc-51 like autophagy activating kinase 1 (ULK1) has been demonstrated, but its role is incompletely understood. Here, we study the effect of ULK1 inhibition in different models of lesion-induced axonal degeneration in vitro and in vivo. Overexpression of a dominant negative of ULK1 (ULK1.DN) in primary rat cortical neurons attenuates axotomy-induced AAD in vitro. Both ULK1.DN and the ULK1 inhibitor SBI-0206965 protect against AAD after rat optic nerve crush in vivo. ULK1.DN additionally attenuates long-term axonal degeneration after rat spinal cord injury in vivo. Mechanistically, ULK1.DN decreases autophagy and leads to an mTOR-mediated increase in translational proteins. Consistently, treatment with SBI-0206965 results in enhanced mTOR activation. ULK1.DN additionally modulates the differential splicing of the degeneration-associated genes Kif1b and Ddit3 . These findings uncover ULK1 as an important mediator of axonal degeneration in vitro and in vivo, and elucidate its function in splicing, defining it as a putative therapeutic target." @default.
• W3020408885 created "2020-05-01" @default.
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• W3020408885 date "2020-04-27" @default.
• W3020408885 modified "2023-10-07" @default.
• W3020408885 title "Inhibition of the autophagic protein ULK1 attenuates axonal degeneration in vitro and in vivo, enhances translation, and modulates splicing" @default.
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• W3020408885 doi "https://doi.org/10.1038/s41418-020-0543-y" @default.
• W3020408885 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7493890" @default.
• W3020408885 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32341448" @default.
• W3020408885 hasPublicationYear "2020" @default.
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