WldS requires Nmnat1 enzymatic activity and N16–VCP interactions to suppress Wallerian degeneration
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چکیده
منابع مشابه
WldS requires Nmnat1 enzymatic activity and N16–VCP interactions to suppress Wallerian degeneration
Slow Wallerian degeneration (Wld(S)) encodes a chimeric Ube4b/nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) fusion protein that potently suppresses Wallerian degeneration, but the mechanistic action of Wld(S) remains controversial. In this study, we characterize Wld(S)-mediated axon protection in vivo using Drosophila melanogaster. We show that Nmnat1 can protect severed axons fro...
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The slow Wallerian degeneration protein (WldS), a fusion protein containing amino-terminal E4B and full-length nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1), delays axon degeneration caused by physical damages, toxins and genetic mutations which result in patients being diagnosed with neurodegenerative diseases. It is still controversial whether the suppression of axonal degenerati...
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Wallerian degeneration is the degeneration of the distal stump of an injured axon. It normally occurs over a time course of around 24 hr but it is delayed in the slow Wallerian degeneration mutant mouse (C57BL/Wlds) for up to 3 weeks. The gene, which protects from rapid Wallerian degeneration, Wld, previously has been mapped to distal chromosome 4. This paper reports the fine genetic mapping of...
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An emerging hypothesis in Parkinson's disease (PD) is that dopaminergic (DA) neurons degenerate through a " dying back " axonopathy wherein degeneration begins in the distal axon and progresses over time towards the cell body. Impaired axonal transport also appears to play an early, pivotal role in PD. Thus processes that delay axonal transport dysfunction and/or axonal degeneration might slow ...
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ژورنال
عنوان ژورنال: Journal of Cell Biology
سال: 2009
ISSN: 1540-8140,0021-9525
DOI: 10.1083/jcb.200808042