NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration.

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Research Abstract Details 

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NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Abstract Text:

L Conforti,G Fang,B Beirowski,M S Wang,L Sorci,S Asress,R Adalbert,A Silva,K Bridge,X P Huang,G Magni,J D Glass,M P Coleman,

The slow Wallerian degeneration protein (Wld(S)), a fusion protein incorporating full-length nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1), delays axon degeneration caused by injury, toxins and genetic mutation. Nmnat1 overexpression is reported to protect axons in vitro, but its effect in vivo and its potency remain unclear. We generated Nmnat1-overexpressing transgenic mice whose Nmnat activities closely match that of Wld(S) mice. Nmnat1 overexpression in five lines of transgenic mice failed to delay Wallerian degeneration in transected sciatic nerves in contrast to Wld(S) mice where nearly all axons were protected. Transected neurites in Nmnat1 transgenic dorsal root ganglion explant cultures also degenerated rapidly. The delay in vincristine-induced neurite degeneration following lentiviral overexpression of Nmnat1 was significantly less potent than for Wld(S), and lentiviral overexpressed enzyme-dead Wld(S) still displayed residual neurite protection. Thus, Nmnat1 is significantly weaker than Wld(S) at protecting axons against traumatic or toxic injury in vitro, and has no detectable effect in vivo. The full protective effect of Wld(S) requires more N-terminal sequences of the protein.

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Publishing Authors By Initials

L Conforti,G Fang,B Beirowski,MS Wang,L Sorci,S Asress,R Adalbert,A Silva,K Bridge,XP Huang,G Magni,JD Glass,MP Coleman,

For similar pathological conditions, signs and symptoms: pathologic processes: nerve degeneration: wallerian degeneration research abstracts see: pathological conditions, signs and symptoms: pathologic processes: nerve degeneration: wallerian degeneration research

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NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Cell death and differentiation

VOLUME: 14

Page Numbers: 116-27

Journal Abbreviation: Cell Death Differ.

ISSN: 1350-9047

DAY: 28

MONTH: 04

YEAR: 2006

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9437445

NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Keywords Mesh Terms:

KEYWORDS: Wallerian Degeneration

MESH TERMS: prevention & control

Chemical & Substance for Abstract: NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Information

Substance Name: Nmnat1 protein, mouse

Registry Number: EC 2.7.7.1

Grant and Affiliation Information for NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration.

AFFILIATION: The Babraham Institute, Cambridge CB2 4AT, UK.

Country: England

AGENCY: United States NINDS

GRANT: NS40405

ACRONYM: NS

MEDLINETA: Cell Death Differ

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