Human homologue of a gene mutated in the slow Wallerian degeneration (C57BL/Wld(s)) mouse (Q28206635)

2

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Sabrina Tosi

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A David Smith

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Michael P Coleman

Basic local alignment search tool

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language of work or name

English

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publication date

6 February 2002

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published in

Gene

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volume

284

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issue

1-2

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page(s)

23-9

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cites work

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Role of the proteasome in Alzheimer’s disease

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An 85-kb tandem triplication in the slow Wallerian degeneration (Wlds) mouse

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A Ufd2/D4Cole1e chimeric protein and overexpression of Rbp7 in the slow Wallerian degeneration (WldS) mouse

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Structure of nicotinamide mononucleotide adenylyltransferase: a key enzyme in NAD(+) biosynthesis

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Molecular cloning, chromosomal localization, tissue mRNA levels, bacterial expression, and enzymatic properties of human NMN adenylyltransferase

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Prevention of β-Amyloid Neurotoxicity by Blockade of the Ubiquitin-Proteasome Proteolytic Pathway

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Prolonged survival of transected nerve fibres in C57BL/Ola mice is an intrinsic characteristic of the axon

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A proteolytic pathway that recognizes ubiquitin as a degradation signal

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A novel ubiquitination factor, E4, is involved in multiubiquitin chain assembly.

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Point mutations define a sequence flanking the AUG initiator codon that modulates translation by eukaryotic ribosomes

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Delayed wallerian degeneration in the central nervous system of Ola mice: an ultrastructural study

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Absence of Wallerian Degeneration does not Hinder Regeneration in Peripheral Nerve

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A gene affecting Wallerian nerve degeneration maps distally on mouse chromosome 4

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Evidence that the Rate of Wallerian Degeneration is Controlled by a Single Autosomal Dominant Gene

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Characterization of recombinant human nicotinamide mononucleotide adenylyl transferase (NMNAT), a nuclear enzyme essential for NAD synthesis

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Loss of the compound action potential: an electrophysiological, biochemical and morphological study of early events in axonal degeneration in the C57BL/Ola mouse

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