Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene. (Q34107309)

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5 December 2019

title

Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene (English)

1 reference

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5 December 2019

author

Thomas H. Gillingwater

8

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5 December 2019

Felipe A Court

9

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5 December 2019

author name string

T G Mack

1

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5 December 2019

M Reiner

2

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5 December 2019

B Beirowski

3

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5 December 2019

W Mi

4

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5 December 2019

M Emanuelli

5

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5 December 2019

D Wagner

6

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5 December 2019

D Thomson

7

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5 December 2019

L Conforti

10

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5 December 2019

F S Fernando

11

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5 December 2019

A Tarlton

12

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5 December 2019

C Andressen

13

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5 December 2019

K Addicks

14

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5 December 2019

G Magni

15

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5 December 2019

R R Ribchester

16

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5 December 2019

V H Perry

17

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5 December 2019

M P Coleman

18

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5 December 2019

language of work or name

English

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publication date

1 December 2001

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5 December 2019

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5 December 2019

volume

4

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5 December 2019

page(s)

1199-1206

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5 December 2019

issue

12

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https://scigraph.springernature.com/pub.10.1038/nn770

5 December 2019

exact match

0 references

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Experiments on the Section of the Glossopharyngeal and Hypoglossal Nerves of the Frog, and Observations of the Alterations Produced Thereby in the Structure of Their Primitive Fibres

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Neurites can remain viable after destruction of the neuronal soma by programmed cell death (apoptosis).

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Evidence that Wallerian degeneration and localized axon degeneration induced by local neurotrophin deprivation do not involve caspases

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Absence of Wallerian Degeneration does not Hinder Regeneration in Peripheral Nerve

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

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Very Slow Retrograde and Wallerian Degeneration in the CNS of C57BL/Ola Mice

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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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The rate of Wallerian degeneration in cultured neurons from wild type and C57BL/WldS mice depends on time in culture and may be extended in the presence of elevated K+ levels

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Genetic influences on cellular reactions to spinal cord injury: a wound-healing response present in normal mice is impaired in mice carrying a mutation (WldS) that causes delayed Wallerian degeneration

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Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS).

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The gene for slow Wallerian degeneration (Wld(s)) is also protective against vincristine neuropathy.

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Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease

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

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

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

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GDNF slows loss of motoneurons but not axonal degeneration or premature death of pmn/pmn mice.

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Glial cells are increased proportionally in transgenic optic nerves with increased numbers of axons.

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

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Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice

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Electrically active axons degenerate when exposed to nitric oxide

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Genotyping methods to detect a unique neuroprotective factor (Wld(s)) for axons

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Genetic influences on cellular reactions to spinal cord injury: Activation of macrophages/microglia and astrocytes is delayed in mice carrying a mutation (WldS) that causes delayed Wallerian degeneration

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