(Q52535028)

2 May 2018

title

Neuronal overexpression of APPL, the Drosophila homologue of the amyloid precursor protein (APP), disrupts axonal transport. (English)

1 reference

2 May 2018

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Torroja L

1

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2 May 2018

Chu H

series ordinal

2

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2 May 2018

Kotovsky I

series ordinal

3

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2 May 2018

White K

series ordinal

4

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2 May 2018

language of work or name

English

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publication date

1 May 1999

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2 May 2018

published in

Current Biology

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2 May 2018

volume

9

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2 May 2018

issue

9

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2 May 2018

page(s)

489-492

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2 May 2018

Role of the beta-amyloid protein in Alzheimer's disease.

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Overexpression of tau protein inhibits kinesin-dependent trafficking of vesicles, mitochondria, and endoplasmic reticulum: implications for Alzheimer's disease

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Kinesin heavy chain is essential for viability and neuromuscular functions in Drosophila, but mutants show no defects in mitosis

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Human amyloid precursor protein ameliorates behavioral deficit of flies deleted for Appl gene

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Behavioral and anatomical deficits in mice homozygous for a modified beta-amyloid precursor protein gene

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beta-Amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity

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Disruption of a behavioral sequence by targeted death of peptidergic neurons in Drosophila

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Multiple antigenic peptides designed to structurally related Drosophila peptides.

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Differential display reveals transcriptional up-regulation of the motor molecules for both anterograde and retrograde axonal transport during nerve regeneration.

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Rapid appearance of beta-amyloid precursor protein immunoreactivity in damaged axons and reactive glial cells in rat brain following needle stab injury.

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Effects of PS1 deficiency on membrane protein trafficking in neurons.

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APPL, the Drosophila member of the APP-family, exhibits differential trafficking and processing in CNS neurons.

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7 January 2021

10.1016/S0960-9822(99)80215-2

Identifiers

DOI

1 reference

2 May 2018

PubMed ID

10322116

1 reference

2 May 2018