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Article

Disruption of axonal transport and neuronal viability by amyloid precursor protein mutations in Drosophila.

Neuron - 8 Nov 2001

Gunawardena S, Goldstein L S

Abstract excerpt

We tested the hypothesis that amyloid precursor protein (APP) and its relatives function as vesicular receptor proteins for kinesin-I. Deletion of the Drosophila APP-like gene (Appl) or overexpression of human APP695 or APPL constructs caused axonal transport phenotypes similar to kinesin and dynein mutants. Genetic reduction of kinesin-I expression enhanced while genetic reduction of dynein expression suppressed...

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Source

Identifiers

PMID: 11709151
DOI: 10.1016/s0896-6273(01)00496-2

Genes

APP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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