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- W2014763931 endingPage "947" @default.
- W2014763931 startingPage "931" @default.
- W2014763931 abstract "Mutations in genes essential for protein homeostasis have been identified in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) patients. Why mature neurons should be particularly sensitive to such perturbations is unclear. We identified mutations in Rab8 in a genetic screen for enhancement of an FTD phenotype associated with ESCRT-III dysfunction. Examination of Rab8 mutants or motor neurons expressing a mutant ESCRT-III subunit, CHMP2B(Intron5), at the Drosophila melanogaster neuromuscular junction synapse revealed synaptic overgrowth and endosomal dysfunction. Expression of Rab8 rescued overgrowth phenotypes generated by CHMP2B(Intron5). In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TGF-β signaling were overactivated and acted synergistically to potentiate synaptic growth. We identify novel roles for endosomal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation in Rab8 mutants. Our data uncover Rab8, POSH, and TAK1 as regulators of synaptic growth responses and point to recycling endosome as a key compartment for synaptic growth regulation during neurodegenerative processes." @default.
- W2014763931 created "2016-06-24" @default.
- W2014763931 creator A5002861186 @default.
- W2014763931 creator A5027525943 @default.
- W2014763931 creator A5049312443 @default.
- W2014763931 creator A5078430949 @default.
- W2014763931 creator A5091582016 @default.
- W2014763931 date "2015-03-23" @default.
- W2014763931 modified "2023-09-30" @default.
- W2014763931 title "Rab8, POSH, and TAK1 regulate synaptic growth in a <i>Drosophila</i> model of frontotemporal dementia" @default.
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