当前位置： SCI文献检索 > Cell Reports期刊下所有文献 > Endophilin-A Deficiency Induces the Foxo3a-Fbxo32 Network in the Brain and Causes Dysregulation of Autophagy and the Ubiquitin-Proteasome System.

Endophilin-A Deficiency Induces the Foxo3a-Fbxo32 Network in the Brain and Causes Dysregulation of Autophagy and the Ubiquitin-Proteasome System.

Abstract：

:Endophilin-A, a well-characterized endocytic adaptor essential for synaptic vesicle recycling, has recently been linked to neurodegeneration. We report here that endophilin-A deficiency results in impaired movement, age-dependent ataxia, and neurodegeneration in mice. Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A. FBXO32 overexpression triggers apoptosis in cultured cells and neurons but, remarkably, coexpression of endophilin-A rescues it. FBXO32 interacts with all three endophilin-A proteins. Similarly to endophilin-A, FBXO32 tubulates membranes and localizes on clathrin-coated structures. Additionally, FBXO32 and endophilin-A are necessary for autophagosome formation, and both colocalize transiently with autophagosomes. Our results point to a role for endophilin-A proteins in autophagy and protein degradation, processes that are impaired in their absence, potentially contributing to neurodegeneration and ataxia.

journal_name

Cell Rep

journal_title

Cell reports

authors

Murdoch JD,Rostosky CM,Gowrisankaran S,Arora AS,Soukup SF,Vidal R,Capece V,Freytag S,Fischer A,Verstreken P,Bonn S,Raimundo N,Milosevic I

doi

10.1016/j.celrep.2016.09.058

subject

Has Abstract

pub_date

2016-10-18 00:00:00

pages

1071-1086

issue

4

issn

2211-1247

pii

S2211-1247(16)31314-6

journal_volume

17

pub_type

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