C9orf72’s Interaction with Rab GTPases—Modulation of Membrane Traffic and Autophagy

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C9orf72’s Interaction with Rab GTPases—Modulation of Membrane Traffic and Autophagy

Hexanucleotide repeat expansion in an intron of Chromosome 9 open reading frame 72 (C9orf72) is the most common genetic cause of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). While functional haploinsufficiency of C9orf72 resulting from the mutation may play a role in ALS/FTD, the actual cellular role of the protein has been unclear. Recent findings have now shown that ...

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Role of Rab GTPases in membrane traffic and cell physiology.

Intracellular membrane traffic defines a complex network of pathways that connects many of the membrane-bound organelles of eukaryotic cells. Although each pathway is governed by its own set of factors, they all contain Rab GTPases that serve as master regulators. In this review, we discuss how Rabs can regulate virtually all steps of membrane traffic from the formation of the transport vesicle...

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Structural mechanisms for regulation of membrane traffic by rab GTPases.

In all eukaryotic organisms, Rab GTPases function as critical regulators of membrane traffic, organelle biogenesis and maturation, and related cellular processes. The numerous Rab proteins have distinctive yet overlapping subcellular distributions throughout the endomembrane system. Intensive investigation has clarified the underlying molecular and structural mechanisms for several ubiquitous R...

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Role of rab proteins in epithelial membrane traffic.

Small GTPase rab proteins play an important role in various aspects of membrane traffic, including cargo selection, vesicle budding, vesicle motility, tethering, docking, and fusion. Recent data suggest also that rabs, and their divalent effector proteins, organize organelle subdomains and as such may define functional organelle identity. Most rabs are ubiquitously expressed. However, some rabs...

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ژورنال

عنوان ژورنال: Frontiers in Cellular Neuroscience

سال: 2016

ISSN: 1662-5102

DOI: 10.3389/fncel.2016.00228