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Rab Cascades01:25

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Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
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Rab Proteins01:14

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Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Coat Assembly and GTPases01:33

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Vesicles incorporate different coat protein subunits in different cell locations, which changes the properties of the coat, such as the shape and geometry of the transport vesicles. Thus, vesicle coat proteins also play a significant role in cargo selection.
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The recycling endosome, also known as the endosomal recycling compartment (ERC), is a part of the slow-recycling process of the endocytic pathway. Molecules internalized through receptor-mediated endocytosis are either degraded in the lysosomes or are recycled to the plasma membrane through the fast- or slow-recycling route.
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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C9orf72's Interaction with Rab GTPases-Modulation of Membrane Traffic and Autophagy.

Bor L Tang1

  • 1Department of Biochemistry, Yong Loo Lin School of Medicine, National University of SingaporeSingapore, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of SingaporeSingapore, Singapore.

Frontiers in Cellular Neuroscience
|October 25, 2016
PubMed
Summary
This summary is machine-generated.

The C9orf72 protein, linked to ALS and FTD, regulates cell membrane traffic and autophagy. Its interaction with Rab GTPases is crucial for these cellular processes.

Keywords:
ALSC9orf72Rabautophagymembrane trafficking

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • The C9orf72 gene mutation is the leading genetic cause of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD).
  • The precise cellular function of the C9orf72 protein has remained largely undetermined, despite its association with neurodegenerative diseases.

Approach:

  • Investigated the physical and functional interactions of C9orf72 with Rab small GTPases.
  • Examined the impact of C9orf72 loss on cellular membrane traffic, including endocytosis.
  • Assessed the role of C9orf72 in the process of autophagy and autophagosome formation.

Key Points:

  • C9orf72 interacts with Rab GTPases, influencing cellular membrane transport and autophagy.
  • Loss of C9orf72 function impairs endocytosis and reduces autophagosome formation in neuronal cells.
  • C9orf72 modulates autophagy through a Guanine nucleotide exchange factor (GEF) complex and as a Rab effector for the Ulk1 complex.

Conclusions:

  • C9orf72 plays a significant role in regulating cellular membrane traffic and autophagy.
  • Understanding C9orf72's cellular functions provides insights into the molecular mechanisms underlying ALS and FTD.