Abstract
The Rab family of GTPases contains over 60 genes in the human genome and contributes to regulation of intracellular membrane trafficking along endocytic and exocytic pathways as well as specialized pathways in specific cell types. It has become increasingly clear that disruption of the intracellular membrane trafficking system at different stages can cause various diseases. In the past decade, altered expression levels and mutations of Rab GTPases have been associated with diseases such as cancer, Alzheimers disease, and various genetic disorders. This review discusses the specific Rab GTPases and their involvement in the diseases.
Keywords: Rab, GTPase, GTP-binding protein, cancer, genetic disorder, Alzheimer's disease, Carpenter syndrome, Griscelli syndrome, Hermansky-Pudlak Syndrome, mental retardation
Current Drug Targets
Title: Rab GTPases, Membrane Trafficking and Diseases
Volume: 12 Issue: 8
Author(s): Guangpu Li
Affiliation:
Keywords: Rab, GTPase, GTP-binding protein, cancer, genetic disorder, Alzheimer's disease, Carpenter syndrome, Griscelli syndrome, Hermansky-Pudlak Syndrome, mental retardation
Abstract: The Rab family of GTPases contains over 60 genes in the human genome and contributes to regulation of intracellular membrane trafficking along endocytic and exocytic pathways as well as specialized pathways in specific cell types. It has become increasingly clear that disruption of the intracellular membrane trafficking system at different stages can cause various diseases. In the past decade, altered expression levels and mutations of Rab GTPases have been associated with diseases such as cancer, Alzheimers disease, and various genetic disorders. This review discusses the specific Rab GTPases and their involvement in the diseases.
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Cite this article as:
Li Guangpu, Rab GTPases, Membrane Trafficking and Diseases, Current Drug Targets 2011; 12 (8) . https://dx.doi.org/10.2174/138945011795906561
DOI https://dx.doi.org/10.2174/138945011795906561 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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