title: Rab7 may be a novel therapeutic target for neurologic diseases as a key regulator in autophagy.
abstract: Macroautophagy is an evolutionally conserved membrane trafficking pathway that delivers intracellular materials to lysosomes for degradation and recycling. Rab7, as a member of the Rab GTPase superfamily, has a unique role in the regulation of macroautophagy, especially in modulating autophagy flux. The functional states of Rab7 generally switch between GTP-bound and GDP-bound states under the control of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Activated GTP-Rab7 is capable of regulating autophagosome formation, autophagosome transportation along microtubules, endosome and autophagosome maturation, as well as lysosome biogenesis via interacting with its effector molecules. Rab7-mediated macroautophagy is closely associated with various pathological processes of several neurologic diseases, such as Parkinson's disease, Huntington's disease, Alzheimer's disease, Charcot-Marie-Tooth type 2B disease, and cerebral ischemic diseases. Considering that macroautophagy can be the prime therapeutic target in certain nervous system diseases, in-depth study of Rab7 in the regulation of macroautophagy may be helpful to identify novel strategies for the treatment of autophagy-related neurologic diseases. © 2017 Wiley Periodicals, Inc.
authors.affiliation: Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
authors.forename: Haixia
authors.initials: H
authors.lastname: Wen
authors.affiliation: Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
authors.forename: Lixuan
authors.initials: L
authors.lastname: Zhan
authors.affiliation: Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
authors.forename: Siyuan
authors.initials: S
authors.lastname: Chen
authors.affiliation: Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
authors.forename: Long
authors.initials: L
authors.lastname: Long
authors.affiliation: Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University and Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
authors.forename: En
authors.identifier: 0000-0003-4874-6373
authors.initials: E
authors.lastname: Xu
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D006801:Humans; D009422:Nervous System Diseases / Q000378:metabolism* / Q000473:pathology*; D020691:rab GTP-Binding Proteins / Q000378:metabolism*; D000090802:rab7 GTP-Binding Proteins
chemical_list: D000090802:rab7 GTP-Binding Proteins; C000716463:rab7 GTP-binding proteins, human; D020691:rab GTP-Binding Proteins
keywords: Rab7; autophagosome maturation; autophagy; neurologic diseases