Rab GTPases regulating receptor trafficking at the late endosome-lysosome membranes

• Published in: Cell biochemistry and function Vol. 30; no. 6; pp. 515 - 523
• Main Authors: Ng, Ee Ling, Gan, Bin Qi, Ng, Fanny, Tang, Bor Luen
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01-08-2012; Wiley Subscription Services, Inc
• Subjects: Animals; Endosomes - metabolism; epidermal growth factor receptor (EGFR); Humans; Intracellular Membranes - metabolism; late endosome/multi-vesicular body (MVB); lysosome; Lysosomes - metabolism; mannose 6-phosphate receptor (M6PR); Protein Transport; rab GTP-Binding Proteins - metabolism; Rab GTPase; Receptor, Epidermal Growth Factor - metabolism; Receptor, IGF Type 2 - metabolism; trans-Golgi network (TGN)
• ISSN: 0263-6484; 1099-0844
• DOI: 10.1002/cbf.2827

Lysosomes serve key degradative functions for the turnover of membrane lipids and protein components. Its biogenesis is principally dependent on exocytic traffic from the late endosome via the trans‐Golgi network, and it also receives cargo to be degraded from the endocytic pathway. Membrane trafficking to the late endosome–lysosome is tightly regulated to maintain the amplitude of signalling events and cellular homeostasis. Key coordinators of lysosomal traffic include members of the Rab small GTPase family. Amongst these, Rab7, Rab9 and the more recently studied Rab22B/31 have all been reported to regulate membrane trafficking processed at the late endosome–lysosome system. We discuss what is known about the roles of these Rab proteins and their interacting partners on the regulation of traffic of important receptor proteins such as the epidermal growth factor receptor (EGFR) and the mannose 6‐phosphate receptor (M6PR), in association with the late endosome–lysosome system. Better knowledge of EGFR and M6PR traffic in this regard may aid in understanding the pathological processes, such as oncogenic transformations associated with these receptors. Copyright © 2012 John Wiley & Sons, Ltd.