Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2007.07.076
Title: Rab22B's role in trans-Golgi network membrane dynamics
Authors: Ng, E.L. 
Wang, Y. 
Tang, B.L. 
Keywords: Rab22B
Small GTPase
trans-Golgi network (TGN)
Issue Date: 2007
Source: Ng, E.L.,Wang, Y.,Tang, B.L. (2007). Rab22B's role in trans-Golgi network membrane dynamics. Biochemical and Biophysical Research Communications 361 (3) : 751-757. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2007.07.076
Abstract: The small GTPase Rab22B (or Rab31) has been suspected to be involved in trafficking at trans-Golgi network. However, its exact cellular localization, tissue expression profile, and functions have not been uncharacterized. Specific antibody raised against Rab22B's protein revealed that Rab22B is brain-enriched, but is also present in substantial levels in spleen and intestine. In HeLa cells, endogenous Rab22B is largely associated with the trans-Golgi network (TGN). Over-expression of a GDP-binding mutant (Rab22BSN), but not wild-type Rab22B, specifically disrupts the TGN localization of TGN46, a dynamic marker which cycles between the TGN and the plasma membrane. The TGN resident membrane protein syntaxin 16, cis-Golgi markers such as GM130 and syntaxin 5, as well as the TGN/late endosome marker mannose 6-phosphate receptor (M6PR) are not affected by Rab22BSN, neither was endosomal-TGN transport of the Shiga toxin B subunit. The disruption of TGN46 staining by Rab22BSN could be specifically attributed to a domain at the C-terminal portion of Rab22B, where its sequence deviates the most from Rab22A. Over-expression of Rab22BSN inhibits the cell surface transport of the vesicular stomatitis virus G protein. Thus, Rab22B may have a role in anterograde exit from the TGN. © 2007 Elsevier Inc. All rights reserved.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/28645
ISSN: 0006291X
10902104
DOI: 10.1016/j.bbrc.2007.07.076
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