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Rab22B is expressed in the CNS astroglia lineage and plays a role in epidermal growth factor receptor trafficking in A431 cells
Author(s) -
Ng Ee Ling,
Ng Jun Jie,
Liang Fengyi,
Tang Bor Luen
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21911
Subject(s) - biology , microbiology and biotechnology , glial fibrillary acidic protein , epidermal growth factor , nestin , epidermal growth factor receptor , astrocyte , receptor , neural stem cell , immunology , biochemistry , stem cell , neuroscience , immunohistochemistry , central nervous system
The expression profile and functions of the brain‐enriched Rab22B/Rab31 small GTPase had remained uncharacterized. Using specific antibodies against Rab22B, we found the protein to be exceptionally enriched in nestin and RC2‐positive radial glia of the embryonic mouse brain. In the adult brain, Rab22B is rather specifically expressed in glial fibrillary acidic protein (GFAP)‐positive mature astrocytes, but is not clearly detectable in either 2′,3′‐cyclic nucleotide 3′‐phosphodiesterase (CNPase)‐positive mature oligodendrocytes or βIII‐tubulin (TuJ)‐positive neurons. In probing for specific functions of Rab22B, we found that Rab22B silencing in A431 cells resulted in abnormal trafficking of the epidermal growth factor receptor (EGFR), Texas‐red‐labeled EGF, and the cation‐independent mannose 6‐phosphate receptor (M6PR). Affinity pull‐down assays and co‐immunoprecipitation analysis indicated that Rab22B could associate with EGFR in a GTP‐dependent manner. Rab22B is thus a Rab protein specifically expressed in the astroglia lineage and may have a role in regulating EGFR trafficking in some cell types. Given that EGFR signaling modulates astrocyte development and oncogenesis of multiple cell types, Rab22B may thus have specific developmental or pathophysiological roles in cell types which it is enriched in. J. Cell. Physiol. 221: 716–728, 2009. © 2009 Wiley‐Liss, Inc.