ICA69 is a novel Rab2 effector regulating ER-Golgi trafficking in insulinoma cells
Research output: Contribution to journal › Research article › Contributed › peer-review
Contributors
Abstract
Islet cell autoantigen of 69 kDa (ICA69) is a small GTPase-binding protein of unknown function. ICA69 is enriched in the Golgi complex and its N-terminal half contains a BAR domain, a module that can bind/bend membranes and interacts with phospholipids. Here we show that in insulinoma INS-1 cells ICA69 binds to the small GTPase Rab2, which regulates the transport of COPI vesicles between the endoplasmic reticulum and the Golgi complex. Rab2 binds to ICA69 in a GTP-dependent fashion and recruits it to membranes. Over-expression of either Rab2 or ICA69 in INS-1 cells results in a phenotype characterized by: (i) impaired anterograde transport of the secretory granule protein precursors pro-ICA512 and chromogranin A; (ii) reduction of stimulated insulin secretion. Taken together, these data identify ICA69 as a novel Rab2 effector and point to its role in regulating the early transport of insulin secretory granule proteins.
Details
Original language | English |
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Pages (from-to) | 197-209 |
Number of pages | 13 |
Journal | European journal of cell biology |
Volume | 87 |
Issue number | 4 |
Publication status | Published - 18 Apr 2008 |
Peer-reviewed | Yes |
External IDs
PubMed | 18187231 |
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Keywords
Sustainable Development Goals
ASJC Scopus subject areas
Keywords
- β-COP, Diabetes T1D, ER, Golgi, ICA69, Intermediate compartment, Rab2, Trafficking