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Buffa, L.* ; Fuchs, E.* ; Pietropaolo, M.* ; Barr, F.* ; Solimena, M.*

ICA69 is a novel Rab2 effector regulating ER-Golgi trafficking in insulinoma cells.

Eur. J. Cell Biol. 87, 197-209 (2008)
DOI PMC
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Islet cell autoantigen of 69kDa (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.
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Publication type Article: Journal article
Document type Scientific Article
ISSN (print) / ISBN 0171-9335
e-ISSN 1618-1298
Quellenangaben Volume: 87, Issue: 4, Pages: 197-209 Article Number: , Supplement: ,
Publisher Elsevier
Reviewing status Peer reviewed
Institute(s) Institute of Pancreatic Islet Research (IPI)