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

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Buffa,  Laura
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Solimena,  Michele
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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引用

Buffa, L., Fuchs, E., Pietropaolo, M., Barr, F., & Solimena, M. (2008). ICA69 is a novel Rab2 effector regulating ER-Golgi trafficking in insulinoma cells. European Journal of Cell Biology, 87(4), 197-209.


引用: http://hdl.handle.net/21.11116/0000-0001-0E2A-2
要旨
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.