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Please use this identifier to cite or link to this item: http://hdl.handle.net/10027/5595

Title: Transport of PIP3 by GAKIN, a kinesin-3 family protein, regulates neuronal cell polarity
Authors: Horiguchi, Kaori
Hanada, Toshihiko
Fukui, Yasuhisa
Chishti, Athar H.
Keywords: rhodamine-phosphatidylethanolamine
phosphatidylcholine
MAGUK, membrane-associated guanylate kinase
FHA, forkhead-associated
Issue Date: 24-Jul-2006
Publisher: Rockefeller University Press
Citation: Horiguchi, K., T. Hanada, Y. Fukui, and A. H. Chishti, 2006, Transport of PIP3 by GAKIN, a kinesin-3 family protein, regulates neuronal cell polarity: Journal of Cell Biology, v. 174, no. 3, p. 425-436. http://www.jcb.org.proxy.cc.uic.edu/cgi/content/full/174/3/425
Abstract: Phosphatidylinositol-(3,4,5)-trisphosphate (PIP3), a product of phosphatidylinositol 3-kinase, is an important second messenger implicated in signal transduction and membrane transport. In hippocampal neurons, the accumulation of PIP3 at the tip of neurite initiates the axon specification and neuronal polarity formation. We show that guanylate kinase - associated kinesin (GAKIN), a kinesin-like motor protein, directly interacts with a PIP3-interacting protein, PIP3BP, and mediates the transport of PIP3-containing vesicles. Recombinant GAKIN and PIP3BP form a complex on synthetic liposomes containing PIP3 and support the motility of the liposomes along microtubules in vitro. In PC12 cells and cultured hippocampal neurons, transport activity of GAKIN contributes to the accumulation of PIP3 at the tip of neurites. In hippocampal neurons, altered accumulation of PIP3 by overexpression of GAKIN constructs led to the loss of the axonally differentiated neurites. Together, these results suggest that, in neurons, the GAKIN-PIP3BP complex transports PIP3 to the neurite ends and regulates neuronal polarity formation.
Description: Copyright: http://www.jcb.org/misc/copyright.pdf
URI: http://hdl.handle.net/10027/5595
ISSN: 0021-9525
Appears in Collections:Publications - Pharmacology

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