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CLIC4 interacts with histamine H3 receptor and enhances the receptor cell surface expression.

Abstract：

:Histamine H3 receptor (H3R), one of G protein-coupled receptors (GPCRs), has been known to regulate neurotransmitter release negatively in central and peripheral nervous systems. Recently, a variety of intracellular proteins have been identified to interact with carboxy (C)-termini of GPCRs, and control their intracellular trafficking and signal transduction efficiencies. Screening for such proteins that interact with the C-terminus of H3R resulted in identification of one of the chloride intracellular channel (CLIC) proteins, CLIC4. The association of CLIC4 with H3R was confirmed in in vitro pull-down assays, coimmunoprecipitation from rat brain lysate, and immunofluorescence microscopy of rat cerebellar neurons. The data from flowcytometric analysis, radioligand receptor binding assay, and cell-based ELISA indicated that CLIC4 enhanced cell surface expression of wild-type H3R, but not a mutant form of the receptor that failed to interact with CLIC4. These results indicate that, by binding to the C-terminus of H3R, CLIC4 plays a critical role in regulation of the receptor cell surface expression.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Maeda K,Haraguchi M,Kuramasu A,Sato T,Ariake K,Sakagami H,Kondo H,Yanai K,Fukunaga K,Yanagisawa T,Sukegawa J

doi

10.1016/j.bbrc.2008.02.071

subject

Has Abstract

pub_date

2008-05-02 00:00:00

pages

603-8

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)00320-3

journal_volume

369

pub_type

杂志文章

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