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J. Biol. Chem., Vol. 283, Issue 18, 12241-12247, May 2, 2008

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MAGI-1a Functions as a Scaffolding Protein for the Distal Renal Tubular Basolateral K⁺ Channels^*

From the Division of Nephrology, Hypertension, and Endocrinology, Department of Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-857, Japan

As the K⁺ recycling pathway for renal Na⁺ reabsorption, renal tubular K⁺ channels participate in the fluid and electrolyte homeostasis. Previously, we showed that the Kir5.1/Kir4.1 heteromer, which is a heteromeric assembly of two inwardly rectifying K⁺ channels, composes the principal basolateral K⁺ channels in distal renal tubules and that two motifs in the carboxyl-terminal portion of the Kir4.1 subunit regulate its functional expression. In this study, by using yeast two-hybrid screening, we identified a new isoform of membrane-associated guanylate kinase with inverted domain structure 1 (MAGI-1a-long) as a scaffolding protein for the basolateral K⁺ channels. MAGI-1a-long interacted with the PSD-95/Dlg/ZO-1 (PDZ)-binding motif of Kir4.1 by its fifth PDZ domain, and a high salt diet, which could suppress mineralocorticoid secretion, facilitated the interaction. The phosphorylation of serine 377 in the PDZ-binding motif disrupted the interaction, and the disruption of the interaction altered the intracellular localization of the channels from the basolateral side to perinuclear components. These results demonstrate that the phosphorylation-dependent scaffolding of the basolateral K⁺ channels by MAGI-1a-long participates in the renal regulation of the fluid and electrolyte homeostasis.

Received for publication, September 14, 2007 , and in revised form, February 7, 2008.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AY598952 [GenBank] and AY598951.

^* This work was supported by grants-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (to M. T., T. A., and S. I.), by grants from Mishima Kaiun Memorial Foundation (to M. T.), Mochida Memorial Foundation for Medical and Pharmaceutical Research (to M. T.), Japan Heart Foundation/Pfizer Japan Inc. grant for cardiovascular disease research (to M. T.), and Salt Science Research Foundation Grants 0639 and 0734 (to M. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. S1–S3.

¹ To whom correspondence should be addressed: Division of Nephrology, Hypertension, and Endocrinology, Dept. of Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan. Fax: 81-22-717-7168; E-mail: mtanemoto-tky{at}umin.ac.jp.

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