Regulation of Expression and Function of Scavenger Receptor Class B, Type I (SR-BI) by Na+/H+ Exchanger Regulatory Factors (NHERFs)

• Type of Material: Article
• Authors: Zhigang Hu, Veterans Affairs Palo Alto Health Care System; Jie Hu, Veterans Affairs Palo Alto Health Care System; Zhonghua Zhang, Veterans Affairs Palo Alto Health Care System; Wen-Jun Shen, Veterans Affairs Palo Alto Health Care System; Changhyon Yun, Emory University; Catherine H Berlot, Weis Center for Research; Fredric B Kraemer, Veterans Affairs Palo Alto Health Care System; Salman Azhar, Veterans Affairs Palo Alto Health Care System
• Language: English
• Date: 2013-04-19
• Publisher: American Society forBiochemistry and Molecular Biology
• Publication Version: Final Published Version
• Copyright Statement: © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.
• Final Published Version (URL): http://dx.doi.org/10.1074/jbc.M112.437368
• Title of Journal or Parent Work: Journal of Biological Chemistry
• Volume: 288
• Issue: 16
• Start Page: 11416
• End Page: 11435
• Grant/Funding Information: This work was supported, in whole or in part, by National Institutes of Health, NHLBI, Grant 2R01HL33881.; This work was also supported by the Office of Research and Development, Medical Service, Department of Veterans Affairs.
• Keywords: BETA(2)-ADRENERGIC RECEPTOR; H+ EXCHANGER; CHOLESTERYL ESTER UPTAKE; DOMAIN-CONTAINING PROTEIN; SELECTIVE UPTAKE; OVARIAN GRANULOSA-CELLS; CAMP-MEDIATED INHIBITION; Science & Technology; PDZ PROTEINS; PROTEIN-COUPLED-RECEPTORS; Life Sciences & Biomedicine; HIGH-DENSITY-LIPOPROTEIN; Biochemistry & Molecular Biology
• Research Categories: Health Sciences, Medicine and Surgery; Health Sciences, General

Abstract

Background: SR-BI mediates selective delivery of lipoprotein-CE to the liver, adrenals, and gonads for product formation. Results: NHERFs interact with and down-regulate SR-BI protein levels to inhibit selective CE uptake and steroidogenesis. Conclusion: Two protein domains (PDZ and MERM) are required for NHERF1/2-mediated inhibition of SR-BI expression and function. Significance: This work reveals a novel mechanism of translational/posttranslational regulation of SR-BI. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.