Work

New perspective of ClC-Kb/2 Cl−channel physiology in the distal renal tubule

Year: 2016

Type: review

Abstract: Since its identification as the underlying molecular cause of Bartter's syndrome type 3, ClC-Kb (ClC-K2 in rodents, henceforth it will be referred as ClC-Kb/2) is proposed to play an important role in systemic electrolyte balance and blood pressure regulation by controlling basolateral Cl(-) exit in the distal renal tubular segments from the cortical thick ascending limb to the outer medullary collecting duct. Considerable experimental and clinical effort has been devoted to the identification and characterization of disease-causing mutations as well as control of the channel by its cofactor, barttin. However, we have only begun to unravel the role of ClC-Kb/2 in different tubular segments and to reveal the regulators of its expression and function, e.g., insulin and IGF-1. In this review we discuss recent experimental evidence in this regard and highlight unexplored questions critical to understanding ClC-Kb/2 physiology in the kidney.

Source: American Journal of Physiology-Renal Physiology

DOI: 10.1152/ajprenal.00577.2015

Authors: Oleg Zaika, Viktor Tomilin, Mykola Mamenko, Vivek Bhalla, Oleh Pochynyuk

Institutions: The University of Texas Health Science Center at Houston, Stanford Medicine, Stanford University

Language: English

Topic: Ion Transport and Channel Regulation

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funders: American Heart Association, National Institute of Diabetes and Digestive and Kidney Diseases