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- W2299692973 endingPage "F930" @default.
- W2299692973 startingPage "F923" @default.
- W2299692973 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." @default.
- W2299692973 created "2016-06-24" @default.
- W2299692973 creator A5011483450 @default.
- W2299692973 creator A5014657118 @default.
- W2299692973 creator A5025348068 @default.
- W2299692973 creator A5034674216 @default.
- W2299692973 creator A5064579974 @default.
- W2299692973 date "2016-05-15" @default.
- W2299692973 modified "2023-10-15" @default.
- W2299692973 title "New perspective of ClC-Kb/2 Cl<sup>−</sup>channel physiology in the distal renal tubule" @default.
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