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our study provides in vivo evidence that, in response to a low-potassium diet, ClC-K and barttin play important roles in the activation of the WNK4-SPAK-NCC cascade and blood pressure regulation.
molecular substrate of a chloride channel previously detected in the mouse thick ascending limb
the major component of Cl(-) transport sensitive to NPPB or pH is mediated by CLC-K1 in the tAL.
Gene expression profiling in the collecting tubules of aquaporin-1 and CLC-Nk1 knockout mice.
induction of SGK1, CLC-K1 and barttin by high osmolarity and change in intracellular volume in distal renal tubular cells in vivo and in vitro
Increasing expression of barttin over that of ClC-K partially recovered this insufficiency, indicating that N-terminal modifications of barttin alter both binding affinities and gating properties
Single loci of tag Single Nucleotide Polymorphisms of CLCNKA_B are not enough to increase the Essential Hypertension susceptibility, the combination of CLCNKA SNP, salt, marine products, meat, edible oil consumption is associated with elevated risk.
R8W and G47R, two naturally occurring barttin mutations identified in patients with Bartter syndrome type IV, reduce barttin palmitoylation and CLC-K/barttin channel activity.
HEK293 cells the potentiating effect of niflumic acid (NFA) on CLC-Ka/barttin and CLC-Kb/barttin channels seems to be absent while the blocking efficacy of niflumic acid and benzofuran derivatives observed in oocytes is preserved
following variables were significantly associated with an estimated glomerular filtration rate: age, type 2 diabetes, total cholesterol, LDL-cholesterol, and the CLCNKA GG genotype
The variant CLCNKA risk allele, telegraphed by linked variants in the adjacent HSPB7 gene, uncovers a previously overlooked genetic mechanism affecting the cardio-renal axis.
Identify a protein region that is involved in calcium binding and that is likely undergoing conformational changes underlying the complex gating of CLC-K channels.
Combined impairment of ClC-Ka and ClC-Kb results in phenotype that mimics neonatal Barrter's syndrome with deafness
Barttin modulates trafficking and function of ClC-K1 and ClC-Kb channels
CLCNKA genetic variants may have roles in salt-sensitive hypertension
The structure of the cytoplasmic domain of CLCNKA reveals a conserved interaction interface.
Disruption of the gene encoding Barttin, BSND, results in a 'double knockout' of the functions of both ClCKA and ClCKB, manifesting as Bartter syndrome type IV with sensorineural deafness and an especially severe salt-losing phenotype.
ClC-Ka and ClC-Kb differ in how conformational changes are translated to the extracellular domain, despite the fact that the cytoplasmic domains share the same quaternary structure
This gene is a member of the CLC family of voltage-gated chloride channels. The encoded protein is predicted to have 12 transmembrane domains, and requires a beta subunit called barttin to form a functional channel. It is thought to function in salt reabsorption in the kidney and potassium recycling in the inner ear. The gene is highly similar to CLCNKB, which is located 10 kb downstream from this gene. Multiple transcript variants encoding different isoforms have been found for this gene.
chloride channel Ka
, chloride channel protein ClC-Ka-like
, chloride channel K1
, chloride channel protein ClC-Ka
, putative basolateral cTAL chloride channel ClC-Ka
, chloride channel, kidney, A
, Chloride channel protein ClC-Kb
, chloride channel Kb