CLCNKB is a voltage-gated chloride channel that may modulate reabsorption of renal salts. Genetic variations in CLCNKB have been implicated in Gitelman and Bartter syndromes, as well as in the induction of ClC-Kb chloride channel functions. Rabbit Anti-CLCNKB antibody recognizes human, mouse, rat, canine, rabbit, and bovineCLCNKB.
Immunogen
Synthetic peptide directed towards the C terminal region of human CLCNKB
Application
Rabbit Anti-CLCNKB antibody is suitable for western blot applications at a concentration of 0.5 μg/ml.
Biochem/physiol Actions
Chloride channel Kb (CLCNKB) is a member of the CLC family of voltage-gated chloride channels, which comprises at least 9 mammalian chloride channels. Each is believed to have 12 transmembrane domains and intracellular N and C termini. Mutations in CLCNKB result in the autosomal recessive Type III Bartter Syndrome. CLCNKA and CLCNKB are closely related (94% sequence identity), tightly linked (separated by 11 kb of genomic sequence) and are both expressed in mammalian kidney.
Sequence
Synthetic peptide located within the following region: ILAAGCPTEPVTLKLSPETSLHEAHNLFELLNLHSLFVTSRGRAVGCVSW
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Tubular transepithelial reabsorption of chloride along the nephron is a major determinant of body salt and water homeostasis and blood pressure regulation. About 40% of the glomerulary filtered sodium chloride are reabsorbed in the distal nephrons. Vectorial transepithelial sodium chloride
Gitelman syndrome (GS) and Bartter syndrome (BS) are hereditary hypokalemic tubulopathies with distinct phenotypic features. GS has been considered a genetically homogeneous disorder caused by mutation in the gene encoding the NaCl cotransporter (TSC) of the distal convoluted tubule. In
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