C7597
Anti-Chloride Channel-K (CLC-K) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
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Conjugate:
unconjugated
Clone:
polyclonal
Application:
IHC, IP, WB CL
Citations:
6
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
rat
technique(s)
immunohistochemistry: suitable, immunoprecipitation (IP): suitable, western blot (chemiluminescent): 1:200
UniProt accession no.
storage temp.
−20°C
Gene Information
rat ... Clcnkb(79430)
General description
The gene Chloride channel Kb (CLCNKB) is mapped to human chromosome 1p36. It is a kidney specific protein and is present in basolateral membranes of renal tubules.
Immunogen
synthetic peptide corresponding to amino acids 674-687 of rat longer form CLC-K2L (with additional C-terminal cysteine). The epitope sequence corresponds to the CLC-K2 isotype. It differs by only one residue from rat CLC-K1, or from corresponding human or mouse CLC-Ka or CLC-Kb.
Application
Anti-Chloride Channel-K (CLC-K) antibody produced in rabbit is suitable for the following applications:
- Immunohistochemistry
- Immunoprecipitation
- Western blotting (chemiluminescent) at a dilution of 1:200
Biochem/physiol Actions
Mutations in chloride channel Kb (CLCNKB) gene cause Bartter syndrome (is a salt-losing renal tubulopathy) and is associated with hypertension (EH). Two classes of CLCNKB mutants are distinguished namely, nonconducting mutants associated with low total protein expression and partially conducting mutants with unaltered channel properties and ClC-Kb protein abundance.
Physical form
Lyophilized at ~0.6 mg/ml from phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin, 5% sucrose, and 0.025% sodium azide.
Disclaimer
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.
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Xiulan Su et al.
Clinical and experimental hypertension (New York, N.Y. : 1993), 34(7), 482-487 (2012-05-15)
We investigated a possible association between genetic variations in chloride channel Kb (CLCNKB) gene and essential hypertension (EH) in the Mongolian and Han populations in Inner Mongolia. Our study included 414 unrelated Mongolian herdsmen and 524 Han farmers. Two tagSNPs
S Adachi et al.
The Journal of biological chemistry, 269(26), 17677-17683 (1994-07-01)
Complementary DNAs encoding rat kidney chloride channels (ClC-K2L and ClC-K2S) were isolated by a polymerase chain reaction cloning strategy. Degenerate primers were designed based on the significant amino acid identity of the previously cloned chloride channels (ClC-0, -1, -2, and
Barttin is a Cl- channel beta-subunit crucial for renal Cl- reabsorption and inner ear K+ secretion.
R Estévez et al.
Nature, 414(6863), 558-561 (2001-12-06)
Renal salt loss in Bartter's syndrome is caused by impaired transepithelial transport in the loop of Henle. Sodium chloride is taken up apically by the combined activity of NKCC2 (Na+-K--2Cl- cotransporters) and ROMK potassium channels. Chloride ions exit from the
S Kieferle et al.
Proceedings of the National Academy of Sciences of the United States of America, 91(15), 6943-6947 (1994-07-19)
We have cloned two closely related putative Cl- channels from both rat kidney (designated rClC-K1 and rClC-K2) and human kidney (hClC-Ka and hClC-Kb) by sequence homology to the ClC family of voltage-gated Cl- channels. While rClC-K1 is nearly identical to
Mathilde Keck et al.
Human mutation, 34(9), 1269-1278 (2013-05-25)
Mutations in the CLCNKB gene encoding the ClC-Kb Cl(-) channel cause Bartter syndrome, which is a salt-losing renal tubulopathy. Here, we investigate the functional consequences of seven mutations. When expressed in Xenopus laevis oocytes, four mutants carried no current (c.736G>C
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