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Merck
CN

C7597

Sigma-Aldrich

Anti-Chloride Channel-K (CLC-K) antibody produced in rabbit

affinity isolated antibody, lyophilized powder

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MDL编号:
UNSPSC代码:
12352203
NACRES:
NA.41
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生物来源

rabbit

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

lyophilized powder

种属反应性

rat

技术

immunohistochemistry: suitable
immunoprecipitation (IP): suitable
western blot (chemiluminescent): 1:200

UniProt登记号

储存温度

−20°C

基因信息

rat ... Clcnkb(79430)

一般描述

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.

免疫原

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.

应用

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

生化/生理作用

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.

外形

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.

免责声明

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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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
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
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
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
N Jeck et al.
Pediatric research, 48(6), 754-758 (2000-12-05)
Gitelman syndrome is an inherited renal disorder characterized by impaired NaCl reabsorption in the distal convoluted tubule and secondary hypokalemic alkalosis. In clinical practice, it is distinguished from other hypokalemic tubulopathies by the presence of both hypomagnesemia and normocalcemic hypocalciuria.

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