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Gene Review

Clcnkb  -  chloride channel, voltage-sensitive Kb

Rattus norvegicus

Synonyms: Chloride channel Kb, Chloride channel protein ClC-Kb, ClC-K2, ClC-K2L, Clck2, ...
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Disease relevance of Clcnkb

  • Patients who harbour CLCNKB mutations are characterized by hypokalaemic alkalosis with salt-wasting, low blood pressure, normal magnesium and hyper- or normocalciuria; they define a distinct subset of patients with Bartter's syndrome in whom nephrocalcinosis is absent [1].

High impact information on Clcnkb

  • These findings demonstrate the critical role of CLCNKB in renal salt reabsorption and blood-pressure homeostasis, and demonstrate the potential role of specific CLCNKB antagonists as diuretic antihypertensive agents [1].
  • These results suggest that ClC-K2L and -K2S are chloride channels in the thick ascending limb and collecting ducts and may be important routes for transcellular chloride transport like ClC-K1 [2].
  • Complementary DNAs encoding rat kidney chloride channels (ClC-K2L and ClC-K2S) were isolated by a polymerase chain reaction cloning strategy [2].
  • To understand the molecular mechanisms of kidney-specific and nephron-segment-specific expression of CLC-K channel genes, the rat ClC-K2 gene promoter was cloned and compared with that of CLC-K1 [3].
  • Three new members, named ClC-K1, ClC-K2, ClC-3, have been isolated [4].

Other interactions of Clcnkb

  • The 687-amino acid protein encoded by ClC-K2L is about 80% identical to rat ClC-K1 and about 40% identical to ClC-0, -1, and -2 [2].

Analytical, diagnostic and therapeutic context of Clcnkb

  • Northern blot with total ClC-K2L as a probe under high stringency revealed its message predominantly in kidney, especially in the outer and inner medulla [2].
  • Northern blot and immunohistochemistry showed that ClC-K1 and ClC-K2 are selectively expressed in the kidney, while ClC-3 distributes in a variety of organs such as brain, lung, and kidney [4].
  • Dietary salt loading down-regulated CIC-K2 mRNA in the outer medulla 0.6-fold versus control whilst furosemide treatment, but not the low-salt diet, increased ClC-K2 mRNA in the outer (1.6-fold) and inner medulla (2.0-fold) [5].


  1. Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III. Simon, D.B., Bindra, R.S., Mansfield, T.A., Nelson-Williams, C., Mendonca, E., Stone, R., Schurman, S., Nayir, A., Alpay, H., Bakkaloglu, A., Rodriguez-Soriano, J., Morales, J.M., Sanjad, S.A., Taylor, C.M., Pilz, D., Brem, A., Trachtman, H., Griswold, W., Richard, G.A., John, E., Lifton, R.P. Nat. Genet. (1997) [Pubmed]
  2. Two isoforms of a chloride channel predominantly expressed in thick ascending limb of Henle's loop and collecting ducts of rat kidney. Adachi, S., Uchida, S., Ito, H., Hata, M., Hiroe, M., Marumo, F., Sasaki, S. J. Biol. Chem. (1994) [Pubmed]
  3. Isolation and characterization of kidney-specific CLC-K2 chloride channel gene promoter. Rai, T., Uchida, S., Sasaki, S., Marumo, F. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  4. ClC family in the kidney. Sasaki, S., Uchida, S., Kawasaki, M., Adachi, S., Marumo, F. Jpn. J. Physiol. (1994) [Pubmed]
  5. Differential gene regulation of renal salt entry pathways by salt load in the distal nephron of the rat. Wolf, K., Castrop, H., Riegger, G.A., Kurtz, A., Krämer, B.K. Pflugers Arch. (2001) [Pubmed]
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