A common sequence variation of the CLCNKB gene strongly activates ClC-Kb chloride channel activity

This publication has 18 references indexed in Scilit:

• Barttin increases surface expression and changes current properties of ClC-K channels
  Pflügers Archiv - European Journal of Physiology, 2002
• Molecular Structure and Physiological Function of Chloride Channels
  Physiological Reviews, 2002
• X-ray structure of a ClC chloride channel at 3.0 Å reveals the molecular basis of anion selectivity
  Nature, 2002
• Barttin is a Cl- channel β-subunit crucial for renal Cl- reabsorption and inner ear K+ secretion
  Nature, 2001
• Mutation of BSND causes Bartter syndrome with sensorineural deafness and kidney failure
  Nature Genetics, 2001
• Impaired solute accumulation in inner medulla ofClcnk1−/− mice kidney
  American Journal of Physiology-Renal Physiology, 2001
• In vivo role of CLC chloride channels in the kidney
  American Journal of Physiology-Renal Physiology, 2000
• Overt nephrogenic diabetes insipidus in mice lacking the CLC-K1 chloride channel
  Nature Genetics, 1999
• Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III
  Nature Genetics, 1997
• Two highly homologous members of the ClC chloride channel family in both rat and human kidney.
  Proceedings of the National Academy of Sciences, 1994