Expression and regulation of ClC-5 chloride channels: Effects of antisense and oxidants

T. X. Weng, L. Mo, H. L. Hellmich, A. S.L. Yu, T. Wood, N. K. Wills

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Genetic mutations of the Cl- channel ClC-5 cause Dent's disease in humans. We recently cloned an amphibian ortholog of Xenopus ClC-5 (xClC-5) from the A6 cell line. We now compare the properties and regulation of ClC-5 currents expressed in mammalian (COS-7) cells and Xenopus oocytes. Whole cell currents in COS-7 cells transfected with xClC-5 cDNA had strong outward rectification, Cl- > I- anion sensitivity, and were inhibited at low pH, similar to previous results in oocytes. In oocytes, antisense xClC-5 cRNA injection had no effect on endogenous membrane currents or the heterologous expression of human ClC-5. Activators of cAMP and protein kinase C inhibitors had no significant effects on ClC-5 currents expressed in either COS-7 cells or oocytes, whereas H-89, a cAMP-dependent protein kinase (PKA) inhibitor, and hydrogen peroxide decreased the currents. We conclude that the basic properties of ClC-5 currents were independent of the host cell type used for expression. In addition, ClC-5 channels may be modulated by PKA and reactive oxygen species.

Original languageEnglish (US)
Pages (from-to)C1511-C1520
JournalAmerican Journal of Physiology - Cell Physiology
Issue number6 49-6
StatePublished - 2001
Externally publishedYes


  • Dent's disease
  • Hydrogen peroxide
  • Mammalian COS-7 cells
  • Patch clamp
  • Xenopus oocytes

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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