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The neglected ion: HCO3

Most research into the function of the cystic fibrosis transmembrane conductance regulator has focused on its role in Cl transport. New findings suggest that we may have been focusing on the wrong ion.

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Figure 1: In normal wild-type (WT) cells, both Cl and HC03 are transported at high rates through the plasma membrane of epithelial cells expressing the CFTR Cl channel protein (top).

References

  1. Zielenski, J. Genotype and phenotype in cystic fibrosis. Respiration 67, 117–133 (2000).

    Article  CAS  Google Scholar 

  2. Riordan, J.R. et al. Identification of the cystic fibrosis gene: cloning and characterization of complementary DNA. Science 245, 1066–1072 (1989).

    Article  CAS  Google Scholar 

  3. Frizzell, R., ed. Physiology of cystic fibrosis. Physiol. Rev. 79 (1999).

  4. Knowles, M.R., Friedman, K.J. & Silverman, L.M. Genetics, diagnosis, and clinical phenotypes. in Cystic Fibrosis in Adults (eds. Yankaskas, J.R. & Knowles, M.R.) 27–42 (Lipencott-Raven, Philadelphia, Pennsylvania, 1999).

    Google Scholar 

  5. Choi, J.Y. et al. Aberrant CFTR-dependent HCO3 transport in mutations associated with cystic fibrosis. Nature (in the press).

  6. Hadorn, B.G. et al. Quantitative assessment of exocrine pancreatic function in infants and children. J. Pediatr. 73, 3950 (1968).

    Article  Google Scholar 

  7. Durie, P.R. & Forstner, G.G. The exocrine pancreas. in Cystic Fibrosis in Adults (eds. Yankaskas, J.R. & Knowles, M.R.) 261–287 (Lippincott-Raven, Philadelphia, Pennsylvania, 1999).

    Google Scholar 

  8. Kopelman, H., Durie, P., Gaskin, K., Weizman, Z. & Forstner, G. Pancreatic fluid secretion and protein hyperconcentration in cystic fibrosis. N. Engl. J. Med. 312, 329–334 (1985).

    Article  CAS  Google Scholar 

  9. Kartner, N., Augustinas, O., Jensen, T.J., Naismith, A.L. & Riordan, J.R. Mislocalization of ΔF508 CFTR in cystic fibrosis sweat gland. Nature Genet. 1, 321–327 (1992).

    Article  CAS  Google Scholar 

  10. Kopito, R.R. Biosynthesis and degradation of CFTR. Physiol. Rev. 79, S167–S173 (1999).

    Article  CAS  Google Scholar 

  11. Denning, G.M. et al. Processing of mutant cystic fibrosis transmembrane conductance regulator is temperature-sensitive. Nature 358, 761–764 (1992).

    Article  CAS  Google Scholar 

  12. Holma, B. & Hegg, P.O. pH- and protein-dependent buffer capacity and viscosity of respiratory mucus. Their interrelationships and influence on health. Sci. Total Environ. 84, 71–82 (1989)

    Article  CAS  Google Scholar 

  13. Illek, B., Yankaskas, J.R. & Machen, T.E. cAMP and genistein stimulate HCO3 conductance through CFTR in human airway epithelia. Am. J. Physiol. 16, L752–L761 (1997).

    Google Scholar 

  14. Linsdell, P. et al. Permeability of wild-type and mutant cystic fibrosis transmembrane conductance regulator chloride channels to polyatomic anions. J. Gen. Physiol. 110, 355–364 (1997).

    Article  CAS  Google Scholar 

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Quinton, P. The neglected ion: HCO3. Nat Med 7, 292–293 (2001). https://doi.org/10.1038/85429

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