Cl- channel activity in Xenopus oocytes expressing the cystic fibrosis gene
The expression of the cystic fibrosis (CF) gene on its introduction into nonepithelial somatic cells has recently been shown to result in the appearance of distinctive low conductance chloride channels stimulated by cyclic AMP (Kartner, N., Hanrahan, J.W., Jensen, T.J., Naismith, A.L., Sun, S., Acke...
Gespeichert in:
Veröffentlicht in: | The Journal of biological chemistry 1991-10, Vol.266 (29), p.19142-19145 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | The expression of the cystic fibrosis (CF) gene on its introduction into nonepithelial somatic cells has recently been shown
to result in the appearance of distinctive low conductance chloride channels stimulated by cyclic AMP (Kartner, N., Hanrahan,
J.W., Jensen, T.J., Naismith, A.L., Sun, S., Ackerley, C.A., Reyes, E.F., Tsui, L.-C., Rommens, J.M., Bear, C.E., and Riordan,
J.R. (1991) Cell 64, 681-691; Anderson, M. P., Rich, D.P., Gregory, R.J., Smith, A.E., and Welsh, M.J. (1991) Science 251,
679-682). Since Xenopus oocytes provide a powerful system for ion channel characterization, we have examined whole cell and
single channel currents in them after injection of cRNA to program the synthesis of the cystic fibrosis transmembrane conductance
regulator (CFTR). This has enabled the direct demonstration that the cyclic AMP activation is mediated by protein kinase A
and that CFTR is without effect on the endogenous calcium-activated chloride channels of the oocyte, which have been well
characterized previously and widely used as reporters of the expression of G-protein-coupled receptors. These findings strengthen
the argument that the CF gene codes for a novel regulated chloride channel rather than a regulatory protein which can modulate
separate chloride channel molecules. |
---|---|
ISSN: | 0021-9258 1083-351X |
DOI: | 10.1016/S0021-9258(18)54971-1 |