Gray, M. A., O'Reilly, C., Winpenny, J. P. and Argent, B. (2001) Functional interactions of HCO3 with cystic fibrosis transmembrane conductance regulator. JOP - Journal of the Pancreas, 2 (Suppl 4). pp. 207-211.
Full text not available from this repository.Abstract
Disruption of normal cystic fibrosis transmembrane conductance regulator- (CFTR)-mediated Cl(-) transport is associated with cystic fibrosis (CF). CFTR is also required for HCO(3)(-) transport in many tissues such as the lungs, gastro-intestinal tract, and pancreas, although the exact role CFTR plays is uncertain. Given the importance of CFTR in HCO(3)(-) transport by so many CF-affected organ systems, it is perhaps surprising that relatively little is known about the interactions of HCO(3)(-) ions with CFTR. We have used patch clamp recordings from native pancreatic duct cells to study HCO(3)(-) permeation and interaction with CFTR. Ion selectivity studies shows that CFTR is between 3-5 times more selective for Cl(-) over HCO(3)(-). In addition, extracellular HCO(3)(-) has a novel inhibitory effect on cAMP-stimulated CFTR currents carried by Cl(-). The block by HCO(3)(-) was rapid, relatively independent of voltage and occurred over the physiological range of HCO(3)(-) concentrations. These data show that luminal HCO(3)(-) acts as a potent regulator of CFTR, and suggests that inhibition involves an external anion-binding site on the channel. This work has implications not only for elucidating mechanisms of HCO(3)(-) transport in epithelia, but also for approaches used to treat CF.
Item Type: | Article |
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Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
Related URLs: | |
Depositing User: | EPrints Services |
Date Deposited: | 25 Nov 2010 11:09 |
Last Modified: | 20 Jun 2024 10:30 |
URI: | https://ueaeprints.uea.ac.uk/id/eprint/12676 |
DOI: |
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