Enteric oxalate secretion is not directly mediated by the human CFTR chloride channel
Urological Research, ISSN: 0300-5623, Vol: 36, Issue: 3-4, Page: 127-131
2008
- 9Citations
- 5Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations9
- Citation Indexes9
- CrossRef6
- Captures5
- Readers5
Article Description
The secretion of the oxalate anion by intestinal epithelia is a functionally significant component of oxalate homeostasis and hence a relevant factor in the etiology and management of calcium oxalate urolithiasis. To test the hypothesis that human cystic fibrosis transmembrane conductance regulator (hCFTR) can directly mediate the efflux of the oxalate anion, we compared cAMP-stimulated Cl, C-oxalate, and SO efflux from Xenopus oocytes expressing hCFTR with water-injected control oocytes. hCFTR-expressing oocytes exhibited a large, reversible cAMP-dependent increase in whole cell conductance measured using a two-electrode voltage clamp and a 13-fold increase in rate of cAMP-stimulated Cl efflux. In contrast, the rate constants of oxalate and sulfate efflux were low and unaffected by cAMP in either control or hCFTR-expressing oocytes. We conclude that the human CFTR gene product does not directly mediate oxalate efflux in secretory epithelia and hence is not directly involved in oxalate homeostasis in humans. © 2008 Springer-Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=48349144487&origin=inward; http://dx.doi.org/10.1007/s00240-008-0142-8; http://www.ncbi.nlm.nih.gov/pubmed/18563405; http://link.springer.com/10.1007/s00240-008-0142-8; https://dx.doi.org/10.1007/s00240-008-0142-8; https://link.springer.com/article/10.1007/s00240-008-0142-8; http://www.springerlink.com/index/10.1007/s00240-008-0142-8; http://www.springerlink.com/index/pdf/10.1007/s00240-008-0142-8
Springer Science and Business Media LLC
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