Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4209782 | Journal of Cystic Fibrosis | 2007 | 4 Pages |
Abstract
CFTR was reported to regulate ENaC channel opening, decreasing ENaC activity in airways and increasing it in sweat ducts. We generated MDCK-I cell lines stably expressing tagged αβγENaC + CFTR or ENaC alone, and developed an assay to quantify cell-surface half-life of ENaC. Surprisingly, we found that co-expressed CFTR stabilizes ENaC at the plasma membrane, suggesting that CFTR regulates ENaC stability, not just opening.
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Authors
C. Lu, C. Jiang, S. Pribanic, D. Rotin,