Population
Oocyte model expressing wild-type and mutant inward rectifying renal K(+) channels (Kir 1.1a / ROMK)
Comparison
Expression of truncated mutant channels and… vs Wild-type Kir 1.1a channels
Design
Preclinical
Authors
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No immediate clinical implications for Bartter syndrome; leaves open therapeutic targeting of the Kir1.1 COOH terminus.
The study identifies the extreme COOH terminus of the Kir 1.1a channel as a critical domain for subunit oligomerization and open-state stabilization, providing a mechanistic basis for the loss of function in a Bartter's syndrome mutation.
Flagg et al. (1999) studied this question.
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