Article
Enhanced Ca2+ signaling, mild primary aldosteronism, and hypertension in a familial hyperaldosteronism mouse model (Cacna1hM1560V/+ ).
Proceedings of the National Academy of Sciences of the United States of America - 27 Apr 2021
Seidel Eric, Schewe Julia, Zhang Junhui, Dinh Hoang An, Forslund Sofia K, Markó Lajos, Hellmig Nicole, Peters Jörg, Muller Dominik N, Lifton Richard P, Nottoli Timothy, Stölting Gabriel, Scholl Ute I
Abstract excerpt
Gain-of-function mutations in the CACNA1H gene (encoding the T-type calcium channel CaV3.2) cause autosomal-dominant familial hyperaldosteronism type IV (FH-IV) and early-onset hypertension in humans. We used CRISPR/Cas9 to generate Cacna1hM1560V/+ knockin mice as a model of the most common FH-IV mutation, along with corresponding knockout mice (Cacna1h-/- ). Adrenal morphology of both Cacna1hM1560V/+ and...
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