Utilization of a Mutagenesis Screen to Generate Mouse Models of Hyperaldosteronism

Author:

Spyroglou Ariadni1,Wagner Sibylle2,Gomez-Sanchez Celso3,Rathkolb Birgit24,Wolf Eckhard4,Manolopoulou Jenny1,Reincke Martin1,Bidlingmaier Martin1,Hrabé de Angelis Martin25,Beuschlein Felix1

Affiliation:

1. Department of Medicine (A.S., J.M., M.R., M.B., F.B.), Endocrine Research, University Hospital Innenstadt, Ludwig Maximilians University, D-80336 Munich, Germany

2. Institute of Experimental Genetics (S.W., B.R.,M.H.d.A.), Helmholtz Center Munich, D-85746 Neuherberg, Germany

3. G.V. Montgomery Veterans Affairs Medical Center and University of Mississippi Medical Center (C.G.S.), Division of Endocrinology, Jackson, Mississippi 39216

4. Chair of Molecular Animal Breeding and Biotechnology (B.R., E.W.), Gene Center, Ludwig Maximilians University, D-81377 Munich, Germany

5. Chair of Experimental Genetics (M.H.d.A.), Technical University Munich, D-85350 Freising-Weihenstephan, Germany

Publisher

The Endocrine Society

Subject

Endocrinology

Reference28 articles.

1. Primary hyperaldosteronism in essential hypertensives: prevalence, biochemical profile, and molecular biology.;Fardella;J Clin Endocrinol Metab,2000

2. Primary aldosteronism: current knowledge and controversies in Conn’s syndrome.;Schirpenbach;Nat Clin Pract Endocrinol Metab,2007

3. [Therapy-resistant hypertension—the endocrinological view].;Beuschlein;MMW Fortschr Med,2007

4. Invalidation of TASK1 potassium channels disrupts adrenal gland zonation and mineralocorticoid homeostasis.;Heitzmann;EMBO J,2008

5. TASK channel deletion in mice causes primary hyperaldosteronism.;Davies;Proc Natl Acad Sci USA,2008

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