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Literature DB >> 24702011

Channels and pumps in aldosterone-producing adenomas.

Celso E Gomez-Sanchez¹.

Abstract

Entities: Disease

Mesh：

Substances：

Year: 2014 PMID： 24702011 PMCID： PMC3973779 DOI： 10.1210/jc.2014-1062

Source DB: PubMed Journal: J Clin Endocrinol Metab ISSN： 0021-972X Impact factor: 5.958

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26 in total

1. The role of TASK1 in aldosterone production and its expression in normal adrenal and aldosterone-producing adenomas.

Authors: Edson F Nogueira; Daniel Gerry; Franco Mantero; Barbara Mariniello; William E Rainey
Journal: Clin Endocrinol (Oxf) Date: 2009-10-28 Impact factor: 3.478

2. KCNJ5 mutations in European families with nonglucocorticoid remediable familial hyperaldosteronism.

Authors: Paolo Mulatero; Philipp Tauber; Maria-Christina Zennaro; Silvia Monticone; Katharina Lang; Felix Beuschlein; Evelyn Fischer; Davide Tizzani; Anna Pallauf; Andrea Viola; Laurence Amar; Tracy Ann Williams; Tim M Strom; Elisabeth Graf; Sascha Bandulik; David Penton; Pierre-François Plouin; Richard Warth; Bruno Allolio; Xavier Jeunemaitre; Franco Veglio; Martin Reincke
Journal: Hypertension Date: 2011-12-27 Impact factor: 10.190

3. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension.

Authors: Murim Choi; Ute I Scholl; Peng Yue; Peyman Björklund; Bixiao Zhao; Carol Nelson-Williams; Weizhen Ji; Yoonsang Cho; Aniruddh Patel; Clara J Men; Elias Lolis; Max V Wisgerhof; David S Geller; Shrikant Mane; Per Hellman; Gunnar Westin; Göran Åkerström; Wenhui Wang; Tobias Carling; Richard P Lifton
Journal: Science Date: 2011-02-11 Impact factor: 47.728

4. Lower expression of the TWIK-related acid-sensitive K+ channel 2 (TASK-2) gene is a hallmark of aldosterone-producing adenoma causing human primary aldosteronism.

Authors: Livia Lenzini; Brasilina Caroccia; Abril González Campos; Ambrogio Fassina; Anna S Belloni; Teresa M Seccia; Maniselvan Kuppusamy; Silvia Ferraro; Ghizlane Skander; Michael Bader; William E Rainey; Gian Paolo Rossi
Journal: J Clin Endocrinol Metab Date: 2013-11-27 Impact factor: 5.958

5. Microribonucleic acid-21 increases aldosterone secretion and proliferation in H295R human adrenocortical cells.

Authors: Damian G Romero; Maria W Plonczynski; Cristian A Carvajal; Elise P Gomez-Sanchez; Celso E Gomez-Sanchez
Journal: Endocrinology Date: 2008-01-24 Impact factor: 4.736

6. Invalidation of TASK1 potassium channels disrupts adrenal gland zonation and mineralocorticoid homeostasis.

Authors: Dirk Heitzmann; Renaud Derand; Stefan Jungbauer; Sascha Bandulik; Christina Sterner; Frank Schweda; Abeer El Wakil; Enzo Lalli; Nicolas Guy; Raymond Mengual; Markus Reichold; Ines Tegtmeier; Saïd Bendahhou; Celso E Gomez-Sanchez; M Isabel Aller; William Wisden; Achim Weber; Florian Lesage; Richard Warth; Jacques Barhanin
Journal: EMBO J Date: 2007-11-22 Impact factor: 11.598

Channels and pumps in aldosterone-producing adenomas.

1. The role of TASK1 in aldosterone production and its expression in normal adrenal and aldosterone-producing adenomas.

2. KCNJ5 mutations in European families with nonglucocorticoid remediable familial hyperaldosteronism.

3. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension.

4. Lower expression of the TWIK-related acid-sensitive K+ channel 2 (TASK-2) gene is a hallmark of aldosterone-producing adenoma causing human primary aldosteronism.

5. Microribonucleic acid-21 increases aldosterone secretion and proliferation in H295R human adrenocortical cells.

6. Invalidation of TASK1 potassium channels disrupts adrenal gland zonation and mineralocorticoid homeostasis.

Review 7. TASK1 and TASK3 potassium channels: determinants of aldosterone secretion and adrenocortical zonation.

8. Single K+ channels in adrenal zona glomerulosa cells. II. Inhibition by angiotensin II.

Review 9. Control of aldosterone secretion: a model for convergence in cellular signaling pathways.

10. TASK channel deletion in mice causes primary hyperaldosteronism.

Review 1. Potassium and Its Discontents: New Insight, New Treatments.

2. ARMC5 mutation analysis in patients with primary aldosteronism and bilateral adrenal lesions.