Molecular and Electrophysiological Analyses of ATP2B4 Gene Variants in Bilateral Adrenal Hyperaldosteronism-Reference-Cited by-同舟云学术

Molecular and Electrophysiological Analyses of ATP2B4 Gene Variants in Bilateral Adrenal Hyperaldosteronism

Published:2020-01-30 Issue:1 Volume:11 Page:52-62
ISSN:1868-8497
Container-title:Hormones and Cancer
language:en
Short-container-title:HORM CANC

Author:

Hattangady Namita Ganesh,Foster Jessica,Lerario Antonio Marcondes,Ponce-Balbuena Daniela,Rege Juilee,Monticone Silvia,Rainey William E.,Mulatero Paolo,Else Tobias^ORCID

Funder

American Heart Association

National Heart, Lung, and Blood Institute

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Endocrine and Autonomic Systems,Endocrinology,Oncology,Endocrinology, Diabetes and Metabolism

Link

http://link.springer.com/content/pdf/10.1007/s12672-019-00375-0.pdf

Reference45 articles.

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2. Azizan EA, Murthy M, Stowasser M, Gordon R, Kowalski B, Xu S, Brown MJ, O'Shaughnessy KM (2012) Somatic mutations affecting the selectivity filter of KCNJ5 are frequent in 2 large unselected collections of adrenal aldosteronomas. Hypertension 59(3):587–591

3. Azizan EA, Poulsen H, Tuluc P, Zhou J, Clausen MV, Lieb A, Maniero C, Garg S, Bochukova EG, Zhao W, Shaikh LH, Brighton CA, Teo AE, Davenport AP, Dekkers T, Tops B, Kusters B, Ceral J, Yeo GS, Neogi SG, McFarlane I, Rosenfeld N, Marass F, Hadfield J, Margas W, Chaggar K, Solar M, Deinum J, Dolphin AC, Farooqi IS, Striessnig J, Nissen P, Brown MJ (2013) Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat Genet 45(9):1055–1060

4. Beuschlein F, Boulkroun S, Osswald A, Wieland T, Nielsen HN, Lichtenauer UD, Penton D, Schack VR, Amar L, Fischer E, Walther A, Tauber P, Schwarzmayr T, Diener S, Graf E, Allolio B, Samson-Couterie B, Benecke A, Quinkler M, Fallo F, Plouin PF, Mantero F, Meitinger T, Mulatero P, Jeunemaitre X, Warth R, Vilsen B, Zennaro MC, Strom TM, Reincke M (2013) Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension. Nat Genet 45(4):440–4–444e1–2

5. Charmandari E, Sertedaki A, Kino T, Merakou C, Hoffman DA, Hatch MM, Hurt DE, Lin L, Xekouki P, Stratakis CA, Chrousos GP (2012) A novel point mutation in the KCNJ5 gene causing primary hyperaldosteronism and early-onset autosomal dominant hypertension. J Clin Endocrinol Metab 97(8):E1532–E1539

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1. Somatic SLC30A1 mutations altering zinc transporter ZnT1 cause aldosterone-producing adenomas and primary aldosteronism;Nature Genetics;2023-09-14

2. Zinc transporter somatic gene mutations cause primary aldosteronism;2022-07-25

3. Update on the Genetics of Primary Aldosteronism and Aldosterone-Producing Adenomas;Current Cardiology Reports;2022-07-16

4. Pathophysiology of bilateral hyperaldosteronism;Current Opinion in Endocrinology, Diabetes & Obesity;2022-06

5. Progress on Genetic Basis of Primary Aldosteronism;Biomedicines;2021-11-17