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1. Full Text Genetic Diagnosis by Whole Exome Capture and Massively Parallel DNA Sequencing
by Murim Choi and Ute I. Scholl and Weizhen Ji and Tiewen Liu and Irina R. Tikhonova and Paul Zumbo and Ahmet Nayir and Ayşin Bakkaloğlu and Seza Özen and Sami Sanjad and Carol Nelson-Williams and Anita Farhi and Shrikant Mane and Richard P. Lifton
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2009, Volume 106, Issue 45, pp. 19096 - 19101
Protein coding genes constitute only approximately 1% of the human genome but harbor 85% of the mutations with large effects on disease-related traits.... 
Exome | Bartter syndrome | DNA | Medical genetics | Diarrhea | Genetic loci | Gastrointestinal tract | Genomes | Genetic mutation | Sequencing | Next-generation sequencing | Personal genomes | Congenital chloride diarrhea | Whole-exome sequencing | CONTRIBUTE | VARIANTS | next-generation sequencing | MULTIDISCIPLINARY SCIENCES | SUSCEPTIBILITY | LOSING DIARRHEA | LOCI | congenital chloride diarrhea | COMMON | MUTATIONS | whole-exome sequencing | SLC26A3 | personal genomes | GENOME-WIDE ASSOCIATION | Molecular Diagnostic Techniques - methods | Humans | Computational Biology | Genetic Diseases, Inborn - genetics | Molecular Sequence Data | Open Reading Frames - genetics | Mutation, Missense - genetics | Algorithms | Diarrhea - genetics | Base Sequence | Chlorides | Antiporters - genetics | Chloride-Bicarbonate Antiporters | Genomics - methods | Sequence Analysis, DNA - methods | Hyperaldosteronism | Genetic aspects | Nucleotide sequencing | Diagnosis | Identification and classification | Methods | Proteins | Genomics | Genes | Mutation | Medical diagnosis | Deoxyribonucleic acid--DNA | Index Medicus | Biological Sciences
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2. Full Text Genetic Spectrum and Clinical Correlates of Somatic Mutations in Aldosterone-Producing Adenoma
by Fernandes-Rosa, Fabio Luiz and Williams, Tracy Ann and Riester, Anna and Steichen, Olivier and Beuschlein, Felix and Boulkroun, Sheerazed and Strom, Tim M and Monticone, Silvia and Amar, Laurence and Meatchi, Tchao and Mantero, Franco and Cicala, Maria-Verena and Quinkler, Marcus and Fallo, Francesco and Allolio, Bruno and Bernini, Giampaolo and Maccario, Mauro and Giacchetti, Gilberta and Jeunemaitre, Xavier and Mulatero, Paolo and Reincke, Martin and Zennaro, Maria-Christina
Hypertension, ISSN 0194-911X, 08/2014, Volume 64, Issue 2, pp. 354 - 361
Primary aldosteronism is the most common form of secondary hypertension. Somatic mutations in KCNJ5, ATP1A1, ATP2B3, and CACNA1D have been described in... 
aldosteronism | mutation | adrenal cortex | mineralocorticoids | aldosterone | potassium channels | DIAGNOSIS | ADRENAL-CORTEX | ATP2B3 | ATP1A1 | PREVALENCE | SURGICALLY CORRECTABLE FORMS | KCNJ5 MUTATIONS | PERIPHERAL VASCULAR DISEASE | CHANNEL MUTATIONS | HYPERTENSION | EXPRESSION | Adrenal Cortex Neoplasms - complications | Genetic Predisposition to Disease | Sodium-Potassium-Exchanging ATPase - genetics | Age Factors | Genetic Association Studies | Plasma Membrane Calcium-Transporting ATPases - genetics | Humans | Middle Aged | Hyperaldosteronism - genetics | Male | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Adrenocortical Adenoma - metabolism | Adrenal Cortex Neoplasms - genetics | Aldosterone - metabolism | Calcium Channels, L-Type - genetics | Hyperaldosteronism - etiology | Sex Factors | Adrenocortical Adenoma - genetics | Adult | Female | Potassium - blood | Mutation | Adrenocortical Adenoma - complications | Adrenal Cortex Neoplasms - metabolism | Index Medicus
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3. Full Text EXAMINATION OF CHROMOSOME 7p22 CANDIDATE GENES RBaK, PMS2 AND GNA12 IN FAMILIAL HYPERALDOSTERONISM TYPE II
by Jeske, YWA and So, A and Kelemen, L and Sukor, N and Willys, C and Bulmer, B and Gordon, RD and Duffy, D and Stowasser, M
Clinical and Experimental Pharmacology and Physiology, ISSN 0305-1870, 04/2008, Volume 35, Issue 4, pp. 380 - 385
SUMMARY • There are two types of familial hyperaldosteronism (FH): FH-I and FH-II. FH-I is caused by a hybrid CYP11B1/CYP11B2 gene mutation. The genetic cause... 
PMS2 | familial hyperaldosteronism type II | genetics | RBaK | hypertension | GNA12 | Hypertension | Genetics | Familial hyperaldosteronism type II | APOPTOSIS | PHYSIOLOGY | NO EVIDENCE | MISMATCH REPAIR | PREVALENCE | CANCER | PRIMARY ALDOSTERONISM | RENIN RATIO | PRODUCT | PHARMACOLOGY & PHARMACY | MUTATIONS | Genetic Predisposition to Disease | RNA Splice Sites - genetics | Humans | Middle Aged | DNA Repair Enzymes - genetics | Hyperaldosteronism - genetics | Repressor Proteins - genetics | Male | 5' Untranslated Regions - genetics | Genetic Markers | DNA-Binding Proteins - genetics | Promoter Regions, Genetic - genetics | Adult | Female | Adenosine Triphosphatases - genetics | Aged | Mismatch Repair Endonuclease PMS2 | Polymorphism, Single Nucleotide | Chromosomes, Human, Pair 7 - genetics | Intracellular Signaling Peptides and Proteins - genetics | Chromosomes, Human, Pair 7, genetics | Adenosine Triphosphatases, genetics | Promoter Regions (Genetics), genetics | Repressor Proteins, genetics | 5' Untranslated Regions, genetics | DNA Repair Enzymes, genetics | Intracellular Signaling Peptides and Proteins, genetics | RNA Splice Sites, genetics | DNA-Binding Proteins, genetics | Hyperaldosteronism, genetics | Genetic research | Genetic aspects | DNA binding proteins | Hyperaldosteronism | Index Medicus
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4. Full Text Somatic ATP1A1, ATP2B3, and KCNJ5 Mutations in Aldosterone-Producing Adenomas
by Williams, Tracy Ann and Monticone, Silvia and Schack, Vivien R and Stindl, Julia and Burrello, Jacopo and Buffolo, Fabrizio and Annaratone, Laura and Castellano, Isabella and Beuschlein, Felix and Reincke, Martin and Lucatello, Barbara and Ronconi, Vanessa and Fallo, Francesco and Bernini, Giampaolo and Maccario, Mauro and Giacchetti, Gilberta and Veglio, Franco and Warth, Richard and Vilsen, Bente and Mulatero, Paolo
Hypertension, ISSN 0194-911X, 01/2014, Volume 63, Issue 1, pp. 188 - 195
Aldosterone-producing adenomas (APAs) cause a sporadic form of primary aldosteronism and somatic mutations in the KCNJ5 gene, which encodes the... 
Hypertension | Potassium channels | Sodium-potassium-exchanging ATPase | Adrenal glands | Conn adenoma | Aldosterone | CELLS | APOPTOSIS | DIAGNOSIS | sodium-potassium-exchanging ATPase | K+-ATPASE | TRANSMEMBRANE SEGMENT M1 | aldosterone | NA,K-ATPASE | adrenal glands | potassium channels | GLOMERULOSA | PERIPHERAL VASCULAR DISEASE | SECRETION | hypertension | EXPRESSION | Adrenal Cortex Neoplasms - complications | Gene Expression | Sodium-Potassium-Exchanging ATPase - genetics | Plasma Membrane Calcium-Transporting ATPases - genetics | Aldosterone - biosynthesis | Humans | Middle Aged | Hyperaldosteronism - genetics | Male | Hyperaldosteronism - metabolism | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Hypertension - etiology | Hypertension - metabolism | Adrenal Cortex Neoplasms - genetics | Aldosterone - genetics | Hyperaldosteronism - etiology | Adrenocortical Adenoma - genetics | Adult | Female | Hypertension - genetics | Mutation | Adrenocortical Adenoma - complications | Cytochrome P-450 CYP11B2 - genetics | Index Medicus
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5. Full Text Case Report: Nodule Development From Subcapsular Aldosterone-Producing Cell Clusters Causes Hyperaldosteronism
by Nishimoto, Koshiro and Seki, Tsugio and Kurihara, Isao and Yokota, Kenichi and Omura, Masao and Nishikawa, Tetsuo and Shibata, Hirotaka and Kosaka, Takeo and Oya, Mototsugu and Suematsu, Makoto and Mukai, Kuniaki
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 01/2016, Volume 101, Issue 1, pp. 6 - 9
Context: We previously reported that the human adrenal cortex remodels to form subcapsular aldosterone-producing cell clusters (APCCs). Some APCCs were... 
DIAGNOSIS | ENDOCRINOLOGY & METABOLISM | COMMON | CHANNEL MUTATIONS | ATP1A1 | HYPERTENSION | SOMATIC MUTATIONS | ADENOMAS | Thyroid Nodule - genetics | Sodium-Potassium-Exchanging ATPase - genetics | Aldosterone - biosynthesis | Humans | Hyperaldosteronism - genetics | Steroid 11-beta-Hydroxylase - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Mutation - genetics | Adrenal Cortex Neoplasms - genetics | DNA - genetics | Hyperaldosteronism - etiology | Thyroid Nodule - pathology | Adrenocortical Adenoma - genetics | Adult | Female | Thyroid Nodule - complications | Cytochrome P-450 CYP11B2 - genetics | Index Medicus | Abridged Index Medicus
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6. Full Text Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits
by Evangelou, Evangelos and Warren, Helen R and Mosen-Ansorena, David and Mifsud, Borbala and Pazoki, Raha and Gao, He and Ntritsos, Georgios and Dimou, Niki and Cabrera, Claudia P and Karaman, Ibrahim and Ng, Fu Liang and Evangelou, Marina and Witkowska, Katarzyna and Tzanis, Evan and Hellwege, Jacklyn N and Giri, Ayush and Velez Edwards, Digna R and Sun, Yan V and Cho, Kelly and Gaziano, J. Michael and Wilson, Peter W. F and Tsao, Philip S and Kovesdy, Csaba P and Esko, Tonu and Mägi, Reedik and Milani, Lili and Almgren, Peter and Boutin, Thibaud and Debette, Stéphanie and Ding, Jun and Giulianini, Franco and Holliday, Elizabeth G and Jackson, Anne U and Li-Gao, Ruifang and Lin, Wei-Yu and Luan, Jian’an and Mangino, Massimo and Oldmeadow, Christopher and Prins, Bram Peter and Qian, Yong and Sargurupremraj, Muralidharan and Shah, Nabi and Surendran, Praveen and Thériault, Sébastien and Verweij, Niek and Willems, Sara M and Zhao, Jing-Hua and Amouyel, Philippe and Connell, John and de Mutsert, Renée and Doney, Alex S. F and Farrall, Martin and Menni, Cristina and Morris, Andrew D and Noordam, Raymond and Paré, Guillaume and Poulter, Neil R and Shields, Denis C and Stanton, Alice and Thom, Simon and Abecasis, Gonçalo and Amin, Najaf and Arking, Dan E and Ayers, Kristin L and Barbieri, Caterina M and Batini, Chiara and Bis, Joshua C and Blake, Tineka and Bochud, Murielle and Boehnke, Michael and Boerwinkle, Eric and Boomsma, Dorret I and Bottinger, Erwin P and Braund, Peter S and Brumat, Marco and Campbell, Archie and Campbell, Harry and Chakravarti, Aravinda and Chambers, John C and Chauhan, Ganesh and Ciullo, Marina and Cocca, Massimiliano and Collins, Francis and Cordell, Heather J and Davies, Gail and Borst, Martin H. de and Geus, Eco J. de and Deary, Ian J and Deelen, Joris and Del Greco M, Fabiola and Demirkale, Cumhur Yusuf and Dörr, Marcus and Ehret, Georg B and Elosua, Roberto and Enroth, Stefan and Erzurumluoglu, A. Mesut and Ferreira, Teresa and Frånberg, Mattias and Franco, Oscar H and Gandin, Ilaria and ... and Million Vet Program and Million Veteran Program and the Million Veteran Program and Stockholms universitet and Matematiska institutionen and Naturvetenskapliga fakulteten
Nature Genetics, ISSN 1061-4036, 10/2018, Volume 50, Issue 10, pp. 1412 - 1425
High blood pressure is a highly heritable and modifiable risk factor for cardiovascular disease. We report the largest genetic association study of blood... 
CARDIOVASCULAR-DISEASE RISK | UK BIOBANK | METAANALYSIS | VARIANTS | RARE | HYPERALDOSTERONISM | GENETICS & HEREDITY | COMMON | HEALTH | HYPERTENSION | GENOME-WIDE ASSOCIATION | Human Umbilical Vein Endothelial Cells | Genetic Predisposition to Disease | Genome-Wide Association Study | Life Style | Blood Pressure - genetics | Humans | Middle Aged | Risk Factors | Cells, Cultured | Male | Genetic Loci | Cardiovascular Diseases - genetics | Genetic Testing - methods | Genetics, Population - methods | Aged, 80 and over | Cardiovascular Diseases - epidemiology | Adult | Female | Aged | Polymorphism, Single Nucleotide | Hypertension - genetics | Quantitative Trait Loci | Hypertension | Health risks | Cardiovascular disease | Genomes | Risk analysis | Loci | Blood | Risk factors | Meta-analysis | Studies | Consortia | Genetic analysis | Blood pressure | Gene loci | Lifestyles | Cardiovascular diseases | Health risk assessment | Index Medicus | Biological Sciences | Naturvetenskap | Natural Sciences | Biologiska vetenskaper
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7. Full Text Screening for membrane hormone receptor expression in primary aldosteronism
by Zwermann, O and Suttmann, Y and Bidlingmaier, M and Beuschlein, F and Reincke, Martin
European Journal of Endocrinology, ISSN 0804-4643, 2009, Volume 160, Issue 3, pp. 443 - 451
Objective: The investigation of expression and functional relevance of G-protein Coupled receptors in primary aldosteronism (PA) by molecular and clinical... 
DEPENDENT CUSHINGS-SYNDROME | IN-VITRO | ADRENOCORTICAL FUNCTION | VIVO | MACRONODULAR ADRENAL-HYPERPLASIA | CORTISOL HYPERSECRETION | ENDOCRINOLOGY & METABOLISM | V-1A RECEPTOR | VASOPRESSIN | SECRETION | GASTRIC-INHIBITORY POLYPEPTIDE | Receptors, Glucagon - genetics | Receptors, LHRH - genetics | Receptors, Thyrotropin - genetics | Genetic Testing | Adenoma - genetics | Humans | Middle Aged | Aldosterone - blood | Hyperaldosteronism - genetics | Receptors, Serotonin, 5-HT4 - genetics | Reverse Transcriptase Polymerase Chain Reaction | Receptor, Melanocortin, Type 2 - genetics | Receptor, Angiotensin, Type 1 - genetics | Receptors, LH - genetics | Receptors, Gastrointestinal Hormone - genetics | Receptors, Vasopressin - genetics | Adult | Aged | Receptors, G-Protein-Coupled - genetics | Receptors, Thyrotropin-Releasing Hormone - genetics | Adrenal Gland Neoplasms - genetics | Index Medicus
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8. Full Text Stress-induced Aldosterone Hyper-Secretion in a Substantial Subset of Patients With Essential Hypertension
by Markou, Athina and Sertedaki, Amalia and Kaltsas, Gregory and Androulakis, Ioannis I and Marakaki, Chrisanthi and Pappa, Theodora and Gouli, Aggeliki and Papanastasiou, Labrini and Fountoulakis, Stelios and Zacharoulis, Achilles and Karavidas, Apostolos and Ragkou, Despoina and Charmandari, Evangelia and Chrousos, George P and Piaditis, George P
The Journal of Clinical Endocrinology & Metabolism, ISSN 0021-972X, 08/2015, Volume 100, Issue 8, pp. 2857 - 2864
Context: Aldosterone (ALD) secretion is regulated mainly by angiotensin II, K+, and adrenocorticotropic hormone (ACTH). Mineralocorticoid receptor antagonists... 
RESPONSES | SIGNALING PATHWAYS | HYPERALDOSTERONISM TYPE-I | HEREDITARY HYPERTENSION | ENDOCRINOLOGY & METABOLISM | KCNJ5 MUTATIONS | ADRENOCORTICOTROPIN | PREVALENCE | FAMILIAL HYPERALDOSTERONISM | EXERCISE | GUIDELINE | Adenoma - genetics | Humans | Middle Aged | Mutant Chimeric Proteins - genetics | Hyperaldosteronism - complications | Hyperaldosteronism - metabolism | Steroid 11-beta-Hydroxylase - genetics | Case-Control Studies | Adenoma - metabolism | Aldosterone - metabolism | Adenoma - complications | Stress, Psychological - metabolism | Hypertension - genetics | Essential Hypertension | Hydrocortisone - blood | Adrenocorticotropic Hormone - blood | Aldosterone - blood | Hyperaldosteronism - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Renin - blood | Hypertension - metabolism | Stress, Psychological - genetics | Adrenal Gland Neoplasms - complications | Adrenal Gland Neoplasms - metabolism | Hypertension - complications | Adrenal Gland Neoplasms - genetics | Cytochrome P-450 CYP11B2 - genetics | Index Medicus | Abridged Index Medicus
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9. Full Text Novel somatic mutations in primary hyperaldosteronism are related to the clinical, radiological and pathological phenotype
by Scholl, Ute I and Healy, James M and Thiel, Anne and Fonseca, Annabelle L and Brown, Taylor C and Kunstman, John W and Horne, Matthew J and Dietrich, Dimo and Riemer, Jasmin and Kücükköylü, Seher and Reimer, Esther N and Reis, Anna‐Carinna and Goh, Gerald and Kristiansen, Glen and Mahajan, Amit and Korah, Reju and Lifton, Richard P and Prasad, Manju L and Carling, Tobias
Clinical Endocrinology, ISSN 0300-0664, 12/2015, Volume 83, Issue 6, pp. 779 - 789
Aldosterone-producing adenomas (APAs) and bilateral adrenal hyperplasia are important causes of secondary hypertension. Somatic mutations in KCNJ5, CACNA1D,... 
ALDOSTERONE-PRODUCING ADENOMAS | K+ CHANNEL MUTATIONS | ENDOCRINOLOGY & METABOLISM | KCNJ5 MUTATIONS | ATP2B3 | PREVALENCE | ATP1A1 | HYPERTENSION | EXPRESSION | ADRENAL-HYPERPLASIA | Sodium-Potassium-Exchanging ATPase - genetics | Plasma Membrane Calcium-Transporting ATPases - genetics | Humans | Hyperaldosteronism - pathology | Middle Aged | Hyperaldosteronism - genetics | Male | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Mutation - genetics | beta Catenin - genetics | Calcium Channels, L-Type - genetics | Hyperaldosteronism - etiology | Hyperaldosteronism - diagnostic imaging | Adult | Female | Retrospective Studies | Hypertension | Genetic aspects | Index Medicus | computed tomography | KCNJ5 | CACNA1D | ATPase | primary aldosteronism
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10. Full Text K⁺ Channel Mutations in Adrenal Aldosterone-Producing Adenomas and Hereditary Hypertension
by Murim Choi and Ute I. Scholl and Peng Yue and Peyman Björklund and Bixiao Zhao and Carol Nelson-Williams and Weizhen Ji and Yoonsang Cho and Aniruddh Patel and Clara J. Men and Elias Lolis and Max V. Wisgerhof and David S. Geller and Shrikant Mane and Per Hellman and Gunnar Westin and Göran Åkerström and Wenhui Wang and Tobias Carling and Richard P. Lifton and Medicinska fakulteten and Medicinska och farmaceutiska vetenskapsområdet and Uppsala universitet and Institutionen för kirurgiska vetenskaper
Science, ISSN 0036-8075, 2/2011, Volume 331, Issue 6018, pp. 768 - 772
Endocrine tumors such as aldosterone-producing adrenal adenomas (APAs), a cause of severe hypertension, feature constitutive hormone production and... 
Depolarization | Hypertension | Somatic mutation | Cell growth | Hyperaldosteronism | REPORTS | Loss of heterozygosity | Adenoma | Genetic mutation | Sequencing | Tumors | REMEDIABLE ALDOSTERONISM | HUMAN BREAST | COLORECTAL CANCERS | ADRENOCORTICAL-CELLS | MULTIDISCIPLINARY SCIENCES | CONDUCTION | GLOMERULOSA CELLS | IDENTIFICATION | MOLECULAR-BASIS | SELECTIVITY | POTASSIUM CHANNEL | Adrenal Glands - pathology | Potassium - metabolism | Cell Proliferation | Humans | Hyperaldosteronism - pathology | Hyperplasia | Protein Multimerization | Zona Glomerulosa - pathology | Male | Hyperaldosteronism - metabolism | Sodium - metabolism | Aldosterone - metabolism | Adrenocortical Adenoma - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - metabolism | Female | Hypertension - genetics | Adrenal Cortex Neoplasms - metabolism | Cell Line | G Protein-Coupled Inwardly-Rectifying Potassium Channels - chemistry | Hyperaldosteronism - genetics | Mutant Proteins - genetics | Mutant Proteins - metabolism | Zona Glomerulosa - metabolism | Adrenal Cortex Neoplasms - pathology | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Adrenocortical Adenoma - pathology | Adrenocortical Adenoma - metabolism | Hypertension - metabolism | Adrenal Cortex Neoplasms - genetics | Mutant Proteins - chemistry | Mutation | Index Medicus | Medical and Health Sciences | MEDICINE | Medicin och hälsovetenskap | MEDICIN
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11. Primary aldosteronism
: molecular genetics, endocrinology, and translational medicine
by Hellman, Per
2014, ISBN 1493905090
genetics | Hyperaldosteronism | Renin-Angiotensin System | therapy | metabolism
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12. Full Text Immunohistochemical, genetic and clinical characterization of sporadic aldosterone-producing adenomas
by Monticone, Silvia and Castellano, Isabella and Versace, Karine and Lucatello, Barbara and Veglio, Franco and Gomez-Sanchez, Celso E and Williams, Tracy A and Mulatero, Paolo
Molecular and Cellular Endocrinology, ISSN 0303-7207, 08/2015, Volume 411, Issue C, pp. 146 - 154
Adrenal glands removed for unilateral primary aldosteronism (PA) display marked histological heterogeneity. Recently reported somatic mutations in KCNJ5,... 
KCNJ5 | CACNA1D | CYP11B1 immunohistochemistry | ATP1A1 | CYP11B2 immunohistochemistry | Aldosterone producing adenoma | ANTIBODIES | DIAGNOSIS | ADRENAL-CORTEX | HYPERPLASIA | SOMATIC MUTATIONS | CELL BIOLOGY | ZONA GLOMERULOSA | ENDOCRINOLOGY & METABOLISM | KCNJ5 MUTATIONS | UPRIGHT POSTURE | HYPERTENSION | Sodium-Potassium-Exchanging ATPase - genetics | Plasma Membrane Calcium-Transporting ATPases - genetics | Adenoma - genetics | Humans | Hyperaldosteronism - pathology | Middle Aged | Adrenal Cortex - metabolism | Male | Hyperaldosteronism - metabolism | Adrenal Cortex - pathology | Adenoma - metabolism | Plasma Membrane Calcium-Transporting ATPases - metabolism | Aldosterone - metabolism | Adrenocortical Adenoma - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - metabolism | Adult | Female | Cytochrome P-450 CYP11B2 - metabolism | Hyperaldosteronism - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Adrenocortical Adenoma - pathology | Adrenocortical Adenoma - metabolism | Sodium-Potassium-Exchanging ATPase - metabolism | Calcium Channels, L-Type - genetics | Steroid 11-beta-Hydroxylase - metabolism | Adenoma - pathology | Calcium Channels, L-Type - metabolism | Genetic aspects | Corticosteroids | Aldosterone | Steroids | Index Medicus | ATP2B3
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13. Full Text Clinical characteristics of somatic mutations in Chinese patients with aldosterone-producing adenoma
by Zheng, Fang-Fang and Zhu, Li-Min and Nie, Ai-Fang and Li, Xiao-Ying and Lin, Jing-Rong and Zhang, Ke and Chen, Jing and Zhou, Wen-Long and Shen, Zhou-Jun and Zhu, Yi-Chun and Wang, Ji-Guang and Zhu, Ding-Liang and Gao, Ping-Jin
Hypertension, ISSN 0194-911X, 03/2015, Volume 65, Issue 3, pp. 622 - 628
Recent studies have shown that somatic mutations in the KCNJ5, ATP1A1, ATP2B3, and CACNA1D genes are associated with the pathogenesis of aldosterone-producing... 
KCNJ5 | potassium channel | somatic mutation | hypertension | aldosterone | DIAGNOSIS | HYPERALDOSTERONISM | ATP1A1 | SELECTIVITY FILTER | LEFT-VENTRICULAR HYPERTROPHY | KCNJ5 MUTATIONS | PERIPHERAL VASCULAR DISEASE | CHANNEL MUTATIONS | POTASSIUM | EXPRESSION | Sodium-Potassium-Exchanging ATPase - genetics | Prevalence | Plasma Membrane Calcium-Transporting ATPases - genetics | Humans | Middle Aged | Asian Continental Ancestry Group - genetics | Molecular Sequence Data | Male | Tumor Burden | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | Mutation - genetics | Adrenocortical Adenoma - metabolism | Adrenal Cortex Neoplasms - genetics | Aldosterone - metabolism | Phenotype | Calcium Channels, L-Type - genetics | Base Sequence | Sex Factors | Adrenocortical Adenoma - genetics | Adult | Female | Potassium - blood | Retrospective Studies | Adrenal Cortex Neoplasms - metabolism | Index Medicus
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