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Nature Genetics, ISSN 1061-4036, 03/2018, Volume 50, Issue 3, pp. 349 - 354
Journal Article
Journal of Human Hypertension, ISSN 0950-9240, 09/2011, Volume 25, Issue 9, pp. 560 - 564
Journal Article
Clinical and Experimental Pharmacology and Physiology, ISSN 0305-1870, 04/2008, Volume 35, Issue 4, pp. 380 - 385
Journal Article
European Journal of Endocrinology, ISSN 0804-4643, 03/2018, Volume 178, Issue 3, pp. R101 - R111
Aldosterone is the main mineralocorticoid hormone in humans and plays a key role in maintaining water and electrolyte homeostasis. Primary aldosteronism (PA),... 
HYPERALDOSTERONISM TYPE-II | GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM | K+ CHANNEL MUTATIONS | ENDOCRINOLOGY & METABOLISM | KCNJ5 MUTATIONS | BETA-CATENIN | FAMILIAL HYPERALDOSTERONISM | SOMATIC MUTATIONS | ADRENAL-HYPERPLASIA | ADENOMAS | POTASSIUM CHANNEL
Journal Article
MOLECULAR AND CELLULAR ENDOCRINOLOGY, ISSN 0303-7207, 12/2015, Volume 418, pp. 207 - 219
GPER possesses structural and functional characteristics shared by members of the G-protein-coupled receptor (GPCR) superfamily, the largest class of plasma... 
G protein-coupled receptor | HYPERALDOSTERONISM TYPE-II | PRIMARY BREAST-CANCER | INDUCED APOPTOSIS | ACETYLCHOLINE-RELEASE | PLASMA-MEMBRANE | ENDOTHELIAL NITRIC-OXIDE | CELL BIOLOGY | GROWTH-FACTOR RECEPTOR | 30 GPR30 | GPER | ENDOCRINOLOGY & METABOLISM | Membrane estrogen receptor | G-PROTEIN-COUPLED-RECEPTOR-30 GPR30 | MOLECULAR-MECHANISMS
Journal Article
Journal Article
eLife, ISSN 2050-084X, 04/2015, Volume 4, pp. e06315 - e06315
Many Mendelian traits are likely unrecognized owing to absence of traditional segregation patterns in families due to causation by de novo mutations,... 
human biology | incomplete penetrance | de novo mutation | voltage-gated calcium channel | exome sequencing | genes | chromosomes | adrenal gland | medicine | CaV3.2 | human | CHILDHOOD ABSENCE EPILEPSY | GENETIC-VARIATION | HYPERALDOSTERONISM TYPE-II | GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM | BIOLOGY | WHOLE-GENOME ASSOCIATION | CA2+ CHANNEL | T-TYPE | GLOMERULOSA CELLS | FAMILIAL HYPERALDOSTERONISM | SOMATIC MUTATIONS | Recurrence | Aldosterone - biosynthesis | Calcium - metabolism | Humans | Hyperaldosteronism - pathology | Middle Aged | Hyperaldosteronism - complications | Child, Preschool | Molecular Sequence Data | Zona Glomerulosa - pathology | Infant | Male | Hyperaldosteronism - metabolism | Calcium Channels, T-Type - metabolism | Adult | Female | Calcium Channels, T-Type - genetics | Hypertension - genetics | Child | Calcium Signaling | Amino Acid Sequence | Gene Expression | Hyperaldosteronism - genetics | Aldosterone - secretion | Genotype | Zona Glomerulosa - metabolism | Hypertension - pathology | Hypertension - metabolism | Phenotype | Sequence Alignment | Membrane Potentials | Adolescent | Age of Onset | Hypertension - complications | Heterozygote | Mutation | Hypertension | Haplotypes | Pediatrics | Nephrology | Calcium (intracellular) | Statistical analysis | Genomics | Genes | Calcium channels (voltage-gated) | Genomes | Aldosterone | Morbidity | Calcium signalling | Consortia | Pathology | Children | Age | Index Medicus
Journal Article