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Hypertension, ISSN 0194-911X, 11/2010, Volume 56, Issue 5, pp. 885 - 892
Journal Article
Molecular and Cellular Endocrinology, ISSN 0303-7207, 03/2014, Volume 383, Issue 1-2, pp. 111 - 117
Journal Article
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 | Medical and Health Sciences | MEDICINE | Medicin och hälsovetenskap | MEDICIN
Journal Article
eLife, ISSN 2050-084X, 04/2015, Volume 4, p. 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
Journal Article
Molecular and Cellular Endocrinology, ISSN 0303-7207, 2010, Volume 317, Issue 1, pp. 99 - 105
Journal Article