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Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause

Sequence analysis identifies gain-of-function somatic mutations in GNA11 or GNAQ in CTNNB1-mutant aldosterone-producing adenomas. Most patients with these mutations presented during puberty, pregnancy or menopause, with elevated LHCGR expression.

Junhua Zhou
Elena A. B. Azizan
Morris J. Brown
Research12 Aug 2021
Nature Genetics

Volume: 53, P: 1360-1372
Somatic mutations of CADM1 in aldosterone-producing adenomas and gap junction-dependent regulation of aldosterone production

Recurrent somatic mutations altering residues in the transmembrane domain of CADM1 are identified in aldosterone-producing adenomas. Follow-up studies implicate a role of gap junction communication in regulating aldosterone production.

Xilin Wu
Elena A. B. Azizan
Morris J. Brown
ResearchOpen Access08 Jun 2023
Nature Genetics

Volume: 55, P: 1009-1021
Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension

Morris Brown and colleagues identify somatic mutations in ATP1A1 and CACNA1D in aldosterone-producing adenomas with features resembling zonaglomerulosa cells. They further show that the ATP1A1 mutations cause inward leak currents under physiological conditions, whereas the CACNA1D mutations induce a shift of voltage-dependent gating to more negative potentials and suppress channel inactivation.

Elena A B Azizan
Hanne Poulsen
Morris J Brown
Research04 Aug 2013
Nature Genetics

Volume: 45, P: 1055-1060
Regulation of aldosterone secretion by Ca_v1.3

Catherine B. Xie
Lalarukh Haris Shaikh
Morris J. Brown
ResearchOpen Access21 Apr 2016
Scientific Reports

Volume: 6, P: 1-10
Primary aldosteronism: molecular medicine meets public health

Primary aldosteronism is the most common cause of endocrine arterial hypertension and is characterized by the autonomous production of aldosterone from one or both adrenal glands. This Review describes the molecular discoveries and developments that have the potential to transform the clinical management of patients with this disease.

Elena A. B. Azizan
William M. Drake
Morris J. Brown
Reviews23 Aug 2023
Nature Reviews Nephrology

Volume: 19, P: 788-806

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Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause

Somatic mutations of CADM1 in aldosterone-producing adenomas and gap junction-dependent regulation of aldosterone production

Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension

Regulation of aldosterone secretion by Ca_v1.3

Primary aldosteronism: molecular medicine meets public health

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Somatic mutations of GNA11 and GNAQ in CTNNB1-mutant aldosterone-producing adenomas presenting in puberty, pregnancy or menopause

Somatic mutations of CADM1 in aldosterone-producing adenomas and gap junction-dependent regulation of aldosterone production

Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension

Regulation of aldosterone secretion by Cav1.3

Primary aldosteronism: molecular medicine meets public health

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Regulation of aldosterone secretion by Ca_v1.3