IndraLab

Statements

CACNA1D activates aldosterone. 5 / 5
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"As outlined above, somatic CACNA1D variants in APAs and APCCs cause excess aldosterone production and primary aldosteronism although they seem not to directly contribute to abnormal cell proliferation and adenoma formation [XREF_BIBR]."
32583268
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"Aldosterone producing adenoma (APA) is a subtype of primary aldosteronism, and somatic mutations in KCNJ5, ATP1A1, ATP2B3, CACNA1D, CLCN2, or CTNNB1 were identified and recognized to drive aldosterone production and/or contribute to tumorigenesis in APA."
32968034
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"Mutations in KCNJ5, ATP1A1, ATP2B3, CACNA1D, and CTNNB1 are thought to cause the excessive autonomous aldosterone secretion of aldosterone producing adenomas (APAs)."
28584016
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"Aldosterone-producing adenoma (APA) is a subtype of primary aldosteronism, and somatic mutations in KCNJ5, ATP1A1, ATP2B3, CACNA1D, CLCN2, or CTNNB1 were identified and recognized to drive aldosterone production and/or contribute to tumorigenesis in APA."
32968034
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"In contrast, CACNA1D mutated aldosterone producing micronodules or aldosterone producing nodules were frequently detected not only in primary aldosteronism patients but also in the zona glomerulosa of normal adrenal glands, which could eventually lead to an autonomous aldosterone production resulting in normotensive or overt primary aldosteronism, but their details have remained unknown."
34011803