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Summary of genetic and molecular mechanisms implicated in Cushing's syndrome

Summary of genetic and molecular mechanisms implicated in Cushing's syndrome
For each cause, the various genetic mutations or abnormal protein expression believed to play a part in the pathophysiology are shown. The most frequent mechanisms are highlighted in blue characters; the well-characterized mechanisms are highlighted in bold characters, and other potential mechanisms are in normal characters; a question mark shows an unconfirmed association or genetic predisposition.
ACTH: corticotropin; AC: adenylate cyclase; GPCR: G-protein-coupled receptor; Gs-alpha: alpha subunit of Gs; ATP: adenosine triphosphate; cAMP: cyclic adenosine monophosphate; PDEs: phosphodiesterases; GEP-NETs: gastroenteropancreatic neuroendocrine tumors; PKA: protein kinase; R1-alpha: type 1-alpha regulatory subunit of PKA; C-alpha: catalytic subunit of PKA; BMAH: bilateral macronodular adrenal hyperplasia; PPNAD: primary pigmented nodular adrenocortical disease.
From: Lacroix A, Feelders RA, Stratakis CA, Nieman LK. Cushing's syndrome. Lancet 2015; 386:913. Illustration used with the permission of Elsevier Inc. All rights reserved.
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