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خرید پکیج
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Summary of genetic and molecular mechanisms implicated in Cushing syndrome

Summary of genetic and molecular mechanisms implicated in Cushing 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.
AC: adenylate cyclase; ACTH: corticotropin; ATP: adenosine triphosphate; BMAH: bilateral macronodular adrenal hyperplasia; C-alpha: catalytic subunit of PKA; cAMP: cyclic adenosine monophosphate; GEP-NETs: gastroenteropancreatic neuroendocrine tumors; GPCR: G-protein-coupled receptor; Gs-alpha: alpha subunit of Gs; PDEs: phosphodiesterases; PKA: protein kinase; PPNAD: primary pigmented nodular adrenocortical disease; R1-alpha: type 1-alpha regulatory subunit of PKA.
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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