7m8v
From Proteopedia
Human CYP11B2 in complex with LCI699
Structural highlights
DiseaseC11B2_HUMAN Familial hyperreninemic hypoaldosteronism type 1;Familial hyperaldosteronism type I. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The molecular defect causing hyperaldosteronism familial 1 is an anti-Lepore-type fusion of the CYP11B1 and CYP11B2 genes. The hybrid gene has the promoting part of CYP11B1, ACTH-sensitive, and the coding part of CYP11B2. FunctionC11B2_HUMAN Preferentially catalyzes the conversion of 11-deoxycorticosterone to aldosterone via corticosterone and 18-hydroxycorticosterone.[1] Publication Abstract from PubMed[Figure: see text]. Aldosterone Synthase Structure With Cushing Disease Drug LCI699 Highlights Avenues for Selective CYP11B Drug Design.,Brixius-Anderko S, Scott EE Hypertension. 2021 Sep;78(3):751-759. doi: 10.1161/HYPERTENSIONAHA.121.17615., Epub 2021 Jul 12. PMID:34247511[2] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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