Glucocorticoid resistance conferring mutation in the C-terminus of GR alters the receptor conformational dynamics

被引:5
作者
Kaziales, Anna [1 ]
Ruehrnoel, Florian [1 ]
Richter, Klaus [1 ]
机构
[1] Tech Univ Munich, Ctr Integrated Prot Sci Munich, Dept Chem, Lichtenbergstr 4, D-85748 Garching, Germany
关键词
GENERAL FORCE-FIELD; LIGAND-BINDING; POINT MUTATION; MOLECULAR CHAPERONES; HSP90; DOMAIN; HETEROCOMPLEX; VISUALIZATION; MECHANISMS; SYSTEM;
D O I
10.1038/s41598-021-92039-9
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The glucocorticoid receptor is a key regulator of essential physiological processes, which under the control of the Hsp90 chaperone machinery, binds to steroid hormones and steroid-like molecules and in a rather complicated and elusive response, regulates a set of glucocorticoid responsive genes. We here examine a human glucocorticoid receptor variant, harboring a point mutation in the last C-terminal residues, L773P, that was associated to Primary Generalized Glucocorticoid Resistance, a condition originating from decreased affinity to hormone, impairing one or multiple aspects of GR action. Using in vitro and in silico methods, we assign the conformational consequences of this mutation to particular GR elements and report on the altered receptor properties regarding its binding to dexamethasone, a NCOA-2 coactivator-derived peptide, DNA, and importantly, its interaction with the chaperone machinery of Hsp90.
引用
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页数:14
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