Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/4041
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dc.contributor.authorVojnović Milutinović, D.en_US
dc.contributor.authorMacut, D.en_US
dc.contributor.authorBožić, I.en_US
dc.contributor.authorNestorov, J.en_US
dc.contributor.authorDamjanović, S.en_US
dc.contributor.authorMatić, Gordanaen_US
dc.date.accessioned2021-04-16T18:00:50Z-
dc.date.available2021-04-16T18:00:50Z-
dc.date.issued2011-
dc.identifier.issn0947-7349-
dc.identifier.issn1439-3646-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/4041-
dc.description.abstractMolecular mechanisms underlying pathophysiology of polycystic ovary syndrome (PCOS), especially those related to cortisol signaling, are poorly understood. We hypothesized that modulation of glucocorticoid receptor (GR) expression and function, may underlie possible PCOS-related impairment of feedback inhibition of hypothalamic-pituitary-adrenocortical (HPA) axis activity and thus contribute to increased adrenal androgen production in women with PCOS.en_US
dc.language.isoenen_US
dc.relation.ispartofExperimental and Clinical Endocrinology & Diabetesen_US
dc.relation.ispartofseries119;636-643-
dc.titleHypothalamic-Pituitary-Adrenocortical Axis Hypersensitivity and Glucocorticoid Receptor Expression and Function in Women with Polycystic Ovary Syndromeen_US
dc.typeArticleen_US
dc.identifier.doi10.1055/s-0031-1283122-
dc.identifier.pmid22068557-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.fulltextWith Fulltext-
item.grantfulltextrestricted-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of Biochemistry and Molecular Biology-
crisitem.author.orcid0000-0002-0142-1056-
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