Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/4021
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dc.contributor.authorSavic, Dankaen_US
dc.contributor.authorKnezevic, Goranen_US
dc.contributor.authorDamjanovic, Svetozaren_US
dc.contributor.authorAntic, Jadrankaen_US
dc.contributor.authorMatić, Gordanaen_US
dc.date.accessioned2021-04-16T15:42:36Z-
dc.date.available2021-04-16T15:42:36Z-
dc.date.issued2014-
dc.identifier.issn0165-0327-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/4021-
dc.description.abstractThe hypothalamo-pituitary-adrenocortical (HPA) axis self-regulation is achieved via cortisol binding to mineralocorticoid (MR) and glucocorticoid receptors (GR). It is often disturbed in mental disorders, particularly in those where traumatic stress has been implicated, such as posttraumatic stress disorder and depression. Although dexamethasone suppression test (DST) is often used as diagnostic aid, the findings still vary. In search of the factors influencing the DST outcome, we examined the glucocorticoid receptor (GR) gene BclI polymorphism.en_US
dc.language.isoenen_US
dc.relation.ispartofJournal of Affective Disordersen_US
dc.relation.ispartofseries168;1-4-
dc.subjectDexamethasone suppression testen_US
dc.subjectGR gene snp BclIen_US
dc.subjectGlucocorticoid receptoren_US
dc.subjectMineralocorticoid receptoren_US
dc.titleGR gene BclI polymorphysm changes the path, but not the level, of dexamethasone-induced cortisol suppressionen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.jad.2014.06.046-
dc.identifier.pmid25033471-
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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