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dc.creatorJovicic, Milica J.
dc.creatorLukić, Iva
dc.creatorRadoičić, Marija B.
dc.creatorAdžić, Miroslav
dc.creatorMaric, Nadja P.
dc.date.accessioned2018-03-01T16:23:24Z
dc.date.available2018-03-01T16:23:24Z
dc.date.issued2015
dc.identifier.issn0306-9877 (print)
dc.identifier.issn1532-2777 (electronic)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/723
dc.description.abstractGlucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. (C) 2015 Elsevier Ltd. All rights reserved.en
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41029/RS//
dc.rightsopenAccessen
dc.sourceMedical Hypothesesen
dc.titleModulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depressionen
dc.typearticleen
dcterms.abstractЈовициц, Милица Ј.; Радоичић Марија; Мариц, Надја П.; Aджић Мирослав; Лукиц, Ива;
dc.citation.volume85
dc.citation.issue3
dc.citation.spage291
dc.citation.epage294
dc.identifier.wos000360868100011
dc.identifier.doi10.1016/j.mehy.2015.05.015
dc.citation.rankM23
dc.identifier.pmid26052031
dc.identifier.scopus2-s2.0-84939563269
dc.identifier.fulltexthttp://vinar.vin.bg.ac.rs//bitstream/id/13901/719.pdf


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