Differential regulation of Akt phosphorylation in endometriosis

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dc.authoridcinar, ozgur/0000-0003-2901-1910
dc.authoridSEVAL CELIK, Yasemin/0000-0002-6516-6285
dc.authoridUz, Yesim/0000-0002-0381-4590
dc.authorwosidcinar, ozgur/ABI-5190-2020
dc.authorwosidSEVAL ÇELİK, Yasemin/IQS-9427-2023
dc.contributor.authorCinar, Ozgur
dc.contributor.authorSeval, Yasemin
dc.contributor.authorUz, Yesim H.
dc.contributor.authorCakmak, Hakan
dc.contributor.authorUlukus, Murat
dc.contributor.authorKayisli, Umit A.
dc.contributor.authorArici, Aydin
dc.date.accessioned2024-06-12T10:51:05Z
dc.date.available2024-06-12T10:51:05Z
dc.date.issued2009
dc.departmentTrakya Üniversitesien_US
dc.description.abstractProtein kinase B (PKB/Akt), a serine/threonine kinase, regulates the function of many cellular proteins involved in apoptosis and proliferation. It was postulated that there is a higher Akt activity in endometriosis compared with normal endometrium, and that oestrogen may be one of the factors responsible for the high Akt activation in endometriotic cells. Phospho-Akt (pAkt) concentrations in normal, eutopic and ectopic endometrial tissues were compared by immunohistochemistry, and a higher pAkt immunoreactivity was revealed in eutopic and ectopic endometrium compared with normal endometrium, in vivo. Higher Akt phosphorylation in stromal cells from eutopic endometrium was observed, when compared with normal, ill vitro (P < 0.05). Akt phosphorylation was rapidly (2-10 min) stimulated when endometrial stromal cells from normal and endometriosis patients were treated with 17 beta-oestradiol. In endometrial stromal cells from the endometriosis group, ICI 182,780 (10, a specific oestrogen receptor antagonist) failed to antagonize the effect of oestradiol when combined with oestradiol, and revealed a stimulatory effect on Akt phosphorylation when given alone (P < 0.05). In Conclusion, since Akt affects cell survival, it is suggested that increased Akt phosphorylation may be related to the altered apoptosis/proliferation harmony in endometriosis, and therefore Akt may play a critical role in the pathogenesis of endometriosis.en_US
dc.identifier.doi10.1016/j.rbmo.2009.10.001
dc.identifier.endpage871en_US
dc.identifier.issn1472-6483
dc.identifier.issn1472-6491
dc.identifier.issue6en_US
dc.identifier.pmid20031030en_US
dc.identifier.scopus2-s2.0-77449109106en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage864en_US
dc.identifier.urihttps://doi.org/10.1016/j.rbmo.2009.10.001
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18241
dc.identifier.volume19en_US
dc.identifier.wosWOS:000273671000017en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Sci Ltden_US
dc.relation.ispartofReproductive Biomedicine Onlineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAkt Phosphorylationen_US
dc.subjectEndometriosisen_US
dc.subjectOestradiolen_US
dc.subjectCell-Cycle Delayen_US
dc.subjectEstrogen-Receptoren_US
dc.subjectStromal Cellsen_US
dc.subjectEndothelial-Cellsen_US
dc.subjectCortical-Neuronsen_US
dc.subjectProtein-Kinaseen_US
dc.subjectApoptosisen_US
dc.subjectExpressionen_US
dc.subjectProgesteroneen_US
dc.subjectActivationen_US
dc.titleDifferential regulation of Akt phosphorylation in endometriosisen_US
dc.typeArticleen_US

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