Dataset on the differentiation of THP-1 monocytes to LPS inducible adherent macrophages and their capacity for NO/iNOS signaling

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dc.authorid0000-0003-0195-3383en_US
dc.authorid0000-0001-8989-8045en_US
dc.authorid0000-0002-1740-4867en_US
dc.authorscopusid57203003221en_US
dc.authorscopusid57211689507en_US
dc.authorscopusid22136607900en_US
dc.authorwosidAAR-5653-2020en_US
dc.authorwosid-en_US
dc.authorwosid-en_US
dc.contributor.authorÖzleyen, Adem
dc.contributor.authorYılmaz, Yakup Berkay
dc.contributor.authorBoyuneğmez Tümer, Tuğba
dc.date.accessioned2024-12-24T08:26:04Z
dc.date.available2024-12-24T08:26:04Z
dc.date.issued2021en_US
dc.departmentEnstitüler, Lisansüstü Eğitim Enstitüsü, Biyomoleküler Bilimler Ana Bilim Dalı
dc.departmentFakülteler, Fen Fakültesi, Moleküler Biyoloji ve Genetik Bölümü
dc.description.abstractWhen THP-1 cells are differentiated into adherent macro-phage-like cells, they respond to inflammatory stimuli by changing their phenotypes to an activation state and altering the expression of inflammation-related genes. Nitric oxide (NO) is a diatomic molecule implicating in various pathological conditions including tissue damage, ER stress, obesity, and cancer. The sustained inflammatory microenvironment leads to increased NO release through the activation of the inducible nitric oxide synthase (iNOS) gene in macrophages. Here, we provide a dataset on the optimized conditions for the THP-1 differentiation and the induction of NO/iNOS signaling under inflammatory stimulus. The human monocytic cells were differentiated into adherent macrophage-like phenotype by phorbol-12-myristate-13-acetate (PMA) stimulation under optimized conditions. In this study, NO/iNOS signaling capacity and the regulation of other pro-inflammatory genes including TNF-α, IL-1β, and COX-2 in the LPS-induced THP-1 were examined.en_US
dc.identifier.citationÖzleyen, A., Yılmaz, Y. B., & Boyuneğmez Tümer, T. (2021). Dataset on the differentiation of THP-1 monocytes to LPS inducible adherent macrophages and their capacity for NO/iNOS signaling. Data in Brief, 35, 106786. https://doi.org/10.1016/j.dib.2021.106786en_US
dc.identifier.doi10.1016/j.dib.2021.106786
dc.identifier.issn2352-3409
dc.identifier.pmid33553532
dc.identifier.scopus2-s2.0-85100179625
dc.identifier.urihttps://doi.org/10.1016/j.dib.2021.106786
dc.identifier.urihttps://hdl.handle.net/20.500.12428/6787
dc.identifier.volume35en_US
dc.identifier.wosWOS:000647430400040
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorÖzleyen, Adem
dc.institutionauthorYılmaz, Yakup Berkay
dc.institutionauthorBoyuneğmez Tümer, Tuğba
dc.language.isoen
dc.publisherElsevier Inc.en_US
dc.relation.ispartofData in Briefen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectInflammationen_US
dc.subjectiNOSen_US
dc.subjectNitric Oxideen_US
dc.subjectPMA differentiationen_US
dc.subjectTHP-1 monocytic cellsen_US
dc.titleDataset on the differentiation of THP-1 monocytes to LPS inducible adherent macrophages and their capacity for NO/iNOS signaling
dc.typeArticle

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