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Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/6758
DC FieldValueLanguage
dc.contributor.authorLi, Peifeien_US
dc.contributor.authorGoh, Ying-Xianen_US
dc.contributor.authorIlic, Bojanaen_US
dc.contributor.authorTai, Cuien_US
dc.contributor.authorDeng, Zixinen_US
dc.contributor.authorChen, Zhaoyanen_US
dc.contributor.authorĐorđević, Markoen_US
dc.contributor.authorOu, Hong-Yuen_US
dc.date.accessioned2023-11-28T09:03:25Z-
dc.date.available2023-11-28T09:03:25Z-
dc.date.issued2023-04-03-
dc.identifier.issn03057453-
dc.identifier.urihttps://biore.bio.bg.ac.rs/handle/123456789/6758-
dc.description.abstractBacterial toxin-antitoxin (TA) modules respond to various stressful conditions. The Gcn5-related N-acetyltransferase-type toxin (GNAT) protein encoded by the GNAT-RHH TA locus is involved in the antibiotic tolerance of Klebsiella pneumoniae.en_US
dc.language.isoenen_US
dc.publisherOxford University Pressen_US
dc.relation.ispartofThe Journal of antimicrobial chemotherapyen_US
dc.titleAntibiotic-induced degradation of antitoxin enhances the transcription of acetyltransferase-type toxin-antitoxin operonen_US
dc.typeJournal Articleen_US
dc.identifier.doi10.1093/jac/dkad048-
dc.identifier.pmid36857516-
dc.identifier.scopus2-s2.0-85151574183-
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/85151574183-
dc.description.rankM21en_US
dc.description.impact5.758en_US
dc.description.startpage1066en_US
dc.description.endpage1075en_US
dc.relation.issn0305-7453en_US
dc.description.volume78en_US
dc.description.issue4en_US
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.deptChair of General Physiology and Biophysics-
crisitem.author.orcid0000-0002-2903-3119-
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