Depletion of Tip60/Kat5 affects the hepatic antioxidant system in mice

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dc.authoridKOCPINAR, ENVER FEHIM/0000-0002-6031-4664
dc.authoridBudak, Harun/0000-0002-7371-8959
dc.contributor.authorKocpinar, Enver Fehim
dc.contributor.authorBaltaci, Nurdan Gonul
dc.contributor.authorAkkemik, Ebru
dc.contributor.authorBudak, Harun
dc.date.accessioned2024-12-24T19:24:11Z
dc.date.available2024-12-24T19:24:11Z
dc.date.issued2023
dc.departmentSiirt Üniversitesi
dc.description.abstractTat-interactive protein 60 kDa (TIP60, also known as lysine acetyltransferase 5 [KAT5]) is a member of the MYST protein family with histone acetyltransferase activity. Recent studies have reported that TIP60 has multiple functions in many signal transduction mechanisms, especially p53-mediated apoptosis. Although the activation of apoptosis signaling pathways requires the presence of cellular reactive oxygen species (ROS) at a certain level, an imbalance between the production and consumption of ROS in cells results in oxidative stress (OS). In this study, we investigated for the first time how the absence of the Tip60 gene in the liver affects gene expression, enzyme activity, and protein expression of the hepatic antioxidant members localized in the cytoplasm, including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione S-transferase (GST). First, we successfully generated liver-specific Tip60 knockout mice (mutants) using Cre/LoxP recombination. The reduced glutathione level and nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) expression, a marker of OS, increased significantly in the Tip60 mutant liver. Gene expression, activity, and protein expression of the enzymatic antioxidant system, including SOD, CAT, GR, GPx, and GST were investigated in mutants and control groups. Despite a significant correlation between the gene, enzyme activity, and protein content for CAT and GR, this was not true for SOD and GPx. The overall results suggest that TIP60 acts on the hepatic antioxidant system both at the gene and protein levels, but the actual effect of the deletion of Tip60 is observed at the protein level, especially for SOD and GPx.
dc.description.sponsorshipAtaturk University Scientific Research Projects Coordination Commission [PRJ2010/279, PRJ2013/293]
dc.description.sponsorshipAtaturk University Scientific Research Projects Coordination Commission, Grant/Award Numbers: PRJ2010/279, PRJ2013/293
dc.identifier.doi10.1002/jcb.30348
dc.identifier.endpage117
dc.identifier.issn0730-2312
dc.identifier.issn1097-4644
dc.identifier.issue1
dc.identifier.pmid36377816
dc.identifier.scopus2-s2.0-85142198361
dc.identifier.scopusqualityQ1
dc.identifier.startpage103
dc.identifier.urihttps://doi.org/10.1002/jcb.30348
dc.identifier.urihttps://hdl.handle.net/20.500.12604/5887
dc.identifier.volume124
dc.identifier.wosWOS:000883529100001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Cellular Biochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241222
dc.subjectactivity
dc.subjectantioxidant system
dc.subjectexpression
dc.subjectknockout mice
dc.subjectliver
dc.subjectTip60
dc.titleDepletion of Tip60/Kat5 affects the hepatic antioxidant system in mice
dc.typeArticle

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