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Sulfasalazine induces apoptosis of HBx-expressing cells in an NF-kappaB-independent manner.

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dc.contributor.authorLee, YM-
dc.contributor.authorKang, M-
dc.contributor.authorHwang, JM-
dc.contributor.authorLee, S-
dc.contributor.authorCho, H-
dc.contributor.authorKim, YS-
dc.date.accessioned2011-04-27T02:20:30Z-
dc.date.available2011-04-27T02:20:30Z-
dc.date.issued2010-
dc.identifier.issn0920-8569-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/2463-
dc.description.abstractThe Hepatitis B virus (HBV) is a causative agent of acute chronic hepatitis, cirrhosis, and hepatocarcinoma. The Hepatitis B virus X protein (HBx) has pleiotypic functions in the regulation of proliferation and apoptosis. It has been suggested that the anti-inflammatory drug sulfasalazine, which is commonly used to treat rheumatoid arthritis and inflammatory bowel disease, inhibits nuclear factor NF-kappaB and induces cell death in HBx-expressing liver cells. In this study, we demonstrate that sulfasalazine induces cell death via apoptosis in HBx-expressing liver cells, as evidenced by characteristic changes in nuclear morphology, cleavage of poly (ADP-ribose) polymerase (PARP), caspase-3 and caspase-9, and activation of caspase-3. We also demonstrate that inhibition of NF-kappaB by siRNA fails to induce apoptosis of HBx-expressing liver cells, indicating that sulfasalazine modulates apoptosis of HBx-expressing cells in an NF-kappaB-independent manner.-
dc.language.isoen-
dc.subject.MESHApoptosis-
dc.subject.MESHCaspase 3-
dc.subject.MESHCaspase 9-
dc.subject.MESHCell Line-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHHepatitis B virus-
dc.subject.MESHHumans-
dc.subject.MESHLiver-
dc.subject.MESHNF-kappa B-
dc.subject.MESHPoly(ADP-ribose) Polymerases-
dc.subject.MESHSulfasalazine-
dc.subject.MESHTrans-Activators-
dc.titleSulfasalazine induces apoptosis of HBx-expressing cells in an NF-kappaB-independent manner.-
dc.typeArticle-
dc.identifier.pmid19859796-
dc.contributor.affiliatedAuthor조, 혜성-
dc.type.localJournal Papers-
dc.identifier.doi10.1007/s11262-009-0416-4-
dc.citation.titleVirus genes-
dc.citation.volume40-
dc.citation.number1-
dc.citation.date2010-
dc.citation.startPage37-
dc.citation.endPage43-
dc.identifier.bibliographicCitationVirus genes, 40(1). : 37-43, 2010-
dc.identifier.eissn1572-994X-
dc.relation.journalidJ009208569-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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