DC Field | Value | Language |
---|---|---|
dc.contributor.author | J Y Kim | - |
dc.contributor.author | E H Song | - |
dc.contributor.author | H J Lee | - |
dc.contributor.author | Y K Oh | - |
dc.contributor.author | K H Choi | - |
dc.contributor.author | Dae Yeul Yu | - |
dc.contributor.author | S I Park | - |
dc.contributor.author | J K Seong | - |
dc.contributor.author | W H Kim | - |
dc.date.accessioned | 2017-04-19T09:18:20Z | - |
dc.date.available | 2017-04-19T09:18:20Z | - |
dc.date.issued | 2010 | - |
dc.identifier.issn | 0022-2836 | - |
dc.identifier.uri | 10.1016/j.jmb.2010.02.016 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/9483 | - |
dc.description.abstract | Hepatitis B virus X (HBx) protein is an important regulator of hepatic steatosis observed in patients with hepatitis B virus; however, its underlying molecular mechanism remains unclear. TNF receptor 1 (TNFR1) is an essential pathway for the HBx-mediated nuclear factor κB (NF-κB) activation involved in hepatic liver injury. Here, we show that HBx-mediated steatosis and apoptosis are regulated by TNFR1- and NF-κB-dependent pathways. HBx-mediated tumor necrosis factor α (TNF-α) production and NF-κB activation were completely diminished in anti-TNF-α-treated cells and TNF-α-/- or TNFR1-/- mice. HBx and TNFR1, which are potentiated by TNF-α, are physically associated and colocalize in the plasma membrane. Similarly, TNFR1 depletion inhibits lipid droplets, and lipogenic genes such as sterol regulatory element binding protein (SREBP) 1 and peroxisome proliferator-activated receptor (PPAR) γ increased in HBx-Tg mice and HepG2-GFPHBx stable cells. Furthermore, lipid accumulation and expression of SREBP1c and PPARγ are significantly increased in AdHBx-GFP-injected (intravenous) wild-type mice, but not in TNFR1-/- mice. HBx-enhanced transcriptional activities of SREBP1 and PPARγ are significantly attenuated by the NF-κB inhibitor Bay 11-7082, as well as by TNFR1 depletion. Also, AdHBx-GFP potentiates TNF-α-induced apoptosis, which is completely inhibited in TNFR1-depleted cells. Our results suggest that HBx-induced NF-κB activation was mediated by direct interaction with TNFR1 and thereby induced TNF-α production. HBx-induced NF-κB activation is also associated with the induction of hepatic steatosis and apoptosis, which is determined by a TNFR1-dependent pathway. | - |
dc.publisher | Elsevier | - |
dc.title | HBx-Induced hepatic steatosis and apoptosis are regulated by TNFR1- and NF-κB-dependent pathways | - |
dc.title.alternative | HBx-Induced hepatic steatosis and apoptosis are regulated by TNFR1- and NF-κB-dependent pathways | - |
dc.type | Article | - |
dc.citation.title | Journal of Molecular Biology | - |
dc.citation.number | 4 | - |
dc.citation.endPage | 931 | - |
dc.citation.startPage | 917 | - |
dc.citation.volume | 397 | - |
dc.contributor.affiliatedAuthor | Dae Yeul Yu | - |
dc.contributor.alternativeName | 김지연 | - |
dc.contributor.alternativeName | 송은현 | - |
dc.contributor.alternativeName | 이현정 | - |
dc.contributor.alternativeName | 오여경 | - |
dc.contributor.alternativeName | 최경희 | - |
dc.contributor.alternativeName | 유대열 | - |
dc.contributor.alternativeName | 박상익 | - |
dc.contributor.alternativeName | 성제경 | - |
dc.contributor.alternativeName | 김원호 | - |
dc.identifier.bibliographicCitation | Journal of Molecular Biology, vol. 397, no. 4, pp. 917-931 | - |
dc.identifier.doi | 10.1016/j.jmb.2010.02.016 | - |
dc.subject.keyword | Apoptosis | - |
dc.subject.keyword | HBx | - |
dc.subject.keyword | NF-κB | - |
dc.subject.keyword | Steatosis | - |
dc.subject.keyword | TNFR1 | - |
dc.subject.local | apoptosis | - |
dc.subject.local | Apoptosis | - |
dc.subject.local | HBX | - |
dc.subject.local | HBx | - |
dc.subject.local | Nuclear factor-kappa B | - |
dc.subject.local | nuclear factor κB | - |
dc.subject.local | Nf-κb | - |
dc.subject.local | NF-kB | - |
dc.subject.local | nuclear factor kappa B | - |
dc.subject.local | NF-κB (nuclear factor kappa-B) | - |
dc.subject.local | NF-kappaB | - |
dc.subject.local | Nuclear factor-κb | - |
dc.subject.local | NF-κ B | - |
dc.subject.local | NF-κB | - |
dc.subject.local | NF-kappa B | - |
dc.subject.local | Nuclear factor κB (NF-κB) | - |
dc.subject.local | Nuclear factor κB | - |
dc.subject.local | NFκB | - |
dc.subject.local | Nf-κB | - |
dc.subject.local | Nuclear factor-κB | - |
dc.subject.local | nuclear factorκB | - |
dc.subject.local | Nuclear factor (NF)-κB | - |
dc.subject.local | Nuclear factor kappa B | - |
dc.subject.local | nuclear factor-κB | - |
dc.subject.local | NF-ΚB | - |
dc.subject.local | Nuclear factor-kappa B (NF-κB) | - |
dc.subject.local | Nuclear factor-kappaB | - |
dc.subject.local | nuclear factor-kappaB | - |
dc.subject.local | nuclear factor-kappaB (NF-κB) | - |
dc.subject.local | NFkappaB | - |
dc.subject.local | Nuclear factor kappaB | - |
dc.subject.local | steatosis | - |
dc.subject.local | Steatosis | - |
dc.subject.local | TNFR1 | - |
dc.description.journalClass | Y | - |
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