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RUVBL1/2 Complex Regulates Pro-Inflammatory Responses in Macrophages via Regulating Histone H3K4 Trimethylation
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Zhang, Rui | - |
dc.contributor.author | Cheung, Chris Y. | - |
dc.contributor.author | Seo, Sang-Uk | - |
dc.contributor.author | Liu, Hang | - |
dc.contributor.author | Pardeshi, Lakhansing | - |
dc.contributor.author | Wong, Koon Ho | - |
dc.contributor.author | Chow, Larry M. C. | - |
dc.contributor.author | Chau, Mary P. | - |
dc.contributor.author | Wang, Yixiang | - |
dc.contributor.author | Lee, Ah Ra | - |
dc.contributor.author | Kwon, Woon Yong | - |
dc.contributor.author | Chen, Sheng | - |
dc.contributor.author | Chan, Bill Kwan-wai | - |
dc.contributor.author | Wong, Kenneth | - |
dc.contributor.author | Choy, Richard K. W. | - |
dc.contributor.author | Ko, Ben C. B. | - |
dc.date.accessioned | 2024-05-27T08:25:47Z | - |
dc.date.available | 2024-05-27T08:25:47Z | - |
dc.date.created | 2021-07-05 | - |
dc.date.created | 2021-07-05 | - |
dc.date.created | 2021-07-05 | - |
dc.date.issued | 2021-06 | - |
dc.identifier.citation | Frontiers in Immunology, Vol.12 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://hdl.handle.net/10371/203692 | - |
dc.description.abstract | Macrophages play an important role in the host defense mechanism. In response to infection, macrophages activate a genetic program of pro-inflammatory response to kill any invading pathogen, and initiate an adaptive immune response. We have identified RUVBL2 - an ATP-binding protein belonging to the AAA+ (ATPase associated with diverse cellular activities) superfamily of ATPases - as a novel regulator in pro-inflammatory response of macrophages. Gene knockdown of Ruvbl2, or pharmacological inhibition of RUVBL1/2 activity, compromises type-2 nitric oxide synthase (Nos2) gene expression, nitric oxide production and anti-bacterial activity of mouse macrophages in response to lipopolysaccharides (LPS). RUVBL1/2 inhibitor similarly inhibits pro-inflammatory response in human monocytes, suggesting functional conservation of RUVBL1/2 in humans. Transcriptome analysis further revealed that major LPS-induced pro-inflammatory pathways in macrophages are regulated in a RUVBL1/2-dependent manner. Furthermore, RUVBL1/2 inhibition significantly reduced the level of histone H3K4me3 at the promoter region of Nos2 and Il6, two prototypical pro-inflammatory genes, and diminished the recruitment of NF-kappaB to the corresponding enhancers. Our study reveals RUVBL1/2 as an integral component of macrophage pro-inflammatory responses through epigenetic regulations, and the therapeutic potentials of RUVBL1/2 inhibitors in the treatment of diseases caused by aberrant activation of pro-inflammatory pathways. | - |
dc.language | 영어 | - |
dc.publisher | Frontiers Media S.A. | - |
dc.title | RUVBL1/2 Complex Regulates Pro-Inflammatory Responses in Macrophages via Regulating Histone H3K4 Trimethylation | - |
dc.type | Article | - |
dc.identifier.doi | 10.3389/fimmu.2021.679184 | - |
dc.citation.journaltitle | Frontiers in Immunology | - |
dc.identifier.wosid | 000662968600001 | - |
dc.identifier.scopusid | 2-s2.0-85108113542 | - |
dc.citation.volume | 12 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Kwon, Woon Yong | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | CHROMATIN REMODELING COMPLEX | - |
dc.subject.keywordPlus | DEPENDENT BINDING | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | METHYLTRANSFERASE | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | TRANSFORMATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | RVB1/RVB2 | - |
dc.subject.keywordPlus | COMPASS | - |
dc.subject.keywordAuthor | RUVBL1 | - |
dc.subject.keywordAuthor | 2 | - |
dc.subject.keywordAuthor | pro-inflammatory | - |
dc.subject.keywordAuthor | macrophages | - |
dc.subject.keywordAuthor | epigenetic modulation | - |
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