DC Field | Value | Language |
---|---|---|
dc.contributor.author | Nguyen Thi Hong Nhung | - |
dc.contributor.author | Hesung Now | - |
dc.contributor.author | Woo-Jong Kim | - |
dc.contributor.author | Nari Kim | - |
dc.contributor.author | Yoo, JY | - |
dc.date.accessioned | 2017-07-19T12:46:45Z | - |
dc.date.available | 2017-07-19T12:46:45Z | - |
dc.date.created | 2016-09-09 | - |
dc.date.issued | 2016-03-21 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/36428 | - |
dc.description.abstract | RIG-I is a key cytosolic RNA sensor that mediates innate immune defense against RNA virus. Aberrant RIG-I activity leads to severe pathological states such as autosomal dominant multi-system disorder, inflammatory myophathies and dermatomyositis. Therefore, identification of regulators that ensure efficient defense without harmful immune-pathology is particularly critical to deal with RIG-I-associated diseases. Here, we presented the inflammatory inducible FAT10 as a novel negative regulator of RIG-Imediated inflammatory response. In various cell lines, FAT10 protein is undetectable unless it is induced by pro-inflammatory cytokines. FAT10 non-covalently associated with the 2CARD domain of RIG-I, and inhibited viral RNA-induced IRF3 and NF-kappa B activation through modulating the RIG-I protein solubility. We further demonstrated that FAT10 was recruited to RIG-I-TRIM25 to form an inhibitory complex where FAT10 was stabilized by E3 ligase TRIM25. As the result, FAT10 inhibited the antiviral stress granules formation contains RIG-I and sequestered the active RIG-I away from the mitochondria. Our study presented a novel mechanism to dampen RIG-I activity. Highly accumulated FAT10 is observed in various cancers with pro-inflammatory environment, therefore, our finding which uncovered the suppressive effect of the accumulated FAT10 during virus-mediated inflammatory response may also provide molecular clue to understand the carcinogenesis related with infection and inflammation. | - |
dc.language | English | - |
dc.publisher | Nature Publishing Group | - |
dc.relation.isPartOf | Scientific Reports | - |
dc.title | Ubiquitin-like modifier FAT10 attenuates RIG-I mediated antiviral signaling by segregating activated RIG-I from its signaling platform | - |
dc.type | Article | - |
dc.identifier.doi | 10.1038/SREP23377 | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | Scientific Reports, v.6, pp.23377 | - |
dc.identifier.wosid | 000372512100001 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.startPage | 23377 | - |
dc.citation.title | Scientific Reports | - |
dc.citation.volume | 6 | - |
dc.contributor.affiliatedAuthor | Woo-Jong Kim | - |
dc.contributor.affiliatedAuthor | Nari Kim | - |
dc.contributor.affiliatedAuthor | Yoo, JY | - |
dc.identifier.scopusid | 2-s2.0-84961784072 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 10 | - |
dc.description.scptc | 9 | * |
dc.date.scptcdate | 2018-05-121 | * |
dc.description.isOpenAccess | Y | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | INNATE IMMUNE-RESPONSES | - |
dc.subject.keywordPlus | HEPATOCELLULAR-CARCINOMA | - |
dc.subject.keywordPlus | PROTEASOMAL DEGRADATION | - |
dc.subject.keywordPlus | ACTIN CYTOSKELETON | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | MODULATION | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
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