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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

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dc.contributor.author김락균-
dc.date.accessioned2021-05-21T17:11:11Z-
dc.date.available2021-05-21T17:11:11Z-
dc.date.issued2020-03-
dc.identifier.issn0036-8075-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/182756-
dc.description.abstractT cells maintain a quiescent state prior to activation. As inappropriate T cell activation can cause disease, T cell quiescence must be preserved. Despite its importance, the mechanisms underlying the "quiescent state" remain elusive. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. BTG1/2-deficient T cells show an increased proliferation and spontaneous activation due to a global increase in messenger RNA (mRNA) abundance, which reduces the threshold to activation. BTG1/2 deficiency leads to an increase in polyadenylate tail length, resulting in a greater mRNA half-life. Thus, BTG1/2 promote the deadenylation and degradation of mRNA to secure T cell quiescence. Our study reveals a key mechanism underlying T cell quiescence and suggests that low mRNA abundance is a crucial feature for maintaining quiescence.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherAmerican Association for the Advancement of Science-
dc.relation.isPartOfSCIENCE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAnimals-
dc.subject.MESHCells, Cultured-
dc.subject.MESHImmediate-Early Proteins / genetics-
dc.subject.MESHImmediate-Early Proteins / physiology*-
dc.subject.MESHLymphocyte Activation*-
dc.subject.MESHMice-
dc.subject.MESHMice, Knockout-
dc.subject.MESHNeoplasm Proteins / genetics-
dc.subject.MESHNeoplasm Proteins / physiology*-
dc.subject.MESHPolyadenylation-
dc.subject.MESHRNA Stability*-
dc.subject.MESHRNA, Messenger / chemistry*-
dc.subject.MESHT-Lymphocytes / immunology*-
dc.subject.MESHTumor Suppressor Proteins / genetics-
dc.subject.MESHTumor Suppressor Proteins / physiology*-
dc.titlemRNA destabilization by BTG1 and BTG2 maintains T cell quiescence-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorSoo Seok Hwang-
dc.contributor.googleauthorJaechul Lim-
dc.contributor.googleauthorZhibin Yu-
dc.contributor.googleauthorPhilip Kong-
dc.contributor.googleauthorEsen Sefik-
dc.contributor.googleauthorHao Xu-
dc.contributor.googleauthorChristian C D Harman-
dc.contributor.googleauthorLark Kyun Kim-
dc.contributor.googleauthorGap Ryol Lee-
dc.contributor.googleauthorHua-Bing Li-
dc.contributor.googleauthorRichard A Flavell-
dc.identifier.doi10.1126/science.aax0194-
dc.contributor.localIdA04520-
dc.relation.journalcodeJ02642-
dc.identifier.eissn1095-9203-
dc.identifier.pmid32165587-
dc.identifier.urlhttps://science.sciencemag.org/content/367/6483/1255.long-
dc.contributor.alternativeNameKim, Lark Kyun-
dc.contributor.affiliatedAuthor김락균-
dc.citation.volume367-
dc.citation.number6483-
dc.citation.startPage1255-
dc.citation.endPage1260-
dc.identifier.bibliographicCitationSCIENCE, Vol.367(6483) : 1255-1260, 2020-03-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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