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Deficiencies of Homer2 and Homer3 accelerate aging-dependent bone loss in mice

DC FieldValueLanguage
dc.contributor.author신동민-
dc.contributor.author양유미-
dc.date.accessioned2020-12-01T17:01:39Z-
dc.date.available2020-12-01T17:01:39Z-
dc.date.issued2020-09-
dc.identifier.issn1226-7155-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/180090-
dc.description.abstractHomer proteins are scaffold proteins that regulate calcium (Ca2+) signaling by modulating the activity of multiple Ca2+ signaling proteins. In our previous report, Homer2 and Homer3 regulated NFATc1 function through its interaction with calcineurin, which then acted to regulate receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis and bone metabolism. However, to date, the role of Homers in osteoclastogenesis remains unknown. In this study, we investigated the roles of Homer2 and Homer3 in aging-dependent bone remodeling. Deletion of Homer2 /Homer3 (Homer2/3 DKO) markedly decreased the bone density of the femur. The decrease in bone density was not seen in mice with Homer2 (Homer2−/−) and Homer3 (Homer3−/−) deletion. Moreover, RANKL treatment of bone marrow-derived monocytes/macrophages in Homer2/3 DKO mice significantly increased the formation of multinucleated cells and resorption areas. Finally, Homer2/3 DKO mice decreased bone density in an aging-dependent manner. These findings suggest a novel potent mode of bone homeostasis regulation through osteoclasts differentiation during aging by Homer proteins, specifically Homer2 and Homer3.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherHarn Rim Won Printing Co.-
dc.relation.isPartOfInternational Journal of Oral Biology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleDeficiencies of Homer2 and Homer3 accelerate aging-dependent bone loss in mice-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학교실)-
dc.contributor.googleauthorJung Yun Kang-
dc.contributor.googleauthorNamju Kang-
dc.contributor.googleauthorDong Min Shin-
dc.contributor.googleauthorYu-Mi Yang-
dc.identifier.doi10.11620/IJOB.2020.45.3.126-
dc.contributor.localIdA02091-
dc.contributor.localIdA05148-
dc.contributor.localIdA05148-
dc.relation.journalcodeJ01144-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.affiliatedAuthor신동민-
dc.contributor.affiliatedAuthor양유미-
dc.contributor.affiliatedAuthor양유미-
dc.citation.volume45-
dc.citation.number3-
dc.citation.startPage126-
dc.citation.endPage133-
dc.identifier.bibliographicCitationInternational Journal of Oral Biology, Vol.45(3) : 126-133, 2020-09-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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