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TRPM7 Is Essential for RANKL-Induced Osteoclastogenesis

DC FieldValueLanguage
dc.contributor.author신동민-
dc.contributor.author양유미-
dc.contributor.author이성준-
dc.contributor.author최형준-
dc.date.accessioned2014-12-18T08:28:20Z-
dc.date.available2014-12-18T08:28:20Z-
dc.date.issued2013-
dc.identifier.issn1226-4512-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/86370-
dc.description.abstractThe transient receptor potential melastatin type 7 (TRPM7) channel is a widely expressed non-selective cation channel with fusion to the C-terminal alpha kinase domain and regarded as a key regulator of whole body Mg2+ homeostasis in mammals. However, the roles of TRPM7 during osteoclastogenesis in RAW264.7 cells and bone marrow-derived monocyte/macrophage precursor cells (BMMs) are not clear. In the present study, we investigate the roles of TRPM7 in osteoclastogenesis using methods of small interfering RNA (siRNA), RT-PCR, patch-clamp, and calcium imaging. RANKL (receptor activator of NF-κB ligand) stimulation did not affect the TRPM7 expression and TRPM7-mediated current was activated in HEK293, RAW264.7, and BMM cells by the regulation of Mg2+. Knock-down of TRPM7 by siTRPM7 reduced intracellular Ca2+ concentration ([Ca2+]i) increases by 0 mM [Mg2+]e in HEK293 cells and inhibited the generation of RANKL-induced Ca2+ oscillations in RAW264.7 cells. Finally, knock-down of TRPM7 suppressed RANKL-mediated osteoclastogenesis such as activation and translocation of NFATc1, formation of multinucleated cells, and the bone resorptive activity, sequentially. These results suggest that TRPM7 plays an essential role in the RANKL-induced [Ca2+]i oscillations that triggers the late stages of osteoclastogenesis.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfKorean Journal of Physiology & Pharmacology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleTRPM7 Is Essential for RANKL-Induced Osteoclastogenesis-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorYu-Mi Yang-
dc.contributor.googleauthorHwi-Hoon Jung-
dc.contributor.googleauthorSung Jun Lee-
dc.contributor.googleauthorHyung-Jun Choi-
dc.contributor.googleauthorMin Seuk Kim-
dc.contributor.googleauthorDong Min Shin-
dc.identifier.doi10.4196/kjpp.2013.17.1.65-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02091-
dc.contributor.localIdA04216-
dc.contributor.localIdA02870-
dc.contributor.localIdA05148-
dc.relation.journalcodeJ02104-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.alternativeNameYang, Yu-Mi-
dc.contributor.alternativeNameLee, Sung Jun-
dc.contributor.alternativeNameChoi, Hyung Jun-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.contributor.affiliatedAuthorChoi, Hyung Jun-
dc.contributor.affiliatedAuthorLee, Sung Jun-
dc.contributor.affiliatedAuthorYang, Yu Mi-
dc.rights.accessRightsfree-
dc.citation.volume17-
dc.citation.number1-
dc.citation.startPage65-
dc.citation.endPage71-
dc.identifier.bibliographicCitationKorean Journal of Physiology & Pharmacology, Vol.17(1) : 65-71, 2013-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Pediatric Dentistry (소아치과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Research Center for Human Natural Defense System (생체방어연구센터) > 1. Journal Papers

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