{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T22:41:01Z","timestamp":1789425661528,"version":"build-2803163510"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2013,6,21]],"date-time":"2013-06-21T00:00:00Z","timestamp":1371772800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,1,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Paget's disease of bone (PDB) is characterized by abnormal osteoclasts with unique characteristics that include increased sensitivity of osteoclast progenitors to 1,25(OH)2D3, receptor activator of NF-\u03baB ligand (RANKL), and TNF-\u03b1; increased osteoclast numbers; and increased expression of IL-6 and several transcription factors. We recently reported that measles virus nucleocapsid protein (MVNP) plays a key role in the development of these abnormal osteoclasts. MVNP can induce the pagetic osteoclast phenotype in vitro and in vivo in TRAP-MVNP transgenic mice. However, the molecular mechanisms by which MVNP generates pagetic osteoclasts have not been determined. TANK-binding kinase 1 (TBK1) and I\u03baB kinase-\u03f5 (IKK\u03f5) are IKK family members that complex with MVNP and activate both IRF3 and NF-\u03baB pathways. MVNP increases the amount of TBK1 protein in bone marrow monocytes (BMM). Interestingly, we found that RANKL increased TBK1 and IKK\u03f5 early in osteoclast differentiation, suggesting a possible role in normal osteoclastogenesis. However, only TBK1 is further increased in osteoclasts formed by TRAP-MVNP BMM owing to increased TBK1 protein stability. TBK1 overexpression induced IL6 promoter reporter activity, and elevated endogenous IL6 mRNA and p65 NF-\u03baB, TAF12, and ATF7 proteins in several cell lines. Overexpression of TBK1 was insufficient to induce pagetic osteoclasts from WT BMM but synergized with MVNP to increase pagetic osteoclast formation from TRAP-MVNP BMM. BX795 inhibition of TBK1 impaired MVNP-induced IL-6 expression in both NIH3T3 cells and BMM, and shRNA knockdown of Tbk1 in NIH3T3 cells impaired IL-6 secretion induced by MVNP and decreased TAF12 and ATF7, factors involved in 1,25(OH)2D3 hypersensitivity of pagetic osteoclasts. Similarly, Tbk1 knockdown in BMM from TRAP-MVNP and WT mice specifically impaired development of the MVNP-induced osteoclast pagetic phenotype. These results demonstrate that TBK1 plays a critical role in mediating the effects of MVNP on osteoclast differentiation and on the expression of IL-6, a key contributor to the pagetic osteoclast phenotype. \u00a9 2014 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2026","type":"journal-article","created":{"date-parts":[[2013,6,21]],"date-time":"2013-06-21T14:01:43Z","timestamp":1371823303000},"page":"90-102","source":"Crossref","is-referenced-by-count":25,"title":["TBK1 Mediates Critical Effects of Measles Virus Nucleocapsid Protein (MVNP) on Pagetic Osteoclast Formation"],"prefix":"10.1093","volume":"29","author":[{"given":"Quanhong","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Medicine\/Hematology-OncologyUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of MedicinePittsburghPAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u00e9n\u00e9dicte","family":"Sammut","sequence":"additional","affiliation":[{"name":"Department of Medicine\/Hematology-OncologyUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of MedicinePittsburghPAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng-Ming","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Medicine\/Hematology-OncologyIndiana UniversityIndianapolisINUSA"},{"name":"Department of Medicine\/Hematology-OncologyUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of MedicinePittsburghPAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noriyoshi","family":"Kurihara","sequence":"additional","affiliation":[{"name":"Department of Medicine\/Hematology-OncologyIndiana UniversityIndianapolisINUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jolene J","family":"Windle","sequence":"additional","affiliation":[{"name":"Department of Human and Molecular GeneticsVirginia Commonwealth UniversityRichmondVAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G David","family":"Roodman","sequence":"additional","affiliation":[{"name":"Veterans Administration Medical CenterIndianapolisINUSA"},{"name":"Department of Medicine\/Hematology-OncologyIndiana UniversityIndianapolisINUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah L","family":"Galson","sequence":"additional","affiliation":[{"name":"Department of Medicine\/Hematology-OncologyUniversity of Pittsburgh Cancer Institute, University of Pittsburgh School of MedicinePittsburghPAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,6,21]]},"reference":[{"issue":"1","key":"2024020318585127500_jbmr2026-bib-0001","doi-asserted-by":"crossref","first-page":"23","DOI":"10.1016\/j.cmet.2010.12.002","article-title":"Contributions of the measles virus nucleocapsid gene and the SQSTM1\/p62(P392L) mutation to Paget's disease","volume":"13","author":"Kurihara","year":"2011","journal-title":"Cell Metab."},{"issue":"1","key":"2024020318585127500_jbmr2026-bib-0002","doi-asserted-by":"crossref","first-page":"46","DOI":"10.1172\/JCI115584","article-title":"Interleukin 6. 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