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Article: TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling

TitleTRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling
Authors
KeywordsOsteopetrosis
TRAF6
CD40
Interleukin-1
Lipopolysaccharide
Issue Date1999
Citation
Genes and Development, 1999, v. 13, n. 8, p. 1015-1024 How to Cite?
AbstractBone resorption and remodeling is an intricately controlled, physiological process that requires the function of osteoclasts. The processes governing both the differentiation and activation of osteoclasts involve signals induced by osteoprotegerin ligand (OPGL), a member of tumor necrosis factor (TNF) superfamily, and its cognate receptor RANK. The molecular mechanisms of the intracellular signal transduction remain to be elucidated. Here we report that mice deficient in TNF receptor-associated factor 6 (TRAF6) are osteopetrotic with defects in bone remodeling and tooth eruption due to impaired osteoclast function. Using in vitro assays, we demonstrate that TRAF6 is crucial not only in IL-1 and CD40 signaling but also, surprisingly, in LPS signaling. Furthermore, like TRAF2 and TRAF3, TRAF6 is essential for perinatal and postnatal survival. These findings establish unexpectedly diverse and critical roles for TRAF6 in perinatal and postnatal survival, bone metabolism, LPS, and cytokine signaling.
Persistent Identifierhttp://hdl.handle.net/10722/291499
ISSN
2023 Impact Factor: 7.5
2023 SCImago Journal Rankings: 5.015
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLomaga, Mark A.-
dc.contributor.authorYeh, Wen Chen-
dc.contributor.authorSarosi, Ildiko-
dc.contributor.authorDuncan, Gordon S.-
dc.contributor.authorFurlonger, Caren-
dc.contributor.authorHo, Alexandra-
dc.contributor.authorMorony, Sean-
dc.contributor.authorCapparelli, Casey-
dc.contributor.authorVan, Gwyneth-
dc.contributor.authorKaufman, Stephen-
dc.contributor.authorVan Der Heiden, Annette-
dc.contributor.authorItie, Annick-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorKhoo, Wilson-
dc.contributor.authorSasaki, Takehiko-
dc.contributor.authorCao, Zhaodan-
dc.contributor.authorPenninger, Josef M.-
dc.contributor.authorPaige, Christopher J.-
dc.contributor.authorLacey, David L.-
dc.contributor.authorDunstan, Colin R.-
dc.contributor.authorBoyle, William J.-
dc.contributor.authorGoeddel, David V.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:30Z-
dc.date.available2020-11-17T14:54:30Z-
dc.date.issued1999-
dc.identifier.citationGenes and Development, 1999, v. 13, n. 8, p. 1015-1024-
dc.identifier.issn0890-9369-
dc.identifier.urihttp://hdl.handle.net/10722/291499-
dc.description.abstractBone resorption and remodeling is an intricately controlled, physiological process that requires the function of osteoclasts. The processes governing both the differentiation and activation of osteoclasts involve signals induced by osteoprotegerin ligand (OPGL), a member of tumor necrosis factor (TNF) superfamily, and its cognate receptor RANK. The molecular mechanisms of the intracellular signal transduction remain to be elucidated. Here we report that mice deficient in TNF receptor-associated factor 6 (TRAF6) are osteopetrotic with defects in bone remodeling and tooth eruption due to impaired osteoclast function. Using in vitro assays, we demonstrate that TRAF6 is crucial not only in IL-1 and CD40 signaling but also, surprisingly, in LPS signaling. Furthermore, like TRAF2 and TRAF3, TRAF6 is essential for perinatal and postnatal survival. These findings establish unexpectedly diverse and critical roles for TRAF6 in perinatal and postnatal survival, bone metabolism, LPS, and cytokine signaling.-
dc.languageeng-
dc.relation.ispartofGenes and Development-
dc.subjectOsteopetrosis-
dc.subjectTRAF6-
dc.subjectCD40-
dc.subjectInterleukin-1-
dc.subjectLipopolysaccharide-
dc.titleTRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1101/gad.13.8.1015-
dc.identifier.pmid10215628-
dc.identifier.pmcidPMC316636-
dc.identifier.scopuseid_2-s2.0-0033561039-
dc.identifier.volume13-
dc.identifier.issue8-
dc.identifier.spage1015-
dc.identifier.epage1024-
dc.identifier.isiWOS:000079983400010-
dc.identifier.issnl0890-9369-

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