File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis

TitleOPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis
Authors
Issue Date1999
Citation
Nature, 1999, v. 397, n. 6717, p. 315-323 How to Cite?
AbstractThe tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and ODF) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph- node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.
Persistent Identifierhttp://hdl.handle.net/10722/291508
ISSN
2021 Impact Factor: 69.504
2020 SCImago Journal Rankings: 15.993
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKong, Young Yun-
dc.contributor.authorYoshida, Hiroki-
dc.contributor.authorSarosi, Ildiko-
dc.contributor.authorTan, Hong Lin-
dc.contributor.authorTimms, Emma-
dc.contributor.authorCapparelli, Casey-
dc.contributor.authorMorony, Sean-
dc.contributor.authorOliveira-dos-Santos, Antonio J.-
dc.contributor.authorVan, Gwyneth-
dc.contributor.authorItie, Annick-
dc.contributor.authorKhoo, Wilson-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorDunstan, Colin R.-
dc.contributor.authorLacey, David L.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorBoyle, William J.-
dc.contributor.authorPenninger, Josef M.-
dc.date.accessioned2020-11-17T14:54:31Z-
dc.date.available2020-11-17T14:54:31Z-
dc.date.issued1999-
dc.identifier.citationNature, 1999, v. 397, n. 6717, p. 315-323-
dc.identifier.issn0028-0836-
dc.identifier.urihttp://hdl.handle.net/10722/291508-
dc.description.abstractThe tumour-necrosis-factor-family molecule osteoprotegerin ligand (OPGL; also known as TRANCE, RANKL and ODF) has been identified as a potential osteoclast differentiation factor and regulator of interactions between T cells and dendritic cells in vitro. Mice with a disrupted opgl gene show severe osteopetrosis and a defect in tooth eruption, and completely lack osteoclasts as a result of an inability of osteoblasts to support osteoclastogenesis. Although dendritic cells appear normal, opgl-deficient mice exhibit defects in early differentiation of T and B lymphocytes. Surprisingly, opgl-deficient mice lack all lymph nodes but have normal splenic structure and Peyer's patches. Thus OPGL is a new regulator of lymph- node organogenesis and lymphocyte development and is an essential osteoclast differentiation factor in vivo.-
dc.languageeng-
dc.relation.ispartofNature-
dc.titleOPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/16852-
dc.identifier.pmid9950424-
dc.identifier.scopuseid_2-s2.0-0033611467-
dc.identifier.volume397-
dc.identifier.issue6717-
dc.identifier.spage315-
dc.identifier.epage323-
dc.identifier.isiWOS:000078324600040-
dc.identifier.issnl0028-0836-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats