| pubmed-article:15936336 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C0018951 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C1622923 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C1159978 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:15936336 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:15936336 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15936336 | pubmed:dateCreated | 2005-6-6 | lld:pubmed |
| pubmed-article:15936336 | pubmed:abstractText | Loss of function mutations in the gene encoding the heparan sulfate proteoglycan Glypican-3 (GPC3) causes an X-linked disorder in humans known as Simpson-Golabi-Behmel Syndrome (SGBS). This disorder includes both pre- and postnatal overgrowth, a predisposition to certain childhood cancers, and a complex assortment of congenital defects including skeletal abnormalities. In this study, we have identified a previously unrecognized delay in endochondral ossification associated with the loss of Gpc3 function. Gpc3 knockout animals show a marked reduction in calcified trabecular bone, and an abnormal persistence of hypertrophic chondrocytes at embryonic day 16.5 (E16.5). These hypertrophic chondrocytes down-regulate Type X collagen mRNA expression and undergo apoptosis, suggesting a normal progression of hypertrophic chondrocyte cell fate. However, replacement of these cells by mineralized bone is delayed in association with a marked delay in the appearance of osteoclasts in the bone in vivo. This delay in vivo correlates with a significant reduction in the capacity to form osteoclasts from bone marrow macrophage precursors in vitro in response to M-CSF and RANKL, and with a reduction in the numbers of bone-marrow-derived cells expressing the markers CD11b and Gr-1. Together, these results indicate selective impairment in the development of the common hematopoietic lineage from which monocyte/macrophages and PMNs are derived. This is the first report of a requirement for heparan sulfate, and specifically Gpc3, in the lineage-specific differentiation of these cell types in vivo. | lld:pubmed |
| pubmed-article:15936336 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15936336 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15936336 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15936336 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15936336 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15936336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15936336 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15936336 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15936336 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:15936336 | pubmed:issn | 0012-1606 | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:GillF TFT | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:Paine-Saunder... | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:VivianoBeth... | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:SaundersScott... | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:SilversteinLa... | lld:pubmed |
| pubmed-article:15936336 | pubmed:author | pubmed-author:PfledererCami... | lld:pubmed |
| pubmed-article:15936336 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15936336 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15936336 | pubmed:volume | 282 | lld:pubmed |
| pubmed-article:15936336 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15936336 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15936336 | pubmed:pagination | 152-62 | lld:pubmed |
| pubmed-article:15936336 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15936336 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15936336 | pubmed:articleTitle | Altered hematopoiesis in glypican-3-deficient mice results in decreased osteoclast differentiation and a delay in endochondral ossification. | lld:pubmed |
| pubmed-article:15936336 | pubmed:affiliation | Department of Pediatrics, Washington University School of Medicine and St. Louis Children's Hospital, St. Louis, MO 63110, USA. | lld:pubmed |
| pubmed-article:15936336 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15936336 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15936336 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15936336 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:15936336 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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