| pubmed-article:20214815 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0021815 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0222645 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C0919538 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:20214815 | lifeskim:mentions | umls-concept:C1513400 | lld:lifeskim |
| pubmed-article:20214815 | pubmed:dateCreated | 2010-4-1 | lld:pubmed |
| pubmed-article:20214815 | pubmed:abstractText | Very little is known about how intervertebral disc (IVD) is formed or maintained. Members of the TGF-beta superfamily are secreted signaling proteins that regulate many aspects of development including cellular differentiation. We recently showed that deletion of Tgfbr2 in Col2a expressing mouse tissue results in alterations in development of IVD annulus fibrosus. The results suggested TGF-beta has an important role in regulating development of the axial skeleton, however, the mechanistic basis of TGF-beta action in these specialized joints is not known. One of the hurdles to understanding development of IVD is a lack of known markers. To identify genes that are enriched in the developing mouse IVD and to begin to understand the mechanism of TGF-beta action in IVD development, we undertook a global analysis of gene expression comparing gene expression profiles in developing mouse vertebrae and IVD. We also compared expression profiles in tissues from wild type and Tgfbr2 mutant mice as well as in sclerotome cultures treated with TGF-beta or BMP4. | lld:pubmed |
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