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Publication : BCL11B regulates sutural patency in the mouse craniofacial skeleton.

First Author  Kyrylkova K Year  2016
Journal  Dev Biol Volume  415
Issue  2 Pages  251-260
PubMed ID  26453795 Mgi Jnum  J:233640
Mgi Id  MGI:5787740 Doi  10.1016/j.ydbio.2015.10.010
Citation  Kyrylkova K, et al. (2016) BCL11B regulates sutural patency in the mouse craniofacial skeleton. Dev Biol 415(2):251-60
abstractText  The transcription factor BCL11B plays essential roles during development of the immune, nervous, and cutaneous systems. Here we show that BCL11B is expressed in both osteogenic and sutural mesenchyme of the developing craniofacial complex. Bcl11b(-/-) mice exhibit increased proliferation of osteoprogenitors, premature osteoblast differentiation, and enhanced skull mineralization leading to synostoses of facial and calvarial sutures. Ectopic expression of Fgfr2c, a gene implicated in craniosynostosis in mice and humans, and that of Runx2 was detected within the affected sutures of Bcl11b(-/-) mice. These data suggest that ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice.
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