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1 to be critical for positioning of the murine coronal suture.
2 genic and non-osteogenic compartments at the coronal suture.
3 (Efna2), ephrin A4 (Efna4) and EphA4 in the coronal suture.
4 red for the exclusion of such cells from the coronal suture.
5 rbital regulatory center, which patterns the coronal suture.
6 rentiated mesoderm of the Twist1(+/-) mutant coronal suture.
7 in the frontal and parietal bones and in the coronal suture.
8 craniosynostosis, particularly affecting the coronal suture.
9 the mesenchymal precursors that generate the coronal suture, an important structural boundary in mamm
10 hat EphA4 mutant mice exhibit defects in the coronal suture and neural crest-mesoderm boundary that p
11 craniosynostosis, specifically involving the coronal sutures, and variable learning disability are th
12 ncluding a plate of cartilage underlying the coronal suture, as well as in osteogenic cells, suggesti
13 he neural crest-mesoderm boundary within the coronal suture, as well as with a reduction in the expre
16 Jagged1 in the mesodermal compartment of the coronal suture, but not in the neural crest compartment,
17 antation of FGF2-soaked beads onto the fetal coronal suture by ex utero surgery resulted in ectopic o
23 tor-1 construct, whereas the normally patent coronal suture fuses when infected with a construct that
28 al tissue juxtaposition that later forms the coronal suture is established at E9.5 as the caudal boun
29 nteract genetically: EphA4 expression in the coronal suture is reduced in Twist1 mutants, and compoun
30 posterior and anterior frontal, sagittal and coronal sutures of early post-natal mutant mice revealed
31 eous insertion of FGF2-soaked beads onto the coronal suture on E15 resulted in up-regulation of osteo
33 ads to expansion of cartilage underlying the coronal sutures, which contribute to suture closure thro
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