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1 genic and non-osteogenic compartments at the coronal suture.
2  (Efna2), ephrin A4 (Efna4) and EphA4 in the coronal suture.
3 red for the exclusion of such cells from the coronal suture.
4 rentiated mesoderm of the Twist1(+/-) mutant coronal suture.
5 in the frontal and parietal bones and in the coronal suture.
6 craniosynostosis, particularly affecting the coronal suture.
7 ion of the frontal and parietal bones at the coronal suture.
8 in postnatal suture mesenchyme, disrupts the coronal suture.
9 to be critical for positioning of the murine coronal suture.
10 Tcf12 in proper formation of the overlapping coronal suture.
11 rbital regulatory center, which patterns the coronal suture.
12 re patency and prevent fusion of the Hhip-/- coronal suture.
13 tingly, Fn1 mutants have premature fusion of coronal sutures.
14 the mesenchymal precursors that generate the coronal suture, an important structural boundary in mamm
15 n shows that descendant cells persist in the coronal suture and contribute to calvarial bone growth.
16 hat EphA4 mutant mice exhibit defects in the coronal suture and neural crest-mesoderm boundary that p
17 is underpinned by the delayed closure of the coronal suture and of the intersphenoidal synchondrosis.
18 rce for understanding the development of the coronal suture and the mechanisms for its loss in cranio
19 craniosynostosis, specifically involving the coronal sutures, and variable learning disability are th
20 ated Hhip-/-;Pthlh-/- embryos and found that coronal sutures are fusing by E18.5.
21 ncluding a plate of cartilage underlying the coronal suture, as well as in osteogenic cells, suggesti
22 t these mice exhibit craniosynostosis of the coronal suture, as well as other cranial sutures.
23 he neural crest-mesoderm boundary within the coronal suture, as well as with a reduction in the expre
24                                 In Hhip(-/-) coronal sutures at E18.5, the osteogenic fronts are clos
25 the wrist and ankle, the middle ear, and the coronal suture between bones in the skull.
26 f supraorbital mesenchymal cells to form the coronal suture between E11.0 and E13.5.
27 Jagged1 in the mesodermal compartment of the coronal suture, but not in the neural crest compartment,
28 antation of FGF2-soaked beads onto the fetal coronal suture by ex utero surgery resulted in ectopic o
29 est that Jagged1 is an effector of Twist1 in coronal suture development.
30          Thus, EphA4 is a Twist1 effector in coronal suture development.
31 ting through Eph-ephrin signaling, regulates coronal suture development.
32 demonstrate that Hhip is required for normal coronal suture development.
33 2-TWIST1 heterodimers is critical for normal coronal suture development.
34  of HH ligands, and we previously identified coronal suture dysgenesis in embryonic Hhip-/- mice, in
35 NeuC/Mes lineage boundary positioning during coronal suture formation.
36 tor-1 construct, whereas the normally patent coronal suture fuses when infected with a construct that
37 of miR-200a in PMIS-miR-200a mice results in coronal suture fusion (craniosynostosis).
38 d mesoderm-derived parietal bone accompanies coronal suture fusion during embryonic development.
39                           We have reassessed coronal suture fusion in an Apert Fgfr2 (S252W) mouse mo
40           On the other hand, the more apical coronal suture initially forms appropriately but then un
41                                          The coronal suture is a major growth center of the skull vau
42 al tissue juxtaposition that later forms the coronal suture is established at E9.5 as the caudal boun
43                                          The coronal suture is most commonly fused in monogenic crani
44 nteract genetically: EphA4 expression in the coronal suture is reduced in Twist1 mutants, and compoun
45 posterior and anterior frontal, sagittal and coronal sutures of early post-natal mutant mice revealed
46 eous insertion of FGF2-soaked beads onto the coronal suture on E15 resulted in up-regulation of osteo
47 pression, may reduce HH signaling to promote coronal suture patency and prevent fusion of the Hhip-/-
48                        We show in mouse that coronal suture progenitors originate from hedgehog-respo
49 substitution (p.R3S), in a male patient with coronal suture synostosis.
50     Nearly all vertebrates have a prominent 'coronal' suture that separates the front and back of the
51  analysis of the embryonic, wild type murine coronal suture to define its population structure.
52 llular diversity within the murine embryonic coronal suture, we generated single-cell transcriptomes
53 ads to expansion of cartilage underlying the coronal sutures, which contribute to suture closure thro