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1 ithelium but a moderate to weak level in the dental mesenchyme.
2 l placode leading to later expression in the dental mesenchyme.
3 cell proliferation levels in the palatal and dental mesenchyme.
4 ning distinct cellular identities within the dental mesenchyme.
5 d for the expression of Bmp4 and Fgf3 in the dental mesenchyme.
6 4 expression is significantly reduced in the dental mesenchyme.
7  that of Fgf3 is not detected in Msx1 mutant dental mesenchyme.
8 is necessary for Fgf3 and Bmp4 expression in dental mesenchyme.
9 la contributes to the inductive potential of dental mesenchyme.
10  the dental lamina epithelium and induce the dental mesenchyme.
11 mes, but only Lef1 expression in Msx1 mutant dental mesenchyme.
12 pivotal role of autonomous regulation of the dental mesenchyme.
13  Smad4 regulate distinct gene sets in murine dental mesenchyme.
14 to regulating the inductive potential of the dental mesenchyme.
15 uce differential Msx1 and Msx2 expression in dental mesenchyme, also differentially induce Dlx1 and D
16                   We conclude that Tgfbr2 in dental mesenchyme and bone is required for tooth develop
17 re all expressed in the neural crest-derived dental mesenchyme and cause tooth agenesis disorder when
18                       In addition, the inter-dental mesenchyme and distal symphysis of Meckel's carti
19  by the re-appearance of expression of early dental mesenchyme and epithelium genes such as dlx2b and
20 P receptor is expressed in both the adjacent dental mesenchyme and in the alveolar bone.
21  been shown to induce morphologic changes in dental mesenchyme and mesenchymal gene expression via Ms
22  transcription factor is highly expressed in dental mesenchyme and preodontoblasts, while in mature,
23 ype-specific gene regulatory networks in the dental mesenchyme and show that Foxp4 is indispensable f
24 nctional redundancy between Msx1 and Msx2 in dental mesenchyme and support a model whereby Msx and Dl
25 he duration of this signal in the developing dental mesenchyme and whether adult dental pulp tissue m
26    We have identified Tbx2 expression in the dental mesenchyme at bud stage and show that this can be
27                             Cell fate of the dental mesenchyme at this stage is therefore determined
28  restricting specific gene expression in the dental mesenchyme, but also for defining gene expression
29 4 and Lef1 expression in explanted wild-type dental mesenchymes, but only Lef1 expression in Msx1 mut
30 FGF signaling in ensuring the proper fate of dental mesenchyme by regulating beta-catenin signaling a
31  of odontogenic potential in the presumptive dental mesenchyme by the Msx1 and Pax9 transcription fac
32 We also found that TM14 preferentially bound dental mesenchyme cells and odontoblasts but not dental
33     We show that although cultured embryonic dental mesenchyme cells are unable to induce tooth forma
34 cells, they inhibit the ability of embryonic dental mesenchyme cells to induce tooth formation.
35 rin beta1 antibody inhibited TM14 binding to dental mesenchyme cells, suggesting that both a heparan
36 ar explants restores mitotic activity in the dental mesenchyme, demonstrating the functional signific
37 lls contribute to the formation of condensed dental mesenchyme, dental papilla, odontoblasts, dentine
38      Ectopic expression of human Bmp4 to the dental mesenchyme driven by the mouse Msx1 promoter rest
39  mechanism that sustains odontogenic fate of dental mesenchyme during tooth development.
40 nd Dlx genes function in parallel within the dental mesenchyme during tooth initiation.
41 maintains odontogenic inductive potential in dental mesenchyme, enabling the identification of crucia
42  Fgf3 nor can FGFs induce Bmp4 expression in dental mesenchyme, even though both signaling molecules
43 f tooth development, Msx1 is required in the dental mesenchyme for tooth formation.
44  of the dental epithelium and its associated dental mesenchyme gives rise to the tooth bud.
45 ow that FGFs induce syndecan-1 expression in dental mesenchyme in a manner that also requires Msx-1.
46 pithelial BMP4 induces its own expression in dental mesenchyme in a manner that requires Msx1.
47 FGF1, FGF2 or FGF8 induce Fgf3 expression in dental mesenchyme in an Msx1-dependent manner.
48 vivo evidence of a deficiency of CNC-derived dental mesenchyme in Msx1 null mutant mouse embryos.
49 monstrate that Msx1 is not only expressed in dental mesenchyme in response to epithelial signals, but
50 iferation or condensation of the CNC-derived dental mesenchyme in the Lef1 null mutant, suggesting th
51 cal WNT pathway in Osr2-IresCre;Smad4(fl/fl) dental mesenchyme in vitro partially rescued the CNC cel
52 lling and tissue grafting, and show that the dental mesenchyme is a much more dynamic population then
53 gly, in the absence of Msx1, the CNC-derived dental mesenchyme misdifferentiates and possesses proper
54                      When implanted into the dental mesenchyme of Msx1 mutants, beads soaked with BMP
55 -mediated non-canonical Wnt signaling in the dental mesenchyme plays a crucial role in cell prolifera
56 netic deletion of the motor protein Kif3a in dental mesenchyme results in an arrest in odontogenesis.
57         We demonstrate that loss of Kif3a in dental mesenchyme results in loss of Hedgehog signaling
58 r (Alk5) in the cranial neural crest-derived dental mesenchyme severely affects the proliferation of
59 ed ectopic Dkk2 expression in the developing dental mesenchyme, similar to Msx1(-/-) embryos, we gene
60 sient functional requirement for Msx1 in the dental mesenchyme that is almost fully supplied by BMP4
61 m receives an Msx1-dependent signal from the dental mesenchyme that is necessary for tooth formation.
62 etwork operating in the neural crest-derived dental mesenchyme that is relevant for many other areas
63 ified an atypical canonical BMP signaling in dental mesenchyme that is Smad4-independent but Smad1/5-
64                                The defective dental mesenchyme then aberrantly signals to the dental
65 as attenuated suggesting that Tgfbr2 acts on dental mesenchyme to indirectly regulate the formation a
66  the protein core of proteoglycans, from the dental mesenchyme using Osr2-Cre, which is also strongly
67                      We have fate mapped the dental mesenchyme, using in vitro tissue culture combine
68 ression of downstream signaling molecules in dental mesenchyme via Msx1.
69         Fgf10, Fgf3, and Fgf9 signals in the dental mesenchyme were downregulated in Wnt1-Cre; Alk5(f
70 can-1 is specifically reduced in Msx1 mutant dental mesenchyme, while expression of the extracellular