ライフサイエンスコーパス: dental mesenchyme

1 l placode leading to later expression in the dental mesenchyme.

2 ning distinct cellular identities within the dental mesenchyme.

3 cell proliferation levels in the palatal and dental mesenchyme.

4 d for the expression of Bmp4 and Fgf3 in the dental mesenchyme.

5 la contributes to the inductive potential of 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 the dental lamina epithelium and induce the dental mesenchyme.

10 mes, but only Lef1 expression in Msx1 mutant dental mesenchyme.

11 to regulating the inductive potential of the dental mesenchyme.

12 uce differential Msx1 and Msx2 expression in dental mesenchyme, also differentially induce Dlx1 and D

13 We conclude that Tgfbr2 in dental mesenchyme and bone is required for tooth develop

14 re all expressed in the neural crest-derived dental mesenchyme and cause tooth agenesis disorder when

15 In addition, the inter-dental mesenchyme and distal symphysis of Meckel's carti

16 P receptor is expressed in both the adjacent dental mesenchyme and in the alveolar bone.

17 been shown to induce morphologic changes in dental mesenchyme and mesenchymal gene expression via Ms

18 transcription factor is highly expressed in dental mesenchyme and preodontoblasts, while in mature,

19 nctional redundancy between Msx1 and Msx2 in dental mesenchyme and support a model whereby Msx and Dl

20 he duration of this signal in the developing dental mesenchyme and whether adult dental pulp tissue m

21 We have identified Tbx2 expression in the dental mesenchyme at bud stage and show that this can be

22 Cell fate of the dental mesenchyme at this stage is therefore determined

23 restricting specific gene expression in the dental mesenchyme, but also for defining gene expression

24 4 and Lef1 expression in explanted wild-type dental mesenchymes, but only Lef1 expression in Msx1 mut

25 FGF signaling in ensuring the proper fate of dental mesenchyme by regulating beta-catenin signaling a

26 of odontogenic potential in the presumptive dental mesenchyme by the Msx1 and Pax9 transcription fac

27 We also found that TM14 preferentially bound dental mesenchyme cells and odontoblasts but not dental

28 We show that although cultured embryonic dental mesenchyme cells are unable to induce tooth forma

29 cells, they inhibit the ability of embryonic dental mesenchyme cells to induce tooth formation.

30 rin beta1 antibody inhibited TM14 binding to dental mesenchyme cells, suggesting that both a heparan

31 ar explants restores mitotic activity in the dental mesenchyme, demonstrating the functional signific

32 lls contribute to the formation of condensed dental mesenchyme, dental papilla, odontoblasts, dentine

33 Ectopic expression of human Bmp4 to the dental mesenchyme driven by the mouse Msx1 promoter rest

34 mechanism that sustains odontogenic fate of dental mesenchyme during tooth development.

35 nd Dlx genes function in parallel within the dental mesenchyme during tooth initiation.

36 Fgf3 nor can FGFs induce Bmp4 expression in dental mesenchyme, even though both signaling molecules

37 f tooth development, Msx1 is required in the dental mesenchyme for tooth formation.

38 of the dental epithelium and its associated dental mesenchyme gives rise to the tooth bud.

39 ow that FGFs induce syndecan-1 expression in dental mesenchyme in a manner that also requires Msx-1.

40 pithelial BMP4 induces its own expression in dental mesenchyme in a manner that requires Msx1.

41 FGF1, FGF2 or FGF8 induce Fgf3 expression in dental mesenchyme in an Msx1-dependent manner.

42 vivo evidence of a deficiency of CNC-derived dental mesenchyme in Msx1 null mutant mouse embryos.

43 monstrate that Msx1 is not only expressed in dental mesenchyme in response to epithelial signals, but

44 iferation or condensation of the CNC-derived dental mesenchyme in the Lef1 null mutant, suggesting th

45 cal WNT pathway in Osr2-IresCre;Smad4(fl/fl) dental mesenchyme in vitro partially rescued the CNC cel

46 lling and tissue grafting, and show that the dental mesenchyme is a much more dynamic population then

47 gly, in the absence of Msx1, the CNC-derived dental mesenchyme misdifferentiates and possesses proper

48 When implanted into the dental mesenchyme of Msx1 mutants, beads soaked with BMP

49 netic deletion of the motor protein Kif3a in dental mesenchyme results in an arrest in odontogenesis.

50 We demonstrate that loss of Kif3a in dental mesenchyme results in loss of Hedgehog signaling

51 r (Alk5) in the cranial neural crest-derived dental mesenchyme severely affects the proliferation of

52 sient functional requirement for Msx1 in the dental mesenchyme that is almost fully supplied by BMP4

53 m receives an Msx1-dependent signal from the dental mesenchyme that is necessary for tooth formation.

54 etwork operating in the neural crest-derived dental mesenchyme that is relevant for many other areas

55 The defective dental mesenchyme then aberrantly signals to the dental

56 as attenuated suggesting that Tgfbr2 acts on dental mesenchyme to indirectly regulate the formation a

57 the protein core of proteoglycans, from the dental mesenchyme using Osr2-Cre, which is also strongly

58 We have fate mapped the dental mesenchyme, using in vitro tissue culture combine

59 ression of downstream signaling molecules in dental mesenchyme via Msx1.

60 Fgf10, Fgf3, and Fgf9 signals in the dental mesenchyme were downregulated in Wnt1-Cre; Alk5(f

61 can-1 is specifically reduced in Msx1 mutant dental mesenchyme, while expression of the extracellular