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1  contribution to odontoblasts during primary dentinogenesis.
2  of newly formed odontoblasts during primary dentinogenesis.
3 ent and DSP is a novel target of MMP9 during dentinogenesis.
4 n an autocrine manner to modulate reparative dentinogenesis.
5 generation of odontoblasts during reparative dentinogenesis.
6    Here, we investigated the role of Msx2 in dentinogenesis.
7  the dynamic Trps1 expression pattern during dentinogenesis.
8 RNA-epigenetic regulatory network to control dentinogenesis.
9 nd important roles in primary and reparative dentinogenesis.
10 might regulate the expression of DSPP during dentinogenesis.
11 tal epithelium does not significantly affect dentinogenesis.
12  molecule that mediates the roles of DMP1 in dentinogenesis.
13 step essential to its biological function in dentinogenesis.
14  the roles of Nma/BAMBI and TGFbeta-1 during dentinogenesis.
15 naling and downstream gene expression during dentinogenesis.
16 expression is tightly regulated during tooth dentinogenesis.
17 t DSPP is probably regulated by DMP-1 during dentinogenesis.
18 hown to play an important role in late stage dentinogenesis.
19 plays a crucial role during osteogenesis and dentinogenesis.
20 tions of odontoblasts at different stages of dentinogenesis.
21 nd function(s) may have a role in regulating dentinogenesis.
22 posure in mouse molars results in reparative dentinogenesis.
23  molars by triggering the natural process of dentinogenesis.
24   Dentin sialoprotein (DSP) is essential for dentinogenesis and processed into fragments in the odont
25 ring odontoblast differentiation, reparative dentinogenesis, and bone.
26 data suggest that Msx2 may act indirectly on dentinogenesis by controlling osteoclast activity and th
27                                       During dentinogenesis, DSPP is proteolytically cleaved into sma
28 es suggest that DMP-1 is essential for later dentinogenesis during postnatal development.
29  primary pulp cultures and during reparative dentinogenesis following pulp exposures.
30  signaling pathway is crucial for reparative dentinogenesis following tooth damage, and the modulatio
31  method of enhancement of natural reparative dentinogenesis has the potential to be translated into a
32 ive effects of Wnt/beta-catenin signaling on dentinogenesis have been reported, but the underlying me
33 gative effects of Wnt/B-catenin signaling on dentinogenesis have been reported, but the underlying me
34                                              Dentinogenesis imperfecta (DGI) and dentin dysplasia (DD
35                                              Dentinogenesis imperfecta (DGI) and dentin dysplasia (DD
36                                              Dentinogenesis imperfecta (DGI) is characterized by disc
37           DSPP mutations in humans may cause dentinogenesis imperfecta (DGI), an autosomal dominant d
38 lt in human hereditary dental disorders like dentinogenesis imperfecta II (MIM 125420) and dentin dys
39 otein (dspp), a candidate gene implicated in dentinogenesis imperfecta II (MIM 125420), is significan
40 ations in this gene were identified in human dentinogenesis imperfecta II (Online Mendelian Inheritan
41  that develop tooth defects similar to human dentinogenesis imperfecta III with enlarged pulp chamber
42 nd shares some features of the human disease dentinogenesis imperfecta III.
43                                              Dentinogenesis Imperfecta type II (DGI-II) is a localize
44 ed to determine if DGI-III co-localized with dentinogenesis imperfecta type II (DGI-II), which has be
45 attering (SAXS) were performed on normal and dentinogenesis imperfecta type II (DI-II) teeth.
46 d Dmp2 genes at a position equivalent to the dentinogenesis imperfecta type II location on human 4q21
47            As recent studies have shown that dentinogenesis imperfecta type II results from mutation
48 tween, and shared chromosomal location with, dentinogenesis imperfecta type II, a second disorder of
49 trong candidate gene for the genetic disease dentinogenesis imperfecta type II.
50                                              Dentinogenesis imperfecta type III (DGI-III) is an autos
51 s classified as dentin dysplasia type II and dentinogenesis imperfecta types II and III.
52 p9-/- teeth displayed a phenotype similar to dentinogenesis imperfecta, including decreased dentin mi
53 s that may be accompanied by bone deformity, dentinogenesis imperfecta, short stature, and shortened
54 ns of a consanguineous family display severe dentinogenesis imperfecta, short stature, various skelet
55 oring the Col1a2(oim) mutation (oim) express dentinogenesis imperfecta.
56 tooth disorders such as dentin dysplasia and dentinogenesis imperfecta.
57 ostnatal development, we analyzed changes of dentinogenesis in Dmp-1 null mice from 3 days after birt
58 ing effect of a sucrose-rich diet on primary dentinogenesis in rat molars.
59                    Although amelogenesis and dentinogenesis initiate in the molar tooth bud, both pro
60                              This reparative dentinogenesis is associated with significant inflammati
61              However, its role in post-natal dentinogenesis is largely unknown.
62 ct evidence to suggest that osteogenesis and dentinogenesis mediated by BMSSCs and DPSCs, respectivel
63       Initial crown dentin formation-primary dentinogenesis-occurred fairly normally in Msx2(-/-) tee
64 essive H3K9me3 and H3K27me3 marks on typical dentinogenesis-related genes.
65             To examine whether DMP1 controls dentinogenesis through the regulation of DSPP in vivo, w
66 beta-catenin signaling pathway in reparative dentinogenesis using an in vivo mouse tooth damage model
67 xposure model in molars to induce reparative dentinogenesis, we demonstrate the contribution of alpha
68  functions as a repressor of later stages of dentinogenesis, we provide functional significance of th
69 insight into the role of Wnt/beta-catenin in dentinogenesis, we used dental pulp cells from a panel o
70 er insight into the role of Wnt/B-catenin in dentinogenesis, we used dental pulp cells from a panel o
71 y a deviation from secondary toward tertiary dentinogenesis with osteodentin formation and impaired d
72 nd important roles in primary and reparative dentinogenesis, with conflicting results regarding their