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1 L is sufficient to induce formation of a new tooth germ.
2 nt role in determining the size and shape of tooth germ.
3 ation and adhesion in different parts of the tooth germ.
4  an increase in programmed cell death in the tooth germ.
5 bles the lamina stage of the mammalian molar tooth germ.
6  while Rspo2 expression is restricted to the tooth germ.
7 ressed in multiple regions of the developing tooth germ.
8 R-24-1/2 were highly expressed in the mature tooth germ.
9 in reptiles can be created from asymmetrical tooth germs.
10 ce supernumerary cusp formation in wild-type tooth germs.
11 ce exhibit early developmental arrest of all tooth germs.
12 ts and modulation of Wnt signaling by Nog in tooth germs.
13 ogenic mesenchymal cells close to developing tooth germs.
14 ack of fgf8 and pax9 expression in zebrafish tooth germs.
15  in the epithelial cells of early developing tooth germs.
16 ng pathway appears not to be active in these tooth germs.
17  prior to grafting, BMP4 rescues Msx1 mutant tooth germs all the way to definitive stages of enamel a
18 x genes is similar between molar and incisor tooth germs, although 3 low-abundance transcripts were f
19 ng molecules are expressed in the developing tooth germ and interact each other to mediate the induct
20 egulating Shh expression in mouse developing tooth germ and limb bud.
21 ular incisor arrested as a single, bud-stage tooth germ and Meckel's cartilage was absent.
22 of exogenous Shh protein directly into early tooth germs and adjacent to tooth germs, resulted in abn
23 ttern surrounding the developing mouse molar tooth germs and mice lacking Osr2 developed supernumerar
24 esenchymal Fgfs in wild-type and Msx1 mutant tooth germs and tested the ability of FGFs to induce Fgf
25 ough proliferation and survival of vestigial tooth germs and that Gas1 function in cranial neural cre
26 tential Msx1 downstream genes in Msx1 mutant tooth germs and we have performed functional experiments
27  we show that these exogenously induced oral tooth germs are able to be at least partly calcified.
28   In this study, we used the embryonic mouse tooth germ as a tool to search for the downstream target
29 /11 (LM-511/521) is the major laminin in the tooth germ basement membrane.
30 iferation, and apoptotic activity within the tooth germ between the wild-type and Lef1 null mutant mi
31 , and second in the development of cap-stage tooth germs by increasing epithelial cell survival.
32  of ectopic MFrzb1 protein on the developing tooth germs by transplanting explants treated with Mfrzb
33 show that addition of BMP4 to Msx1 deficient tooth germs bypasses the requirement for Msx1 and rescue
34 4, by differential hybridization using mouse tooth germ cDNA microarrays.
35 actor, which we named AmeloD, by screening a tooth germ complementary DNA (cDNA) library using a yeas
36 olar tooth germs while their maxillary molar tooth germs completed morphogenesis.
37                                              Tooth germ culture showed that the developing tooth inva
38      The enamel knot, a signaling center for tooth germ development, is defective, and there is a sig
39                                       As the tooth germ develops and proceeds to the cap stage, the e
40 d alveolar bone leads to an expansion of the tooth germ, driven by increased proliferation, indicatin
41              During their early development, tooth germs exhibit many morphological and molecular sim
42  of this increased cell death, the bud stage tooth germ fails to advance to the cap stage in the abse
43 ests that Wnt signaling is required early in tooth germ formation and that interference with signalin
44 s with epithelium during the early stages of tooth germ formation and undergo complex changes which,
45 ing epithelial/mesenchymal cell signaling in tooth germ formation.
46                                       Mutant tooth germs formed multiple dental epithelial buds into
47  of ectomesenchymal cells that surrounds the tooth germ in early stages of tooth development.
48 pithelium but repressed Shh in the wild-type tooth germ in vivo.
49    The degree of mineralization of permanent tooth germs in dental age assessment has been an area of
50  activin betaA mutant embryos is lost in all tooth germs, including the maxillary molars.
51 h development, suggestive of a role in early tooth germ initiation and subsequent epithelial-mesenchy
52 during normal development, the growth of the tooth germ is constrained by the surrounding tissues.
53 atrix protein derived from embryonic porcine tooth germs is used clinically, but the mechanisms by wh
54 not (EK), located at the center of cap stage tooth germs, is a transitory cluster of nondividing epit
55 at activin betaA is expressed in presumptive tooth-germ mesenchyme and is thus a candidate for a sign
56 e mesenchyme in incisor and mandibular molar tooth germs must be carried-out in maxillary molar mesen
57            When isolated from the developing tooth germ, odontoblasts quickly lose their potential to
58 3 was ectopically elevated in the developing tooth germ of Smad7 null mice, indicating the hyperactiv
59 ct the expression in mouse molar and incisor tooth germs of 14 of the 19 known members of the Sox fam
60 erformed protein-soaked bead implantation on tooth germs of the 2 different EK regions and compared t
61 ha5-null mouse primary dental epithelium and tooth germ organ cultures.
62  that when added to explanted Msx1-deficient tooth germs prior to grafting, BMP4 rescues Msx1 mutant
63 nt mice, both mandibular and maxillary molar tooth germs progressed to the early bell stage, with res
64 he enamel knot signalling centre in downless tooth germs provide functional data directly linking the
65 mesenchymal interactions, and the developing tooth germ provides a powerful model for elucidating the
66  experimental manipulation, the murine molar tooth germ provides a powerful system for studying the r
67 ectly into early tooth germs and adjacent to tooth germs, resulted in abnormal epithelial invaginatio
68 tegrin alpha6 antibody and wortmannin reduce tooth germ size and shape.
69 a mandibular remnant that displayed abnormal tooth germs, substandard angiogenesis, and enhanced apop
70 ation and subsequent arrest of supernumerary tooth germs that correlated with downregulation of Msx1
71  study we used early mouse molar and incisor tooth germs that possess distinct tooth-forming capabili
72 essed at embryonic day 14.5 (E14.5) in early tooth germs, then down-regulated from E15.5-E17.5 and re
73 e expression sequence (CAGE-seq) using mouse tooth germ to identify the genes preferentially expresse
74                                              Tooth germs undergo a series of dynamic morphologic chan
75 onditional knockout and YAP transgenic mouse tooth germs using transcriptome sequencing (RNA-Seq) and
76 Whereas Sostdc1 expression in the developing tooth germ was not increased in Msx1(-/-) embryos, genet
77          By adding a soluble form of Edar to tooth germs, we were able to mimic the tabby enamel knot
78                                  Whereas all tooth germs were arrested at the bud stage in Msx1(-/-)
79 To further test this hypothesis, Msx1 mutant tooth germs were first cultured with either BMP4 or with
80  in the dental epithelium of the Msx1 mutant tooth germ where Bmp4 expression is significantly reduce
81                         The developing mouse tooth germ, which is an experimentally accessible model
82 developmental arrest of the mandibular molar tooth germs while their maxillary molar tooth germs comp
83              Lama5-null mice develop a small tooth germ with defective cusp formation and have reduce
84 in the dental epithelium resulted in a small tooth germ with reduced epithelial cell proliferation.
85 hibitor in cell cultures of Smad7(-/-) molar tooth germs, with rescued expression of cyclin D1 and ce