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1 turation ameloblasts compared with secretory ameloblasts.
2 loblasts and then downregulated again in the ameloblasts.
3 d expression of ameloblastin and amelotin in ameloblasts.
4 AP6 is not expressed from these promoters in ameloblasts.
5 ncisor and differentiate into enamel-forming ameloblasts.
6 uoride, must be neutralized by the overlying ameloblasts.
7 rmed localization of ACPT in secretory-stage ameloblasts.
8 amplifying cells that are progenitors of the ameloblasts.
9 on of beta-galactosidase in maturation stage ameloblasts.
10 mouse incisors confirmed DPPI expression by ameloblasts.
11 tracellular localization in maturation-stage ameloblasts.
12 nations demonstrated the complete absence of ameloblasts.
13 to understand the roles of AE2 and NBCe1 in ameloblasts.
14 ly expressed in the early stage of secretory ameloblasts.
15 s also transiently expressed by presecretory ameloblasts.
16 es of tooth-specific cells, odontoblasts and ameloblasts.
17 al cells differentiate into enamel-secreting ameloblasts.
18 rix protein, is expressed by differentiating ameloblasts.
19 l cells; GlcNAc-acylated K5 is identified in ameloblasts.
20 region of CK14, a differentiation marker for ameloblasts.
21 alized tissues like long bone, calvaria, and ameloblasts.
22 has never been specifically demonstrated in ameloblasts.
23 model for studying electrolyte transport by ameloblasts.
24 ulated twice during the normal life cycle of ameloblasts.
25 in components biosynthesized and secreted by ameloblasts.
26 synthesized and secreted by secretory-phase ameloblasts.
27 ization in the Tomes' processes of secretory ameloblasts.
28 sed, almost exclusively, in maturation stage ameloblasts.
29 n the enamel knots and cervical loops and in ameloblasts.
30 ot-forming cervical loops and enamel-forming ameloblasts.
31 apical NaPi-2b and Nckx4 in maturation-stage ameloblasts.
32 peared to be internalized by secretory stage ameloblasts.
33 tems used by secretory- and maturation-stage ameloblasts.
34 24A4 signal specifically in maturation-stage ameloblasts.
35 d potential mechanisms of Ca(2+) handling by ameloblasts.
36 gulates proliferation and differentiation of ameloblasts.
38 forms (55 and 66 kDa) distinctly appeared in ameloblasts after day 1, reached a peak on day 5, and re
39 ctor-beta (TGF-beta) impacting indirectly on ameloblast-ameloblast interactions and proteolytic proce
42 dental epithelial cell differentiation into ameloblasts and activated promoter activity of the ename
43 al cells differentiate into enamel-secreting ameloblasts and dentin-secreting odontoblasts, respectiv
44 s, the most abundant isoform found in murine ameloblasts and developing enamel is the M180 protein.
45 molecular sizes (37, 55, and 66 kDa) in both ameloblasts and enamel matrix during PN development.
46 alyses indicated that Fam20a is expressed in ameloblasts and gingivae, providing biological plausibil
47 ion except for increased retention in mature ameloblasts and immature odontoblasts in the continually
48 examined the profiles of ameloblastin in the ameloblasts and in the enamel matrix during different po
51 lloproteinase that is initially expressed by ameloblasts and odontoblasts immediately prior to the on
53 gans as well as defects in the maturation of ameloblasts and odontoblasts point to an important and n
54 : (1) AMELX contains 2 additional exons; (2) ameloblasts and odontoblasts synthesize amelogenin 8/9;
58 on4 may contribute to the differentiation of ameloblasts and osteoblasts through regulation of Runx2
59 B6 to the distal membrane of differentiating ameloblasts and pre-ameloblasts, and then ITGB6 appeared
60 nd its related STPs are expressed in the pre-ameloblasts and pre-secretory ameloblasts in positions w
61 llular Ca(2+) buffering systems expressed in ameloblasts and provides an up-dated view of current mod
63 eloblasts, then strong staining in secreting ameloblasts and stratum intermedium cells, followed by c
64 t the interface between the maturation-stage ameloblasts and the underlying cells of the stratum inte
65 it-amplifying cells, re-expressed in the pre-ameloblasts and then downregulated again in the amelobla
66 enamel matrix proteins/peptides secreted by ameloblasts and/or epithelial rest cells contribute to t
68 ransporter NBCe1 has been localized in mouse ameloblasts, and has been proposed to have a role in mat
69 inct and specific signal in maturation-stage ameloblasts, and in the junctional epithelium following
70 bnormal cranial dimensions, defective dental ameloblasts, and nasal septal deviation, consistent with
71 brane of differentiating ameloblasts and pre-ameloblasts, and then ITGB6 appeared to be internalized
72 rix, loss of ameloblast phenotype, increased ameloblast apoptosis and formation of multi-cellular mas
75 nes function to ensure that enamel-producing ameloblasts are generated on only one side of the tooth
80 wo major transporters recently identified in ameloblasts are the Na(+)K(+)-dependent calcium transpor
83 blast organelles changes (percent volume per ameloblast) as ameloblasts progress through six defined
84 P-20), kallikrein-4 (KLK-4), and odontogenic ameloblast-associated protein (ODAM) using quantitative
87 normal; presumably due to the UPR modulating ameloblast behaviour and function in an attempt to relie
88 e N-terminal region of the cytokeratin 14 of ameloblasts binds to trityrosyl motif peptide (ATMP) of
89 S17 mRNA was not detected in secretory stage ameloblasts but could be detected in odontoblasts, while
90 usly, we showed that pendrin is expressed in ameloblasts but is not critical for enamel formation.
91 pon the transcellular transport of Ca(2+) by ameloblasts, but little is known about the molecular mec
92 sor that shows that enamelin is expressed by ameloblasts, but not by odontoblasts or other cells in t
93 thelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix
94 the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting pro
100 ad of predominantly locating adjacent to the ameloblast cell membrane, beta-catenin was predominantly
101 inactivation of MMP20 would result in tight ameloblast cell-cell attachments that may cause maturati
106 R-200a-3p expression is activated in the pre-ameloblast cells to enhance epithelial cell differentiat
108 oral epithelial cells to dental epithelial (ameloblast) cells, which can be used in tissue repair an
111 he dentin proteins expressed by presecretory ameloblasts contribute to the unique properties of the d
112 Cre;Fam20C(fl/fl) mice had severe enamel and ameloblast defects, while their dentin and alveolar bone
113 ible for dental enamel formation, we used an ameloblast-derived cell line (LS8) to characterize speci
116 e-rich amelogenin peptide (TgLRAP), in which ameloblasts differentiate earlier, AMG+4 transcripts wer
117 miR-224 was significantly downregulated as ameloblasts differentiated, in parallel with upregulatio
120 ession at the bud stage and exhibit abnormal ameloblast differentiation on both labial and lingual su
121 d to adhere properly to each other, although ameloblast differentiation was unaffected at early stage
127 h occurs at a mineralization front along the ameloblast distal membrane in which amorphous calcium ph
128 its compelling biological role in organizing ameloblasts during amelogenesis, this study strengthens
129 ontoblast cells and the epithelially derived ameloblasts during development is responsible for the fo
131 focal laser scan microscopic observations on ameloblasts during postnatal (PN) growth of the teeth sh
132 ude that EMSP1 is expressed by pig and mouse ameloblasts during the early maturation stage of ameloge
133 encodes a calcium transporter upregulated in ameloblasts during the maturation stage of amelogenesis.
135 protein-1 (XBP1) plays a role in regulating ameloblast ER volume, as has been previously demonstrate
137 continuously deposited by stem cell-derived ameloblasts exclusively on the labial, or outer, surface
141 resent evidence to demonstrate that affected ameloblasts express but fail to secrete full-length amel
142 dy, we tested the hypothesis that maturation ameloblasts express Dra and Slc26a6 to secrete bicarbona
145 ed the first evidence that enamel cells, the ameloblasts, express NBCe1 in a polarized fashion, there
147 f appositional growth (at the cusp tip), (3) ameloblast extension rate, (4) duration of ameloblast ex
148 ) ameloblast extension rate, (4) duration of ameloblast extension, and (5) spreading rate of appositi
149 ) mice, the apical sides of enamel-secreting ameloblasts failed to adhere properly to each other, alt
150 nactivation of Spry4 alone initiates ectopic ameloblast formation in the embryo, the dosage of anothe
151 CK14/amelogenin to the apical region of the ameloblasts from day 1, reaching a peak on days 3-5, and
152 tooth by inhibiting the formation of ectopic ameloblasts from self-renewing stem cells, and that they
155 While epithelial stem cells giving rise to ameloblasts have been well-characterized, cells giving r
157 metalloproteinase-20 (MMP20) is expressed by ameloblasts in developing teeth and MMP20 mutations caus
158 and the localization of EMSP1 expression in ameloblasts in mouse day 14 first and second molars by i
159 sed in the pre-ameloblasts and pre-secretory ameloblasts in positions where they may be able to detec
160 l formation requires the sliding movement of ameloblasts in rows during the secretory stage of develo
162 ression of Cnnm4 in the neural retina and in ameloblasts in the developing tooth, suggesting a hither
163 evidence that AE2 and NBCe1 are expressed in ameloblasts in vivo in a polarized fashion, thereby prov
165 -regulation of NBCe1 in fluorosed maturation ameloblasts in vivo, with no effect of fluoride in vitro
166 t molars localized FAM20A in secretory-stage ameloblasts, in odontoblasts, and in the eruption pathwa
167 y, our results show that integrity of the SI-ameloblast interface is essential for normal enamel mine
171 Amel X(-/-)/Ambn(-/-) mice, not only was the ameloblast layer irregular and detached from the enamel
172 FoxJ1(-/-) mice show a reduced and defective ameloblast layer, revealing a biological effect of these
177 ineered teeth contain dentin and enamel with ameloblast-like cells and rests of Malassez of human ori
178 calization of TIP39 and tuftelin in cultured ameloblast-like cells showed that these two proteins col
187 a stably transfected Tet-Off Mmp20-inducible ameloblast-lineage cell line and found that MMP20 expres
189 is study was to determine whether epithelial ameloblast-lineage cells, derived from the human enamel
192 maturation, indicating that maturation-stage ameloblasts maintain a high level of metabolic activity.
194 ndible of Ctip2(-/-) mice: expression of the ameloblast markers amelogenin, ameloblastin, and enameli
195 n ion levels in enamel fluid near the apical ameloblast membrane may reduce the transport activity of
196 the curvature of the surface from which the ameloblasts migrate (the dentin-enamel junction or DEJ).
197 e conclude that MMP20 plays a role in normal ameloblast migration through tightly controlled Wnt sign
198 el, Ca(2+) is the most abundant ion, yet how ameloblasts modulate Ca(2+) dynamics remains poorly know
201 Therefore, we propose that MMP20 facilitates ameloblast movement by cleaving ameloblast cell-cell con
202 eloblast attachments would also preclude the ameloblast movement necessary to form decussating enamel
205 , and that in Mmp20 ablated mice, high-level ameloblast N-cadherin expression persists during the mat
207 s excess beta-catenin, which translocates to ameloblast nuclei to promote cell migration/invasion.
209 CK14/amelogenin in the perinuclear region of ameloblasts on day 0, migration of the co-assembled CK14
211 gy, polarization, and adhesion properties of ameloblasts on the labial side of these teeth were sever
212 vival but is essential for the generation of ameloblasts, one of the major differentiated cell types
213 potentially NaPi-2b) located in ruffle-ended ameloblasts operate in a coordinated way with the pH-reg
216 on of dental epithelia into enamel-producing ameloblasts or the root epithelial lineage compartmental
220 ein in the developing enamel matrix, loss of ameloblast phenotype, increased ameloblast apoptosis and
222 eceded by a decrease in proliferation of the ameloblast precursor cells and a reduction in amelogenin
224 hat Tbx1 is essential for the maintenance of ameloblast progenitor cells in rodent incisors and that
227 s changes (percent volume per ameloblast) as ameloblasts progress through six defined developmental s
229 the secretory pathway in the enamel-forming ameloblasts, resulting in eruption of malformed tooth en
232 data indicate that the mutation inhibits the ameloblast secretory pathway leading to ER stress and an
238 n blot analysis reveals that tuftelin is not ameloblast-specific but is expressed in multiple tissues
242 -regulated in the K14-cre;Bmp2(f/f);Bmp4(f/f)ameloblasts, suggesting that the reduced MMP20 and KLK4
243 lateral anion exchanger Ae2a,b in maturation ameloblasts suggests that these cells secrete bicarbonat
247 oblasts give rise to tall columnar secretory ameloblasts that direct the enamel to achieve its full t
248 ix proteins was down-regulated in the mutant ameloblasts, the cleavage of ameloblastin was drasticall
249 sx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to un
251 we found no APC staining in differentiating ameloblasts, then strong staining in secreting ameloblas
252 were capable of differentiating to secretory ameloblasts; this process, however, was apparently delay
255 also cleaves junctional complexes present on ameloblasts to foster the cell movement necessary for fo
256 may be an important event necessary for the ameloblasts to start moving in rows that slide by one an
257 nued in the distal ends of the pre-secretory ameloblasts to the beginning of enamel matrix secretion.
260 unolocalized to the apical pole of secretory ameloblasts (Tomes' processes) and to the newly secreted
261 d fashion, thereby providing a mechanism for ameloblast transcellular bicarbonate secretion in the pr
262 nohistochemically (IHC) localized in the pre-ameloblasts up to initial dentin matrix deposition and c
263 iguing possibility that WDR72 is critical to ameloblast vesicle turnover during enamel maturation.
264 ess questions related to HCO3 (-)export from ameloblasts, we have developed a polarized 2-dimensional
268 rolled Bmp4 expression in epithelium-derived ameloblasts were located in the region between 0.26 kb a
271 sed at the basolateral membrane of secretory ameloblasts, whereas AE2 is expressed at the apical memb
272 lysis by PCR showed NBCe1-A present in human ameloblasts, whereas mouse ameloblasts expressed NBCe1-B
273 ted by specialized epithelial cells known as ameloblasts which themselves undergo striking morphologi
274 ynthesized by a highly specialized cell, the ameloblast, which secretes matrix proteins with little h
275 dult epithelial stem cells that give rise to ameloblasts, which generate enamel, and little is known
276 trafficking is important in maturation-stage ameloblasts with respect to secretion into immature enam
277 ferentiation of inner enamel epithelium into ameloblasts, with intense localization in the Tomes' pro
278 hese genes are active only in enamel-forming ameloblasts within the dental organ of the developing to
280 stry localized exons 8/9-encoded proteins in ameloblasts, young odontoblasts, and stratum intermedium
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