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1 gulates proliferation and differentiation of 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 amplifying cells that are progenitors of the ameloblasts.
8 on of beta-galactosidase in maturation stage ameloblasts.
9  mouse incisors confirmed DPPI expression by ameloblasts.
10 tracellular localization in maturation-stage ameloblasts.
11 ppressed after IEE cell differentiation into ameloblasts.
12 nations demonstrated the complete absence of ameloblasts.
13  to understand the roles of AE2 and NBCe1 in ameloblasts.
14 ic tools available to study gene function in ameloblasts.
15 ly expressed in the early stage of secretory ameloblasts.
16 ect conversion of Notch1-expressing cells to ameloblasts.
17 s also transiently expressed by presecretory ameloblasts.
18 es of tooth-specific cells, odontoblasts and ameloblasts.
19 al cells differentiate into enamel-secreting ameloblasts.
20 -mediated recombination in incisor and molar ameloblasts.
21 rix protein, is expressed by differentiating ameloblasts.
22 l cells; GlcNAc-acylated K5 is identified in ameloblasts.
23 region of CK14, a differentiation marker for ameloblasts.
24 alized tissues like long bone, calvaria, and ameloblasts.
25  has never been specifically demonstrated in ameloblasts.
26 ulated twice during the normal life cycle of ameloblasts.
27 in components biosynthesized and secreted by ameloblasts.
28  synthesized and secreted by secretory-phase ameloblasts.
29 turation ameloblasts compared with secretory ameloblasts.
30 rmed localization of ACPT in secretory-stage ameloblasts.
31 n of the IEE and to its differentiation into ameloblasts.
32  model for studying electrolyte transport by ameloblasts.
33 sed, almost exclusively, in maturation stage ameloblasts.
34 n the enamel knots and cervical loops and in ameloblasts.
35 ot-forming cervical loops and enamel-forming ameloblasts.
36 apical NaPi-2b and Nckx4 in maturation-stage ameloblasts.
37 then differentiate into the enamel-producing ameloblasts.
38 peared to be internalized by secretory stage ameloblasts.
39 tems used by secretory- and maturation-stage ameloblasts.
40 24A4 signal specifically in maturation-stage ameloblasts.
41 d potential mechanisms of Ca(2+) handling by ameloblasts.
42                           The end-product of ameloblast activity is a marvel of structural engineerin
43 forms (55 and 66 kDa) distinctly appeared in ameloblasts after day 1, reached a peak on day 5, and re
44                                 Secretory KI ameloblasts also lacked Tomes' processes, consistent wit
45 ctor-beta (TGF-beta) impacting indirectly on ameloblast-ameloblast interactions and proteolytic proce
46 nockout of Wls by Shh-Cre leads to defective ameloblast and odontoblast differentiation.
47 ted and the polarity and organization of the ameloblast and odontoblast layers is disrupted.
48 ters that were associated with pre-secretory ameloblast and odontoblast.
49  dental epithelial cell differentiation into ameloblasts and activated promoter activity of the ename
50 elial progenitors generates enamel-producing ameloblasts and adjacent layers of non-ameloblast cells.
51 al cells differentiate into enamel-secreting ameloblasts and dentin-secreting odontoblasts, respectiv
52 s, the most abundant isoform found in murine ameloblasts and developing enamel is the M180 protein.
53 molecular sizes (37, 55, and 66 kDa) in both ameloblasts and enamel matrix during PN development.
54 alyses indicated that Fam20a is expressed in ameloblasts and gingivae, providing biological plausibil
55 examined the profiles of ameloblastin in the ameloblasts and in the enamel matrix during different po
56 mbinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation.
57 of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.
58 lloproteinase that is initially expressed by ameloblasts and odontoblasts immediately prior to the on
59 n of mouse enamelysin was detectable only in ameloblasts and odontoblasts of developing teeth.
60 gans as well as defects in the maturation of ameloblasts and odontoblasts point to an important and n
61 : (1) AMELX contains 2 additional exons; (2) ameloblasts and odontoblasts synthesize amelogenin 8/9;
62 presence of stem cells capable of generating ameloblasts and odontoblasts.
63 day-old mice detected TIP39 RNA in secretory ameloblasts and odontoblasts.
64               It is expressed exclusively in ameloblasts and odontoblasts.
65 on4 may contribute to the differentiation of ameloblasts and osteoblasts through regulation of Runx2
66 serves as one of the main calcium sensors in ameloblasts and plays a major role in enamel mineralizat
67 B6 to the distal membrane of differentiating ameloblasts and pre-ameloblasts, and then ITGB6 appeared
68 nd its related STPs are expressed in the pre-ameloblasts and pre-secretory ameloblasts in positions w
69 llular Ca(2+) buffering systems expressed in ameloblasts and provides an up-dated view of current mod
70 nse APC staining resumes in maturation-stage ameloblasts and proximal papillary cells.
71 igh amount of Cre recombinase exclusively in ameloblasts and showed developmental stage- and cell-spe
72 eloblasts, then strong staining in secreting ameloblasts and stratum intermedium cells, followed by c
73 t the interface between the maturation-stage ameloblasts and the underlying cells of the stratum inte
74 it-amplifying cells, re-expressed in the pre-ameloblasts and then downregulated again in the amelobla
75  enamel matrix proteins/peptides secreted by ameloblasts and/or epithelial rest cells contribute to t
76 xpressed in dental epithelia, differentiated ameloblasts, and certain ectodermal organs.
77 ransporter NBCe1 has been localized in mouse ameloblasts, and has been proposed to have a role in mat
78 inct and specific signal in maturation-stage ameloblasts, and in the junctional epithelium following
79 bnormal cranial dimensions, defective dental ameloblasts, and nasal septal deviation, consistent with
80 brane of differentiating ameloblasts and pre-ameloblasts, and then ITGB6 appeared to be internalized
81 ained throughout life and endlessly generate ameloblasts, and thus enamel.
82 rix, loss of ameloblast phenotype, increased ameloblast apoptosis and formation of multi-cellular mas
83  the p.Tyr64His amelogenin mutation involves ameloblast apoptosis induced by ER stress.
84                                              Ameloblasts are an attractive study case because mineral
85 nes function to ensure that enamel-producing ameloblasts are generated on only one side of the tooth
86 l the pH of the microenvironment adjacent to ameloblasts are not currently well-understood.
87                                      Because ameloblasts are responsible for dental enamel formation,
88       We also demonstrate that mouse incisor ameloblasts are sensitive to the toxic effects of high d
89                                              Ameloblasts are supported by a host of cell types which
90 wo major transporters recently identified in ameloblasts are the Na(+)K(+)-dependent calcium transpor
91 ct of PDGF on CSF-1 expression using MEOE-3M ameloblasts as a model.
92  osteoblasts, hypertrophic chondrocytes, and ameloblasts as well as odontoblasts.
93 blast organelles changes (percent volume per ameloblast) as ameloblasts progress through six defined
94 P-20), kallikrein-4 (KLK-4), and odontogenic ameloblast-associated protein (ODAM) using quantitative
95 ressed enamel matrix components (Odontogenic ameloblast-associated protein) and dentin dysplasia targ
96     APC staining disappears again in reduced ameloblasts at the conclusion of amelogenesis.
97                                    The tight ameloblast attachments would also preclude the ameloblas
98 normal; presumably due to the UPR modulating ameloblast behaviour and function in an attempt to relie
99 e N-terminal region of the cytokeratin 14 of ameloblasts binds to trityrosyl motif peptide (ATMP) of
100 S17 mRNA was not detected in secretory stage ameloblasts but could be detected in odontoblasts, while
101 usly, we showed that pendrin is expressed in ameloblasts but is not critical for enamel formation.
102 pon the transcellular transport of Ca(2+) by ameloblasts, but little is known about the molecular mec
103 sor that shows that enamelin is expressed by ameloblasts, but not by odontoblasts or other cells in t
104 thelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix
105 the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting pro
106                                          The ameloblast cell layer of the enamel organ is in contact
107  in a protein matrix located proximal to the ameloblast cell layer.
108 late reticulum, stratum intermedium, and the ameloblast cell lineage.
109 4 promoter show robust Cre expression in the ameloblast cell lineage.
110        Co-immunoprecipitation assay of mouse ameloblast cell lysates with either ameloblastin or Psma
111 ad of predominantly locating adjacent to the ameloblast cell membrane, beta-catenin was predominantly
112  inactivation of MMP20 would result in tight ameloblast cell-cell attachments that may cause maturati
113  facilitates ameloblast movement by cleaving ameloblast cell-cell contacts.
114 lel within boundaries fabricated by a single ameloblast cell.
115  that represses amelogenin expression in non-ameloblast cells in vivo.
116  decreased expression in the differentiating ameloblast cells of the mouse lower incisor.
117 R-200a-3p expression is activated in the pre-ameloblast cells to enhance epithelial cell differentiat
118 ucing ameloblasts and adjacent layers of non-ameloblast cells.
119 is an intricate process tightly regulated by ameloblast cells.
120  oral epithelial cells to dental epithelial (ameloblast) cells, which can be used in tissue repair an
121                            The pre-secretory ameloblast cluster exhibited higher activation of inflam
122 is significantly downregulated in maturation ameloblasts compared with secretory ameloblasts.
123 he dentin proteins expressed by presecretory ameloblasts contribute to the unique properties of the d
124 Cre;Fam20C(fl/fl) mice had severe enamel and ameloblast defects, while their dentin and alveolar bone
125                        Enamel is secreted by ameloblasts derived from tooth epithelial stem cells (SC
126 ible for dental enamel formation, we used an ameloblast-derived cell line (LS8) to characterize speci
127                             The secretion of ameloblast-derived Dspp is short-lived, correlates to th
128 th RhoGDI antibody in the irregularly shaped ameloblasts detached from the matrix.
129 e-rich amelogenin peptide (TgLRAP), in which ameloblasts differentiate earlier, AMG+4 transcripts wer
130   miR-224 was significantly downregulated as ameloblasts differentiated, in parallel with upregulatio
131 s showed that NBCe1 mRNA was up-regulated as ameloblasts differentiated.
132          Third, we detected abnormalities in ameloblast differentiation in developing mutant incisors
133 ession at the bud stage and exhibit abnormal ameloblast differentiation on both labial and lingual su
134 d to adhere properly to each other, although ameloblast differentiation was unaffected at early stage
135 ulting from defects in dentin deposition and ameloblast differentiation.
136 dental epithelial markers reveal a defect in ameloblast differentiation.
137 cued teeth exhibit a delayed odontoblast and ameloblast differentiation.
138 tors implicated in the tooth development and ameloblast differentiation.
139 ys a major role in enamel mineralization and ameloblast differentiation.
140 ect, although there is no apparent change in ameloblast differentiation.
141 h occurs at a mineralization front along the ameloblast distal membrane in which amorphous calcium ph
142 its compelling biological role in organizing ameloblasts during amelogenesis, this study strengthens
143 ontoblast cells and the epithelially derived ameloblasts during development is responsible for the fo
144 fects of strain stimulus on the migration of ameloblasts during enamel formation.
145 focal laser scan microscopic observations on ameloblasts during postnatal (PN) growth of the teeth sh
146 ude that EMSP1 is expressed by pig and mouse ameloblasts during the early maturation stage of ameloge
147 encodes a calcium transporter upregulated in ameloblasts during the maturation stage of amelogenesis.
148 ontoblasts and low levels in osteoblasts and ameloblasts during tooth development.
149  protein-1 (XBP1) plays a role in regulating ameloblast ER volume, as has been previously demonstrate
150 correlates positively with percent volume of ameloblast ER.
151  continuously deposited by stem cell-derived ameloblasts exclusively on the labial, or outer, surface
152                     Histologically, Irf6-cKO ameloblasts exhibited disturbances in adhesion and polar
153                                              Ameloblasts express a number of transporters and channel
154                              To regulate pH, ameloblasts express anion exchanger 2 (Ae2a,b), chloride
155 resent evidence to demonstrate that affected ameloblasts express but fail to secrete full-length amel
156 dy, we tested the hypothesis that maturation ameloblasts express Dra and Slc26a6 to secrete bicarbona
157                           Our data show that ameloblasts express Dra, pendrin, or Slc26a6 but each of
158                                              Ameloblasts express transmembrane proteins for transport
159 ed the first evidence that enamel cells, the ameloblasts, express NBCe1 in a polarized fashion, there
160  present in human ameloblasts, whereas mouse ameloblasts expressed NBCe1-B.
161 f appositional growth (at the cusp tip), (3) ameloblast extension rate, (4) duration of ameloblast ex
162 ) ameloblast extension rate, (4) duration of ameloblast extension, and (5) spreading rate of appositi
163 ) mice, the apical sides of enamel-secreting ameloblasts failed to adhere properly to each other, alt
164 nactivation of Spry4 alone initiates ectopic ameloblast formation in the embryo, the dosage of anothe
165  CK14/amelogenin to the apical region of the ameloblasts from day 1, reaching a peak on days 3-5, and
166 tooth by inhibiting the formation of ectopic ameloblasts from self-renewing stem cells, and that they
167 re we asked if Mmp20 overexpression disrupts ameloblast function.
168                                Pre-secretory ameloblasts give rise to tall columnar secretory amelobl
169                                              Ameloblasts had not previously been screened for membran
170   While epithelial stem cells giving rise to ameloblasts have been well-characterized, cells giving r
171 metalloproteinase-20 (MMP20) is expressed by ameloblasts in developing teeth and MMP20 mutations caus
172 ter, Enamelin-tdTomato for identification of ameloblasts in live tissues and cells, and used it to de
173  and the localization of EMSP1 expression in ameloblasts in mouse day 14 first and second molars by i
174 sed in the pre-ameloblasts and pre-secretory ameloblasts in positions where they may be able to detec
175 l formation requires the sliding movement of ameloblasts in rows during the secretory stage of develo
176 ression of Cnnm4 in the neural retina and in ameloblasts in the developing tooth, suggesting a hither
177 ells, and used it to demonstrate presence of ameloblasts in the new 3D co-culture system of dental SC
178 evidence that AE2 and NBCe1 are expressed in ameloblasts in vivo in a polarized fashion, thereby prov
179 tion of NBCe1 mRNA in maturation-stage mouse ameloblasts in vivo, as compared with controls.
180 -regulation of NBCe1 in fluorosed maturation ameloblasts in vivo, with no effect of fluoride in vitro
181 t molars localized FAM20A in secretory-stage ameloblasts, in odontoblasts, and in the eruption pathwa
182 nd enamel crystal growth, and in maintaining ameloblast integrity and function during amelogenesis.
183 y, our results show that integrity of the SI-ameloblast interface is essential for normal enamel mine
184  presumably by HCO3 (-)ions transported from ameloblasts into the developing enamel matrix.
185                                         Each ameloblast is responsible for the formation of one ename
186                MMP20, a protease secreted by ameloblasts, is responsible for processing enamel protei
187 Amel X(-/-)/Ambn(-/-) mice, not only was the ameloblast layer irregular and detached from the enamel
188 FoxJ1(-/-) mice show a reduced and defective ameloblast layer, revealing a biological effect of these
189 e rods are the mineralized trail that moving ameloblasts leave behind.
190         The promoter was analyzed in a mouse ameloblast-like cell line (LS8) and was compared with pr
191           Here, we report that Ambn binds to ameloblast-like cell membranes through a highly evolutio
192                                           An ameloblast-like cell population developed ectopically on
193                                         When ameloblast-like cells (LS8) were transfected with an ame
194 ineered teeth contain dentin and enamel with ameloblast-like cells and rests of Malassez of human ori
195 calization of TIP39 and tuftelin in cultured ameloblast-like cells showed that these two proteins col
196                                       Within ameloblast-like cells, upregulation of miR-153 results i
197 tin promoter activity by greater than 50% in ameloblast-like cells.
198 l, ranging from 20 to 30% of the activity in ameloblast-like cells.
199  and ranged from 8 to 30% of the activity in ameloblast-like cells.
200                                        Using ameloblast-like LS8 cells, we demonstrate that these cel
201  were detected in RNA isolated from cultured ameloblast-like LS8 cells.
202 ed 2.2-kilobase mouse amelogenin promoter in ameloblast-like LS8 cells.
203 romoter was systematically analyzed in mouse ameloblast-like LS8 cells.
204 a stably transfected Tet-Off Mmp20-inducible ameloblast-lineage cell line and found that MMP20 expres
205 ted by low pH, but not by fluoride, in human ameloblast-lineage cells in vitro.
206 is study was to determine whether epithelial ameloblast-lineage cells, derived from the human enamel
207 e multiple effects of micromolar fluoride on ameloblast-lineage cells.
208 gnificantly increased the apoptotic index of ameloblast-lineage cells.
209 maturation, indicating that maturation-stage ameloblasts maintain a high level of metabolic activity.
210         Histologic observations coupled with ameloblast marker analyses suggested that Evc2 mutant pr
211 ndible of Ctip2(-/-) mice: expression of the ameloblast markers amelogenin, ameloblastin, and enameli
212 n ion levels in enamel fluid near the apical ameloblast membrane may reduce the transport activity of
213 croscopy to show colocalization of Ambn with ameloblast membrane surfaces in developing mouse incisor
214  the curvature of the surface from which the ameloblasts migrate (the dentin-enamel junction or DEJ).
215 d abruptly ends at the transition stage when ameloblast migration ceases.
216 e conclude that MMP20 plays a role in normal ameloblast migration through tightly controlled Wnt sign
217 el, Ca(2+) is the most abundant ion, yet how ameloblasts modulate Ca(2+) dynamics remains poorly know
218 age and its localization was associated with ameloblast modulation.
219                                              Ameloblasts move in groups that slide by one another as
220 Therefore, we propose that MMP20 facilitates ameloblast movement by cleaving ameloblast cell-cell con
221 eloblast attachments would also preclude the ameloblast movement necessary to form decussating enamel
222 pecific MMP, enamelysin (MMP20), facilitates ameloblast movements during enamel development.
223                  These data demonstrate that ameloblasts must continuously interact with the developi
224 , and that in Mmp20 ablated mice, high-level ameloblast N-cadherin expression persists during the mat
225     To sustain mineral accretion, maturation ameloblasts need to buffer these protons.
226 s excess beta-catenin, which translocates to ameloblast nuclei to promote cell migration/invasion.
227                                    Secretory ameloblasts of AmelX(-/-) mice, but not wild-type mice,
228 CK14/amelogenin in the perinuclear region of ameloblasts on day 0, migration of the co-assembled CK14
229  Ct-positive granules appeared beaded in the ameloblasts on day 3.
230 gy, polarization, and adhesion properties of ameloblasts on the labial side of these teeth were sever
231 vival but is essential for the generation of ameloblasts, one of the major differentiated cell types
232 potentially NaPi-2b) located in ruffle-ended ameloblasts operate in a coordinated way with the pH-reg
233 gal staining was observed in secretory stage ameloblasts or in odontoblasts.
234 ling is not essential for differentiation of ameloblasts or odontoblasts.
235 on of dental epithelia into enamel-producing ameloblasts or the root epithelial lineage compartmental
236       Here we ask how the volume of selected ameloblast organelles changes (percent volume per amelob
237                        Loss of Fgfr1 affects ameloblast organization at the enamel-secretory stage an
238 e system for HAT-7 cells, a rat cell line of ameloblast origin.
239 ein in the developing enamel matrix, loss of ameloblast phenotype, increased ameloblast apoptosis and
240 sp formation, cervical loop down-growth, and ameloblast polarization, did not occur normally.
241 eceded by a decrease in proliferation of the ameloblast precursor cells and a reduction in amelogenin
242        Both isoforms were immunolocalized in ameloblasts, principally at maturation stage.
243 hat Tbx1 is essential for the maintenance of ameloblast progenitor cells in rodent incisors and that
244       The epithelial stem cells that are the ameloblast progenitors reside in structures called cervi
245                                              Ameloblasts progress through defined stages of developme
246 s changes (percent volume per ameloblast) as ameloblasts progress through six defined developmental s
247 ar machinery involved in Ca2+ homeostasis in ameloblasts remains poorly understood.
248  the secretory pathway in the enamel-forming ameloblasts, resulting in eruption of malformed tooth en
249                                              Ameloblasts secrete amelogenins on the pre-existing enam
250 ma3 co-distribution with ameloblastin at the ameloblast secretory end piece.
251 data indicate that the mutation inhibits the ameloblast secretory pathway leading to ER stress and an
252             During the maturation stage, the ameloblasts shorten and direct the enamel to achieve its
253                     The data suggest that in ameloblasts, Slc26a isoforms can functionally compensate
254 cadherin expression was increased as well as ameloblast specific factors.
255                                              Ameloblast-specific amelogenin gene expression is spatio
256                     Amelogenin expression is ameloblast-specific and developmentally regulated at the
257 n blot analysis reveals that tuftelin is not ameloblast-specific but is expressed in multiple tissues
258                    These results demonstrate ameloblast-specific expression of enamelin and reveal th
259 actopyranoside (X-gal) staining demonstrated ameloblast-specific expression of enamelin.
260 Cre)-recombinase from the locus of the mouse ameloblast-specific gene amelogenin X (Amelx-iCre) with
261 d may serve as a powerful tool for targeting ameloblast-specific gene expression in future investigat
262 n molecule 1 (Stim1) floxed mice to generate ameloblast-specific Stim1 conditional knockout mice (Sti
263 -regulated in the K14-cre;Bmp2(f/f);Bmp4(f/f)ameloblasts, suggesting that the reduced MMP20 and KLK4
264 lateral anion exchanger Ae2a,b in maturation ameloblasts suggests that these cells secrete bicarbonat
265                                              Ameloblasts synthesize and secrete the enamel matrix pro
266 ey regulatory cytokine for amelogenesis, and ameloblasts synthesize CSF-1.
267                               Differentiated ameloblasts synthesizing enamel matrix proteins and odon
268 oblasts give rise to tall columnar secretory ameloblasts that direct the enamel to achieve its full t
269 ix proteins was down-regulated in the mutant ameloblasts, the cleavage of ameloblastin was drasticall
270 sx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to un
271                                       In the ameloblasts, the sequence of expression of these fractio
272  we found no APC staining in differentiating ameloblasts, then strong staining in secreting ameloblas
273 were capable of differentiating to secretory ameloblasts; this process, however, was apparently delay
274                            It is secreted by ameloblasts throughout the secretory stage and can readi
275 tacking while diminishing the ability of the ameloblast to interact with the matrix.
276 also cleaves junctional complexes present on ameloblasts to foster the cell movement necessary for fo
277  may be an important event necessary for the ameloblasts to start moving in rows that slide by one an
278 nued in the distal ends of the pre-secretory ameloblasts to the beginning of enamel matrix secretion.
279 d the dissociation of the co-assembly at the ameloblast Tomes' process.
280 concentrates along the secretory face of the ameloblast Tomes' process.
281 unolocalized to the apical pole of secretory ameloblasts (Tomes' processes) and to the newly secreted
282 d fashion, thereby providing a mechanism for ameloblast transcellular bicarbonate secretion in the pr
283 nohistochemically (IHC) localized in the pre-ameloblasts up to initial dentin matrix deposition and c
284 iguing possibility that WDR72 is critical to ameloblast vesicle turnover during enamel maturation.
285 ess questions related to HCO3 (-)export from ameloblasts, we have developed a polarized 2-dimensional
286  proteins previously described in maturation ameloblasts were also present in HAT-7 cells.
287  amelogenins the enamel would acidify unless ameloblasts were buffered by alternative ways.
288                                              Ameloblasts were immunostained for anion exchanger-2 (Ae
289 rolled Bmp4 expression in epithelium-derived ameloblasts were located in the region between 0.26 kb a
290 tes an ER stress response pathway, and mouse ameloblasts were shown to express activated Ire1.
291  while transition-stage and maturation-stage ameloblasts were strongly positive.
292 sed at the basolateral membrane of secretory ameloblasts, whereas AE2 is expressed at the apical memb
293 lysis by PCR showed NBCe1-A present in human ameloblasts, whereas mouse ameloblasts expressed NBCe1-B
294 ted by specialized epithelial cells known as ameloblasts which themselves undergo striking morphologi
295 ynthesized by a highly specialized cell, the ameloblast, which secretes matrix proteins with little h
296 dult epithelial stem cells that give rise to ameloblasts, which generate enamel, and little is known
297 trafficking is important in maturation-stage ameloblasts with respect to secretion into immature enam
298 hese genes are active only in enamel-forming ameloblasts within the dental organ of the developing to
299          Amelogenin proteins are secreted by ameloblasts within the enamel organ during tooth develop
300 stry localized exons 8/9-encoded proteins in ameloblasts, young odontoblasts, and stratum intermedium

 
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