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1 ge repopulating potential and, eventually, a mature cell).
2 ficiency does not impact the activity of the mature cell.
3 etal structure during the development of the mature cell.
4 escent, proliferate, or differentiate into a mature cell.
5 le intercellular contacts are formed between mature cells.
6 multiple rounds of exchange between EPCs and mature cells.
7 sduction but did not disrupt transduction in mature cells.
8 or survival of oligodendrocyte progenitor or mature cells.
9 somes subsequently damaged by other means in mature cells.
10  normal homeostatic production of functional mature cells.
11 ciated with abnormal maturation or number of mature cells.
12 o display the NK1.1 marker characteristic of mature cells.
13 d in hyperpolarized E(Cl) similar to that of mature cells.
14 cells to an approximately linear relation in mature cells.
15 direct acinar-to-ductal phenotypic switch in mature cells.
16 ic cells (DCs) must differentiate into fully mature cells.
17 rythroblasts and young reticulocytes than in mature cells.
18 munorestorative capacity reflects effects on mature cells.
19 rvous system give rise to different types of mature cells.
20 oietic progenitors that are not expressed in mature cells.
21 tion of new buds and induction of capsule on mature cells.
22 as 27 +/- 9 pN, compared to 54 +/- 14 pN for mature cells.
23 bset, and it decreases to low levels in more mature cells.
24 ase of myeloid progenitors and a decrease of mature cells.
25  in ontogeny, but not for the homeostasis of mature cells.
26 ineage throughout development, as well as on mature cells.
27  reduced, resulting in a much lower yield of mature cells.
28 xpression is restricted to subpopulations of mature cells.
29 ial effects of CD5 signaling in immature and mature cells.
30 he regulation of cytokine gene expression in mature cells.
31 sitional hepatocytes) that have replaced the mature cells.
32 elevant for physiological responses in these mature cells.
33 eutrophils but also modulate the function of mature cells.
34 ge differentiation into single-positive (SP) mature cells.
35 rface density of the coreceptor than do more mature cells.
36  mass than lineage-committed progenitors and mature cells.
37 atopoietic stem cells to the fully developed mature cells.
38 very by targeting the secretory machinery of mature cells.
39 lymphoid progenitors of cDCs/pDCs but not in mature cells.
40 trol self-renewal potential in both stem and mature cells.
41 s local airway eosinophil differentiation to mature cells.
42 ture cells and a defect in THPO clearance in mature cells.
43 yte differentiation that leave an imprint on mature cells.
44 he gene in response to an external signal in mature cells.
45  proliferating followed by a decline in more mature cells.
46 onstrating an anti-inflammatory phenotype in mature cells.
47 nd to systemic feedback from progenitors and mature cells.
48 nsitory stages before terminating into fully mature cells.
49 xt influences forced transdifferentiation of mature cells.
50 days in vitro) against induced apoptosis and mature cells (5+ days in vitro) against glutamate toxici
51 ve embryonic stages from gastrulation to the mature cell, a period of 24 h.
52 he most striking phenotype was cell death in mature cells after a delay of 3-4 weeks.
53 c gain or loss of expression of miR-17-92 in mature cells after activation resulted in striking recip
54  differentiating to produce large numbers of mature cells -- all without depletion of the stem cell p
55 ation complexes but that some, possibly more mature cells also accumulated substantial viral RNA in t
56 h the midacinar region (zone 2), to the most mature cells and apoptotic cells found pericentrally in
57 s that formed cytoplasmic granular bodies in mature cells and during infection of mouse brain.
58 subunit has been shown to be associated with mature cells and is linked to large neurons in the cereb
59 act presynaptic terminals apposing spines on mature cells and on newborn neurons.
60 include the active destruction of the oldest mature cells and possible control by apoptosis.
61 egulation of CD86, CD69, and MHC class II in mature cells and receptor editing in immature cells.
62       Although the production of nonadherent mature cells and their progenitors in nicotine-treated L
63                     The ability to propagate mature cells and tissue from pluripotent stem cells offe
64 these early stages was somewhat less than in mature cells and varied from cell to cell.
65 cess, and 2) Trps1 represses the function of mature cells and, consequently, restricts the extent of
66       In wild-type sepals, ROS accumulate in maturing cells and limit organ growth, suggesting that R
67  cloning capacity, impaired development into mature cells, and HSC and Meg transcription signatures.
68 ge-restricted stem cells, for maintenance of mature cells, and, in the future, for implantable, vascu
69                                   Functional mature cells are continually replenished by stem cells t
70 sion of MDC within the medulla, because more mature cells are found there.
71 es reconstructed from expression profiles of mature cells are not only consistent with current experi
72                                        Fully mature cells are postmitotic, process-bearing cells that
73 y be a potent therapeutic approach to render mature cells arising from transduced stem cells resistan
74 t acts predominantly to reduce the number of mature cells, as well as the function of peripheral iNKT
75  small, immature osteoclasts on day 2 and in mature cells at later times.
76 aturation, ranging from blasts to terminally mature cells belonging to all 3 lineages, were represent
77 f dendritic arborization, and acquisition of mature cell body morphology, we show that granule cell m
78    These results suggest that following ADX, mature cells born during the 1st postnatal week die, whe
79  death is important in controlling activated mature cells, but little is known about possible functio
80 essing cells differentiate into all types of mature cells, but their capacity for endocrine different
81                                 For example, mature cells can access an evolutionarily conserved prog
82 n into active stem cells, or, alternatively, mature cells can de-differentiate into stem-like cells o
83 initiated, as well as the means by which the maturing cell can commit to development along a specific
84 e marrow from hematopoietic progenitors into mature cells capable of a plethora of immunomodulatory r
85 ating oligodendrocytes were transitioning to mature cells capable of generating new myelin sheaths.
86 t least some molecular pathways with that of mature cells (CD18 and PECAM-1), but is differently affe
87 specification of the relative intensities of mature cell-cell adhesions.
88 m cells, throughout their development and as mature cells, cells of the immune system find themselves
89 marker protein transferrin receptor (TfR) in mature cells centers on directed transport to the dendri
90 ly in a fraction of the population to supply mature cells, coincident with maintenance of the undiffe
91 S cell-derived DCs (ES-DCs) represented less mature cells compared with bone marrow-derived DCs.
92 nificant survival advantage relative to more mature cells, consistent with the idea of chemotherapy t
93 ghly chemotactic for 2-wk-old cells, but not mature cells, correlating with a loss of mRNA for the LT
94 es similar to native heart tissue, including mature, cell-cycle-arrested cardiomyocytes.
95 y which promote paligenosis, a process where mature cells de-differentiate to acquire stem cell activ
96 mmit to the osteoclast phenotype and how the mature cell degrades bone.
97 etween the marrow reticulocyte stage and the mature cell, demonstrating that the mechanical stability
98               Block of mito-Ca(2+) uptake in mature cells depresses presynaptic-Ca(2+) influx and imp
99 f SIV-naive monkeys the majority of mDC were mature cells derived from skin that expressed high level
100 ells, indicating that significant numbers of mature cells die in response to ADX.
101                              Neural stem and mature cells differentially expressed CXCL-10, CXCR3, BD
102 did not decrease, suggesting that these less mature cells do not die following ADX.
103 opment, but inhibition of lipid synthesis in mature cells does not involve nuclear ER-alpha.
104 rants (RTEs), contrarily to peripheral naive mature cells, efficiently differentiate into Treg on tra
105  undergoes structural transformation between mature, cell-entry intermediate (A-particle) and empty f
106                                      In less mature cells, EphB4 depleted primitive cells, as measure
107  of human monocyte-derived macrophages, only mature cells exhibited TNF-alpha-induced suppression of
108 it the renin phenotype expressed Akr1b7, and maturing cells expressed angiogenic factors necessary fo
109  of early immigrants rather than entrance of mature cells from the circulation.
110 atopoietic stem/progenitor cells (HSPCs) and mature cells from the myeloid and lymphoid lineages.
111 n the airways relative to the recruitment of mature cells from the peripheral circulation to the deve
112 f hematopoietic progenitors and also affects mature cell function.
113 is, including stem/progenitor cell, and more mature cell, function.
114 f differentiation from stem to progenitor to mature cell has increased from blood to include a variet
115  cell-mediated immunity, whose expression in mature cells has been reported to be restricted to T and
116 rcation membrane system (DMS), a hallmark of mature cells, has been proposed as the source of proplat
117 cell differentiation or dedifferentiation of mature cells have been described in various systems, but
118 er-individual differences in stem-progenitor-mature cell hierarchy in adult organs.
119  phenotypic heterogeneity in stem-progenitor-mature cell hierarchy of the normal breast.
120                    These properties make the mature cell ideally suited for fine intensity discrimina
121  and with a delay in the appearance of fully mature cells in cultures undergoing granulocyte macropha
122 ion of genes enriched in differentiating and mature cells in eight major cell type lineages.
123 omeostatic mechanisms and thus the number of mature cells in most lineages remained within normal lim
124 ting macrophages to allow their induction in mature cells in response to an appropriate stimulus.
125 asal epithelial cells compared with the more mature cells in the superficial layer of the normal stra
126 e peripheral circulation and the re-entry of mature cells in the vessel wall back into cell cycle.
127 oximately 350-fold), with a complete lack of mature cells in thymus, spleen, and liver.
128                                Activation in mature cells instead stimulated hypertrophy, matrix mine
129                            Activation to the mature cell-invasive toxin involves palmitoylation of ly
130  a multipotent stem or progenitor state to a mature cell is critically important.
131   Thus, it remains unclear how feedback from mature cells is conveyed to HSCs to adjust their prolife
132 o develop in the absence of Btk, its role in mature cells is unknown.
133                                           In mature cells, labeling was present in both cell bodies a
134 ts cell number and cyclin expression but not mature cell length, indicating that, in roots, uncheckin
135  stem cells maintain and regenerate multiple mature cell lineages in the olfactory epithelium.
136 em cells, and model 2 for the maintenance of mature cell lineages.
137                                              Mature cell lines produced TNFalpha when stimulated with
138   In conclusion, neither SCC development nor mature cell maintenance is dependent on intact trigemina
139 nuclear antigen but did not express the more mature cell markers NeuN and Hu, suggesting that they we
140 rogenitor cells grown in serum expressed the mature cell markers opsin, but few cells expressed glial
141 ian stem cell systems where large numbers of mature cells must be continuously produced throughout ad
142 structs all distal structures, implying that mature cells near the wound retain positional memory alo
143 e self-renewal and differentiation such that mature cells necessary for tissue function can be genera
144                            The production of mature cells necessitates that lineage-committed progeni
145                 The action potentials of the mature cell occur only on stimulation, and are 10 times
146                  The differentiated state of mature cells of adult organisms is achieved and maintain
147 alysing c-myb(-/-) chimaeras we show that no mature cells of any lymphoid or myeloid lineage can be d
148 aughter cells that are destined to commit to mature cells of different specific lineages.
149 limited by embryonic lethality or absence of mature cells of interest, creating the need for alternat
150 m cells (MSCs), which can differentiate into mature cells of multiple mesenchymal tissues including f
151 essivity factor for DNA polymerase delta, in mature cells of Nicotiana benthamiana.
152  cells have been shown to differentiate into mature cells of nonhematopoietic tissues, such as hepato
153 d with specific cytokine combinations toward mature cells of particular types.
154 tic growth and functions associated with the mature cells of specific daughter lineages (such as mega
155 at display a phenotype characteristic of the mature cells of that tissue.
156 at the apex of a hierarchy that produces all mature cells of the blood.
157 development from hematopoietic stem cells to mature cells of the hematolymphoid system involves progr
158                                 In contrast, mature cells of the lymphoid lineages expressed little t
159  are only released to the plasma membrane in mature cells of the olfactory receptor neuron lineage.
160 s expressed in hematopoietic progenitors and mature cells of the three main hematopoietic lineages.
161 lls with the potential to differentiate into mature cells of various organs.
162 eration is impaired, transdifferentiation of mature cells or differentiation of stem cells allows pro
163   Cancer may arise from dedifferentiation of mature cells or maturation-arrested stem cells.
164 y altered progenitor population function and mature cell output.
165 ed that acinar cells lacking ATF3 maintain a mature cell phenotype during pancreatitis, a finding sup
166 ely 1 week, remaining viable and with stable mature cell phenotypes for more than 8 weeks.
167 and survival, with dose-dependent effects on mature cell phenotypes.
168 rcentage of BrdUrd-labeled cells that showed mature cell phenotypes.
169 role of endocytic membrane remodeling in the maturing cell plate while the plate is stabilized by cal
170 ited from the cytoplasm to the expanding and maturing cell plate.
171 oles that neuronal and glial progenitors and mature cells play in CNS angiogenesis and neurovascular
172 s targeted to the sites of cell division and mature cell poles where, in B.subtilis, it controls the
173 t is targeted to midcell and retained at the mature cell poles.
174 mplete, SP rings exhibited two properties of mature cell poles: they behaved as though composed of in
175 ate copper as they differentiate into a more mature cell population and this accumulation is not refl
176      During organogenesis, the final size of mature cell populations depends on their rates of differ
177  Beyond stem cells, there was a reduction in mature cell populations in the BM and peripheral blood,
178 L), using highly enriched CML stem cells and mature cell populations in vitro.
179  is unknown whether this reflects changes in mature cell populations or whether the IL-23-driven coli
180 omatin accessibility discriminates stem from mature cell populations, enabling the identification of
181 r the transdifferentiation of more plentiful mature cell populations.
182 ning the potential to differentiate into all mature cell populations.
183 ytoplasmic GR, while abventricular NSPCs and mature cells primarily expressed nuclear GR.
184 ve distribution of PAI-2 in the postmitotic, maturing cells prior to terminal keratinization and deat
185 nmemory pool, the number of naive follicular mature cells produced per transitional B cell is 3- to 6
186 poietic progenitors, which dynamically drive mature cell production, and hematopoietic stem cells (HS
187 efects from alterations in the physiology of mature cells, Rbfox1 and Rbfox2 were deleted from mature
188 lication of progenitors and the life-span of mature cells, reflecting the timing of death by apoptosi
189 fic fugetaxis-inducing factors to which only mature cells respond.
190 AML, because induced deletion of the gene in mature cells resulted in a similar phenotype.
191 cells; however, the mechanism by which these mature cells sense systemic insulin demand and initiate
192 the memory CD8+ T cell response suggest that mature cells should be considered as immunotherapeutic a
193  and biomass, as no changes were detected in mature cell size, specific leaf area, or relative photos
194 e cells specialized for antigen capture into mature cells specialized for T cell stimulation.
195 ce expression is restricted primarily to the mature cell stage during development.
196 pressed on B cells from the immature through mature cell stages.
197 e expression of markers associated with more mature cell states was expanded.
198  proliferation and greater expansion of more mature cell subsets.
199 are either required to provide the influx of maturing cells (such as hematopoietic stem cells) or whi
200 ants exhibit a different TCR repertoire than mature cells, suggesting that the iNKT population is sha
201 ein that is proteolytically cleaved to yield mature cell surface glycoproteins gp40 and gp15, which a
202          Finally, we show that the increased mature cell surface LDLR in the presence of RAP coexpres
203 on mice also expressed higher levels of more mature cell surface markers, additionally linking inflam
204 in particular lymphoid cells possessing more mature cell surface markers, comprise the human componen
205 h these stem cells expressed a somewhat more mature cell surface phenotype than the initial yolk sac
206  CD34+/c-kit+ cells or cells expressing more mature cell surface phenotypes.
207 nthesized invariant chain-associated MHC-II, mature cell surface pMHC-II complexes internalize follow
208  135 and 125 kD; the 135-kD band represented mature cell surface receptor containing sialic acid and
209 ity oLH binding component contributed by the mature cell surface receptor.
210  whereas hCG cannot discriminate between the mature cell surface wild-type receptor and an intracellu
211 inities of two populations of rLHR where the mature, cell surface form binds oLH with a higher affini
212  of Notch by furin is required to generate a mature, cell surface heterodimeric receptor that can be
213 52P) selectively increased polyploidization, mature cell-surface marker expression, and apoptosis of
214 and synaptic functions in the developing and mature cell-surface proteomes, respectively.
215  signaling pathways, induced cleavage of the mature cell-surface receptor.
216 steoblast precursor recruitment and promotes mature cell survival.
217 differentiated hematopoietic cells and fewer mature cells than controls.
218 henotype remains necessary, because the most mature cells that can be produced with current systems e
219         Ideal grafts should contain HSC plus mature cells that confer only the benefits of protection
220 ntal differences influence the properties of mature cells that exit the thymus and seed peripheral ly
221  and find CD34+ progenitor cells and various mature cells that harbor preleukemic mutations.
222 direct progeny of mutated stem cells or more mature cells that reacquire stem cell properties during
223                                           In mature cells, the core enhancer had low activity and req
224 ced as myeloid precursors differentiate into mature cells, then drops as monocytes further differenti
225 ay translate into effects on the majority of mature cells, thereby providing a strategy for potentiat
226 of human pluripotent stem cells (hPSCs) into mature cells, tissues and organs holds major promise for
227 ert a diseased cell to a healthy state, or a mature cell to a pluripotent state.
228 frequently requires the dedifferentiation of mature cells to a condensed mesenchymal blastema, from w
229 ed cells and (ii) during the exposure of the mature cells to an actin cytoskeleton disrupting drug.
230 wound healing, stem cells provide functional mature cells to meet acute demands for tissue regenerati
231     However, it is now possible to reprogram mature cells to pluripotency.
232 d and offer an initial strategy for inducing mature cells to switch their fate.
233    Ee-BAM1 also surrounds the amyloplasts in mature cells toward the base of the bud.
234                                        These maturing cells transition from a proliferative state to
235 s had the potential to develop into only one mature cell type ('uni-lineage potential'), bi- and rare
236 equence of fate decisions that leads to each mature cell type in a tissue or organism.
237  mediate differentiation of hPS cells into a mature cell type, independent of soluble inductive facto
238 nes often showed biases towards one or other mature cell type.
239 e and differentiate to replace dead or dying mature cell types and maintain the integrity and functio
240 as appears to lack progenitor cells, and its mature cell types are maintained by the proliferation of
241  Lineage commitment and differentiation into mature cell types are mostly considered to be unidirecti
242 d progenies that are generally applicable to mature cell types as well.
243                            The generation of mature cell types during pancreatic development depends
244 have been functionally shown to generate all mature cell types for the lifetime of the organism.
245           Our results indicate that, whereas mature cell types in each organ may have unique developm
246 n epithelium, and suggest that plasticity of mature cell types may play a role in the generation of n
247 tages of embryogenesis to differentiation of mature cell types of all three germ layers from pluripot
248 enitor cells (TBPCs), which give rise to the mature cell types of chorionic villi-syncytiotrophoblast
249 xpressing progenitor cells contribute to all mature cell types of the retina.
250                     These two phenotypically mature cell types show a high degree of plasticity, whic
251 enewal with differentiation into the various mature cell types to maintain tissue homeostasis.
252 e to at least fourteen functionally distinct mature cell types, and represents the best characterized
253 enriched populations when compared with more mature cell types, and that this gene is essential for t
254            Adult blood contains a mixture of mature cell types, each with specialized functions.
255 enitor cells with their capacity to generate mature cell types.
256 s progenitors but also differentiated toward mature cell types.
257 liferate and differentiate into a variety of mature cell types.
258 intain their potential to differentiate into mature cell types.
259 stimulation they are capable of regenerating mature cell types.
260 ability of myeloblasts to differentiate into mature cell types.
261 ability of myeloblasts to differentiate into mature cell types.
262 s properties to stem-like cells than to more mature cell types.
263 uiescent, proliferate, or differentiate into mature cell types.
264 ntiation, resulting in a failure to generate mature cell types.
265 n the larval lymph gland gives rise to three mature cell types: plasmatocytes, lamellocytes, and crys
266 he theoretical potential to develop into all mature cell types; however, the actual ability to develo
267 ntiation and is not known to be inducible in mature cells under physiological conditions.
268                                   As embryos mature, cells undergo remarkable transitions that are ac
269                                      (1) The matured cells undergo a selective turnover of mRNA encod
270                        New capsule formed by mature cells upon induction of synthesis is added at the
271 n have short NRL ranging from 160 to 189 bp, mature cells usually have longer NRLs ranging between 19
272 t cell population thought to be derived from mature cells via dedifferentiation.
273  STAT5)(2-4) or pre-B-cell receptors in more mature cells (via activation of the protein kinase ERK)(
274 re cross-linked by short peptide chains, the mature cell wall is chemically diverse.
275                                          The mature cell wall of B. anthracis is resistant to digesti
276                We show that incorporation of mature cell wall precursor, UDP-MurNAc-pentapeptide, is
277 reactions of cell wall synthesis, generating mature cell wall-linked surface protein.
278 erial cell wall enzymes cooperate to build a mature cell wall.
279 agine (Asp/Asn, Asx) bridges are specific to mature cell wall.
280 at are subsequently cross-linked to form the mature cell wall.
281 and remain associated with primary PD in the mature cell wall.
282  structure that is not incorporated into the mature cell wall.
283 were polarized to regions of the cell with a mature cell wall; they were absent from small buds and t
284 oteichoic acids is 3:2; and (iii) 50% of the mature cell-wall binding sites for a fluorinated oritava
285                      Molecular models of the mature cell-wall complexes that are consistent with inte
286 scent cross wall or "cell plate" and also in mature cell walls.
287                   In contrast, Ca2+ entry in mature cells was confined to the action potential itself
288 sing higher levels of GSK3beta compared with mature cells was selectively enhanced by stem cell facto
289  expression data available are only from the mature cells, we have some challenges in identifying tra
290 e compared to their corresponding adipocytic maturing cells, we identified a group of genes overexpre
291 okines and chemokines, indicating that these mature cells were functionally competent in the context
292      Nevertheless, the different lineages of mature cells were produced in normal numbers in vitro.
293    Although effector genes characteristic of mature cells were upregulated late, coincident with morp
294 lly, and del(12p) occurs postnatally in more mature cells with a structure that suggests the involvem
295 g and cancer, was particularly widespread in mature cells with an extended lifespan.
296 sult typically in partial differentiation to mature cells with under- or overexpression of adult tiss
297 hown further maturation and ultimate loss of matured cells with continuing therapy.
298 , a carbohydrate antigen expressed on highly mature cells within the CD56(dim)CD16(+) NK cell compart
299 ssular niches, DCs can exist as immature and mature cells within the same tissue, revealing an additi
300  thymocyte development caused an increase in mature cells within the thymus.

 
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