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1 ct of posttranscriptional regulation in stem cell fate specification.
2 ired for FSC maintenance and polar and stalk cell fate specification.
3 ls entered a cell cycle arrest that preceded cell fate specification.
4 pound eye are a classical model for studying cell fate specification.
5 erful system to study the molecular basis of cell fate specification.
6 EAD4 in blastomeres dictates first mammalian cell fate specification.
7 constraints, cell proliferation dynamics and cell fate specification.
8 nd nuclear factors in the establishment of T-cell fate specification.
9 te inner ear morphogenesis without affecting cell fate specification.
10 g convergent extension movements or mesoderm cell fate specification.
11 ranscriptional control mechanisms underlying cell fate specification.
12 stem has been most studied in the context of cell fate specification.
13 is a central regulator required for aleurone cell fate specification.
14  study gene regulatory networks that control cell fate specification.
15 ctor that participates in embryonic neuronal cell fate specification.
16  candidate regulators of hypothalamic neural cell fate specification.
17 yet generates different outcomes in daughter cell fate specification.
18 chanism that generates asymmetry in daughter cell fate specification.
19 germline stem cell totipotency and embryonic cell fate specification.
20 al stem cell self-renewal and neuronal/glial cell fate specification.
21 n of radial glial cell division and daughter cell fate specification.
22 ng aspects of dorsal neural tube closure and cell fate specification.
23 hat loss of plasticity can be uncoupled from cell fate specification.
24 an excellent model system to study epidermal cell fate specification.
25 standing gene regulation and the dynamics of cell fate specification.
26 ly link cell proliferation, pluripotency and cell fate specification.
27 nts and inductive tissue interactions during cell fate specification.
28 spacing rule, reflecting the coordination of cell fate specification.
29 lable for the investigation of photoreceptor cell fate specification.
30 tinogenic potential of progenitor cells, and cell fate specification.
31 ly, and this asymmetry is crucial for proper cell fate specification.
32 n mother cells (PMCs), suggesting defects in cell fate specification.
33 eogenic, and block chondrogenic, programs of cell fate specification.
34 lular morphogenesis, signal transduction and cell fate specification.
35 e anterior localization of Numb and daughter cell fate specification.
36 y for correct regulation of neurogenesis and cell fate specification.
37 way may mediate Numb signaling in asymmetric cell fate specification.
38 on and a substantial alteration in CD4-CD8 T cell fate specification.
39 munication between adjacent cells to control cell fate specification.
40 nner to regulate both cell proliferation and cell fate specification.
41 sis, auditory hair cell differentiation, and cell fate specification.
42  SCARECROW (SCR) control root patterning and cell fate specification.
43 pport an inhibitory role for Kremen1 in hair cell fate specification.
44 rategy for overcoming epigenetic barriers to cell fate specification.
45  results in disrupted cell proliferation and cell fate specification.
46 regulatory networks to control photoreceptor cell fate specification.
47 ams, actively repressed by GSX2/DLX-mediated cell fate specification.
48 s an excellent system to study mechanisms of cell fate specification.
49 d establish an important function for APA in cell fate specification.
50 luences and the interplay between the two in cell fate specification.
51 ity and transcriptional networks controlling cell-fate specification.
52 y be a general mechanism to control terminal cell-fate specification.
53 tone modifications over the course of neural cell-fate specification.
54 -1 causes reciprocal defects in Wnt-mediated cell-fate specification.
55 re we report that ACBD3 is a Numb partner in cell-fate specification.
56 1 and met-2 as negative regulators of vulval cell-fate specification.
57 scription factors plays fundamental roles in cell-fate specification.
58 e programming of cellular age in parallel to cell-fate specification.
59 re inherent to gene expression and can drive cell-fate specification.
60 ions of the different parts of the embryo to cell fate specifications.
61  non-coding RNA epigenetic regulation during cell fate specifications.
62 al regulates patterns of gene expression and cell fate specification along the dorsal-ventral axis.
63 le, the midline cells are involved in neural cell fate specification along the dorso-ventral axis but
64 TRIC LEAVES2 (AS2) gene, which promotes leaf cell fate specification and adaxial polarity.
65                                    Embryonic cell fate specification and axis patterning requires int
66 ediating the abilities of the BMPs to direct cell fate specification and axon outgrowth.
67                Wnt signaling is critical for cell fate specification and cell differentiation in many
68 gene regulatory network involved in aleurone cell fate specification and cell differentiation.
69 upstream regulatory events and helps program cell fate specification and cell invasion.
70        However, its molecular functions in B cell fate specification and commitment have remained elu
71 elopment, but its molecular function(s) in B cell fate specification and commitment is unknown.
72 nt, but its molecular function(s) in early B cell fate specification and commitment is unknown.
73 lysis of genetic networks, which orchestrate cell fate specification and commitment.
74  that is heavily compromised in DS, but also cell fate specification and dendritic maturation.
75 stone modifications accompany the process of cell fate specification and determination.
76 e same transcription factors can function in cell fate specification and differentiated cell behavior
77 netic mechanism by which yki plays a role in cell fate specification and differentiation - a novel as
78  autonomous factors required redundantly for cell fate specification and differentiation during inner
79              The mechanisms of photoreceptor cell fate specification and differentiation have been ex
80       RNA-binding proteins (RBPs) coordinate cell fate specification and differentiation in a variety
81 n UNC-62 plays essential roles in regulating cell fate specification and differentiation in the M lin
82 ch signaling pathway, which is important for cell fate specification and differentiation in various s
83  addition, we revealed a role for Neurog2 in cell fate specification and differentiation of ventromed
84 e first week after loss of miRNA expression, cell fate specification and differentiation were not mar
85  Wnt signaling mediate critical functions in cell fate specification and differentiation, but specifi
86 leolar size was reduced significantly during cell fate specification and differentiation, predominant
87 nt are the underlying mechanisms controlling cell fate specification and differentiation.
88 ption factors, which have been implicated in cell fate specification and differentiation.
89  of morphogenetic movements with progressive cell fate specification and differentiation.
90 s that accompanies developmental competence, cell fate specification and differentiation.
91 a conserved use of closely related bHLHs for cell fate specification and differentiation.
92 tes neural progenitor cell proliferation and cell fate specification and differentiation.
93 llular events, including cell proliferation, cell fate specification and differentiation.
94  system for studying molecular mechanisms of cell fate specification and differentiation.
95 ncreatic acinar cells and critical to acinar cell fate specification and differentiation.
96 identifying regulatory parallels between P12 cell fate specification and egl-5 transcriptional regula
97 pment have illuminated mechanisms underlying cell fate specification and elucidated intercellular sig
98 RL) is an essential transcription factor for cell fate specification and functional maintenance of ro
99 ever, how cells differentially transduce the cell fate specification and guidance activities of morph
100  well as during organ patterning, migration, cell fate specification and hair cell regeneration.
101 to examine the effects of ADAM10 deletion on cell fate specification and intestinal stem cell mainten
102        Notch is required for many aspects of cell fate specification and morphogenesis during develop
103 l events in the vertebrate embryo, affecting cell fate specification and morphogenesis.
104 broad spectrum of genes that are involved in cell fate specification and morphogenesis.
105 recocious polarization as well as subsequent cell fate specification and morphogenesis.
106 two other model systems widely used to study cell fate specification and morphogenesis: the pre-impla
107           Notch signalling is required for T-cell fate specification and must be maintained throughou
108       The transcription factor TLX1 controls cell fate specification and organ expansion during splee
109 but is a target for regulation by Ral during cell fate specification and pattern formation.
110                        During organogenesis, cell fate specification and patterning are regulated by
111          Ea/Ep ingression depends on correct cell fate specification and polarization, apical myosin
112                          The coordination of cell fate specification and proliferation is particularl
113 ural tube is a source of signals that direct cell fate specification and proliferation.
114  control bipolar interneuron and Muller glia cell fate specification and promote proliferative quiesc
115 netic modification with an important role in cell fate specification and reprogramming.
116 is balance is important for axis elongation, cell fate specification and somitogenesis.
117 initial target of Prox1 during the lymphatic cell fate specification and that FGF signaling may play
118  abruptly after germinal and initial somatic cell fate specification and then diminish, whereas 24-nt
119 d applicability in directed differentiation, cell fate specification and therapeutic applications.
120  important model for analyzing mechanisms of cell fate specification and tissue morphogenesis.
121 ling pathways that control unique aspects of cell fate specification and tissue morphogenesis.
122 phogen gradients provide positional cues for cell fate specification and tissue patterning during emb
123 ly conserved signaling pathway that controls cell fate specification and tissue patterning in the emb
124 ens act as graded positional cues to dictate cell fate specification and tissue patterning.
125                  To better understand anther cell fate specification and to provide a resource for th
126 es in the embryo and the adult, ranging from cell-fate specification and cell polarity to social beha
127 ution and represent a mechanism for coupling cell-fate specification and cell-cycle progression.
128 tial and temporal mechanisms governing their cell-fate specification and differential integration int
129 ivation by distal enhancers is essential for cell-fate specification and maintenance of cellular iden
130       These findings forge new links between cell-fate specification and morphogenesis, and they repr
131 LIM homeodomain transcriptional code confers cell-fate specification and neurotransmitter identity in
132 regulatory networks that define neural-crest cell-fate specification and subsequent mesoderm cell lin
133                                It determines cell-fate specification and tissue architecture during a
134  involves extensive lineage diversification, cell-fate specification and tissue patterning(1).
135 cyte meiotic maturation/ovulation, male germ cell fate specification, and a nonessential function of
136 ebellum, gene-expression cascades underlying cell fate specification, and a number of previously unkn
137 itioning of proteins that mediate signaling, cell fate specification, and asymmetric cell division.
138 he other elements, impacting eve expression, cell fate specification, and cardiac function.
139 o aberrant cell proliferation, inappropriate cell fate specification, and excessive Ras pathway activ
140 role of enhancers in controlling patterning, cell fate specification, and morphogenesis during develo
141 by influencing in addition to proliferation, cell fate specification, and neurite development.
142 uencing neural precursor cell proliferation, cell fate specification, and neuronal maturation.
143 sses associated with intestinal development, cell fate specification, and the maintenance of intestin
144  this system, the effects on cell signaling, cell fate specification, and tissue differentiation are
145 TZFs) play pivotal roles in gene expression, cell fate specification, and various developmental proce
146 rdinated program of lineage diversification, cell-fate specification, and morphogenetic movements est
147 of pathways involved in tissue self-renewal, cell-fate specification, and regeneration.
148 duction and functions to canalize aspects of cell-fate specification, animal size regulation, and mol
149  exhibited broader and shorter body axis but cell fate specification appeared normal.
150 isms controlling hypothalamic patterning and cell fate specification are poorly understood.
151            Among the genes required for male cell fate specification are Wnt/beta-catenin pathway mem
152 scale remodelling of the intestinal wall and cell-fate specification are closely linked.
153 downstream of or parallel to lin-12 in AC/VU cell fate specification at an early developmental stage,
154  spatiotemporally complex manner, completing cell-fate specification at the periphery by Hamburger an
155 essential developmental processes, including cell fate specification, axon guidance and anteroposteri
156                    Brg1 was not required for cell fate specification but was required for photorecept
157 ession did not appear to alter photoreceptor cell fate specification, but it inhibited subsequent dif
158                 SHR is also essential for BS cell-fate specification, but it is expressed in the cent
159 ly in the BS cells and act redundantly in BS cell-fate specification, but their expression pattern an
160    These results highlight the complexity of cell fate specification by cell-cell interactions in a r
161  a transcriptional regulator that can affect cell fate specification by controlling Achaete levels.
162 ural plate border, prdm1a acts explicitly on cell fate specification by counteracting olig4 expressio
163         The protein co-factor Ldb1 regulates cell fate specification by interacting with LIM-homeodom
164 e use of canonical Notch signaling for early cell fate specifications by lower organisms may represen
165 homeodomain proteins play essential roles in cell fate specification, cell differentiation, migration
166 and spatial coordination of cell cycle exit, cell fate specification, cell migration and differentiat
167  including tissue patterning, proliferation, cell fate specification, cell polarity and migration.
168 uires precise regulation and coordination of cell fate specification, cell proliferation and differen
169 scence microscopy to study processes such as cell-fate specification, cell death, and transdifferenti
170  (ERK) signaling governs multiple aspects of cell fate specification, cellular transitions, and growt
171 e this with the RTK/N signaling to provide a cell fate specification code that entails both extrinsic
172 4), a receptor kinase implicated in aleurone cell fate specification, colocalized to plasma membrane
173 family of transcription factors orchestrates cell-fate specification, commitment and differentiation
174 m proliferating progenitor cells to terminal cell fate specification, contemporary with regulation of
175 odel organism studies have demonstrated that cell fate specification decisions play an important role
176                                              Cell-fate specification decisions are critical for norma
177                                       Proper cell-fate specification decisions are critical to achiev
178  data identify Ptf1a as a major regulator of cell-fate specification decisions in the developing brai
179                                        After cell fate specification, differentiating cells must ampl
180 provide important data on the proliferation, cell fate specification, differentiation and survival of
181 ficance of differences in the proliferation, cell fate specification, differentiation of survival of
182            N-myc is not required for retinal cell fate specification, differentiation, or survival.
183 hat is a critical modulator of Ras-dependent cell fate specification during C. elegans development.
184 nc-finger RNA-binding proteins that regulate cell fate specification during C. elegans embryogenesis.
185 family of receptors plays important roles in cell fate specification during development and in adult
186                 Sox2 plays critical roles in cell fate specification during development and in stem c
187  Cell proliferation must be coordinated with cell fate specification during development, yet interact
188 ot only normal growth and apoptosis but also cell fate specification during development.
189 egans muscle excess 3 (MEX-3) is involved in cell fate specification during early embryonic developme
190 of genes from this spatial network underlies cell fate specification during early embryonic developme
191          Morphogen signals are essential for cell fate specification during embryogenesis.
192 es in cell proliferation, morphogenesis, and cell fate specification during embryonic development.
193 tered levels of Amun function interfere with cell fate specification during eye and sensory organ dev
194 f mitotic spindle orientation is crucial for cell fate specification during mammalian neurogenesis.
195 ell signaling pathway is used extensively in cell fate specification during metazoan development.
196 unction in the nucleus that is important for cell fate specification during primary neurogenesis.
197 tercellular signaling events that coordinate cell fate specification during stomatal development.
198 rol genes critical for pattern formation and cell fate specification during the development of multic
199 onal elongation is central to the process of cell fate specification during this critical stage of em
200                    However, the mechanism of cell fate specification during this process is unknown.
201              Here, we report that this first cell fate specification event is controlled by glucose.
202 onarily conserved pathway essential for many cell fate specification events during metazoan developme
203  signaling pathway required for a variety of cell fate specification events in many organisms.
204      A functional egg-laying system requires cell fate specification events in the epithelial cells o
205            Notch signaling controls numerous cell-fate specification events in multicellular organism
206 mic transformation but are dispensable for T-cell fate specification from a multipotential precursor.
207 he Notch pathway is a versatile regulator of cell fate specification, growth, differentiation, and pa
208  Many of the genes and pathways that promote cell fate specification have been elucidated.
209 onflicting verbal models of vulval precursor cell fate specification have been proposed: sequential i
210 details of the three-dimensional patterns of cell fate specification have not been investigated in th
211                It is generally believed that cell fate specification in C. elegans is mainly mediated
212                                              Cell fate specification in development requires transcri
213 r maintaining stem cell pluripotency and for cell fate specification in development.
214 maternal mRNAs, which is crucial for correct cell fate specification in early C. elegans embryos, is
215 at tissue-level forces can directly regulate cell fate specification in early human development.
216 s act as graded positional cues that control cell fate specification in many developing tissues.
217 gulation of gene expression is essential for cell fate specification in metazoans.
218                  To identify genes affecting cell fate specification in neural crest, we performed a
219                                              Cell fate specification in the CNS is controlled by the
220 ab-9, a T-box gene known to be important for cell fate specification in the developing C. elegans hin
221             Egfr/Ras signaling promotes vein cell fate specification in the developing Drosophila win
222 o construct a unified model of photoreceptor cell fate specification in the developing vertebrate ret
223 e exhibit normal stem cell proliferation and cell fate specification in the DG but show impaired diff
224 s study, nucleolus size was monitored during cell fate specification in the Drosophila eye imaginal d
225                                              Cell fate specification in the early C. elegans embryo r
226  mls-2 also affects cleavage orientation and cell fate specification in the M lineage.
227                                              Cell fate specification in this region depends on sonic
228      These data suggest a model for aleurone cell fate specification in which DEK1 perceives and/or t
229 CTOR2 (PDF2) are indispensable for epidermal cell-fate specification in Arabidopsis embryos.
230 result from an overt defect in patterning or cell-fate specification in Gbx2 mutants.
231 centration-dependent positional and temporal cell-fate specification in solid tissues.
232 ty in the CNS, but the mechanisms regulating cell-fate specification in the developing brainstem are
233 nical Wnt receptor Ryk regulates interneuron cell-fate specification in vivo and in vitro.
234 ignalling, and that this crosstalk regulates cell-fate specification in vivo during Xenopus developme
235 gulator of pancreatic development and acinar cell fate specification, induced the expression of endoc
236                       A derepression mode of cell-fate specification involving the transcriptional re
237                                Developmental cell fate specification is a unidirectional process that
238 eveals that this "master regulator" of glial cell fate specification is also required (gasp!) to gene
239  What controls Hippo pathway activity during cell fate specification is incompletely understood.
240           The role of microRNAs in embryonic cell fate specification is largely unknown.
241                                              Cell fate specification is mediated primarily through th
242                       The dynamic process of cell fate specification is regulated by networks of regu
243 the mechanisms underlying prdm1a function in cell fate specification is unknown.
244                                       Neural cell fate specification is well understood in the embryo
245 sting that this developmental pathway for BS cell-fate specification is likely to be evolutionarily c
246 n of neural progenitors in proliferation and cell fate specification, is largely unknown.
247 t mixed-lineage states are obligatory during cell-fate specification, manifest differing frequencies
248 mbly of gene regulatory networks involved in cell fate specification may facilitate the efficient and
249 ans) is an ideal model organism to study the cell fate specification mechanisms during embryogenesis.
250 a systematic and comprehensive analysis from cell fate specification, migration, and connectivity, to
251 velopment has been used extensively to study cell fate specification, migration, proliferation, survi
252 oan origin of a beta-catenin-mediated binary cell-fate specification module.
253                       The genetic control of cell fate specification, morphogenesis and expansion of
254 g aspects of human NC development, including cell fate specification, multipotency and cell migration
255         In larval imaginal discs, growth and cell fate specification occur normally in mutant cells,
256 en though cardiac cell migration and initial cell fate specification occur normally.
257  fluorescence markers, we show that aleurone cell fate specification occurs exclusively in response t
258 ndicates that prdm1 functions to promote the cell fate specification of both neural crest cells and R
259 hods for regulating self-renewal and initial cell fate specification of hESCs.
260  roles for these molecules: an early role in cell fate specification of multiple neural progenitors a
261                     These proteins influence cell fate specification of neural lineages and different
262 d novel transcriptional programs controlling cell fate specification of populations arising from the
263 4/MKK5 or MPK3/MPK6 disrupts the coordinated cell fate specification of stomata versus pavement cells
264                                          The cell fate specification of subcutaneous preadipocytes by
265 n of SMADs 2 and 3 at the floor plate, while cell fate specification of the notochord and the floor p
266 the transcriptional networks that govern the cell fate specification of these progenitors are incompl
267  elegans where CeTwist is required to direct cell fate specifications of a subset of mesodermal cells
268 uration of newborn neurons without affecting cell-fate specification of neural stem cells/neural prog
269 ila eye, Frizzled (Fz)/PCP signaling induces cell-fate specification of the R3/R4 photoreceptors thro
270 lls hyperproliferative, and caused defective cell fate specification or differentiation both in vitro
271 ling is not required in mammals for earliest cell fate specifications or for formation of the three g
272 cal processes, including cell proliferation, cell fate specification, organogenesis, and epithelial-m
273                             The far reach of cell fate specification pathways makes it particularly c
274 gration of Wnt-dependent and Wnt-independent cell fate specification pathways within the Caenorhabdit
275  different Wnt pathways converge on the same cell fate specification process, our data suggest they m
276 ng the irreversibility of the patterning and cell fate specification process.
277                        Wnt signaling affects cell-fate specification processes throughout embryonic d
278 he relationships among cell types in diverse cell-fate specification processes.
279 B signaling is essential in vivo for Schwann cell fate specification, proliferation, survival, migrat
280  the BS cells, but the molecular basis of BS cell-fate specification remains unclear.
281                                  This binary cell fate specification requires input from both the Wnt
282                                              Cell fate specification requires precise coordination of
283 on of asymmetric cell divisions and stomatal cell fate specification, resulting in a lack of stomatal
284 , convergent extension of the cochlear duct, cell fate specification, synaptogenesis, and the establi
285 ional organ requires coordinated programs of cell fate specification, terminal differentiation and mo
286 Ras pathway also functions in cell survival, cell-fate specification, terminal differentiation, and p
287 nally, by controlling the timing and pace of cell fate specification, the embryo temporally modulates
288 erall tempo of retinogenesis, by integrating cell fate specification, the wave of neurogenesis and th
289 nsic transcription factor Ngn2 cooperate for cell fate specification through their synergistic activi
290  encodes a transcription factor that governs cell fate specification throughout development and tissu
291 totic precision fundamentally contributes to cell fate specification, tissue development and homeosta
292 conserved Notch pathway regulates asymmetric cell fate specification to daughters of ganglion mother
293 rocesses ranging from cell proliferation and cell fate specification to differentiation over embryoni
294  has been difficult to assign later roles in cell fate specification to specific BMP ligands.
295 B size could be an important parameter in ES cell fate specification via differential gene expression
296                     TGF-beta ligands control cell fate specification via Smad-mediated signaling.
297      To determine whether prdm8 controls pMN cell fate specification, we used zebrafish as a model sy
298  and expansion of pavement cells and stomata cell fate specification; we also observed severe alterat
299 gregates known as embryoid bodies (EBs), yet cell fate specification within EBs is generally consider
300                       Mechanisms that govern cell-fate specification within developing epithelia have

 
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