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1 stem cells, embryonal carcinomas and induced pluripotent cells).
2 growth factor GDF9 can reprogram hADFs into pluripotent cells.
3 and effectiveness of cell differentiation of pluripotent cells.
4 ning the culture requirements of naive human pluripotent cells.
5 ay to drive mesendodermal differentiation of pluripotent cells.
6 ry meristems can be traced back to groups of pluripotent cells.
7 es that have bivalent chromatin structure in pluripotent cells.
8 ng loci were bound by Mediator or cohesin in pluripotent cells.
9 lation, suggesting it is a pivotal marker of pluripotent cells.
10 engraftment of blood progenitors from human pluripotent cells.
11 ry program at the G(1)/S-phase transition in pluripotent cells.
12 cations at the Oct4 locus in fibroblasts and pluripotent cells.
13 tive way to induce CPCs from mouse and human pluripotent cells.
14 is the key feature of murine totipotent and pluripotent cells.
15 lture can also induce abnormalities in these pluripotent cells.
16 ith endoderm promotes induction of CPCs from pluripotent cells.
17 aining the differentiation responsiveness of pluripotent cells.
18 erences between in vitro and ex vivo primate pluripotent cells.
19 ion between embryonic stem cells and induced pluripotent cells.
20 tified proteins and phosphorylation sites in pluripotent cells.
21 n the formation of teratomas by transplanted pluripotent cells.
22 C/C substrates are also present during G1 of pluripotent cells.
23 ariants affecting the transcriptome of human pluripotent cells.
24 on in a broad range of cell types, including pluripotent cells.
25 lls and in epigenetic remodeling of germ and pluripotent cells.
26 cle structure and transcriptional network of pluripotent cells.
27 feeders for both autologous and heterologous pluripotent cells.
28 tional regulator of differentiation in these pluripotent cells.
29 y novel peptides that bind to the surface of pluripotent cells.
30 dynamics during lineage commitment of human pluripotent cells.
31 via diploid aggregation, unique to bona fide pluripotent cells.
32 tained the matrix signal for differentiating pluripotent cells.
33 ns methylated differently in fibroblasts and pluripotent cells.
34 ing networks that control differentiation of pluripotent cells.
35 n epigenetic mechanism of gene repression in pluripotent cells.
36 tween Oct4/Sox2 and cell cycle regulation in pluripotent cells.
37 microRNAs expressed specifically in ESCs and pluripotent cells.
38 or genetic studies of human pre-implantation pluripotent cells.
39 ether are sufficient to generate retina from pluripotent cells.
40 y in controlling early neural development of pluripotent cells.
41 he role of the transcription factor Foxd3 in pluripotent cells.
42 alance between transcriptional programmes in pluripotent cells.
43 ction in gene expression regulation in mouse pluripotent cells.
44 the genetic regulation of gene expression in pluripotent cells.
45 ure cell types of all three germ layers from pluripotent cells.
46 in the transcriptional regulatory network of pluripotent cells.
47 we show that this instability only occurs in pluripotent cells.
48 ed in undifferentiated hPSCs compared to non-pluripotent cells.
49 ns of the endogenous Oct4 distal enhancer in pluripotent cells.
50 fic genome structures and gene expression in pluripotent cells.
51 ted, contractile fibers from mouse and human pluripotent cells.
52 omatic cells, resulting in the generation of pluripotent cells.
53 required to produce cellular diversity from pluripotent cells.
54 ating that they were fully reprogrammed into pluripotent cells.
57 tand the role of this molecular pathway in a pluripotent cell and the impact of CSB mutation during h
58 of up to 100 cardiomyocytes for every input pluripotent cell and was effective in 11 hiPSC lines tes
59 w that Jarid2/Jumonji, a protein enriched in pluripotent cells and a founding member of the Jumonji C
60 he grafted cells by separating contaminating pluripotent cells and committed neural cells using fluor
64 Tet1 and Tet2 are highly expressed in mouse pluripotent cells and downregulated to different extents
65 chanism of histone methylation regulation in pluripotent cells and during early cell-fate transitions
66 f the mutated cell; earlier mutations target pluripotent cells and generate more widespread disease a
68 mportance of post-transcriptional control in pluripotent cells and identify miRNAs and RNA-binding pr
70 aling potently induces SMC-specific genes in pluripotent cells and prevents dedifferentiation of arte
71 ty to detect chromosomal gains and losses in pluripotent cells and their derivatives, as well as meio
72 n of haemangioblasts and cardiomyocytes from pluripotent cells, and for the origins of stem cells in
73 limiting requirement for differentiation of pluripotent cells, and that experimental suppression of
74 oportion of the protein kinase complement of pluripotent cells, and there is accumulating evidence th
77 ow intracellular signaling pathways in human pluripotent cells are coordinated and how they maintain
78 ylation during reprogramming, while ESC-like pluripotent cells are distinguished by extension of deme
81 t silence retrotransposons in germ cells and pluripotent cells are important for limiting the accumul
82 fferentiation, which could shed light on why pluripotent cells are only receptive to differentiation
85 of the distal TSS is highly active in naive pluripotent cells, autonomously reports Tet1 expression
86 complex cell and environmental regulation of pluripotent cell behaviour, and suggest simple determini
88 loci indicates that a subset is expressed in pluripotent cells but not in diverse fetal and adult tis
90 iated hPS cells, had little or no binding on pluripotent cells, but preferential binding to certain e
92 henomenon of somatic cell reprogramming into pluripotent cells by exposure to sublethal stimuli, whic
93 he strictest of all developmental assays for pluripotent cells by generating completely iPSC-derived
94 Secondary growth is initiated from groups of pluripotent cells, called meristems, which are establish
103 reporter-based studies of gene expression in pluripotent cells can be significantly influenced by the
104 However, much work remains to be done before pluripotent cells can be used for preclinical and clinic
106 tracellular matrix populated with autologous pluripotent cells can result in de-novo organogenesis, b
111 hether endothelial cells differentiated from pluripotent cells could serve as surrogates to test emer
120 neurons made from PD patient-derived induced pluripotent cells, dramatically reduced LRRK2-dependent
122 ein network (PluriNet) that is shared by the pluripotent cells (embryonic stem cells, embryonal carci
123 pecification occurs either by induction from pluripotent cells (epigenesis) or by a cell-autonomous m
124 preimplantation embryonic lethality because pluripotent cells fail to form and all cells differentia
125 se embryonic stem cells (ESCs) and defined a pluripotent cell fate (PCF) gene signature associated wi
127 richardii, the WUS pro-orthologue marks the pluripotent cell fate of immediate descendants of the ro
128 cells (ESCs) provide an unlimited supply of pluripotent cells for articular cartilage tissue enginee
131 prior to and independently of Cdh1 to prime pluripotent cells for mesoderm differentiation, thus hel
134 ERK signalling, which promotes exit of naive pluripotent cells from self-renewal, does not prevent JA
137 ell lines and interrogated to understand how pluripotent cells generate distinct fates during early d
139 mine the trajectories connecting somatic and pluripotent cells, genetic and chemical methodologies fo
141 fects in a dataset profiling differentiating pluripotent cells (GSE32923) and another from human brai
145 for precise genome editing in human-induced pluripotent cells (hiPSCs) will enable sophisticated gen
146 (NuRD) is required for lineage commitment of pluripotent cells; however, the mechanism through which
148 that geminin is present in G1 phase of mouse pluripotent cells in contrast to somatic cells, where an
149 Nanog orthologs supported self-renewal of pluripotent cells in the absence of leukemia inhibitory
151 key role in choreographing the responses of pluripotent cells in the early embryo to the signals tha
152 Its inhibition lowers the percentage of pluripotent cells in the early mouse embryo and signific
154 ed-specific, proteins were also expressed by pluripotent cells in the human preimplantation embryo.
156 hereas Oct3/4 is expressed in totipotent and pluripotent cells in the mouse life cycle, Rex1 expressi
158 portance of Mbd3/NuRD for the development of pluripotent cells in vivo and for their ex vivo progress
159 iew recent insights into the nature of human pluripotent cells in vivo, obtained by the deep sequenci
161 riNet seems to be a common characteristic of pluripotent cells, including mouse embryonic stem and in
164 ial for driving the differentiation of human pluripotent cells into cell types useful for clinical ap
167 upport a role for Wnts in differentiation of pluripotent cells into profibrotic fibroblasts and the p
169 ssue or neural cultures derived from induced pluripotent cells (iPS), in conjunction with transcripto
170 Knockdown of SETDB1 in PWS-specific induced pluripotent cells (iPSCs) causes a decrease in the accum
173 uman embryonic stem cells (ESCs) and induced pluripotent cells (iPSCs) into neurons are often cumbers
174 Reprogramming somatic cells into induced-pluripotent cells (iPSCs) provides new access to all som
175 iving lung progenitors from patient-specific pluripotent cells is a key step in producing differentia
177 generation of differentiated DA neurons from pluripotent cells is a prerequisite for the use of hiPSC
180 n vitro and in vivo differentiation of human pluripotent cells, likely through defects in the silenci
181 oduct, the HERVK accessory protein Rec, in a pluripotent cell line is sufficient to increase IFITM1 l
182 scle that is potentially applicable to other pluripotent cell lines and to generating other forms of
184 epiblast stem cells (EpiSCs), self-renewing pluripotent cell lines equivalent to the postimplantatio
189 of both enzymes in tandem results in viable, pluripotent cell lines with distinct effects on the DNA
190 aled 23 distinguishing candidate genes among pluripotent cell lines with divergent cardiogenic potent
191 ranscriptional and epigenetic comparisons of pluripotent cell lines, explaining some of the previousl
192 ubstantial variation has been reported among pluripotent cell lines, which could affect their utility
193 cells (EGCs) represent two classic types of pluripotent cell lines, yet their molecular equivalence
196 NT2 cell population density; levels of Oct4 (pluripotent cell marker) and HCMV genome penetration are
197 e the level of HCMV genomes in nuclei, Oct4 (pluripotent cell marker), or hDaxx (cellular repressor o
201 activating EMT, and that the Nanog marker of pluripotent cells may act as the primary transcription f
204 rom a specified germ cell to a population of pluripotent cells occurs rapidly following fertilization
205 omplex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to ac
207 through regulation of the polyamine pool in pluripotent cells of the embryo, whether they are in a p
209 transcription factor Mga is expressed in the pluripotent cells of the inner cell mass (ICM) and epibl
210 Both lin28a and lin28b are expressed in pluripotent cells of the Xenopus embryo and are enriched
212 factors to reprogram somatic cells to become pluripotent cells, offers a significant technical simpli
213 icient for neural induction, Tbx3-expressing pluripotent cells only form retina in the context of the
214 uivalent to a certain developmental stage of pluripotent cells or a heterogeneous population composed
215 Whether regeneration is accomplished by pluripotent cells or by the collective activity of multi
216 the cells retained spectroscopic features of pluripotent cells or developed spectroscopic features su
219 analysed and their silencing in germ cells, pluripotent cells or somatic cells remains poorly unders
220 nown whether there are additional classes of pluripotent cells, or what the spectrum of reprogrammed
221 scription factors that maintain an important pluripotent cell population called the shoot apical meri
222 ex vivo fail to expand their Oct4-positive, pluripotent cell population despite producing robust end
223 e first two lineages to differentiate from a pluripotent cell population during mammalian development
224 d that the Msx1-expressing cells represent a pluripotent cell population for the regenerating digit.
225 rived from the blastema, an undifferentiated pluripotent cell population thought to be derived from m
226 stricted to the ICM, and is downregulated in pluripotent cell populations in the later stages, i.e. t
227 minates in the establishment of two distinct pluripotent cell populations: the shoot apical meristem
229 sient downregulation of Nanog in a subset of pluripotent cells predisposes them toward differentiatio
230 d proliferative characteristics of embryonic pluripotent cells, reduces expression of pluripotency fa
231 tion as both a repressor and an activator in pluripotent cells, regulating expression of developmenta
232 re of embryonic development, but the role of pluripotent cell regulation in somatic tissue regenerati
233 argeted single-copy genomic integration into pluripotent cells, reporter assays and flow cytometry ar
235 er specification of definitive endoderm from pluripotent cells results in a highly enriched AFE popul
236 mming and the pooled selection of polyclonal pluripotent cells results in high-quality, stable iPSCs.
239 differentiation-promoting conditions, these pluripotent cells showed the same general trends of gene
240 ated derivatives of fatty acids (NO2-FA) are pluripotent cell-signaling mediators that display anti-i
242 scription factors, DNA methylation status at pluripotent cell-specific genes, and the capacity to dif
248 ifferentiated cells can be reprogrammed into pluripotent cells, suggesting that in vitro reprogrammin
249 e, neither class of contacts was observed in pluripotent cells, suggesting that lineage-specific chro
250 s suggest a mechanism whereby Mga influences pluripotent cell survival through regulation of the poly
251 Lin28, can reprogram somatic cells back into pluripotent cells, termed induced pluripotent stem cells
254 s differentiation and enable self-renewal of pluripotent cells that are ex vivo counterparts of naive
255 nique relationship between the germ line and pluripotent cells that are present during the earliest s
256 mbryonic stem (hES) cells are self-renewing, pluripotent cells that are valuable research tools and h
257 he recent discovery of novel means to derive pluripotent cells that avoid embryo destruction, includi
258 ells (hiPSCs) provides a potential supply of pluripotent cells that avoid immune rejection and could
259 The ability to reprogram somatic cells into pluripotent cells that can be differentiated in vitro pr
261 low us to manipulate the germ line to create pluripotent cells that could serve as a critical tool in
262 During early mammalian development, as the pluripotent cells that give rise to all of the tissues o
265 f mammalian embryos, which has favored using pluripotent cells that recapitulate cardiac myogenesis.
267 by triggering genetic variation in germ and pluripotent cells through mutation followed by natural s
268 studies have aimed to convert cultured human pluripotent cells to a naive state, but it remains uncle
271 uently, Foxd3 needs to be silenced in primed pluripotent cells to allow re-activation of relevant gen
272 ic biology underlying the differentiation of pluripotent cells to cardiac lineages and describe curre
273 ellite cells and directed differentiation of pluripotent cells to mature skeletal muscle have proved
276 f7l1 as a unique factor that is necessary in pluripotent cells to prepare them for lineage specificat
277 ly development is governed by the ability of pluripotent cells to retain the full range of developmen
278 essary for a rapid switch in the response of pluripotent cells to Wnt/beta-catenin stimulation, from
279 imary human cells, including multipotent and pluripotent cells, to uncover both the underlying mechan
280 method for directed differentiation of human pluripotent cells toward neural crest stem cells has yet
281 lar mechanisms found in germ cells and other pluripotent cell types and identify genetic regulators o
283 nocytic stem cells in the hair follicle, and pluripotent cell types from the hair follicle and papill
285 lled stem cells, even though they range from pluripotent cells-typified by embryonic stem cells, whic
286 During embryonic development, uncommitted pluripotent cells undergo progressive epigenetic changes
287 e 3D chromatin landscape of naive and primed pluripotent cells, unveiling common features as well as
288 efficient targeting of three genes in human pluripotent cells using zinc-finger nuclease (ZFN)-media
289 x: How is cell-cycle progression possible in pluripotent cells when oscillations of key regulatory pr
291 ligase III, SSrp1, Xrcc-6/Ku70, and Parp2 in pluripotent cells, which decreased during the differenti
292 s transition coincides with the formation of pluripotent cells, which in mammals can be used to gener
295 is possible to apply genome editing to human pluripotent cells with minimal impact on genomic mutatio
296 e site-specific genome modification in human pluripotent cells with similar efficiency and precision
298 approach is accomplished directly from human pluripotent cells without the need for coculture on feed
299 generate hematopoietic stem cells from human pluripotent cells would enable many biomedical applicati
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