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1 we show that this instability only occurs in pluripotent cells.
2 ed in undifferentiated hPSCs compared to non-pluripotent cells.
3 ns of the endogenous Oct4 distal enhancer in pluripotent cells.
4 to enhance reprogramming of fibroblasts into pluripotent cells.
5 fic genome structures and gene expression in pluripotent cells.
6 ted, contractile fibers from mouse and human pluripotent cells.
7 omatic cells, resulting in the generation of pluripotent cells.
8 germ cells given their similarities to naive pluripotent cells.
9 ating that they were fully reprogrammed into pluripotent cells.
10 growth factor GDF9 can reprogram hADFs into pluripotent cells.
11 and effectiveness of cell differentiation of pluripotent cells.
12 ning the culture requirements of naive human pluripotent cells.
13 ry meristems can be traced back to groups of pluripotent cells.
14 es that have bivalent chromatin structure in pluripotent cells.
15 ng loci were bound by Mediator or cohesin in pluripotent cells.
16 lation, suggesting it is a pivotal marker of pluripotent cells.
17 engraftment of blood progenitors from human pluripotent cells.
18 ry program at the G(1)/S-phase transition in pluripotent cells.
19 cations at the Oct4 locus in fibroblasts and pluripotent cells.
20 tive way to induce CPCs from mouse and human pluripotent cells.
21 is the key feature of murine totipotent and pluripotent cells.
22 lture can also induce abnormalities in these pluripotent cells.
23 sands of somatic regulatory sequences within pluripotent cells.
24 ith endoderm promotes induction of CPCs from pluripotent cells.
25 aining the differentiation responsiveness of pluripotent cells.
26 erences between in vitro and ex vivo primate pluripotent cells.
27 ion between embryonic stem cells and induced pluripotent cells.
28 tified proteins and phosphorylation sites in pluripotent cells.
29 n the formation of teratomas by transplanted pluripotent cells.
30 C/C substrates are also present during G1 of pluripotent cells.
31 on in a broad range of cell types, including pluripotent cells.
32 lls and in epigenetic remodeling of germ and pluripotent cells.
33 cle structure and transcriptional network of pluripotent cells.
34 feeders for both autologous and heterologous pluripotent cells.
35 ibody repertoires and the differentiation of pluripotent cells.
36 tional regulator of differentiation in these pluripotent cells.
37 y novel peptides that bind to the surface of pluripotent cells.
38 via diploid aggregation, unique to bona fide pluripotent cells.
39 tained the matrix signal for differentiating pluripotent cells.
40 ns methylated differently in fibroblasts and pluripotent cells.
41 genetic differences between naive and primed pluripotent cells.
42 reater in ESC-differentiated neurons than in pluripotent cells.
43 in establishing neural lineage commitment in pluripotent cells.
44 the genetic regulation of gene expression in pluripotent cells.
45 required to produce cellular diversity from pluripotent cells.
46 may contribute to its biological activity in pluripotent cells.
47 ay to drive mesendodermal differentiation of pluripotent cells.
48 ariants affecting the transcriptome of human pluripotent cells.
49 dynamics during lineage commitment of human pluripotent cells.
50 ether are sufficient to generate retina from pluripotent cells.
51 he role of the transcription factor Foxd3 in pluripotent cells.
52 alance between transcriptional programmes in pluripotent cells.
53 ction in gene expression regulation in mouse pluripotent cells.
54 ure cell types of all three germ layers from pluripotent cells.
55 in the transcriptional regulatory network of pluripotent cells.
56 How is end protection achieved in pluripotent cells?
59 tand the role of this molecular pathway in a pluripotent cell and the impact of CSB mutation during h
60 of up to 100 cardiomyocytes for every input pluripotent cell and was effective in 11 hiPSC lines tes
61 w that Jarid2/Jumonji, a protein enriched in pluripotent cells and a founding member of the Jumonji C
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
67 CNA proteins are expressed across eukarya in pluripotent cells and have conserved functions in fertil
68 mportance of post-transcriptional control in pluripotent cells and identify miRNAs and RNA-binding pr
71 ning gene 9 (Sox9) is expressed initially in pluripotent cells and subsequently in ectodermal, endode
72 enriched at polycomb and stem cell genes in pluripotent cells and that TRF1 abrogation results in in
73 ty to detect chromosomal gains and losses in pluripotent cells and their derivatives, as well as meio
74 n of haemangioblasts and cardiomyocytes from pluripotent cells, and for the origins of stem cells in
75 limiting requirement for differentiation of pluripotent cells, and that experimental suppression of
76 oportion of the protein kinase complement of pluripotent cells, and there is accumulating evidence th
79 ow intracellular signaling pathways in human pluripotent cells are coordinated and how they maintain
80 ylation during reprogramming, while ESC-like pluripotent cells are distinguished by extension of deme
83 t silence retrotransposons in germ cells and pluripotent cells are important for limiting the accumul
84 fferentiation, which could shed light on why pluripotent cells are only receptive to differentiation
86 the major binding partner of Id proteins in pluripotent cells as the basic helix-loop-helix (bHLH) t
89 use epiblast stem cells, which correspond to pluripotent cells at a late post-implantation stage of e
90 of the distal TSS is highly active in naive pluripotent cells, autonomously reports Tet1 expression
91 complex cell and environmental regulation of pluripotent cell behaviour, and suggest simple determini
93 loci indicates that a subset is expressed in pluripotent cells but not in diverse fetal and adult tis
95 iated hPS cells, had little or no binding on pluripotent cells, but preferential binding to certain e
97 henomenon of somatic cell reprogramming into pluripotent cells by exposure to sublethal stimuli, whic
98 he strictest of all developmental assays for pluripotent cells by generating completely iPSC-derived
99 Secondary growth is initiated from groups of pluripotent cells, called meristems, which are establish
105 reporter-based studies of gene expression in pluripotent cells can be significantly influenced by the
106 However, much work remains to be done before pluripotent cells can be used for preclinical and clinic
108 tracellular matrix populated with autologous pluripotent cells can result in de-novo organogenesis, b
113 hether endothelial cells differentiated from pluripotent cells could serve as surrogates to test emer
115 er with image analysis of single embryos and pluripotent cell culture, we have found that Notch is ac
119 between GBA and CTSB and GBA p.N370S induced pluripotent cell-derived neurons were shown to have decr
125 y developmental event during which embryonic pluripotent cells diversify into lineage-specific precur
126 neurons made from PD patient-derived induced pluripotent cells, dramatically reduced LRRK2-dependent
130 pecification occurs either by induction from pluripotent cells (epigenesis) or by a cell-autonomous m
131 ficient to drive robust neural commitment in pluripotent cells, even under non-permissive conditions.
132 preimplantation embryonic lethality because pluripotent cells fail to form and all cells differentia
133 se embryonic stem cells (ESCs) and defined a pluripotent cell fate (PCF) gene signature associated wi
135 richardii, the WUS pro-orthologue marks the pluripotent cell fate of immediate descendants of the ro
136 cells (ESCs) provide an unlimited supply of pluripotent cells for articular cartilage tissue enginee
139 prior to and independently of Cdh1 to prime pluripotent cells for mesoderm differentiation, thus hel
141 CX43) gap junction communication in cultured pluripotent cells from human dental follicles (hDFC).
142 ERK signalling, which promotes exit of naive pluripotent cells from self-renewal, does not prevent JA
146 mine the trajectories connecting somatic and pluripotent cells, genetic and chemical methodologies fo
148 fects in a dataset profiling differentiating pluripotent cells (GSE32923) and another from human brai
152 for precise genome editing in human-induced pluripotent cells (hiPSCs) will enable sophisticated gen
153 d the concept of co-culture of human induced pluripotent cells (hiPSCs) with various types of support
154 (NuRD) is required for lineage commitment of pluripotent cells; however, the mechanism through which
156 that geminin is present in G1 phase of mouse pluripotent cells in contrast to somatic cells, where an
157 oincides with loss of epiblast pluripotency, pluripotent cells in development and in vitro can adopt
158 Nanog orthologs supported self-renewal of pluripotent cells in the absence of leukemia inhibitory
160 key role in choreographing the responses of pluripotent cells in the early embryo to the signals tha
161 Its inhibition lowers the percentage of pluripotent cells in the early mouse embryo and signific
163 ed-specific, proteins were also expressed by pluripotent cells in the human preimplantation embryo.
165 curs during differentiation of Dnmt3a(W326R) pluripotent cells in vitro, and is also evident in Dnmt3
167 iew recent insights into the nature of human pluripotent cells in vivo, obtained by the deep sequenci
171 ial for driving the differentiation of human pluripotent cells into cell types useful for clinical ap
174 fibroblast growth factor (FGF) drives naive pluripotent cells into extraembryonic lineages before im
175 upport a role for Wnts in differentiation of pluripotent cells into profibrotic fibroblasts and the p
177 ssue or neural cultures derived from induced pluripotent cells (iPS), in conjunction with transcripto
178 Knockdown of SETDB1 in PWS-specific induced pluripotent cells (iPSCs) causes a decrease in the accum
181 uman embryonic stem cells (ESCs) and induced pluripotent cells (iPSCs) into neurons are often cumbers
182 Reprogramming somatic cells into induced-pluripotent cells (iPSCs) provides new access to all som
183 iving lung progenitors from patient-specific pluripotent cells is a key step in producing differentia
185 generation of differentiated DA neurons from pluripotent cells is a prerequisite for the use of hiPSC
189 n vitro and in vivo differentiation of human pluripotent cells, likely through defects in the silenci
190 oduct, the HERVK accessory protein Rec, in a pluripotent cell line is sufficient to increase IFITM1 l
191 scle that is potentially applicable to other pluripotent cell lines and to generating other forms of
192 epiblast stem cells (EpiSCs), self-renewing pluripotent cell lines equivalent to the postimplantatio
196 of both enzymes in tandem results in viable, pluripotent cell lines with distinct effects on the DNA
197 aled 23 distinguishing candidate genes among pluripotent cell lines with divergent cardiogenic potent
198 ranscriptional and epigenetic comparisons of pluripotent cell lines, explaining some of the previousl
199 ubstantial variation has been reported among pluripotent cell lines, which could affect their utility
200 cells (EGCs) represent two classic types of pluripotent cell lines, yet their molecular equivalence
203 NT2 cell population density; levels of Oct4 (pluripotent cell marker) and HCMV genome penetration are
204 e the level of HCMV genomes in nuclei, Oct4 (pluripotent cell marker), or hDaxx (cellular repressor o
207 H3K4me2 during formation of the intermediate pluripotent cell mass known as callus derived from Arabi
209 activating EMT, and that the Nanog marker of pluripotent cells may act as the primary transcription f
211 the insights into telomere end protection in pluripotent cells mean for the t-loop model of end prote
213 rom a specified germ cell to a population of pluripotent cells occurs rapidly following fertilization
214 omplex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to ac
216 through regulation of the polyamine pool in pluripotent cells of the embryo, whether they are in a p
217 transcription factor Mga is expressed in the pluripotent cells of the inner cell mass (ICM) and epibl
218 Both lin28a and lin28b are expressed in pluripotent cells of the Xenopus embryo and are enriched
220 factors to reprogram somatic cells to become pluripotent cells, offers a significant technical simpli
221 icient for neural induction, Tbx3-expressing pluripotent cells only form retina in the context of the
222 Whether regeneration is accomplished by pluripotent cells or by the collective activity of multi
223 the cells retained spectroscopic features of pluripotent cells or developed spectroscopic features su
226 analysed and their silencing in germ cells, pluripotent cells or somatic cells remains poorly unders
227 nown whether there are additional classes of pluripotent cells, or what the spectrum of reprogrammed
228 scription factors that maintain an important pluripotent cell population called the shoot apical meri
229 d that the Msx1-expressing cells represent a pluripotent cell population for the regenerating digit.
230 rived from the blastema, an undifferentiated pluripotent cell population thought to be derived from m
231 minates in the establishment of two distinct pluripotent cell populations: the shoot apical meristem
233 sient downregulation of Nanog in a subset of pluripotent cells predisposes them toward differentiatio
235 d proliferative characteristics of embryonic pluripotent cells, reduces expression of pluripotency fa
236 re of embryonic development, but the role of pluripotent cell regulation in somatic tissue regenerati
237 argeted single-copy genomic integration into pluripotent cells, reporter assays and flow cytometry ar
239 er specification of definitive endoderm from pluripotent cells results in a highly enriched AFE popul
240 mming and the pooled selection of polyclonal pluripotent cells results in high-quality, stable iPSCs.
244 scription factors, DNA methylation status at pluripotent cell-specific genes, and the capacity to dif
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 (pESCs) and bi-parental ESCs, establishing a pluripotent cell system of distinct parental backgrounds
253 Lin28, can reprogram somatic cells back into pluripotent cells, termed induced pluripotent stem cells
256 s differentiation and enable self-renewal of pluripotent cells that are ex vivo counterparts of naive
257 ells (hiPSCs) provides a potential supply of pluripotent cells that avoid immune rejection and could
258 The ability to reprogram somatic cells into pluripotent cells that can be differentiated in vitro pr
260 During early mammalian development, as the pluripotent cells that give rise to all of the tissues o
263 PRC2-bound elements function as silencers in pluripotent cells, they can transition into active tissu
264 by triggering genetic variation in germ and pluripotent cells through mutation followed by natural s
265 studies have aimed to convert cultured human pluripotent cells to a naive state, but it remains uncle
268 uently, Foxd3 needs to be silenced in primed pluripotent cells to allow re-activation of relevant gen
269 early development, extrinsic triggers prompt pluripotent cells to begin the process of differentiatio
270 ic biology underlying the differentiation of pluripotent cells to cardiac lineages and describe curre
271 ellite cells and directed differentiation of pluripotent cells to mature skeletal muscle have proved
274 f7l1 as a unique factor that is necessary in pluripotent cells to prepare them for lineage specificat
275 ly development is governed by the ability of pluripotent cells to retain the full range of developmen
276 essary for a rapid switch in the response of pluripotent cells to Wnt/beta-catenin stimulation, from
277 imary human cells, including multipotent and pluripotent cells, to uncover both the underlying mechan
278 method for directed differentiation of human pluripotent cells toward neural crest stem cells has yet
279 lar mechanisms found in germ cells and other pluripotent cell types and identify genetic regulators o
281 nocytic stem cells in the hair follicle, and pluripotent cell types from the hair follicle and papill
283 lled stem cells, even though they range from pluripotent cells-typified by embryonic stem cells, whic
284 During embryonic development, uncommitted pluripotent cells undergo progressive epigenetic changes
285 e 3D chromatin landscape of naive and primed pluripotent cells, unveiling common features as well as
286 efficient targeting of three genes in human pluripotent cells using zinc-finger nuclease (ZFN)-media
287 x: How is cell-cycle progression possible in pluripotent cells when oscillations of key regulatory pr
289 ligase III, SSrp1, Xrcc-6/Ku70, and Parp2 in pluripotent cells, which decreased during the differenti
290 s transition coincides with the formation of pluripotent cells, which in mammals can be used to gener
291 pically upregulated, both in male and female pluripotent cells, while Tsix expression aberrantly pers
292 mbryos, where EPHA receptors are enriched in pluripotent cells whilst surrounding lineage-specified t
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