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1 ntrol and L1CAM-deficient neurons from these ES cells.
2 ues the differentiation defects of aneuploid ES cells.
3 so contributes to the rapid proliferation of ES cells.
4 nt promoter genes were reduced in BAF250a KO ES cells.
5 3K79me2, H3K36me3, H3K9me3, and H4K20me3, in ES cells.
6 d promoters were bivalent in human and mouse ES cells.
7 omote de novo methylation in differentiating ES cells.
8 ocesses that establish healthy pregnancy and ES cells.
9 ongation, and alternative splicing events in ES cells.
10  essential for the proper differentiation of ES cells.
11 anisms in human prostate cancer versus mouse ES cells.
12 e of the most rapidly induced transcripts in ES cells.
13 h may support the diverse mRNA repertoire in ES cells.
14 l to the pluripotency and differentiation of ES cells.
15 rons derived from these conditionally mutant ES cells.
16 g wild-type Lsh but not the ATP mutant in KO ES cells.
17 hment XCI during in vitro differentiation of ES cells.
18 a genome-wide basis in differentiating mouse ES cells.
19 enes or more) after a single transfection of ES cells.
20 ased targeting vectors introduced into mouse ES cells.
21 ensable for global gene expression in murine ES cells.
22 restored SHF gene expression in Casp3 mutant ES cells.
23 ich is the preferred SOX2 binding partner in ES cells.
24 derepressed pluripotency-associated genes in ES cells.
25 dinate binding of SOX2 and p63 was absent in ES cells.
26  determining the developmental plasticity of ES cells.
27 regulated in Drosha- but not Dicer-deficient ES cells.
28  RNAPII elongation rates and RNA splicing in ES cells.
29  Tet triple KO fibroblast derived from mouse ES cells.
30 ns between LIF-independent iOCT4 and control ES cells.
31 ty as well as the developmental potential of ES cells.
32 GC-like cells (PGCLCs) in EpiLCs, but not in ES cells.
33 g the levels of expression driven by CREs in ES cells.
34 ssion in murine Mesp1(Cre/+); Rosa26(EYFP/+) ES cells.
35 s in early mouse embryos and embryonic stem (ES) cells.
36 critical for self-renewal in embryonic stem (ES) cells.
37 expression programs in mouse embryonic stem (ES) cells.
38 ogonia, growing oocytes, and embryonic stem (ES) cells.
39 1, at bivalent loci in human embryonic stem (ES) cells.
40 strongly suppressed in mouse embryonic stem (ES) cells.
41 hd9, Brg1 and Ep400 in mouse embryonic stem (ES) cells.
42 ed their expression in mouse embryonic stem (ES) cells.
43 s of the HH pathway in mouse embryonic stem (ES) cells.
44               We further demonstrate that in ES cells, 1) both RARgamma and RXRalpha are present at t
45 some occupancy in KO ES cells compared to WT ES cells after differentiation.
46                                    The mouse ES cells also differentiate into Pax7(+) cells with sate
47 osome inactivation and XIST transcription in ES cells, also plays a role in maintenance of the inacti
48 gene targeting in mice using embryonic stem (ES) cells, although suitable for generating sophisticate
49 ethodology that utilizes the differentiating ES cell and embryoid body system to define the modules a
50 analysis revealed that LIF-independent iOCT4 ES cells and control ES cells exhibit similar transcript
51 n, we purified native nucleosomes from mouse ES cells and detect that Suv39h1 and Suv39h2 exclusively
52 K27me3) of ChIP sequencing datasets in human ES cells and eight pairs in murine ES cells, and predict
53 de changes in NANOG-binding patterns between ES cells and EpiLCs, indicating epigenetic resetting of
54 otency-associated gene transcription both in ES cells and in differentiating embryoid bodies.
55                                      Both NT ES cells and iPS cells derived from the same somatic cel
56 (TRIM28; also known as TIF1beta and KAP1) in ES cells and orchestrates retroviral silencing activity
57 se phenotypes were mimicked by SHANK3-edited ES cells and rescued by transduction with a Shank3 expre
58  Pausing can be induced directly in cultured ES cells and sustained for weeks without appreciable cel
59 sing quantitative live-cell imaging in mouse ES cells and tumor cells, we demonstrate that, although
60 9 trimethylation (H3K9me3) profiles in mouse ES cells and uncovered two distinct classes of SETDB1 bi
61 s involved in maintenance of embryonic stem (ES) cells and early embryonic development of the mouse.
62 omatin interactions in human embryonic stem (ES) cells and four human ES-cell-derived lineages, we un
63  lentiviral vector in murine embryonic stem (ES) cells and human inducible pluripotent stem (iPS) cel
64              We show that in embryonic stem (ES) cells and in some tissues, the Stra6 gene encodes tw
65 mpetent-able to give rise to embryonic stem (ES) cells and live, fertile mice.
66 L4 enzyme-dead knock-in (KI) embryonic stem (ES) cells and mice, which carry Y5477A/Y5523A/Y5563A mut
67  is expressed in pluripotent embryonic stem (ES) cells and regulates ES cell differentiation.
68 re malignant counterparts of embryonic stem (ES) cells and serve as useful models for investigating c
69  activity in differentiating embryonic stem (ES) cells and that hearts from Wnt5a(-/-); Wnt11(-/-) em
70            Neurogenesis was reduced in BERKO ES cells, and oligodendrogliogenesis was enhanced.
71  in human ES cells and eight pairs in murine ES cells, and predicted high-confidence (HC) bivalent pr
72 tion: immature Xenopus laevis oocytes, mouse ES cells, and the transition state of proliferating mamm
73 precise control of the forces experienced by ES cells, and therefore provided at least one explanatio
74  promoter region are lost in embryonic stem (ES) cells, and ES-cloned embryos show RNF12-dependent Xi
75 o compare the gene expression profile of the ES cell- and adult progenitor-derived, GM-CSF-instructed
76 oduce the dramatic rearrangements underlying ES-cell- and PGC-specific transcriptional programs remai
77                      In this protocol, mouse ES cells are aggregated in 96-well plates in medium cont
78 cated genome engineering in species in which ES cells are not available.
79                        Mouse embryonic stem (ES) cells are a popular model system to study biological
80                              Embryonic stem (ES) cells are in a dynamic equilibrium of distinct funct
81                        Mouse embryonic stem (ES) cells are locked into self-renewal by shielding from
82 mice as well as the differentiation of mouse ES cells as a model with which to address this issue.
83 gramming in which repression of pre-existing ES cell-associated gene expression program is followed b
84 we found thatGli1andNanogare co-expressed in ES cells at high levels.
85  of BAF250a, a key regulatory subunit of the ES cell ATP-dependent Brahma-associated factor (BAF) chr
86             In this setting, we inquired how ES cells avoid the potentially deleterious consequences
87 such models are generated by embryonic stem (ES) cell-based targeted insertion, or pronuclear injecti
88  combinations sufficient to explain observed ES cell behavior.
89 ly, we find the strongest gene clustering in ES cells between transcription factor genes that control
90 enes that are transcriptionally repressed in ES cells but ready to be activated in response to differ
91 ficient to support enhanced proliferation of ES cells, but not to maintain their undifferentiated phe
92 t characteristics similar to embryonic stem (ES) cells, but the genetic drivers underlying malignant
93 a disrupted the differentiation potential of ES cells by altering the expression timing of key develo
94 fects of aneuploidy on mouse embryonic stem (ES) cells by generating a series of cell lines that each
95 HDR-mediated events in mouse embryonic stem (ES) cells by more than 20-fold through the use of co-inc
96                                 Conventional ES cells can be derived and maintained in vitro with med
97                                 Nonetheless, ES cells can seemingly acquire TS-like characteristics u
98            Mouse pluripotent embryonic stem (ES) cells can exist in distinct yet interchangeable epig
99 rogrammed STAP cells, unlike embryonic stem (ES) cells, can contribute to both embryonic and placenta
100  SCNT embryos developed into blastocysts and ES cells capable of contributing to traditional germline
101                      Here we show that mouse ES cells carrying a hypomorphic Gpc4 allele, in a single
102     Here, we generated human embryonic stem (ES) cells carrying a conditional L1CAM loss-of-function
103 ry through which pluripotent embryonic stem (ES) cells choose between self-renewal and differentiatio
104 alyzing two independent conditionally mutant ES cell clones, we found that deletion of L1CAM dramatic
105 ndings highlight a unique mechanism by which ES cells communicate with trophoblasts within the blasto
106 we found distinct nucleosome occupancy in KO ES cells compared to WT ES cells after differentiation.
107                           In vitro data from ES cells confirmed that bexarotene-activated RXR affecte
108                                Despite this, ES cells consume high levels of exogenous glutamine when
109                          Poised chromatin in ES cells contains both H3 Lys-4 trimethylation (H3K4me3)
110         Many of the transcription factors in ES cells control both host and retroviral genes coordina
111 methylation and transcriptome profiles of NT ES cells corresponded closely to those of IVF ES cells,
112 ly similar to those of their embryonic stem (ES) cell counterparts, and both are typical of aneural m
113 on of the Romk1-specific first exon using an ES cell Cre-LoxP strategy and examined the renal phenoty
114 ntional serum plus LIF medium phenocopy male ES cells cultured in 2i/L.
115             Furthermore, we find that female ES cells cultured in conventional serum plus LIF medium
116 ts long-term LIF-independent self-renewal of ES cells cultured in media containing fetal bovine serum
117 , in which naive pluripotent embryonic stem (ES) cells cultured in basic fibroblast growth factor (bF
118 factor 4) plays an unappreciated role in the ES cell cycle by forming a complex with cyclin-Cdk1 and
119 educes endogenous H3K4 methylation levels in ES cells, decreases the protein stability of MLL3 and ML
120  RECQL5 and BLM has on mouse embryonic stem (ES) cells deleted for FANCB, a member of the FA core com
121                              Map3k1(m) (PHD) ES cells demonstrate that the MEKK1 PHD controls p38 and
122     Here we demonstrate that embryonic stem (ES) cells derived from the ICM generate and shed microve
123  iPS cells and nuclear transfer ES cells (NT ES cells) derived by somatic cell nuclear transfer (SCNT
124 s stably maintained in embryonic stem cells (ES cells) derived from most embryos.
125 to steer directional differentiation because ES cell-derived cells are typically immature with impair
126 istent with this notion, we found that mouse ES cell-derived DCs (ES-DCs) represented less mature cel
127 etry, microscopic imaging, and RNA-Seq, that ES cell-derived macrophages responded to S. Typhimurium,
128 eproducible strategy to exponentially expand ES cell-derived megakaryocyte-erythroid progenitors that
129 ously using fetus-derived NPCs, infection of ES cell-derived pNSCs with HCMV was nonprogressive.
130                              Embryonic Stem (ES) cell-derived EphrinB2(+) cells are enriched with hem
131                  Here, human embryonic stem (ES) cell-derived neural progenitor cells, endothelial ce
132                We used human embryonic stem (ES) cell-derived primitive prerosette neural stem cells
133                                        Using ES-cell-derived human neurons, we show that ApoE secrete
134 man embryonic stem (ES) cells and four human ES-cell-derived lineages, we uncover extensive chromatin
135                     Here, we generated human ES cells designed to conditionally express heterozygous
136                           In embryonic stem (ES) cells, developmental regulators have a characteristi
137                                           In ES cells, differentially expressed genes after perturbat
138  is one of the most rapidly induced genes in ES cell differentiation and it is the earliest expressed
139 plays a critical role in the early stages of ES cell differentiation and the reprogramming of somatic
140                               We showed that ES cell differentiation induces selective alteration of
141 oth the mRNA and protein levels during mouse ES cell differentiation into SMCs (ESC-SMC differentiati
142 y Hoxa1-bound regions during early stages of ES cell differentiation into the neuro-ectoderm.
143  also improves, in addition to murine, human ES cell differentiation to blood cells.
144 t are recapitulated by existing protocols of ES cell differentiation, these data indicate that mouse
145 tent embryonic stem (ES) cells and regulates ES cell differentiation.
146  widely applied protocols of embryonic stem (ES) cell differentiation have been developed to enable i
147 Both the MEKK1 PHD and TAB1 are critical for ES-cell differentiation and tumourigenesis.
148                          We show that paused ES cells display a remarkable global suppression of tran
149             Drosha-deficient embryonic stem (ES) cells display genomic hypomethylation that is not ac
150 renewal of pluripotent mouse embryonic stem (ES) cells downstream of the cytokine leukemia inhibitory
151            Finally, in differentiating human ES cells, endodermal markers were more efficiently induc
152 nes based on their likelihood of determining ES cell (ESC) identity.
153 st cancer model, using our novel female GEMM ES cell (ESC) pipeline.
154 derivation of somatic motoneurons (MNs) from ES cells (ESCs) after exposure to sonic hedgehog (SHH) a
155 from mutant p53-induced transformation using ES cells (ESCs) that express a conformational mutant of
156                                    Unlike in ES cells, Esrrb interacts in TS cells with the histone d
157 occupancy of pluripotency-associated loci in ES cells, Esrrb sustains the stemness of TS cells by dir
158                          Consequently, naive ES cells exhibit an elevated alphaKG to succinate ratio
159  TGF-beta- or EGF-stimulated Map3k1(m) (PHD) ES cells exhibit defective non-canonical ubiquitination
160                               Setdb1 ablated ES cells exhibit severe growth inhibition, which is not
161 t LIF-independent iOCT4 ES cells and control ES cells exhibit similar transcriptional programs relati
162                                Haploid human ES cells exhibited typical pluripotent stem cell charact
163                              Embryonic stem (ES) cells express pluripotency-associated genes and repr
164  eight genes including Braf, Mitf, and ERas (ES-cell expressed Ras) as candidate resistance genes.
165 ycle stage between the transplanted nucleus (ES cell, fetal fibroblast or terminally differentiated c
166 d using the data to deconvolute a mixture of ES cells, fibroblasts and hematopoietic progenitors into
167 uld aid efforts to generate autologous human ES cells for regenerative applications, as donated or di
168                          Here, we engineered ES cells from WT mice to express a doxycycline-regulated
169 pulation has yielded haploid embryonic stem (ES) cells from several mammalian species, but haploid hu
170               Although embryonic stem cells (ES cells) from in vitro fertilized embryos (IVF ES cells
171        Endogenous cyclin D1 enhanced Wnt and ES cell gene expression and expanded a prostate stem cel
172 gulates pivotal transcription factors in the ES cell gene regulatory network to sustain naive identit
173                              Embryonic stem (ES) cells go though embryo-like cell cycles regulated by
174      Here we show that mouse embryonic stem (ES) cells grown under conditions that maintain naive plu
175 or expression of a functional RNAi-cassette, ES-cell handling, or screening for mice with the desired
176 several mammalian species, but haploid human ES cells have yet to be reported.
177 9(-/-) relative to Rad9(+/+) embryonic stem (ES) cells have reduced levels of Neil1 protein.
178 although short-term suppression of Mek1/2 in ES cells helps to maintain an ICM-like epigenetic state,
179 f a unique stem cell phenotype by both human ES cells (hESCs) and induced pluripotent stem cells (iPS
180 routes to generate nontransgenic naive human ES cells (hESCs).
181 he absence of proliferation (embryonic stem [ES] cell heterokaryons) or DNA replication (nuclear tran
182                              Embryonic stem (ES) cells, however, characteristically suppress transcri
183                                Extinction of ES cell identity in single cells is acute.
184               We propose that propagation of ES cell identity is not determined by a vast interactome
185 ed that Patz1 is required for maintenance of ES cell identity.
186 we show that prolonged culture of male mouse ES cells in 2i/L results in irreversible epigenetic and
187 19 is critical for proper differentiation of ES cells in collaboration with Rnf20.
188                                   Thus, even ES cells in ground-state pluripotency cannot fully overc
189 s unclear how sustained propagation of naive ES cells in vitro affects their stability and functional
190 irst' allele and identify essential genes in ES cells, including the histone methyltransferase Setdb1
191 ption factors in common with embryonic stem (ES) cells, including OCT4 (encoded by Pou5f1), SOX2, NAN
192 urther show that injecting MVs isolated from ES cells into blastocysts results in an increase in thei
193                 Here we differentiated mouse ES cells into macrophages in vitro and showed, through a
194 e genetically modified mouse embryonic stem (ES) cells into functional macrophages provides a potenti
195  monolayer cultures of mouse embryonic stem (ES) cells into PSM-like cells without the introduction o
196 ethod, genetically matched sets of human IVF ES cells, iPS cells and nuclear transfer ES cells (NT ES
197   Our strategy to generate null mutant mouse ES cells is applicable to thousands of genes and repurpo
198            The unique chromatin signature of ES cells is fundamental to the pluripotency and differen
199   Interestingly, enzyme-dead MLL4 protein in ES cells is highly unstable.
200  that using engineered human embryonic stem (ES) cells is a viable approach to studying disease-assoc
201 ization both in the inducible Xist transgene ES cell line and in normal XX somatic cells.
202 cing of EC cell lines and their nonmalignant ES cell line counterparts.
203     We constructed a homozygous mutant mouse ES cell line in the Traf2 gene that is known to play a r
204               We have therefore generated an ES cell line in which Hdac1 and Hdac2 can be inactivated
205                                   Using this ES cell line, we observed that the first primitive eryth
206 operties, we used a modified embryonic stem (ES) cell line that emulates the early embryonic demethyl
207  engineered a new transgenic embryonic stem (ES) cell line, where eGFP expression is driven by the re
208 ndrial localization of MRP-1 was examined in ES cell lines by differential centrifugation and membran
209                                However, some ES cell lines demonstrated gradual loss of donor mtDNA a
210 es in an allele-specific manner using hybrid ES cell lines from reciprocal crosses between C57BL/6J a
211 alysed a collection of human parthenogenetic ES cell lines originating from haploid oocytes, leading
212 differentiation competence is more common in ES cell lines than in induced pluripotent stem cell line
213 uccessful isolation and maintenance of human ES cell lines with a normal haploid karyotype.
214 elf-renewal, but failed to expand as iPSC or ES cell lines.
215 n in conditional-ready IKMC 'knockout-first' ES cell lines.
216 ogenic SHANK3 knockout human embryonic stem (ES) cell lines.
217 ) drives TE-like transcriptional programs in ES cells, maintains trophoblast stem (TS) cell self-rene
218 ng key pluripotency pathways associated with ES cell maintenance and self-renewal.
219 phectoderm (TE) lineage by repression of the ES cell master regulator Oct4 or activation of the TE ma
220                           Like Mll4 knockout ES cells, Mll4(KI/KI) ES cells show reduced levels of H3
221 ring the onset of Hox gene expression in the ES cell model and during body segment identity specifica
222 rrogated the progression of reprogramming in ES cell models with regulatable Oct4 and Cdx2 transgenes
223 IVF ES cells, iPS cells and nuclear transfer ES cells (NT ES cells) derived by somatic cell nuclear t
224                          Fibers derived from ES cells of mdx mice exhibit an abnormal branched phenot
225 dress this issue, we cultured Ewing sarcoma (ES) cells on electrospun poly(epsilon-caprolactone) 3D s
226 d that co-culture of wild-type and aneuploid ES cells or supplementation with extracellular BMP4 resc
227 ges but retain an epigenetic memory of their ES cell origin.
228 nscriptome upon conditional KAP1 knockout in ES cells overlapped with the changes during embryoid bod
229               IalphaI is not produced by the ES cells per se but is added to the cells via the cell c
230 nd PRC2 reveals a novel mechanism underlying ES cell pluripotency and differentiation regulation.
231 aling in a LIF-independent manner to promote ES cell pluripotency and self-renewal.
232  expression patterns can serve as markers of ES cell pluripotency.
233       Erk1/2 activation contributes to mouse ES cell pluripotency.
234                              Embryonic stem (ES) cell pluripotency is governed by OCT4-centric transc
235 pose that after the dissolution of the naive ES-cell pluripotency network during establishment of Epi
236                                          The ES cell population behaves asynchronously.
237 ese functions, we used mouse embryonic stem (ES) cells, primary neurons, and APOE3 and APOE4 mice tre
238  gene profiles in multiple SCC cell lines to ES cell profiles and determined that SOX2 binds to disti
239 more, we found that a PKA inhibitor impaired ES cell proliferation, tumor growth and metastasis, whic
240 ly, Wnt5a/Wnt11 treatment of differentiating ES cells reduced both phosphorylated and total Akt throu
241     In contrast, pluripotent embryonic stem (ES) cells represent an inexhaustible source for DC produ
242 cells) from in vitro fertilized embryos (IVF ES cells) represent the 'gold standard', they are alloge
243                       Although haploid human ES cells resembled their diploid counterparts, they also
244 on of Tet1 and Tet2 in mouse embryonic stem (ES) cells results in an apparent loss of H3K27me3 at biv
245              Moreover, LIF-independent iOCT4 ES cells retain the capacity to differentiate in vitro a
246        Transcriptome sequencing of the Ctcfl ES cells revealed 14 genes deregulated by Ctcfl expressi
247       In contrast to the in-depth studies of ES cell self-renewal and pluripotency, few TE-specific r
248 SALL4, a gene involved in the maintenance of ES cell self-renewal, is aberrantly expressed in 47.7% o
249 critical role in controlling embryonic stem (ES) cell self-renewal and pluripotency.
250 ription factor implicated in embryonic stem (ES) cell self-renewal, yet its knockout causes intrauter
251 ith cell-permeable alphaKG directly supports ES-cell self-renewal while cell-permeable succinate prom
252 is study demonstrates shear stress-dependent ES cell sensitivity to dalotuzumab, highlighting the imp
253       Aggressive cancers and embryonic stem (ES) cells share a common gene expression signature.
254     Like Mll4 knockout ES cells, Mll4(KI/KI) ES cells show reduced levels of H3K4me1/2.
255 changes using inducible CDX2 embryonic stem (ES) cells, so that we could predict which CDX2-bound gen
256   However, it is not known whether there are ES cell-specific mechanisms regulating mitotic fidelity.
257 enced by a large complex bound to DNA by the ES cell-specific zinc-finger protein ZFP809.
258 Oct4) play a seminal role in embryonic stem (ES) cell-specific gene regulation.
259                Cells newly departed from the ES cell state display features of early post-implantatio
260                              The human naive ES cell state has eluded derivation without the use of t
261 e Ctcfl transgene reproduce the phenotype in ES cell-tetraploid chimeras.
262                              Embryonic stem (ES) cells that have the remarkable capability to differe
263 duces a naive state in mouse embryonic stem (ES) cells that resembles the inner cell mass (ICM) of th
264 se model cell line and mouse embryonic stem (ES) cells that this library can be used for genetic resc
265 e all-trans-retinoic acid (RA)-responsive in ES cells, the downstream promoter contains a half-site R
266                           In differentiating ES cells, the presence of NANOG reduces the transcriptio
267  used successfully in murine embryonic stem (ES) cells, there remain a set of nearly two thousand gen
268                                           In ES cells, they are predicted to act as transcriptional a
269 2 and NANOG promote the pluripotent state in ES cells, they show contrasting roles in EpiLCs, as Sox2
270  extensive demethylation, we subjected mouse ES cells to chemically defined hypomethylating culture c
271 n a rate-dependent manner the sensitivity of ES cells to IGF-1R inhibitor dalotuzumab (MK-0646) and s
272 s, cohesin depletion enhanced the ability of ES cells to initiate somatic cell reprogramming in heter
273  states are vital for the differentiation of ES cells to multipotent stem cells, little is known rega
274              Neural differentiation of human ES cells to NPs is concurrent with a threefold elevation
275 the differentiation of mouse embryonic stem (ES) cells to both primitive and definitive haematopoieti
276  this link, we have used NOD embryonic stem (ES) cells to generate a novel NOD transgenic line with t
277 mes at the edge of NFRs, where they regulate ES cell transcriptional programs.
278                    Dnmt3a/b deletion retards ES cell transition, correlating with delayed Nanog promo
279 issue is produced from mouse embryonic stem (ES) cells under chemically defined conditions.
280 in from the inner cell mass, embryonic stem (ES) cells undergo differentiation to the trophectoderm (
281                We investigated whether mouse ES cells undergoing largely undirected neocortical diffe
282 mparison to more differentiated cells, naive ES cells utilize both glucose and glutamine catabolism t
283 isingly, inhibition of either Akt or PI3K in ES cells was an equally effective means of increasing SH
284            However, by assaying thousands of ES cells, we identify a spectrum of subpopulations defin
285          To dissect Pol II dynamics in mouse ES cells, we inhibited Pol II transcription at either in
286                              In Oga KO mouse ES cells, we observed pronounced changes in expression o
287 ts, as well as 115 co-expression clusters in ES cells, we validate the utility of this approach.
288 e high in wild-type (WT) and Nf1 23aIN/23aIN ES cells, where the Nf1 exon 23a inclusion level is high
289 S cells corresponded closely to those of IVF ES cells, whereas iPS cells differed and retained residu
290 equired for Neil1 protein stability in mouse ES cells, whereas it regulates NEIL1 transcription in th
291 ablish the poised chromatin configuration in ES cells, which is essential for the proper differentiat
292 d c-Myc (Myc) expression in cohesin-depleted ES cells, which promoted DNA replication-dependent repro
293  that uses the immense regenerative power of ES cells while avoiding the risks associated with direct
294 ore, SHF markers are reduced in Casp3 mutant ES cells while the treatment of wild type ES cells with
295 ncreases the level of global H2Bub1 in mouse ES cells, while down-regulation of Fbxl19 reduces the le
296                 We expect that haploid human ES cells will provide novel means for studying human fun
297 nt ES cells while the treatment of wild type ES cells with Caspase inhibitors blocked the ability of
298      Here we generated mouse embryonic stem (ES) cells with a constitutive endogenous Nf1 exon 23a in
299 datasets in murine and human embryonic stem (ES) cells with over 1000 mammalian TF sequence motifs.
300                              Embryonic stem (ES) cells with the Ctcfl transgene reproduce the phenoty

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