戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 limiting the replicative potential of normal human somatic cells.
2 alignant cells, and is absent in most normal human somatic cells.
3 e activity is repressed in almost all normal human somatic cells.
4 leus depended on KAP1 in both mouse ESCs and human somatic cells.
5 unctional consequences of mtDNA mosaicism in human somatic cells.
6 gf6 enhanced reprogramming in both mouse and human somatic cells.
7 clock-like mutational processes operating in human somatic cells.
8 pluripotency gene Oct4 (Pou5f1) in mouse and human somatic cells.
9 ther radiation or the endonuclease I-PpoI in human somatic cells.
10 f homologous chromosomes at sites of DSBs in human somatic cells.
11 he stable repressive status of hTERT gene in human somatic cells.
12 fficient, nonviral methods for reprogramming human somatic cells.
13 ly increased the reprogramming efficiency of human somatic cells.
14 uclear reprogramming towards pluripotency in human somatic cells.
15 the functional inactivation of DNA-PK(cs) in human somatic cells.
16  the key to routine nuclear reprogramming of human somatic cells.
17 frequency of rAAV-mediated gene targeting in human somatic cells.
18 monstrated that Ku70 is an essential gene in human somatic cells.
19 t a single polycistronic virus can reprogram human somatic cells.
20 s can be used for specific gene targeting in human somatic cells.
21 limits the replicative life span of cultured human somatic cells.
22 nterference reduces mitotic recombination in human somatic cells.
23 hypersensitivity, and genetic instability in human somatic cells.
24 efore, ATR is essential for the viability of human somatic cells.
25 malignant tumor cells but not in most normal human somatic cells.
26 The purpose of this review is to outline how human somatic cell ancestral trees can organize many old
27 f the L1 element into differentiated primary human somatic cells and G1/S-arrested cells, resulting i
28 ns at developmental gene loci differ between human somatic cells and hPSCs, and that changes in the c
29 *TTC)n sequence, which is highly unstable in human somatic cells and in the germline.
30 reprogram the nuclei of fully differentiated human somatic cells, apparently conferring on them a plu
31         Our data demonstrate that non-neural human somatic cells, as well as pluripotent stem cells,
32           Thus, Ku86 is an essential gene in human somatic cells because of its requirement, not in N
33                        Thus, the patterns of human somatic cell birth and death are measurable with f
34   Telomerase is not expressed in most normal human somatic cells but is active in stabilizing telomer
35  elongates telomeres, is repressed in normal human somatic cells but is reactivated during tumor prog
36 ressively shorten with each cell division in human somatic cells, but the mechanisms governing telome
37 radually shorten during replicative aging in human somatic cells by Southern analysis.
38 his work, we attempted to generate Ku70-null human somatic cells by using a rAAV-based gene knockout
39 tem cells have been generated from mouse and human somatic cells by viral expression of the transcrip
40                   Reprogramming of mouse and human somatic cells can be achieved by ectopic expressio
41                                        Thus, human somatic cells can be faithfully reprogrammed to pl
42                                              Human somatic cells can be reprogrammed into induced plu
43 merase catalytic component, hTERT, in normal human somatic cells can reconstitute telomerase activity
44                                         Most human somatic cells can undergo only a limited number of
45                                              Human somatic cells cannot regenerate in this way and di
46                                     Thus, in human somatic cells, ch-TOG appears to play a major role
47 l to the recovery of gene-targeted clones in human somatic cells comprising only 0.02-0.17% of cells
48      Combined with reprogramming technology, human somatic cell-derived NSCs and their progeny can mo
49               Telomeres gradually shorten as human somatic cells divide and a correlation has been ob
50 cers express telomerase activity, while most human somatic cells do not have detectable telomerase ac
51 These results demonstrate that reprogramming human somatic cells does not require genomic integration
52 plicating episomes that can be maintained in human somatic cells for weeks to months were used.
53 discrete islands during the reprogramming of human somatic cells from skin biopsies and blood draws o
54    By constructing stable and complete human-human somatic cell fusions between a highly metastatic,
55 extension of adeno-associated virus-mediated human somatic cell gene targeting technology is describe
56 ological and clinical relevance of p53 loss, human somatic cell gene targeting was used to delete the
57 n SCNT, and that, as in mice, H3K9me3 in the human somatic cell genome is an SCNT reprogramming barri
58 trate that during the reprogramming process, human somatic cells go through a transient state that re
59 prevention of replicative senescence in some human somatic cells grown in vitro.
60                        Here, we show that in human somatic cells, H4K16ac does not substantially affe
61  small interfering RNAs (siRNAs) in infected human somatic cells has been controversial.
62 last years, but their direct conversion from human somatic cells has not yet been reported.
63                                    Recently, human somatic cells have been reprogrammed directly to p
64  a chromosome 11-specific YAC library from a human somatic cell hybrid line that has retained chromos
65                    PCR screening of a rodent-human somatic cell hybrid panel by ECK-specific primers
66                                  In a rodent-human somatic cell hybrid panel, the hITF (HGMW-approved
67 mapped to human chromosome 14 using a rodent/human somatic cell hybrid panel.
68 itutions are also present in N23HA, a rodent-human somatic cell hybrid that contains only the PKD1 ho
69                                        Human-human somatic cell hybridization studies carried out bet
70 spectively, by analysis of a panel of rodent-human somatic cell hybrids and yeast artificial chromoso
71 sis of a panel of multiple independent mouse/human somatic cell hybrids containing a normal human Xi
72         Here we have tested a panel of mouse-human somatic cell hybrids for production of infectious
73 el of monochromosomal mouse/human or hamster/human somatic cell hybrids localized two AUF1 loci to hu
74 cific expression of DLX5 and DLX6 in mouse x human somatic cell hybrids, lymphoblastoid cell lines, a
75 pression of 33 X-linked genes in eight mouse/human somatic-cell hybrids that contain either the human
76 riptional activity, are maintained in rodent/human somatic-cell hybrids, such hybrids have been used
77                           Analyses of rodent-human somatic-cell hybrids, YAC contigs, and FISH of nor
78 genes in either human somatic cells or mouse/human somatic-cell hybrids.
79 nced its transcriptional activity in diverse human somatic cells, implying the possible benefit from
80 hich may limit the proliferative capacity of human somatic cells in epithelia and blood.
81 ms of loss of heterozygosity (LOH) in normal human somatic cells in vivo.
82                                              Human somatic cells, including hepatocytes, exhibit no t
83 anscription-factor-mediated reprogramming of human somatic cells, indicate a role for the trophectode
84                  Recently, the conversion of human somatic cells into induced pluripotent stem cells
85 ng of steady-state telomere length in normal human somatic cells is a promising biomarker for age-ass
86            Programmed telomere shortening in human somatic cells is thought to act as a tumor suppres
87 el in vitro model system was generated using human somatic cell knockout technologies.
88 be an improved approach to the generation of human somatic-cell knockouts, which we have used to gene
89  Hsa21 and transferred the chromosome from a human somatic cell line into mouse embryonic stem (ES) c
90 d virus-mediated gene targeting to produce a human somatic cell line that expresses a conditionally n
91                      Using a panel of rodent-human somatic cell lines and fluorescence in situ hybrid
92  issue, we describe here the construction of human somatic cell lines containing a targeted disruptio
93 iruses have been investigated in a series of human somatic cell lines deficient in IFN signaling prot
94 ional inactivation of either Ku70 or Ku86 in human somatic cell lines is lethal.
95 ard, can be applied to many loci and several human somatic cell lines, and can facilitate many functi
96 gene in a panel of seven different mouse and human somatic cell lines.
97                                              Human somatic cells may contain up to seven histone H1 v
98                     Telomerase repression in human somatic cells may therefore have evolved as a powe
99                             In vitro, normal human somatic cells must overcome two proliferative bloc
100                                              Human somatic cell nuclear transfer (SCNT) holds great p
101                   We can now safely say that human somatic cell nuclear transfer is alive and well.
102  mechanical properties of the spheroids from human somatic cells of different phenotypes: mesenchymal
103 joining, performs the additional function in human somatic cells of suppressing genomic instability t
104 nges after the induction of reprogramming in human somatic cells on day 7 from the 20-24 day process.
105  dosage compensation--is extremely stable in human somatic cells; only fetal germ cells have a develo
106 he cell types are directly reprogrammed from human somatic cells or differentiated from an iPSC inter
107 reviously reported for other genes in either human somatic cells or mouse/human somatic-cell hybrids.
108                                           In human somatic cells or yeast cells lacking telomerase, t
109              However, in some species and in human somatic cells, Piwil proteins bind primarily to tR
110 nstrated that p53 silences L1 transposons in human somatic cells, potentially acting as a tumor-suppr
111             Here, we demonstrate that mature human somatic cells produce abundant virus-derived siRNA
112 diated genome editing in clinically relevant human somatic cells remains untested.
113 thologs hsa-miR-302b and hsa-miR-372 promote human somatic cell reprogramming.
114 ellular identity and constitute a barrier to human somatic cell reprogramming; yet a comprehensive un
115 at the lack of telomerase expression in most human somatic cells results from its repressive genomic
116 ctivation of even a single allele of Ku86 in human somatic cells results in profound telomere loss, w
117 type B-Raf is critical for normal mitosis of human somatic cells, suggesting that mutational activati
118                                      In most human somatic cells, telomerase expression is repressed,
119                               In most normal human somatic cells, telomerase is repressed and telomer
120                                    In normal human somatic cells, telomere dysfunction causes cellula
121                   In contrast to most normal human somatic cells that do not express telomerase due t
122                                           In human somatic cells, the major mechanism controlling mit
123 RT is sufficient to drive a number of normal human somatic cells to a tumorigenic fate.
124            Epigenetic reprogramming of adult human somatic cells to alternative fates, such as the co
125 y reduces the efficiency of reprogramming of human somatic cells to an ESC-like state.
126 throughout primed and naive reprogramming of human somatic cells to hiPS cells.
127     Here we describe a protocol to reprogram human somatic cells to hiPSCs with high efficiency in 15
128                             Reprogramming of human somatic cells to induced pluripotent stem cells (i
129 teins (Nanog and Sox2), together can convert human somatic cells to pluripotency.
130 ANOG, and LIN28) are sufficient to reprogram human somatic cells to pluripotent stem cells that exhib
131                         The reprogramming of human somatic cells to primed or naive induced pluripote
132 ned transgene expression in multiple primary human somatic cell types, thereby representing a highly
133             By employing RNA interference in human somatic cells, we found that severe reduction of M
134         Here, using Xenopus egg extracts and human somatic cells, we show that actin dynamics and for
135 cate that a Piwi-piRNA pathway is present in human somatic cells, with an uncharacterised function li
136 rated directly from fewer than 1,000 primary human somatic cells, without requiring stable genetic ma

 
Page Top