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

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