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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
29 reprogram the nuclei of fully differentiated human somatic cells, apparently conferring on them a plu
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
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
40 merase catalytic component, hTERT, in normal human somatic cells can reconstitute telomerase activity
44 l to the recovery of gene-targeted clones in human somatic cells comprising only 0.02-0.17% of cells
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
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
59 a chromosome 11-specific YAC library from a human somatic cell hybrid line that has retained chromos
63 itutions are also present in N23HA, a rodent-human somatic cell hybrid that contains only the PKD1 ho
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
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
74 nced its transcriptional activity in diverse human somatic cells, implying the possible benefit from
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
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
88 ard, can be applied to many loci and several human somatic cell lines, and can facilitate many functi
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.
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
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
119 cate that a Piwi-piRNA pathway is present in human somatic cells, with an uncharacterised function li
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