ライフサイエンスコーパス: cell reprogramming

1 ong with active transcription during somatic cell reprogramming.

2 ing ground state pluripotency during somatic cell reprogramming.

3 enetic barrier during the process of somatic cell reprogramming.

4 rticipates in induced pluripotent stem (iPS) cell reprogramming.

5 can partially substitute for Ascl1 during iN cell reprogramming.

6 s in the subset of nucleolar proteins during cell reprogramming.

7 ecosystem management, emergency response and cell reprogramming.

8 on presents a roadblock to efficient somatic cell reprogramming.

9 ctivity favors the entire process of somatic cell reprogramming.

10 maintenance of ESC self-renewal and somatic cell reprogramming.

11 g mechanisms of ESC pluripotency and somatic cell reprogramming.

12 nduction at pluripotency loci during somatic cell reprogramming.

13 them from embryonic stem cells or by somatic cell reprogramming.

14 was indentified to be induced during somatic cell reprogramming.

15 examination of mechanisms governing somatic cell reprogramming.

16 f self-renewal, differentiation, and somatic cell reprogramming.

17 ficient to cause Arx-dependent beta-to-alpha-cell reprogramming.

18 R-302b and hsa-miR-372 promote human somatic cell reprogramming.

19 otency factors with the capacity for somatic cell reprogramming.

20 ntenance of ES cell self-renewal and somatic cell reprogramming.

21 l-mediated tumorigenic mechanism involving B cell reprogramming.

22 self-renewal and differentiation and somatic cell reprogramming.

23 ration, differentiation, apoptosis, and stem cell reprogramming.

24 evated during induced pluripotent stem (iPS) cell reprogramming.

25 f hES cells is acquired as an early event in cell reprogramming.

26 ike factor 4 (Klf4) is essential for somatic cell reprogramming.

27 ing a critical difference in human and mouse cell reprogramming.

28 Pluripotency can be recreated by somatic cell reprogramming.

29 recapitulated in the culmination of somatic cell reprogramming.

30 hift is predominantly caused by a B-2 to B-1 cell reprogramming.

31 a (MEL) cells is a dramatic example of tumor-cell reprogramming.

32 cient to increase p53 levels and impair stem cell reprogramming.

33 ll regeneration therapies relying upon alpha-cell reprogramming.

34 nd, conversely, acts as a barrier to somatic-cell reprogramming.

35 tion (TD) is a recent advancement in somatic cell reprogramming.

36 y of embryonic stem cells (ESCs) and somatic cell reprogramming.

37 velopmental differentiation can help improve cell reprogramming.

38 e splicing regulatory network during somatic cell reprogramming.

39 (MBNL) RNA binding proteins, is involved in cell reprogramming.

40 fate, such as disease therapeutics and stem cell reprogramming.

41 complex in stem cell maintenance and somatic cell reprogramming.

42 ing has been implicated in promoting somatic cell reprogramming.

43 erexpression of Tet2 enhances OSKM-induced B-cell reprogramming.

44 slation of p21, a known inhibitor of somatic cell reprogramming.

45 lated molecular mechanisms affecting somatic cell reprogramming.

46 and the molecular pathways governing somatic cell reprogramming.

47 eling of dementia disorders based on somatic cell reprogramming.

48 nic stem cell (ESC) self-renewal and somatic cell reprogramming.

49 embryonic and somatic stem cell biology and cell reprogramming.

50 ntrolling stem cell pluripotency and somatic cell reprogramming.

51 ation of embryonic stem cells or via somatic cell reprogramming.

52 the contexts of stem cell specification and cell reprogramming.

53 Identifying means to enhance Schwann cell reprogramming after nerve injury could be used to f

54 Somatic cell reprogramming also has been achieved more recently

55 induced plasticity of respiratory epithelial cells, reprogramming alveolar cells into epithelial cell

56 Tet2 provides a mechanistic link between iPS cell reprogramming and B-cell transdifferentiation.

57 Recent advances in cell reprogramming and beta cell differentiation now all

58 ency, because its depletion inhibits somatic cell reprogramming and blastocyst development.

59 rs in biological processes including somatic cell reprogramming and guided differentiation.

60 The advent of cell reprogramming and induced pluripotent stem cells (i

61 Thus, this unexpected link between cell reprogramming and infection opens up a new premise

62 ion of true hiPSCs immediately after somatic cell reprogramming and involves column-based positive se

63 genomic manipulation could provide a path to cell reprogramming and novel cell replacement-based ther

64 f certain mechanisms, such as acinar-to-beta-cell reprogramming and pancreatitis.

65 enes, cell differentiation, stem and somatic cell reprogramming and response to environmental stimuli

66 10) controls stem cell self-renewal, somatic cell reprogramming and senescence, and tumorigenesis.

67 nisms of pluripotency, cell differentiation, cell reprogramming and transdifferentiation, among other

68 ellular plasticity in the context of somatic cell reprogramming and tumorigenesis.

69 atin remodeler, in ESC self-renewal, somatic cell reprogramming, and blastocyst development.

70 ulator in embryonic stem (ES) cells, somatic cell reprogramming, and cancer.

71 s multistage developmental defects, impaired cell reprogramming, and hematopoietic malignancies.

72 nally, Rif1 acts as a barrier during somatic cell reprogramming, and its depletion significantly enha

73 ld open a new avenue for immunotherapy, stem cell reprogramming, and other therapeutic applications.

74 ing non-viral and non-integrating methods of cell reprogramming, and using novel gene editing techniq

75 Although isolated examples of adult cell reprogramming are known, there is no general unders

76 RNA metabolism, the roles of RBPs in somatic cell reprogramming are poorly understood.

77 Non-invasive evaluation of cell reprogramming by advanced image analysis is require

78 n of the pluripotency network during somatic cell reprogramming by exogenous transcription factors in

79 onic stem (ES) to trophoblast stem (TS)-like cell reprogramming by introducing individual TS cell-spe

80 e importance of defining trajectories during cell reprogramming by various methods.

81 nt in vitro and, increasingly due to somatic cell reprogramming, cellular and molecular mechanisms of

82 enomic findings suggested that alpha to beta cell reprogramming could be promoted by manipulating the

83 his article reviews landmark developments in cell reprogramming, current knowledge, and technological

84 Somatic cell reprogramming, directed differentiation of pluripot

85 oses, reflecting common mechanisms for plant cell reprogramming during endosymbiosis.

86 Because somatic cell reprogramming during induced pluripotent stem cell

87 ions showed differential effects on the stem cell reprogramming efficiency in a c-Myc dependent manne

88 ctivation induces a 100-fold increase in iPS cell reprogramming efficiency, involving 95% of the popu

89 Recent advances in cell reprogramming enable investigators to generate plur

90 indicating that this is a true irreversible cell reprogramming event.

91 ine transcription factors, including somatic cell reprogramming factors (Oct4, Sox2, Klf4, and c-Myc)

92 ancreatic beta cells, and expression of beta cell reprogramming factors in vivo converts antral cells

93 al. show that the cyclic expression of stem cell reprogramming factors in vivo increases the lifespa

94 ganization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1.

95 stem and progenitor cell biology and somatic cell reprogramming for applications directed to the vess

96 Cell reprogramming from a quiescent to proliferative sta

97 f similarities between cancer genes and stem cell reprogramming genes, widespread mutations in epigen

98 ion compromises ESC self-renewal and somatic cell reprogramming, globally increases m(6)A RNA levels,

99 Somatic cell reprogramming has generated enormous interest, foll

100 In vivo cell reprogramming has the potential to enable more-effe

101 Therefore, a detailed study of cell reprogramming has the potential to shed light on un

102 Recent advances in cell reprogramming have permitted the development of dif

103 atin responses in leukemic and host CD4(+) T cells, reprogramming host T cells toward normalcy.

104 Glycolysis is critical for cancer stem cell reprogramming; however, the underlying regulatory m

105 ck of cell intermediates and enables somatic cell reprogramming in absence of otherwise essential plu

106 t cell types, and have implications for beta-cell reprogramming in diabetes and diagnosis of beta-cel

107 as a novel marker for reversible human beta-cell reprogramming in diabetes.

108 the ability of ES cells to initiate somatic cell reprogramming in heterokaryons.

109 elopment and give further insights into germ cell reprogramming in mice.

110 Nanog enables somatic cell reprogramming in serum-free medium supplemented wit

111 miRNAs in the regulation of pluripotency and cell reprogramming in the laboratory rat.

112 These findings support a model of host cell reprogramming in which a bacterial pathogen uses th

113 Cell reprogramming, in which a differentiated cell is ma

114 pathway, a central regulator of the Schwann cell reprogramming induced by nerve injury.

115 MicroRNAs (miRNAs) are critical to somatic cell reprogramming into induced pluripotent stem cells (

116 scovered an unexpected phenomenon of somatic cell reprogramming into pluripotent cells by exposure to

117 izing IL-6-specific antibody prevented iTreg cell reprogramming into TH17-like cells and protected ag

118 Thus, injury-induced Schwann cell reprogramming involves down-regulation of myelin ge

119 Somatic cell reprogramming involves epigenomic reconfiguration,

120 ed pluripotent stem cells (iPSCs) by somatic cell reprogramming involves global epigenetic remodellin

121 These findings indicate that somatic cell reprogramming is associated with marked increases i

122 Cell reprogramming is largely mediated by DNA and RNA.

123 Patient-specific somatic cell reprogramming is likely to have a large impact on m

124 ulate this process and contribute to somatic cell reprogramming is not clear.

125 architecture is reconfigured during somatic cell reprogramming is poorly understood.

126 Research in stem cell biology and cell reprogramming is rapidly advancing, with the hope o

127 4 regulates ES cell self-renewal and somatic cell reprogramming is still poorly understood.

128 in bypass of cellular senescence and somatic cell reprogramming, is markedly overexpressed in human P

129 PDAC because it induces a process of acinar cell reprogramming known as acinar-to-ductal metaplasia

130 es promotes beta-cell regeneration and liver cell reprogramming, leading to restoration of normoglyce

131 prehension of the complex process of somatic cell reprogramming, many questions regarding the molecul

132 Somatic cell reprogramming may afford models of nonfamilial "spo

133 Our results raise the prospect that blood cell reprogramming may be a strategy for derivation of t

134 drive cell killing by SFB, while glycolytic cell reprogramming may represent a resistance strategy p

135 However, during somatic cell reprogramming, mesenchymal-epithelial transition (M

136 ntext of most induced pluripotent stem (iPS) cell reprogramming methods, heterogeneous populations of

137 Cell reprogramming models appear particularly promising

138 o, we applied induced pluripotent stem (iPS) cell reprogramming of aged hematopoietic progenitors and

139 ed both pluripotency in ES cells and somatic cell reprogramming of fibroblasts to induced pluripotent

140 Interruption of Th2 cell reprogramming of Treg cells might thus provide cand

141 ation and expansion, which in turn drove Th2 cell reprogramming of Treg cells.

142 such abnormalities are intrinsic to somatic cell reprogramming or secondary to the reprogramming met

143 ent of early epigenetic marks during somatic cell reprogramming: Parp1 functions in the regulation of

144 hting broad and general roles for SMAD2/3 as cell-reprogramming potentiators.

145 ribe an early and essential stage of somatic cell reprogramming, preceding the induction of transcrip

146 keletal remodeling in modulating the somatic cell reprogramming process.

147 fic protease 26 negatively regulates somatic cell-reprogramming process by stabilizing chromobox (CBX

148 Cell reprogramming promises to make characterization of

149 tity was the result of lymphatic endothelial cell reprogramming rather than replacement by blood endo

150 Even though different methods of somatic cell reprogramming result in stem cell lines that are mo

151 ty with a sialyltransferase inhibitor during cell reprogramming resulted in a dose-dependent reductio

152 enhanced global demethylation during somatic cell reprogramming (SCR) of hHFCs.

153 highly accurate discrimination based on the cell reprogramming status.

154 Human cell reprogramming technologies offer access to live hum

155 The advent of somatic cell reprogramming technologies-which enables the genera

156 limits of current knowledge in the field of cell reprogramming, the mechanistic elements that underl

157 rily arrested in mitosis can support somatic cell reprogramming, the production of embryonic stem cel

158 actors, our approach achieves acinar-to-beta-cell reprogramming through transient cytokine exposure r

159 Somatic cell reprogramming to a pluripotent state continues to c

160 The recent description of somatic cell reprogramming to an embryonic stem (ES) cell-like p

161 Although somatic cell reprogramming to generate inducible pluripotent ste

162 In this review, we explore the RNA-mediated cell reprogramming to induce specific target cell genera

163 ouble-strand breaks, is required for somatic cell reprogramming to induced pluripotent stem cells (iP

164 is to identify kinases that regulate somatic cell reprogramming to iPSCs.

165 Somatic cell reprogramming to pluripotency requires an immediate

166 ncy of embryonic stem cells, and for somatic cell reprogramming to the pluripotent state.

167 ound that during the early stages of somatic cell reprogramming toward a pluripotent state, specific

168 MicroRNAs are potential candidates for cell reprogramming toward a proregenerative phenotype.

169 Treg cell reprogramming, vaccine efficacy, and antitumor CD8(

170 In hosts with established tumors, Treg cell reprogramming was suppressed by tumor-induced indol

171 ng shore dynamics through embryonic and germ cell reprogramming, we found evidence of bookmarking, a

172 Using conditional cell reprogramming, we generated a stable cell culture o

173 Directed somatic cell reprogramming, which does not pass through typical

174 l importance of the NHEJ pathway for somatic cell reprogramming, with a major role for LIG4 and DNA-P

175 nd suggests a general paradigm for directing cell reprogramming without reversion to a pluripotent st