ライフサイエンスコーパス: multipotency

1 eir unique dual properties (self-renewal and multipotency).

2 uished by the properties of self-renewal and multipotency.

3 binding without effects on cell viability or multipotency.

4 ed a clear adipogenic ability with increased multipotency.

5 Oct4 that control stem cell self renewal and multipotency.

6 rve as an important mechanism to control HSC multipotency.

7 utes of stem cells, including quiescence and multipotency.

8 nction of this class of proteins to maintain multipotency.

9 tures of stem cells, namely self-renewal and multipotency.

10 s revealed the capacity for self-renewal and multipotency.

11 s biased; the remaining progenitors maintain multipotency.

12 tor p63; eliminating DeltaNp63 unleashes HBC multipotency.

13 markers CD73, CD90 and CD105, and displayed multipotency.

14 twork that underpin NS cell self-renewal and multipotency.

15 ct to self-replication, stemness traits, and multipotency.

16 nally activate Notch in daughters to control multipotency.

17 otype that maintain replicative capacity and multipotency.

18 ignature resulting in reprogramming cells to multipotency.

19 gene, protein, and functional signatures of multipotency.

20 ially enlarging the potential for pancreatic multipotency.

21 ar cells is sufficient for HBC activation to multipotency.

22 hematopoietic stem cell (HSC) quiescence and multipotency.

23 ro-effector genes in MP cells, indicative of multipotency.

24 uclear lamina, which thereby preserved their multipotency.

25 astrocytes and oligodendrocytes, indicating multipotency.

26 em cell protein to regulate self-renewal and multipotency.

27 ecipients, confirming their self renewal and multipotency.

28 ciated and conserved function in maintaining multipotency.

29 Consistent with this multipotency, a significant portion of these tumor cells

30 ystem occurs at mitotic exit when cells lose multipotency and begin to develop stable connections tha

31 elopment, including cell fate specification, multipotency and cell migration.

32 materials chemistry in maintaining stem-cell multipotency and controlling differentiation.

33 ed decreased senescence and maintained their multipotency and differentiation potential until passage

34 a process associated with loss of stem cell multipotency and engraftment potential.

35 rapid downregulation of genes that maintain multipotency and establish NPCs' neural identity.

36 crest-derived progenitors for self-renewal, multipotency and establishment of multiple neural crest-

37 udy was to determine their origin, degree of multipotency and heterogeneity, and contribution to vess

38 unknown whether they contribute to oncogenic multipotency and metastasis.

39 profile of transcription factors regulating multipotency and neural crest progenitor characteristics

40 the normally quiescent HBCs are activated to multipotency and proliferate when sustentacular cells ar

41 We conclude that the balance between multipotency and selective neuropotency, which is charac

42 of cell types, yet molecules controlling NC multipotency and self-renewal and factors mediating cell

43 cell characteristics such as clonogenicity, multipotency and self-renewal capacity.

44 ty to instructive signals, while maintaining multipotency and self-renewal capacity.

45 BCG2 expressing side population demonstrates multipotency and self-renewal properties indicating stem

46 n GABPbeta subunit, critically regulates HSC multipotency and self-renewal via controlling an essenti

47 and Foxg1 cooperation to maintenance of NSC multipotency and self-renewal, and establish a useful me

48 ly progenitors is not at the expense of full multipotency and support the current model of hematopoie

49 of cells that are endowed with self-renewal, multipotency, and a unique potential for tumor initiatio

50 st strike a balance between self-renewal and multipotency, and differentiation.

51 aBMSCs exhibited multipotency, and karyotypes were normal up to 30 PDs, w

52 eneration as a result of their self-renewal, multipotency, and paracrine capabilities.

53 ers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity following injection in

54 The deficits in self-renewal and multipotency are restored by expression of Notch1-ICD or

55 The hallmarks of HSCs, self-renewal and multipotency, are observed in in vitro assays and cell t

56 e TICs possess stem cell characteristics and multipotency as demonstrated by in vitro sphere-formatio

57 n in the absence of cell division, and their multipotency at the population level reflects collective

58 ted to provide a cellular memory to maintain multipotency but also stabilize cell fate decisions and

59 NCDPs displayed multipotency by differentiating into microtubule-associa

60 tes hematopoietic stem cell self-renewal and multipotency by limiting stem cell proliferation and dif

61 at neural potential can be separated from NC multipotency by the action of a single gene, and establi

62 its ability to restore the self-renewal and multipotency defects of Ars2 knockout NSCs.

63 ic programs compatible with self-renewal and multipotency downstream of the HSC.

64 with as few as 200 cells, self-renewability, multipotency, drug resistance, metastatic potential, and

65 fied in C. elegans, underlie progenitor cell multipotency during the development of diverse bilateria

66 occurring in human breast cancer, to induce multipotency during tumorigenesis in the mammary gland.

67 r signatures characterising pluripotency and multipotency exist, there is, as yet, no single quantita

68 ion (PDL) caused facultative reactivation of multipotency factors (Sox9 and Hnf1beta) in Ptf1a(+) aci

69 pressing the cell cycle and regulating other multipotency factors such as vasa.

70 -cell level, that self-renew without loss of multipotency for more than 140 population doublings and

71 Dnmt3a-null HSCs upregulate HSC multipotency genes and downregulate differentiation fact

72 F1 deficiency also reduced the expression of multipotency genes, including Slamf1, Mecom, Hoxa9, Hlf,

73 possess stem cell characteristics, including multipotency, high proliferative potential, and their ca

74 sion is closely associated with pluripotency/multipotency in both mouse and human embryonic stem cell

75 t bidirectional Notch signaling may regulate multipotency in other systems.

76 lude that the acquisition and maintenance of multipotency in the small micromere lineage requires nan

77 To assess their multipotency in vivo, periosteal cells were injected int

78 opulation-doubling rate, cell proliferation, multipotency, in vivo dentin regeneration, and immunosup

79 eterogeneous cells that expressed markers of multipotency, including Sox2, Sca1, and Rex1 (Zfp42).

80 MSCs to retain their stem-cell phenotype and multipotency, independent of differentiation-promoting m

81 r culture conditions favoring maintenance of multipotency, infection caused NPCs to quickly and abnor

82 GBC is a multipotent progenitor cell, whose multipotency is activated after destruction of both neur

83 and Ldb2, and promotes RPC proliferation and multipotency; it also controls specification of mammalia

84 y of cell behavior and identity owing to its multipotency, motility and ability to form a broad array

85 tion during embryonic development due to its multipotency, motility, and ability to form a broad arra

86 f et al. (2014) demonstrate self-renewal and multipotency of a single CD62L(+) memory T cell across s

87 DNA-binding) genes maintain self-renewal and multipotency of adult neural stem cells.

88 , we evaluate evidence for the existence and multipotency of axial stem cells.

89 ely dependent on the ability to maintain the multipotency of cells and control their differentiation.

90 is the full manifestation of the pluri- and multipotency of embryonic and adult stem cells, thus the

91 are orchestrated to regulate maintenance and multipotency of HSCs.

92 e, we investigated self-renewal capacity and multipotency of individual memory lymphocytes by in vivo

93 In this way, Mbd3/NuRD protects the multipotency of lymphoid progenitors, preventing B cell-

94 Our results suggest that MBD1 maintains the multipotency of NSCs by restraining the onset of differe

95 VPCs) offer a paradigm for investigating how multipotency of progenitor cells is maintained during pe

96 as floating cultures, thereby revealing the multipotency of RPCs generated from integration-free hiP

97 e mechanisms that establish and maintain the multipotency of stem cells are poorly understood.

98 into how epigenetic regulation preserves the multipotency of stem cells for subsequent differentiatio

99 ated from human PPE cells, demonstrating the multipotency of the human ES-derived PPE cells.

100 We suggest that multipotency of the nerve-associated progenitors lasting

101 Multipotency of these cells was demonstrated by their ca

102 Multipotency of these cells was demonstrated by their ca

103 fication of surfaces that allow retention of multipotency of this key regenerative cell type have rem

104 demonstrated the proliferative capacity and multipotency of this population.

105 is little definitive information about their multipotency or extent of contribution to the axis.

106 lineage tracing, allowing the definition of multipotency potential to be achieved with high confiden

107 lies the existence of an underlying germline multipotency program in these cell types that has a prev

108 that are hallmark characters of the germline multipotency program.

109 signals organize epigenetic marks to confer multipotency remain to be uncovered.

110 an aortic endothelial cells in vitro acquire multipotency rendering the cells susceptible to osteoind

111 Stemness, as "self-renewal and multipotency," seems not to be limited to a particular c

112 multiple histologic phenotypes indicative of multipotency suggests a stem cell-like etiology of ovari

113 They exhibit clonal multipotency that can give rise to myogenic, melanocytic

114 hysical property robustly predicts stem cell multipotency, there exists a unique and minimal set of t

115 ect reprogramming to maintain or reestablish multipotency; they acquire an active block to signal tra

116 as a stem cell niche to maintain prohemocyte multipotency through Hedgehog and JAK/STAT signaling.

117 ld be expanded extensively while maintaining multipotency to differentiate into cardiomyocytes, smoot

118 e time and place in which cells transit from multipotency to one of several differentiated lineages.

119 s, we show that only some progenitors regain multipotency to produce de novo ductal and glandular str

120 th the ability of long-term self-renewal and multipotency to reconstitute all blood lineages.

121 ch T cell precursors progress from primitive multipotency to T lineage commitment.

122 s successfully negotiate the transition from multipotency to unipotency, including the loss of self-r

123 Here we investigated MG multipotency using injury paradigms that target differen

124 rity was assessed by flow cytometry and TMSC multipotency was examined by induction of neural cells,

125 Multipotency was required for Th17 cell-mediated tumor e

126 Neural stem cells proliferate and maintain multipotency when cultured in the presence of FGF2, but

127 Some of these cells exhibit multipotency, whereas others do not.