ライフサイエンスコーパス: cell plasticity

1 n the regulation of cell-cycle-mediated stem cell plasticity.

2 ve disputed the notion of hematopoietic stem cell plasticity.

3 ovascularization to test human hematopoietic cell plasticity.

4 t widely studied and debated example of stem cell plasticity.

5 ell biology including the phenomenon of stem cell plasticity.

6 gesting parity for inhibitory and excitatory cell plasticity.

7 if the adjuvant used is one that supports T-cell plasticity.

8 AZA is also known to induce cell plasticity.

9 ation senses metabolic changes and modulates cell plasticity.

10 eterogeneity in cancer--clonal evolution and cell plasticity.

11 as a central regulator of pancreatic cancer cell plasticity.

12 lti-phenotypic cell population dynamics with cell plasticity.

13 ppressor T-cell population, and limited Th17 cell plasticity.

14 oblems pertaining to tissue regeneration and cell plasticity.

15 netic modification may underlie regulatory T-cell plasticity.

16 well as a new strategy for controlling T reg cell plasticity.

17 e on the role of miR302 in the regulation of cell plasticity.

18 ndings reveal a dramatic delay in inhibitory cell plasticity.

19 aggressive melanoma cells, causing melanoma cell plasticity.

20 nvestigators challenging the notion of these cells' plasticity.

21 e found that senescence does not alter alpha-cell plasticity: alpha-cells can reprogram to produce in

22 ative paradigm of CSC theory with reversible cell plasticity among cancer cells has received much att

23 38 MAPK as an important regulator of Schwann cell plasticity and differentiation.

24 d the highly dynamic mechanisms that control cell plasticity and fate.

25 in the expression of critical genes promotes cell plasticity and has a critical role in accurately or

26 Accordingly, tumor cell plasticity and how it affects disease progression h

27 n animal models and clinically, is that of T-cell plasticity and how lymphocytic responses are determ

28 ransfer can regulate the maintenance of stem cell plasticity and induce beneficial cell phenotype mod

29 , via the viral protein Tax, exploits CD4+ T cell plasticity and induces transcriptional changes in i

30 epigenetic regulators in determining cancer cell plasticity and metastatic progression.

31 lies that refinement of the concepts of stem cell plasticity and of the stem cell niche is warranted.

32 , we studied the role of Hes1 in both acinar cell plasticity and pancreatic regeneration after caerul

33 Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking c

34 The switch in cell plasticity and protein expression was confirmed by

35 Our findings suggest that cell plasticity and remodeling responses such as deforma

36 demyelinated adult CNS, which has decreased cell plasticity and scarring.

37 generative response through the induction of cell plasticity and stemness.

38 erarchical signaling network regulating PDAC cell plasticity and suggest that the molecular decision

39 ignant properties that affect both the tumor cell plasticity and the endothelial cell behavior.

40 nd beneficial role for the SASP in promoting cell plasticity and tissue regeneration and introduces t

41 ng the molecular mechanisms underlying plant cell plasticity and totipotency.

42 Thus, PRC2-targeted therapy may reduce tumor cell plasticity and tumor heterogeneity, offering a new

43 t Nodal signaling has a key role in melanoma cell plasticity and tumorigenicity, thereby providing a

44 he molecular mechanisms that control Schwann cell plasticity and underlie nerve pathology, including

45 ithelial traits, an increase in stemness and cell plasticity, and the acquisition of more aggressive

46 ampered by their intrinsic autofluorescence, cell plasticity, and the complexities of monocyte-MPhi c

47 erative potential, the demonstration of stem cell plasticity, and the creation of human embryonic ste

48 y in melanoma progression, metastasis, tumor cell plasticity, and tumor therapeutic resistance.

49 However, data supporting stem cell plasticity are extensive and cannot be easily dismi

50 The mechanisms that mediate epithelial cell plasticity are only beginning to be understood.

51 t be used to characterize T cell phenotype/T cell plasticity as a function of seasonality, or as a re

52 and show that PDGFRalpha targets progenitor cell plasticity as a profibrotic mechanism.

53 invasion and migration in addition to tumor cell plasticity as shown by vasculogenic mimicry.

54 bolic reprogramming not only promotes cancer cell plasticity, but also provides novel insights for tr

55 rovide insights into the regulation of tumor cell plasticity by an embryonic milieu, which may hold s

56 results suggest an avenue for promoting stem cell plasticity by targeting barriers of latent lineage

57 Pancreatic exocrine cell plasticity can be observed during development, panc

58 lls in human autoimmunity and show that Treg cell plasticity can be tissue specific.

59 conceivable that changes in stem/progenitor cell plasticity contribute to the loss of this capacity,

60 T helper 17 (Th17) cell plasticity contributes to both immunity and autoimm

61 Tumor cell plasticity contributes to functional and morphologi

62 scriptional events that determine epithelial cell plasticity controlled by TGF-beta.

63 Therefore, we investigated whether liver cell plasticity could contribute to IHBD regeneration in

64 This endocrine cell plasticity could have implications for islet develo

65 Deregulated cell plasticity could result in the development of debil

66 are an essential manifestation of epithelial cell plasticity during morphogenesis, wound healing, and

67 tivation of BMP signaling governs epithelial cell plasticity, EMT, and tumorigenicity during breast c

68 ZEB1 is also a key determinant of cell plasticity, endowing cells with the capacity to wit

69 will we be able to fully harness adult stem cell plasticity for clinical purposes.

70 dicating how difficult it will be to exploit cell plasticity for therapeutic purposes.

71 A rush of papers proclaiming adult stem cell plasticity has fostered the notion that there is es

72 led to clinical trials in humans, true stem cell plasticity has not rigorously been established in m

73 This concept of stem-cell "plasticity" has helped to galvanize research on st

74 al evidence supporting the existence of stem-cell plasticity have been refuted because stem cells hav

75 molecular and cellular mechanisms of cancer cell plasticity in a conditional oncogenic Kras mouse mo

76 tes the in vivo study of stem and progenitor cell plasticity in disease and regeneration.

77 ) that regulates cholesterol homeostasis and cell plasticity in endodermal-derived tissues.

78 e investigated the time course of inhibitory cell plasticity in mouse primary visual cortex by using

79 Cancer cell plasticity in response to evolutionary pressures is

80 set of development also has implications for cell plasticity in somatic cell nuclear transfer, genomi

81 the endocardium reveal extensive endothelial cell plasticity in the infarct zone and identify the end

82 The molecular mechanisms regulating Schwann cell plasticity in the PNS remain to be elucidated.

83 hese studies and provide evidence for single-cell plasticity in the primary motor cortex of primates.

84 el permits comprehensive study of human stem cell plasticity in vivo.

85 The discovery of Th17 cell plasticity, in which CD4(+) IL-17-producing Th17 ce

86 We conclude that stem-cell plasticity is a true characteristic of NSCs and tha

87 hing and provide proof that targeting tumour cell plasticity is a viable therapeutic opportunity.

88 We conclude that liver cell plasticity is competent for regeneration of IHBDs i

89 Smooth muscle cell plasticity is considered a prerequisite for atheros

90 The observed cell plasticity is dependent on ZEB1, a key regulator of

91 This mitral cell plasticity is odor specific, recovers gradually ove

92 accepted that dynamic and reversible tumour cell plasticity is required for metastasis, however, in

93 The evidence for and against stem-cell plasticity is reviewed here as well as some of the

94 lead to a disturbance of later events in Th cell plasticity, leading to autoimmune diseases or other

95 regeneration results from diminished Schwann cell plasticity, leading to slower myelin clearance.

96 vitro and in vivo, a function known as "stem cell plasticity", makes them an appealing cell source fo

97 Immune cell plasticity may augment suppression of Th2 cells by

98 heses regarding the mechanisms by which Th17-cell plasticity may be controlled in vivo.

99 This novel mechanism for CNS cell plasticity may operate in wider contexts.

100 Additional Purkinje cell plasticity mechanisms may also contribute to eyebli

101 Thus, it is unknown whether Th17 cell plasticity merely reflects change in expression of

102 ntigen 1 (FRA-1) as a central node in tumour cell plasticity networks, and discuss mechanisms regulat

103 We hypothesized that AZA-induced cell plasticity occurs via a transient multipotent cell

104 onal consequences of this mode of epithelial cell plasticity on targeted cell lysis by cytotoxic T ly

105 ractile force as a determinant of epithelial cell plasticity, particularly in cancer cells that can s

106 ear events could be shared between different cell plasticity phenomena across phyla.

107 alysis of our model, it is found that cancer cell plasticity plays an essential role in maintaining t

108 r model reveals that the delay in inhibitory cell plasticity potently accelerates Hebbian plasticity

109 asing evidence supports the idea that cancer cell plasticity promotes metastasis and tumor recurrence

110 This high degree of stem cell plasticity prompted us to test whether dead myocard

111 porting the notion that clonal selection and cell plasticity represent two sides of the same coin.

112 l-to-mesenchymal transitions (EMTs) underlie cell plasticity required in embryonic development and fr

113 ts and, therefore, may have consequences for cell plasticity, resilience, and survival in patients wi

114 revealed a remarkable dichotomy in RS and IB cell plasticity; spared whisker potentiation occurred in

115 In truth, stem cell plasticity, strictly defined, has yet to be rigorou

116 licate genome-reprogramming studies and stem-cell plasticity studies, but could also reveal clues abo

117 umor microenvironments (TMEs) induce stromal cell plasticity that affects tumorigenesis.

118 s, and may provide new perspectives on tumor cell plasticity that could be exploited for novel therap

119 ly a dynamic and reversible phenotypic tumor cell plasticity that renders a proportion of cells both

120 microenvironment (TME) contributes to cancer cell plasticity, the specific TME factors most actively

121 In addition to the changes in cell plasticity, these studies demonstrated that chronic

122 Human B cells exploit CD4(+) T-cell plasticity to create flexibility in the effector T-

123 Translating the promise inherent in tumor cell plasticity to the clinical arena remains a major ch

124 fore each mating session; thus, VTA dopamine cell plasticity was dependent on action of endogenous op

125 Cell plasticity, which includes transdifferentiation and

126 egulation by PRC2 is a key mediator of tumor cell plasticity, which is required for the adaptation of

127 of the PAF-Wnt signalling axis in modulating cell plasticity, which is required for the maintenance o

128 notypic heterogeneity is the result of tumor cell plasticity, which-together with the genetic backgro

129 multi-phenotypic cancer model by integrating cell plasticity with the conventional hierarchical struc