ライフサイエンスコーパス: transit-amplifying cell

1 istent with the founder cell being a stem or transit amplifying cell.

2 op, in which stem cells regulate the fate of transit amplifying cells.

3 from the limited developmental potential of transit amplifying cells.

4 ate-stage progenitor cells (IPCs), a type of transit amplifying cells.

5 in regulating the switch from stem cells to transit-amplifying cells.

6 quiescent and activated V-SVZ stem cells and transit-amplifying cells.

7 the transition from quiescent stem cells to transit-amplifying cells.

8 nd induces periclinal formative divisions in transit-amplifying cells.

9 dent increase in the proliferative output of transit-amplifying cells.

10 toward early differentiation and are likely transit-amplifying cells.

11 esponses, and are proposed to be the liver's transit-amplifying cells.

12 known mechanism, triggering proliferation of transit-amplifying cells.

13 ation allowing homotypic interaction between transit-amplifying cells.

14 al homeostasis: 1) asymmetric division (stem-transit amplifying cell); 2) populational asymmetry (pro

15 Neural progenitors (transit amplifying cells and neuroblasts) but not NSCs (

16 strate that connexin (Cx) 45 is expressed in transit-amplifying cells and neuroblasts in the postnata

17 se in the number of dividing cells including transit-amplifying cells and neuroblasts.

18 Transit-amplifying cells and progenitor cells were then

19 Actively cycling, transit-amplifying cells and quiescent cells including s

20 r follicles is composed of actively cycling, transit-amplifying cells and quiescent cells including s

21 Cancer stem cells then give rise to transit-amplifying cells and terminally differentiated c

22 cells are highly responsive, whereas type C "transit-amplifying" cells and type A neuroblasts are rem

23 me severely affects the proliferation of TA (transit-amplifying) cells and the maintenance of dental

24 ulb neuronal lineage, Ascl1 is restricted to transit amplifying cells, and by 30 d all cells matured

25 d genes that represent differentiated cells, transit-amplifying cells, and residents of stem cell nic

26 than small intestine, containing stem cells, transit-amplifying cells, and the expected spectrum of d

27 that restrict the developmental potential of transit amplifying cells are poorly understood.

28 Such signaling is required for survival of transit-amplifying cells as shown by the death of transi

29 herin-mediated homotypic interaction between transit-amplifying cells as shown by their prevention in

30 ut did not affect the proportion of stem and transit-amplifying cells, as judged by clonal growth cha

31 tified OLIG2-expressing glial progenitors as transit-amplifying cells at the tumorigenic onset.

32 stem cells (SCs) give rise to proliferating transit-amplifying cells before terminal differentiation

33 The GRFs are expressed in transit-amplifying cells but are excluded from the stem

34 Rapid cell proliferation is a hallmark of transit amplifying cells, but the mechanisms of this loc

35 lates the transition of root stem cells into transit-amplifying cells by interacting with GROWTH-REGU

36 or SHOOTMERISTEMLESS (STM), is surrounded by transit amplifying cells competent to respond to auxin h

37 Thus, in the appropriate microenvironment, transit-amplifying cells dedifferentiate, becoming funct

38 erate cell populations expressing markers of transit-amplifying cells (DeltaNp63), intermediate cells

39 rs are required for suppression of indirect, transit amplifying cell-driven neurogenesis by promoting

40 l subpopulation of actively dividing type C (transit-amplifying) cells expressed oligodendrocyte line

41 arious levels of differentiation, the cancer transit-amplifying cells fail to differentiate normally

42 EC cluster 1 exhibits transit-amplifying cell features with preferential proli

43 by an ordered replication of stem cells and transit amplifying cells followed by terminal differenti

44 pecific changes, and observed an increase in transit amplifying cells following ethanol exposure that

45 )), niche astrocytes (GFP(+)EGFR(-)CD24(-)), transit amplifying cells (GFP(-)EGFR(+)CD24(-)), and neu

46 development wherein a heterogeneous pool of transit-amplifying cells gives rise to Aire- and Ccl21a-

47 Here, we discover that hair follicle transit-amplifying cells (HF-TACs) play an essential rol

48 g necrosis in rapidly dividing hair follicle transit-amplifying cells (HF-TACs) while sparing most ha

49 cells that exit the stem cell domain acquire transit amplifying cell identity before they are incorpo

50 osine (5-hmC) in keratinocyte stem cells and transit amplifying cells in human psoriasis and in imiqu

51 m and progenitor cells reminiscent of type C transit-amplifying cells in germinal zones of the adult

52 tivity and modulating the differentiation of transit-amplifying cells in the colon.

53 tions highlight an underappreciated role for transit-amplifying cells in the tuning of differentiated

54 cer stem cells in vitro and proliferation of transit-amplifying cells in vivo.

55 In infant small bowel, survivin in transit amplifying cells increased 71% after SBR.

56 it-amplifying cells as shown by the death of transit-amplifying cells induced by treatment with a ser

57 n of the Paneth cell population and that the transit amplifying cell is likely the main progenitor re

58 Specification of new organs from transit amplifying cells is critical for higher eukaryot

59 We propose that the regulated elimination of transit-amplifying cells is essential to preserve stem c

60 those comprising the ciliary marginal zone, transit-amplifying cells, limbal epithelial stem cells,

61 inal stem cell located at position 0 and the transit amplifying cell located at position +4 in the cr

62 nd frequently coexpress Neurog1, but not the transit amplifying cell marker MASH1, nor the neuronal m

63 method, as cells isolated using the modified transit amplifying cell method could not be re-directed

64 e patterning of the basal layer implies that transit amplifying cells migrate over the basement membr

65 senchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs).

66 In addition, transit-amplifying cells not contacting other cells unde

67 proximal region of prostatic ducts while the transit-amplifying cells occupy the distal region of the

68 ressed in intermediate progenitor cells, the transit amplifying cell of the cerebral cortex.

69 The nMRTF cell state resembles transit-amplifying cells of the hair follicle matrix, wi

70 hogenesis and spindle orientation within the transit-amplifying cells of the matrix.

71 Keratinocytes can be enriched for stem or transit amplifying cells on the basis of beta1 integrin

72 human epidermal cells, designated as stem or transit-amplifying cells on the basis of Delta1 and mela

73 ition from neural stem or precursor cells to transit-amplifying cells or neurons.

74 neuronal lineage commitment and expands the transit-amplifying cell population, increasing neuron pr

75 nophen to accomplish "washout" of label from transit amplifying cell populations.

76 it maintained by a central stem cell and its transit amplifying cell progeny.

77 Importantly, we found that modulation of transit-amplifying cell proliferation changes the ratio

78 gulate dental epithelial stem cell activity, transit-amplifying cell proliferation, and enamel format

79 The subsequent increase in survivin among transit amplifying cells promotes epithelial cell prolif

80 ssed in the stem cells, downregulated in the transit-amplifying cells, re-expressed in the pre-amelob

81 primarily at the crypt side walls where the transit amplifying cell resides and not at the crypt bas

82 cluding both quiescent neural stem cells and transit-amplifying cells) responds to Shh in regions und

83 We conclude that transit-amplifying cells retain stem cell competence und

84 he early SC descendents en route to becoming transit-amplifying cells retain stemness and slow-cyclin

85 include a stem cell and multiple progenitor (transit-amplifying) cell stages, which ultimately give r

86 eraction, but low cell density nonaggregated transit-amplifying cells still survived because Notch-1

87 In contrast to growth inhibition of normal transit-amplifying cells, supplementation of low-Ca(2+)-

88 k of contribution from highly proliferative "transit-amplifying" cells supports a model whereby alpha

89 system behaves similarly to niche/stem cell/transit amplifying cell systems in other organisms.

90 Hair follicle stem cells (HFSCs) and their transit amplifying cell (TAC) progeny sense BMPs at defi

91 rapidly dividing, yet genotoxicity-sensitive transit-amplifying cells (TAC) that maintain hair growth

92 NSCs) become activated (aNSCs), and generate transit amplifying cells (TACs), which give rise to neur

93 Transit-amplifying cells (TACs) are an early intermediat

94 Stem cells self-renew or give rise to transit-amplifying cells (TACs) that differentiate into

95 ated, SCs typically give rise to short-lived transit-amplifying cells (TACs), which then progress to

96 originated from limbus, and gave rise to the transit amplifying cells that migrated centripetally to

97 r stem cells and short-lived, maintaining or transit amplifying cells that support the papilla and sp

98 ccompanied by decreased proliferation of the transit-amplifying cells that are progenitors of the ame

99 Secretory cells also act as transit-amplifying cells that eventually differentiate i

100 cortex involves a lineage of neural stem and transit-amplifying cells that forms the outer subventric

101 Initial cells generate a population of transit-amplifying cells that undergo a limited number o

102 lls in the cancer cell lineage or hierarchy (transit-amplifying cells), the property of malignancy an

103 d these molecules is particularly evident in transit amplifying cells, the immediate derivatives of s

104 s, with unlimited self-renewal capacity, and transit amplifying cells, those daughters of stem cells

105 target of miR-124 at the transition from the transit amplifying cell to the neuroblast stage.

106 accumulation of nestin and FABP5-expressing transit amplifying cells to produce classic psoriatic ep

107 icted apoptosis would occur in both stem and transit-amplifying cells to account for plaque clearance

108 gands and Notch-1 receptors between adjacent transit-amplifying cells to activate their survival sign

109 HDT1 and HDT2, regulate a second switch from transit-amplifying cells to expanding cells.

110 genitor cells (nIPCs) are a neuron-producing transit-amplifying cell type born in the germinal zones

111 s, with this population behaving strictly as transit amplifying cells under homeostatic conditions.

112 normal tissue renewal is that whereas normal transit amplifying cells usually differentiate and die,

113 fication, and inhibition of proliferation of transit-amplifying cells via contact inhibition-induced

114 Mash1 nor anti-Neurog1) and neuron-committed transit amplifying cells (which express Mash1).

115 ctivity than the more actively proliferating transit amplifying cells, which are destined to differen

116 iding Nkx2.5-positive myocytes correspond to transit amplifying cells, which condition the replicativ

117 wing stem cells; and their progeny, known as transit amplifying cells, which differentiate after seve

118 y in the germinative zone and represents the transit amplifying cells, which have a limited prolifera

119 sist in early wound healing by engrafting as transit-amplifying cells, which then differentiate into

120 the meristem are generated by stem cells and transit-amplifying cells, which together determine RM ce