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 from the limited developmental potential of transit amplifying cells.

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

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

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

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

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

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

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

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

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

12 ation allowing homotypic interaction between transit-amplifying cells.

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

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

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

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

17 Transit-amplifying cells and progenitor cells were then

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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