ライフサイエンスコーパス: osteoblast lineage

1 dependent upon expression of Gsalpha in the osteoblast lineage.

2 rentiation of mesenchymal stem cells towards osteoblast lineage.

3 accompanied by reduced Wnt signaling in the osteoblast lineage.

4 of mesenchymal cell differentiation into the osteoblast lineage.

5 lls, which some evidence suggests are of the osteoblast lineage.

6 es of these pathways in specification of the osteoblast lineage.

7 sB mice is independent of the changes in the osteoblast lineage.

8 ions downstream of Ihh in development of the osteoblast lineage.

9 its complex actions in bone to cells of the osteoblast lineage.

10 Cells of the osteoblast lineage affect the homing and the number of l

11 blasts, allowing the conditional ablation of osteoblast lineage after treatment with ganciclovir (GCV

12 we identify two distinct roles for RA in the osteoblast lineage: an early role in blocking the recrui

13 ons in BMP receptor function targeted to the osteoblast lineage and demonstrate a necessary role of B

14 skeletal phenotype is cell autonomous to the osteoblast lineage and independent of adipocyte formatio

15 he mesenchymal maturation program toward the osteoblast lineage and is mechanistically distinct from

16 senchymal stem cell (hMSC) commitment to the osteoblast lineage and modulates Wnt/beta-catenin signal

17 Signals that govern development of the osteoblast lineage are not well understood.

18 ell migration and differentiation toward the osteoblast lineage as measured by mineralized nodule for

19 ises from mesenchymal cells induced into the osteoblast lineage by essential transcription factors an

20 Wnt10b shifts cell fate toward the osteoblast lineage by induction of the osteoblastogenic

21 the mouse osteocalcin 2 promoter in several osteoblast lineage cell lines.

22 e production of trophic factors required for osteoblast lineage cell maintenance, ultimately leading

23 dherin expression was efficiently ablated in osteoblast lineage cells as assessed by mRNA expression

24 C/EBP transcription factors was disrupted in osteoblast lineage cells by overexpressing a naturally o

25 on the skeleton, but the role of ERalpha in osteoblast lineage cells has remained elusive.

26 In conclusion, N-cadherin expression in osteoblast lineage cells is dispensable for HSC maintena

27 nce suggesting that N-cadherin expression on osteoblast lineage cells regulates hematopoietic stem ce

28 receptor (EGFR) specifically inactivated in osteoblast lineage cells revealed that EGFR stimulates b

29 nesis indirectly by enhancing the ability of osteoblast lineage cells to stimulate osteoclastogenesis

30 By deleting the receptor Bmpr1a in osteoblast lineage cells with Dmp1-Cre, we observed a dr

31 ugh PHEX/Phex expression occurs primarily in osteoblast lineage cells, transgenic Phex expression in

32 on of osteoclasts secondary to activation of osteoblast lineage cells, which expressed increased RANK

33 ressed by a variety of cell types, including osteoblast lineage cells.

34 ifferent stages of differentiation in murine osteoblast lineage cells.

35 llow the fates of stage-selective subsets of osteoblast lineage cells.

36 CXCL12 expression is secondary to a loss of osteoblast lineage cells.

37 in osteoclast precursors and indirectly via osteoblast lineage cells.

38 nsgenic mice that express Cre recombinase in osteoblast lineage cells.

39 tion factor that is first expressed in early osteoblast-lineage cells and represents a primary determ

40 nce suggests that only a minuscule number of osteoblast-lineage cells are present in peripheral blood

41 Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT

42 Osteoblast-lineage cells circulate in physiologically si

43 ne-specific proteins to identify circulating osteoblast-lineage cells in 11 adolescent males and 11 a

44 However, the osteoblast-lineage cells isolated from these mice exhibi

45 ociated athanogene-1 (BAG-1) is expressed by osteoblast-lineage cells; early embryonic lethality in B

46 poietic (e.g. T and B-cell) and mesenchymal (osteoblast lineage, chondrocyte) cell types.

47 Runx2 is indispensable for osteoblast lineage commitment and early differentiation

48 ctor Maf (also known as c-Maf) is central to osteoblast lineage commitment.

49 ncluding minimal association with osterix(+) osteoblast-lineage committed mesenchymal cells in wild-t

50 an important role in regulating BMP9-induced osteoblast lineage differentiation of MSCs.

51 coordinate beta-catenin signaling within the osteoblast lineage during embryonic and postnatal bone d

52 rect pluripotent mesenchymal cells toward an osteoblast lineage, exert their osteoinductive effects t

53 Mice lacking G(s)alpha in cells of the osteoblast lineage exhibit a reduction in pro-B and pre-

54 active G alpha(q) transgene in cells of the osteoblast lineage exhibited severe osteopenia in cortic

55 dependent signaling pathways in cells of the osteoblast lineage extrinsically regulate bone marrow B

56 In the absence of Ihh, cells of the osteoblast lineage fail to activate the expression of Ru

57 ndifferentiated MPCs and MPCs induced to the osteoblast lineage for 1-7 days by cDNA microarray analy

58 ubunit G(s)alpha is required in cells of the osteoblast lineage for normal postnatal B lymphocyte pro

59 otency, we measured the expression levels of osteoblast lineage genes in synovial and periosteal clon

60 Donor cells found in the bone expressed osteoblast lineage genes, and produced the extracellular

61 oreover, mice with loss of RNF146 within the osteoblast lineage had increased fat stores and were glu

62 Mice lacking Atg7 in the entire osteoblast lineage had low bone mass and fractures assoc

63 teriparatide's actions on early cells of the osteoblast lineage has been demonstrated.

64 increases the numbers of early cells of the osteoblast lineage, hastens their differentiation into o

65 hondrium; the latter were early cells of the osteoblast lineage immediately descended from their prog

66 omoter-driven cre to mark early cells of the osteoblast lineage in adult mice.

67 commitment of mesenchymal progenitors to the osteoblast lineage in association with enhanced Wnt sign

68 t Ihh signaling is directly required for the osteoblast lineage in the developing long bones and that

69 Ihh) is indispensable for development of the osteoblast lineage in the endochondral skeleton.

70 modulates cellular functions in cells of the osteoblast lineage in vitro and in vivo.

71 e of Gsalpha signaling in cells of the early osteoblast lineage in vivo by conditionally deleting Gsa

72 n of osteoclast precursors with cells of the osteoblast lineage is a prerequisite for osteoclast form

73 these results suggest that commitment to the osteoblast lineage is not a requirement for RANKL gene t

74 ession in cells from different stages of the osteoblast lineage isolated by FACS sorting showed that

75 tivation of Wnt/betacatenin signaling in the osteoblast lineage leads to an increase in bone mass thr

76 Taken together, our data indicate that osteoblast lineage maturation is a critical aspect under

77 le of RUNX2 activity and its function during osteoblast lineage maturation.

78 mmitment of mesenchymal cells ex vivo to the osteoblast lineage occurred in Runx2-II(-/-) mice, but o

79 Postnatal removal of Gsalpha in the osteoblast lineage (P-Gsalpha(OsxKO) mice) yielded marke

80 ents may be necessary to regulate Osx during osteoblast lineage progression.

81 P-2 and IGF-1 regulate Osx expression during osteoblast lineage progression.

82 Selective deletion of Smurf2 in the osteoblast lineage recapitulates the phenotype of germli

83 data demonstrate that commitment within the osteoblast lineage requires sequential, stage-specific,

84 Deletion of G(s)alpha early in the osteoblast lineage results in a 59% decrease in the perc

85 Id expression may be critical to BMP-induced osteoblast lineage-specific differentiation of mesenchym

86 Osteoblast lineage-specific differentiation of mesenchym

87 ated by applying it to an important study of osteoblast lineage-specific differentiation.

88 kers [alkaline phosphatase, osteopontin, and osteoblast lineage-specific transcription factor (Cbfa-1

89 activity of this suppressor in cells of the osteoblast lineage suggest that it is expressed with oth

90 iption factor required for commitment to the osteoblast lineage, supporting the idea that osteoclast-

91 Cells of the osteoblast lineage that reside in the endosteal niche ha

92 eton, is strictly restricted to cells of the osteoblast lineage thereafter, and is regulated by BMP7

93 Although differentiation of the osteoblast lineage was not disturbed, the proliferation

94 es cell-specific gene expression in cells of osteoblast lineage, we constructed a recombinant adenovi

95 hown that Sox2 maintains self-renewal in the osteoblast lineage while inhibiting differentiation.