ライフサイエンスコーパス: osteoblastogenesis

1 othesized that estrogen loss also stimulates osteoblastogenesis.

2 plained, at least in part, by an increase in osteoblastogenesis.

3 ntly inhibited adipogenesis whereas promoted osteoblastogenesis.

4 NFATc1 regulates both osteoclastogenesis and osteoblastogenesis.

5 nd increasing adipogenesis while suppressing osteoblastogenesis.

6 1 isoform transcripts is a hallmark of early osteoblastogenesis.

7 s positive for Runx2, a master regulator for osteoblastogenesis.

8 ells and represents a primary determinant of osteoblastogenesis.

9 promoted enhanced adipogenesis and decreased osteoblastogenesis.

10 ctivator critically mediates Ihh function in osteoblastogenesis.

11 expression along various lineages including osteoblastogenesis.

12 ormation of osteoblast precursors to promote osteoblastogenesis.

13 interrelated network of miRNAs that control osteoblastogenesis.

14 nesis and coordinates osteoclastogenesis and osteoblastogenesis.

15 of action of this antiosteoporotic agent in osteoblastogenesis.

16 and hyperactivation of p38 MAPK that favors osteoblastogenesis.

17 erostin expression by the osteocyte favoring osteoblastogenesis.

18 contrast, deletion of Tie2 has no effect on osteoblastogenesis.

19 udies, we evaluated the role of Wnt11 during osteoblastogenesis.

20 ize Wnt signaling, an essential stimulus for osteoblastogenesis.

21 neage determination between adipogenesis and osteoblastogenesis.

22 HES-1 appears to mediate effects of Notch on osteoblastogenesis.

23 osteoclastogenesis and a smaller increase in osteoblastogenesis.

24 c protein 2 (BMP2) and demonstrated enhanced osteoblastogenesis and adipogenesis versus WT MSCs.

25 , identify Bicc1 as a genetic determinant of osteoblastogenesis and BMD and suggest that it does so b

26 nt, at least in part, for the attenuation of osteoblastogenesis and bone formation by the age-depende

27 eoclastosis, and angiogenesis and stimulated osteoblastogenesis and bone formation, whereas ephrinB2-

28 nt activity, and its overexpression inhibits osteoblastogenesis and causes osteopenia.

29 togenesis in a cell-autonomous manner and in osteoblastogenesis and chondrogenesis in non-cell-autono

30 one mass through a dual mechanism: increased osteoblastogenesis and decreased osteoclastogenesis.

31 asts derived from these mice showed impaired osteoblastogenesis and enhanced adipogenesis.

32 MAGP1Delta bone marrow stromal cells undergo osteoblastogenesis and form mineralized nodules.

33 t indispensable for Avp action in inhibiting osteoblastogenesis and gene expression, Avp-stimulated g

34 ticoids depress bone formation by inhibiting osteoblastogenesis and increasing osteoblast apoptosis.

35 he bisphosphonate group, is known to enhance osteoblastogenesis and inhibit osteoclastic bone resorpt

36 ule stimulated polycystin- and TAZ-dependent osteoblastogenesis and inhibited adipogenesis.

37 rate that canonical Wnt signaling stimulates osteoblastogenesis and inhibits adipogenesis of bipotent

38 Runx2-I is sufficient for early osteoblastogenesis and intramembranous bone formation, w

39 ghly expressed during osteoclastogenesis and osteoblastogenesis and is dramatically upregulated in th

40 close to TMEM135, a gene recently linked to osteoblastogenesis and longevity) significantly associat

41 in vivo, the agomir significantly increased osteoblastogenesis and mineralization, reversed bone los

42 In vitro, menin modulates osteoblastogenesis and osteoblast differentiation promot

43 eptor, EphB4, is involved in the coupling of osteoblastogenesis and osteoclastogenesis and in angioge

44 plays a pivotal role in the disregulation of osteoblastogenesis and osteoclastogenesis induced by ovx

45 he Phe377del mutation in ANK causes impaired osteoblastogenesis and osteoclastogenesis resulting in h

46 tetracycline-labeled vertebrae, and impaired osteoblastogenesis and osteoclastogenesis, as determined

47 OVX-Diet rats showed enhanced osteoblastogenesis and osteoclastogenesis.

48 obiota has anti-anabolic effects suppressing osteoblastogenesis and pro-catabolic effects enhancing o

49 gests that some miRs play important roles in osteoblastogenesis and skeletal homeostasis, much less i

50 Mechanistically, FGF21 inhibits osteoblastogenesis and stimulates adipogenesis from bone

51 with severe osteopenia because of defective osteoblastogenesis and subsequent impaired osteocalcin p

52 Tea polyphenols enhance osteoblastogenesis and suppress osteoclastogenesis in vi

53 Knock down of Bicc1 and Pkd2 impaired osteoblastogenesis, and Bicc1 deficiency-dependent osteo

54 d fractures by mediating osteoclastogenesis, osteoblastogenesis, and bone collagen synthesis.

55 whereas ephrinB2-Fc stimulated angiogenesis, osteoblastogenesis, and bone formation but had no effect

56 n of preosteoblast replication, induction of osteoblastogenesis, and inhibition of osteoblast and ost

57 of beta-catenin, inhibits apoptosis, induces osteoblastogenesis, and inhibits adipogenesis.

58 Notch receptors regulate osteoblastogenesis, and Notch activation induces cleavag

59 utralized the negative effect of MM cells on osteoblastogenesis, and reduced IL-6 secretion.

60 is by regulating both osteoclastogenesis and osteoblastogenesis, and they serve as inhibitors for cal

61 he principal site for osteoclastogenesis and osteoblastogenesis; and an increase in the former has be

62 genes that are capable of further affecting osteoblastogenesis, angiogenesis, and the deposition of

63 iously shown that cellular proliferation and osteoblastogenesis are important in the development of v

64 tagonists, namely SR49059 or ADAM, increased osteoblastogenesis, as did the genetic deletion of Avpr1

65 ignaling shifts mesenchymal cell fate toward osteoblastogenesis at the expense of adipogenesis; howev

66 Overexpression of NICD impairs osteoblastogenesis, but the mechanisms are not understoo

67 he lineage determination of adipogenesis and osteoblastogenesis by demethylating Wnt10a gene and upre

68 hibited decreased adipogenesis and increased osteoblastogenesis compared with WT MSCs.

69 associated with the post-commitment stage of osteoblastogenesis, demonstrated by impaired ECM mineral

70 demonstrate that miR-34c is critical during osteoblastogenesis in part by regulating Notch signaling

71 adipogenic potential and causes spontaneous osteoblastogenesis in ST2 cells and mouse embryonic fibr

72 tween low bone mineral density and decreased osteoblastogenesis in the bone marrow and validate the s

73 The role of Wnt signaling in osteoblastogenesis in the embryo remains to be fully est

74 TNFalpha inhibits osteoblastogenesis in the presence of ascorbic acid in c

75 elta signaling is required for Wnt3a-induced osteoblastogenesis in these cells, and PKCdelta homozygo

76 HES1 impaired osteoblastogenesis in vitro, and transgenic osteoblasts

77 it) is a transcription factor that regulates osteoblastogenesis in vitro.

78 mal bone mass or osteopenia due to defective osteoblastogenesis increased bone formation without affe

79 2 expression, Indian hedgehog signaling, and osteoblastogenesis is intact.

80 These findings demonstrate that osteoblastogenesis is limited by an elaborate network of

81 (SAMP6) to test the hypothesis that reduced osteoblastogenesis is linked with decreased bone mass.

82 One mechanism whereby Wnt10b promotes osteoblastogenesis is suppression of PPARgamma expressio

83 on factor proven essential for commitment to osteoblastogenesis, is also expressed in response to BMP

84 another mesenchymal differentiation process, osteoblastogenesis, is enhanced upon HDAC inhibition.

85 ctivated Fz2 does not influence apoptosis or osteoblastogenesis, it inhibits adipogenesis through a m

86 The downregulation of ACC1 on osteoblastogenesis may be the cause for the osteopenia p

87 Runx2, a transcription factor essential for osteoblastogenesis, negatively regulates expression of t

88 pression in multiple myeloma cells inhibited osteoblastogenesis of bone marrow-derived osteoblast pro

89 n in a cellular in vivo context during early osteoblastogenesis of MC3T3-E1 cultures and BMSCs induce

90 nce the stimulating effect of ovariectomy on osteoblastogenesis or osteoclastogenesis.

91 ich p38 signaling in myeloma cells regulates osteoblastogenesis, osteoclastogenesis, and bone destruc

92 sal microbiota's immunoregulatory effects on osteoblastogenesis, osteoclastogenesis, marrow T-cell he

93 d that DeltaFosB transcriptionally regulates osteoblastogenesis, possibly at the expense of adipogene

94 In conclusion, CTGF enhances osteoblastogenesis, possibly by inhibiting Notch signali

95 tructure, increased bone turnover, depressed osteoblastogenesis (Runx2, Sparc), and increased both os

96 ntiated mesenchyme and a marked reduction in osteoblastogenesis that resulted in a high incidence of

97 ecution and completion of BMP2 signaling for osteoblastogenesis through a mechanism that requires RUN

98 take place with the parallel enhancement of osteoblastogenesis, thus providing a novel therapeutic a

99 essential role in cellular proliferation and osteoblastogenesis via the beta-catenin signaling pathwa

100 Osteoblastogenesis was accelerated in ank/ank mesenchyma

101 echanism involved in reduced bone formation, osteoblastogenesis was studied in bone marrow stromal ce

102 G233V mutant marrow was diminished, whereas osteoblastogenesis was unaffected.

103 n, indicating that the stimulatory effect on osteoblastogenesis was unrelated to BMP and Wnt signalin

104 ate the potential role of Notch signaling in osteoblastogenesis, we used conditional alleles to genet

105 s with roles in inhibition of BMP-2-directed osteoblastogenesis were significantly upregulated.

106 cription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma-mediate