ライフサイエンスコーパス: osteoclast precursor

1 ess that culminates in fusion of mononuclear osteoclast precursors.

2 f inducing differentiation and activation of osteoclast precursors.

3 ppressed by Wnt activation in osteoblast and osteoclast precursors.

4 p50 and p52, c-Fos, and NFATc1 expression in osteoclast precursors.

5 entiation at the stage of multinucleation of osteoclast precursors.

6 oduction to expand the number of bone marrow osteoclast precursors.

7 n pump and CLIC-5b to colocalize in cultured osteoclast precursors.

8 and directly stimulating differentiation of osteoclast precursors.

9 , receptor activator of NF-kappaB (RANK), in osteoclast precursors.

10 its cytokine-induced osteoclast formation by osteoclast precursors.

11 n is essential for cell survival in isolated osteoclast precursors.

12 vitro, and therefore are highly enriched in osteoclast precursors.

13 , are required for cell survival in isolated osteoclast precursors.

14 r degradation of TNFR-associated factor 6 in osteoclast precursors.

15 TSH receptor (TSHR) found on osteoblast and osteoclast precursors.

16 es sustained SOCS-3 expression in macrophage/osteoclast precursors.

17 d OPN-stimulated cell migration in RAW 264.7 osteoclast precursors.

18 ptors 1 (p55r) and 2 (p75r), each present on osteoclast precursors.

19 and differentiation (cyclosporine A only) of osteoclast precursors.

20 nase-binding proteins DAP12 and FcRgamma, in osteoclast precursors.

21 with the fusion but not the proliferation of osteoclast precursors.

22 duced osteoclastogenesis from mouse or human osteoclast precursors.

23 nduction of tumor necrosis factor-alpha from osteoclast precursors.

24 TRAP) activity produced by RANK-L-stimulated osteoclast precursors.

25 R1) is responsive to CCL3 in human and mouse osteoclast precursors.

26 on non-MM cells, most likely osteoclasts and osteoclast precursors.

27 ontingent on the state of differentiation of osteoclast precursors.

28 anced the resorptive activity of co-cultured osteoclast precursors.

29 ted activation of ERK, p38, and NF-kappaB in osteoclast precursors.

30 f the IL-27 receptor subunit WSX-1 on murine osteoclast precursors.

31 essed the resorptive activity of co-cultured osteoclast precursors.

32 ounded by a significantly elevated number of osteoclast precursors.

33 ruitment, differentiation, and activation of osteoclast precursors.

34 wed that supporting osteoblasts, rather than osteoclast precursors, accounted for the blunted respons

35 using RAW264.7 cells or bone marrow cells as osteoclast precursors, addition of M1 macrophages signif

36 le of these molecules in the relationship of osteoclast precursors and cells of osteoblastic lineage

37 ity of TGF-beta to induce SOCS expression in osteoclast precursors and examined the effect of SOCS ex

38 08 was confirmed using shRNA interference in osteoclast precursors and GPR40(-/-) primary cell cultur

39 formation of multinucleated osteoclasts from osteoclast precursors and in vitro bone resorption by is

40 ene 5 (atg5) and light chain 3 gene (lc3) in osteoclast precursors and increased LC3-II protein level

41 rption, exerting its effect both directly in osteoclast precursors and indirectly via osteoblast line

42 f cathepsin G reduces the number of CD11b(+) osteoclast precursors and mature osteoclasts at the tumo

43 mediated bone resorption and was produced by osteoclast precursors and mature osteoclasts in response

44 delta, CCR1 and CCR3, were expressed in both osteoclast precursors and mature, bone-resorbing osteocl

45 cate that dynamin function is central to the osteoclast precursors and myoblasts fusion process, and

46 generate dynamin 1- and 2-deficient primary osteoclast precursors and myoblasts, we found that fusio

47 Murine osteoclast precursors and osteoblasts express the integr

48 Mechanistic studies in osteoclast precursors and osteoblasts showed that JWH133

49 Osteoprotegerin ligand (OPGL) targets osteoclast precursors and osteoclasts to enhance differe

50 Like TNF, IL-1 directly targeted osteoclast precursors and promoted the osteoclast phenot

51 d systemic bone loss in CIA mice by reducing osteoclast precursors and promoting immune tolerance.

52 the lack of Wnt activation in osteoblast and osteoclast precursors and subsequently led to defective

53 relative to wild type, in p55r(+/+)p75r(-/-) osteoclast precursors and suppressed in those expressing

54 er the p62(P392L) or WT p62 gene into normal osteoclast precursors and targeted p62(P392L) expression

55 However, the nature of osteoclast precursors and the mechanisms underlying mult

56 d on the inducible release of TNF-alpha from osteoclast precursors and the subsequent increase of ost

57 may contribute directly to the expansion of osteoclast precursors and to the formation and activatio

58 RAF6-induced NF-kappaB activity in wild-type osteoclast precursors and, in keeping with its role as a

59 e induces the expansion of a myeloid lineage osteoclast precursor, and targeting IL-23 pathway may co

60 on, reduces the number of TNFalpha-producing osteoclast precursors, and attenuates the induction of T

61 mol/L), increased the percentage of immature osteoclast precursors, and decreased IL-1beta and tumor

62 s identified as a binding partner of MITF in osteoclast precursors, and overexpression of 14-3-3 in a

63 ent osteoclast-like giant cells, mononuclear osteoclast precursors, and spindle-shaped stromal cells

64 Using mice whose BM stromal cells and osteoclast precursors are chimeric for the presence of T

65 apeutic targeting of both PAR-1 signaling in osteoclast precursors as well as cathepsin G at the tumo

66 d osteoclast number by inducing apoptosis of osteoclast precursors as well as mature osteoclasts.

67 ed that the initial receptor by which murine osteoclast precursors bind matrix is the integrin alphav

68 In vitro treatment of murine osteoclast precursors, both cell line (RAW264.7) and bon

69 oclast formation through direct targeting of osteoclast precursors but indirectly stimulates osteocla

70 nduced NFATc1 expression in freshly isolated osteoclast precursors but stimulated its expression in R

71 ted osteoclastogenesis from freshly isolated osteoclast precursors but stimulated osteoclast formatio

72 ne erosion were examined for the presence of osteoclast precursors by the colocalization of messenger

73 Unexpectedly, however, TLR stimulation of osteoclast precursors by these microbial products strong

74 itive, multinucleated, attached to bone) and osteoclast precursors (cathepsin K-positive, mononucleat

75 ciency hampered activation of IKK complex in osteoclast precursors, causing arrest of osteoclastogene

76 cells secrete potent chemotactic factors for osteoclast precursors, CCL7 was not responsible for this

77 identified via genomic analysis of a primary osteoclast precursor cell cDNA library and is identical

78 Using a murine osteoclast precursor cell line as well as primary human

79 st precursors and the subsequent increase of osteoclast precursor cell numbers with enhanced expressi

80 enesis extended to the conversion of a third osteoclast precursor cell type- dendritic cells.

81 es, MIP-1 delta stimulated chemotaxis of two osteoclast precursor cell types: murine bone marrow mono

82 d NF-kappaB activation in mouse monocyte, an osteoclast precursor cell, through inhibition of activat

83 ty of Traf6 to activate AP-1, and Limd1(-/-) osteoclast precursor cells are defective in the activati

84 TRAP-positive, cathepsin K-positive osteoclast precursor cells are identified in areas of pa

85 Overexpression of RCANs in osteoclast precursor cells attenuated osteoclast differe

86 numerous mononucleated cathepsin K-positive osteoclast precursor cells emerged in the synovial membr

87 VEGF(121)/rGel was selectively cytotoxic to osteoclast precursor cells rather than mature osteoclast

88 Internalization of VEGF(121)/rGel into osteoclast precursor cells was suppressed by pretreatmen

89 ion and up-regulated TNF-alpha production in osteoclast precursor cells.

90 ithin 48 hours of exposure without impacting osteoclast precursor cells.

91 genesis is directly mediated through RANK on osteoclast precursor cells.

92 osis and decreases survival/proliferation of osteoclast precursor cells.

93 severely reduced in RANKL-treated TNFr1-null osteoclast precursors compared with wild type counterpar

94 (1) agonist, SEW2871, stimulated motility of osteoclast precursor-containing monocytoid populations i

95 activator of NF-kappaB ligand in BM-derived osteoclast precursor cultures from KO mice.

96 Furthermore, adding either Bgn or Fmod to osteoclast precursor cultures significantly attenuated t

97 effects of these compounds on the macrophage/osteoclast precursors, DBP-MAF, CSF-1, and the combinati

98 Cultured osteoclast precursors derived from CYLD-deficient mice w

99 irst time, the direct effects of estrogen on osteoclast precursor differentiation and shows that, in

100 sion by stromal cells and directly stimulate osteoclast precursor differentiation under the aegis of

101 , LPS administered to wild-type mice prompts osteoclast precursor differentiation, manifest by profou

102 that S1P controls the migratory behaviour of osteoclast precursors, dynamically regulating bone miner

103 In osteoclast precursors, EphB4-Fc induced ephrinB2 phospho

104 Cells with the properties of osteoclast precursors express functional S1P(1) receptor

105 vide evidence that in the presence of RANKL, osteoclast precursors express TPH(1) and synthesize sero

106 We find that a pure population of murine osteoclast precursors fails to undergo osteoclastogenesi

107 Bone marrow-derived osteoclast precursors from MFG-E8-deficient (Mfge8(-/-))

108 High levels of unprocessed p100 in osteoclast precursors from NIK-/- mice or a nonprocessab

109 Osteoclast precursors from P394L mutant mice had increas

110 Purified osteoclast precursors from PSTPIP2-deficient mice exhibi

111 Osteoclast precursors from Sirt3-/- mice underwent incre

112 expression of nonmuscle myosin IIA inhibits osteoclast precursor fusion and that a temporary, cathep

113 B is significantly enhanced at the onset of osteoclast precursor fusion, and specific inhibition of

114 or PSTPIP2 inhibition of TRAP expression and osteoclast precursor fusion, whereas interaction with PE

115 ts and increases SMAD phosphorylation around osteoclast precursor fusion.

116 Itch(-/-) osteoclast precursors had prolonged RANKL-induced NF-kap

117 0719 reduced the retention of CX3CR1-EGFP(+) osteoclast precursors in bone by increasing their mobili

118 er observed that treatment with ASCs reduced osteoclast precursors in bone marrow, resulting in decre

119 LPS suppressed generation of osteoclast precursors in mice in vivo, and adsorption of

120 ells directly induce osteoclastogenesis from osteoclast precursors in the absence of underlying strom

121 ivation of macrophages, dendritic cells, and osteoclast precursors in the bone marrow may prime the j

122 lation maintained the phagocytic activity of osteoclast precursors in the presence of osteoclastogeni

123 xis in vivo, and RANKL-induced maturation of osteoclast-precursors in vitro, indicate the commensal m

124 by directly promoting the differentiation of osteoclast precursors independent of cytokine-responsive

125 activated kinase-1 (Tak1) in macrophages and osteoclast precursors independently of beta-catenin.

126 phylococcal infection of bone marrow-derived osteoclast precursors induced their differentiation into

127 Loss of MYO10 expression in osteoclast precursors inhibits the ability of mononuclea

128 hese results suggest that TLR stimulation of osteoclast precursors inhibits their differentiation int

129 ating the recruitment and differentiation of osteoclast precursors into mature osteoclasts.

130 tro, amylin inhibits fusion of mononucleated osteoclast precursors into multinucleated osteoclasts in

131 at sphingosine-1 phosphate in blood attracts osteoclast precursors into the bloodstream to keep them

132 In osteoclast precursors, IRE1alpha was transiently activat

133 in bone marrow macrophages (BMMs), which are osteoclast precursors, is tyrosine-phosphorylated by c-S

134 In WT osteoclast precursors, Itch bound to TRAF6 and the deubi

135 ely regulate Wnt signaling in osteoblast and osteoclast precursors, known to regulate bone homeostasi

136 hancing the migration and differentiation of osteoclast precursors, leading to increased osteoclast a

137 s beta(5) basal transcription in macrophage (osteoclast precursor)-like and osteoblast-like cells.

138 oprecipitated from avian marrow macrophages (osteoclast precursors) maintained in the adherent, but n

139 d osteolysis requires a continuous supply of osteoclast precursors migrating into the bone microenvir

140 C-derived Wnt5a/Ror2 signaling in regulating osteoclast precursor migration and differentiation in th

141 es chemotaxis and regulates the migration of osteoclast precursors not only in culture but also in vi

142 ival properties of M-CSF, TNF-alpha enhanced osteoclast precursor number only in the presence of stro

143 Murine osteoclast precursors obtained from mouse bone marrow an

144 factor-alpha (TNFalpha) increases the blood osteoclast precursor (OCP) numbers in arthritic patients

145 ecursors and resorb bone, the identity of an osteoclast precursor (OCP) population in vivo and its re

146 proliferation and beta-catenin activation in osteoclast precursors (OcP) in response to M-CSF.

147 sed to evaluate the frequency of circulating osteoclast precursors (OCPs) and myeloid dendritic cells

148 in radiographs, exhibit a marked increase in osteoclast precursors (OCPs) compared with those from he

149 eoclastogenic cytokine, induces apoptosis of osteoclast precursors (OCPs) in the absence of IKKbeta/N

150 ANKL and TNF activate NF-kappaB signaling in osteoclast precursors (OCPs) to induce osteoclast (OC) f

151 te NF-kappaB canonical signaling directly in osteoclast precursors (OCPs) to induce osteoclast format

152 Like TNF, IL-1 is secreted by osteoclast precursors (OCPs), but unlike TNF, it does no

153 neration and release from the bone marrow of osteoclast precursors (OCPs).

154 ne marrow cells to quantify and characterize osteoclast precursors (OCPs).

155 osteoclasts in the absence of added splenic osteoclast precursors, osteoblasts, or vitamin D/PTH/PTH

156 s or bone and of attachment and spreading of osteoclast precursors plated on vitronectin; 3) inhibiti

157 ture osteoblast can feedback to regulate the osteoclast precursor pool size and play a multifunctiona

158 e the high-turnover bone loss to an expanded osteoclast precursor pool, together with enhanced osteob

159 We showed here that osteoclast precursors prepared from mouse bone marrow ce

160 TNFr1), prompts robust osteoclastogenesis by osteoclast precursors pretreated with RANKL, and deletio

161 These osteoclast precursors proliferate more rapidly than the

162 Genetically, beta-catenin deletion blocks osteoclast precursor proliferation, while beta-catenin c

163 cells causes high bone mass due to impaired osteoclast precursor proliferation.

164 However, EVs from osteoclast precursors promoted 1,25-dihydroxyvitamin D3-

165 cation, such as RANKL, a crucial mediator of osteoclast precursor recruitment and maturation.

166 Moreover, Sirt3-/- osteoclast precursors reduced AMP-activated protein kina

167 Suppressing Tbx3 in osteoclast precursors reduced JDP2 expression and signif

168 Conversely, p100-deficient osteoclast precursors show enhanced sensitivity to RANKL

169 erse signaling networks modulated by PTEN in osteoclast precursors stimulated by RANKL and osteoponti

170 -) mice exhibit higher levels of markers for osteoclast precursors, suggesting altered osteoclast dif

171 Activation of RBP-J selectively in osteoclast precursors suppressed inflammatory osteoclast

172 subsequent targeting of chemoattractants of osteoclast precursors that are up-regulated at the tumor

173 eoclast differentiation through an action on osteoclast precursors that is independent of stromal cel

174 SHIP(-/-) mice contain increased numbers of osteoclast precursors, that is, macrophages, we examined

175 n of chemoattractants that attract monocytic osteoclast precursors, thereby coupling bone formation a

176 been less well studied is the trafficking of osteoclast precursors to and from the bone surface, wher

177 also detected a change in the ability of the osteoclast precursors to form tunneling nanotubes (TNTs)

178 cal for the differentiation of hematopoietic osteoclast precursors to fully differentiated osteoclast

179 io, and the ability of osteocytes to attract osteoclast precursors to induce local bone resorption.

180 nges are required for the differentiation of osteoclast precursors to mature bone-resorbing osteoclas

181 get disease by increasing the sensitivity of osteoclast precursors to osteoclastogenic cytokines.

182 t mechanism that suppresses the responses of osteoclast precursors to RANKL.

183 Iron uptake by osteoclast precursors via the transferrin cycle increase

184 ion assays confirmed that membrane fusion of osteoclast precursors was inhibited.

185 aintained when direct contact between M1 and osteoclast precursors was interrupted by cell culture in

186 precursor cell line as well as primary human osteoclast precursors, we demonstrate that pharmacologic

187 me myeloid lineage as macrophages, which are osteoclast precursors, we hypothesized that MDSC may und

188 of inducing migration and differentiation of osteoclast precursors were enhanced, and these enhanced

189 Osteoclasts and osteoclast precursors were generated by culturing spleno

190 p62(P392L)-transduced osteoclast precursors were hyperresponsive to receptor a

191 When osteoclast precursors were induced by macrophage colony-

192 from NF-kappaB p50/p52 double knockout (dKO) osteoclast precursors when either c-Fos or NFATc1 is exp

193 due to the increased production of committed osteoclast precursors with a subsequent increase in oste

194 er normal conditions, and the interaction of osteoclast precursors with cells of the osteoblast linea

195 cells, we retrovirally transduced authentic osteoclast precursors with chimeric c-Fms constructs con

196 ic cell-cell interactions of the hemopoietic osteoclast precursors with the neighboring osteoblast/st

197 We demonstrate that treatment of wild-type osteoclast precursors with the osteoclastogenic cytokine

198 B ligand (RANKL)-mediated differentiation of osteoclast precursors without affecting proliferation an