ライフサイエンスコーパス: osteoclast precursor

1 g in mouse bone marrow macrophages, known as osteoclast precursors.

2 ruitment, differentiation, and activation of osteoclast precursors.

3 f inducing differentiation and activation of osteoclast precursors.

4 ess that culminates in fusion of mononuclear osteoclast precursors.

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

6 entiation at the stage of multinucleation of osteoclast precursors.

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

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

9 and directly stimulating differentiation of osteoclast precursors.

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

11 its cytokine-induced osteoclast formation by osteoclast precursors.

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

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

14 , are required for cell survival in isolated 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 the capacity of HSPCs to differentiate into osteoclast precursors.

20 itogen-activated protein kinase induction in osteoclast precursors.

21 ppressed by Wnt activation in osteoblast and osteoclast precursors.

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

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

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

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

26 duced osteoclastogenesis from mouse or human osteoclast precursors.

27 ibiting RANKL-induced NF-kappaB signaling in osteoclast precursors.

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

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

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

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

32 ontingent on the state of differentiation of osteoclast precursors.

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

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

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

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

37 ounded by a significantly elevated number of osteoclast precursors.

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

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

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

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

42 08 was confirmed using shRNA interference in osteoclast precursors and GPR40(-/-) primary cell cultur

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

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

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

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

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

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

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

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

51 Murine osteoclast precursors and osteoblasts express the integr

52 Mechanistic studies in osteoclast precursors and osteoblasts showed that JWH133

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

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

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

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

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

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

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

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

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

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

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

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

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

66 enes associated with osteoclast progenitors, osteoclast precursors, and mature cells.

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

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

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

70 RNA-sequencing data showed that EMP-derived osteoclast precursors arose independently of the haemato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 osteoclast cells (bone-resorbing cells) from osteoclast precursor cells (OCPs) and its contribution t

90 sequencing of wild-type and STING-deficient osteoclast precursor cells and differentiating osteoclas

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

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

93 Overexpression of RCANs in osteoclast precursor cells attenuated osteoclast differe

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

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

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

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

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

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

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

101 ogenesis was seen in highly purified PAR1 KO osteoclast precursor cells.

102 1 (PAR1) was transiently induced in cultured osteoclast precursor cells.

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

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

105 osteoclastogenic macrophages (AtoMs)) as the osteoclast precursor-containing population in the inflam

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

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

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

109 Cultured osteoclast precursors derived from CYLD-deficient mice w

110 STING-deficient osteoclast precursors differentiate with greater efficie

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

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

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

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

115 In osteoclast precursors, EphB4-Fc induced ephrinB2 phospho

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

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

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

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

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

121 Osteoclast precursors from P394L mutant mice had increas

122 Purified osteoclast precursors from PSTPIP2-deficient mice exhibi

123 Osteoclast precursors from Sirt3-/- mice underwent incre

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

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

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

127 ts and increases SMAD phosphorylation around osteoclast precursor fusion.

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

129 0719 reduced the retention of CX3CR1-EGFP(+) osteoclast precursors in bone by increasing their mobili

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

131 mprising a subset distinct from conventional osteoclast precursors in homeostatic bone remodeling.

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

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

134 mphoid lineages and an elevated abundance of osteoclast precursors in the BM and osteoclastogenic mac

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

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

137 In addition, osteoclast precursors in untreated cells (CP) were more

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

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

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

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

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

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

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

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

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

147 In osteoclast precursors, IRE1alpha was transiently activat

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

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

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

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

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

153 While GPR109A is highly expressed in osteoclast precursor macrophages, its role in bone devel

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

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

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

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

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

159 Murine osteoclast precursors obtained from mouse bone marrow an

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

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

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

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

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

165 the autophagic response induced by RANKL in osteoclast precursors (OCPs) derived from bone marrow-de

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

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

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

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

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

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

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

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

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

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

176 d an erythromyeloid progenitor (EMP)-derived osteoclast precursor population.

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

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

179 These osteoclast precursors proliferate more rapidly than the

180 e effect of cigarette smoke extract (CSE) on osteoclast precursor proliferation and osteoclast apopto

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

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

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

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

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

186 Suppressing Tbx3 in osteoclast precursors reduced JDP2 expression and signif

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

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

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

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

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

192 Furthermore, EMPs gave rise to long-lasting osteoclast precursors that contributed to postnatal bone

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

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

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

196 ound a diminished crosstalk with circulating osteoclast precursors through the CD244-CD48 coreceptor

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

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

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

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

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

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

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

204 Iron uptake by osteoclast precursors via the transferrin cycle increase

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

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

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

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

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

210 Osteoclasts and osteoclast precursors were generated by culturing spleno

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

212 When osteoclast precursors were induced by macrophage colony-

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

214 lth and disease, are formed by the fusion of osteoclast precursors, where each fusion event raises th

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

216 Finally, infection of macrophages or osteoclast precursors with B. abortus 2308 resulted in g

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

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

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

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

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