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1 to that of its physiological decoy receptor osteoprotegerin.
2 ngiogenesis, which was completely blocked by osteoprotegerin.
3 sible using antibodies to RANKL or synthetic osteoprotegerin.
4 ifically blocked by the RANKL decoy receptor osteoprotegerin.
5 decreased expression of RANKL and increased osteoprotegerin.
6 ) that could be blocked by pretreatment with osteoprotegerin.
7 shed expression of the RANKL decoy receptor, osteoprotegerin.
8 P, fibrinogen, sICAM-1, sTNFRI, sTNFRII, and osteoprotegerin.
9 ing factor-1, and decrease the expression of osteoprotegerin.
10 by concurrent treatment with ibandronate or osteoprotegerin.
11 colony-stimulating factor, RANK ligand, and osteoprotegerin.
12 K on osteoclast surfaces by RANKL similar to osteoprotegerin.
13 es, the most pronounced increase was seen in osteoprotegerin.
14 asma levels of osteopontin, osteocalcin, and osteoprotegerin (204%, 148%, and 55%, respectively; P <
15 cation (fibroblast growth factor-23 and OPG [osteoprotegerin]), 3 inflammatory biomarkers (tumor necr
16 epressed osteoclast progenitor expression of osteoprotegerin, a decoy receptor for RANKL previously t
19 proteins regulates osteoblast expression of Osteoprotegerin, a major inhibitor of osteoclast differe
20 e of the genes identified in this screen was osteoprotegerin, a member of the tumor necrosis factor r
24 king finding was the significant decrease in osteoprotegerin, an osteoclastogenesis inhibitory factor
25 up EP-HN019 presented greater expressions of osteoprotegerin and beta-defensins than group EP (P <0.0
26 vels of biomarkers of vascular inflammation (osteoprotegerin and C-terminal proendothelin-1, adjusted
28 al fibroblasts, increasing the expression of osteoprotegerin and decreasing receptor activator of nuc
29 Group EP-HD100 presented greater levels of osteoprotegerin and gene expression of interleukin (IL)-
31 ow that muscle cells can produce and secrete osteoprotegerin and pharmacologic treatment of dystrophi
34 ys a unique role in osteocytes, up-regulates osteoprotegerin and Wnt signaling, and differentially re
35 -polymerase chain reaction (RT-PCR) for OPG (osteoprotegerin); and RANKL (receptor activator of NF-ka
36 Some of these, including oxidized lipids, osteoprotegerin, and bisphosphonates, appear to regulate
37 rcarboxylated osteocalcin (%ucOC)] and IL-6, osteoprotegerin, and C-reactive protein (CRP) concentrat
39 ces were observed in the 3-y change in IL-6, osteoprotegerin, and CRP concentrations between particip
41 g regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1-34) regulated only s
42 lis infection, while mRNA for interleukin-1, osteoprotegerin, and STAT6 all increased in the suscepti
43 -H+-ATPase inhibitor SB 242784, the cytokine osteoprotegerin, and the amino bisphosphonates alendrona
44 tivator of nuclear factor-kappaB ligand, and osteoprotegerin; and up-regulate osteoclast formation.
46 igand (RANKL) and variable downregulation of osteoprotegerin are implicated, and bone health may impr
47 aB ligand (RANKL) and its receptors RANK and osteoprotegerin are key regulators of bone remodeling bu
48 e investigated whether circulating levels of osteoprotegerin are related to features of CMV disease a
49 ligand RANKL, and the soluble decoy receptor osteoprotegerin are the key regulators of osteoclast dif
51 ctivator of NF kappa B ligand and suppresses osteoprotegerin at concentrations two logs lower than th
52 h the receptor activator of NF-kappaB ligand/osteoprotegerin axis was unaffected, expression of tumor
53 of a distinct program of genes that included osteoprotegerin, BCL-2, and IAP-1 (inhibitor of apoptosi
56 vary biomarkers (especially MMP-8 and -9 and osteoprotegerin) combined with red-complex anaerobic per
58 The association observed between increased osteoprotegerin concentrations and periodontitis was los
61 appaB ligand (RANKL) coupled with decline in osteoprotegerin correlate with decreased bone mineral de
64 Juvenile Paget's disease can result from osteoprotegerin deficiency caused by homozygous deletion
68 nate zoledronic acid and the RANKL inhibitor osteoprotegerin, each blocked GM-CSF-induced tumor growt
69 of the osteoclastogenesis inhibitory factor osteoprotegerin enabled early growth of SS18-SSX2-transf
70 hematical model based on type I collagen and osteoprotegerin expression that predicts the bone-formin
71 aB ligand (RANKL) production, an increase in osteoprotegerin expression, and a decrease in serum tart
72 ANKL and M-CSF, saturating concentrations of osteoprotegerin failed to inhibit approximately 40% of t
75 AT/enhancer-binding protein-beta and -delta, osteoprotegerin, FOXC2 and FOXF2, BMP-2, p75 neurotrophi
76 eceived an injection of anti-RANKL antibody, osteoprotegerin fusion protein (OPG-Fc), or a control fu
77 This effect was antagonized by injection of osteoprotegerin fusion protein into the local gingival t
79 showed that Smad1 activates osteopontin and osteoprotegerin gene expression by dislodging Hoxc-8 fro
80 801, on chromosome 8, near to the TNFRSF11B (osteoprotegerin) gene, and rs3736228, on chromosome 11 i
83 ppa B ligand at day 7 post-treatment, strong osteoprotegerin immunoreactivity was observed at day 15
85 shed novel roles for tumor-derived CCL20 and osteoprotegerin in inducing CCL2 production from macroph
87 ace membrane fibroblasts expressed RANKL and osteoprotegerin in response to stimulation with conditio
91 conjunction with their shared decoy receptor osteoprotegerin, in the bone marrow of infected IFrag(-/
93 (3)-mediated endothelial survival depends on osteoprotegerin induction by NF-kappaB and indicate a ne
97 on SLA and modSLA [e.g., prostaglandin E(2), osteoprotegerin, latent and active TGF-beta1, and stimul
98 osis factor (TNF)-alpha, C-reactive protein, osteoprotegerin, leptin, and adiponectin were determined
99 , a calcium-sensing receptor related factor, osteoprotegerin, leptin, bisphosphonates and oxidized li
100 icipants inoculated with P. vivax, where the osteoprotegerin level correlated with the levels of para
101 Recent observational studies show that serum osteoprotegerin levels are associated with the severity
103 essive atherosclerosis with increased plasma osteoprotegerin levels, consistent with observational st
106 ivator of NF-kappaB (RANK), the receptor for osteoprotegerin ligand (OPGL), also known as RANK ligand
107 tem is enhanced by the addition of exogenous osteoprotegerin ligand (OPGL), an essential Ocl differen
109 insic cell surface determinant that mediates osteoprotegerin ligand effects on bone resorption and re
110 nduced cytokine (TRANCE, also referred to as osteoprotegerin ligand), and kit ligand-1 (KL-1) in vitr
111 enetic interactions between osteoprotegerin, osteoprotegerin ligand, and RANK during bone resorption
112 t differentiation factor (ODF; also known as osteoprotegerin ligand, receptor activator of nuclear fa
113 01 with Bonferroni correction for both), but osteoprotegerin lost significance after age and sex adju
114 differentiation and calcification inhibitors osteoprotegerin, matrix Gla protein, and osteopontin.
115 c and treatment studies in mice suggest that osteoprotegerin may protect against vascular calcificati
116 the generation of bone cancer pain and that osteoprotegerin may provide an effective treatment for t
117 of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates
118 ding macrophage inflammatory protein-1Delta, osteoprotegerin, monokine induced by interferon-gamma (I
126 hosphatase mRNA levels, and potently induced osteoprotegerin mRNA, whereas LiCl was ineffective alone
130 TNF-related apoptosis-inducing ligand; OPG, osteoprotegerin; Omp29, 29-kDa outer membrane protein; P
131 r of nuclear factor kappaBeta ligand (RANKL)/osteoprotegerin (OPG) (2.5 +/- 0.7-fold, p < 0.001) rati
133 ons on structurally conserved ectodomains of osteoprotegerin (OPG) and decoy receptor 3, other two se
136 o compare the activity of TSG-6 with that of osteoprotegerin (OPG) and to investigate its role as an
137 r activator of NF-kappaB) and decoy receptor osteoprotegerin (OPG) are constitutively expressed at al
138 uclear factor-kappabeta ligand (sRANKL), and osteoprotegerin (OPG) at baseline (the date of initiatio
139 tor for NF-kappaB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and expression of the transcr
142 nic markers, alkaline phosphatase (ALP), and osteoprotegerin (OPG) by hMSCs and transcriptome analysi
143 ulatory factors in osteoblasts by decreasing osteoprotegerin (OPG) expression and increasing monocyte
144 ld lower RANKL expression but >2-fold higher osteoprotegerin (OPG) expression than donor-matched ABCs
145 ormone-related protein (PTHrP) down-regulate osteoprotegerin (OPG) gene expression in the dental foll
146 of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) immunohistochemistry was carried o
147 All treatments upregulated mRNA levels for osteoprotegerin (OPG) in comparison to PLAC (P < 0.05).
150 from tumor cells suppress the expression of osteoprotegerin (OPG) in osteoblasts and subsequently po
152 bular molar, a decrease in the expression of osteoprotegerin (OPG) in the dental follicle at day 3 en
153 ukin (IL)-17A, IL-17E, IL-17F, IL-17A/F, and osteoprotegerin (OPG) in women with rheumatoid arthritis
154 lear factor-kappa B ligand (RANKL) inhibitor osteoprotegerin (OPG) inhibits osteoclastogenesis and su
156 ator of Nfkb ligand (RANKL) activates, while osteoprotegerin (OPG) inhibits, osteoclastogenesis.
169 of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) levels and RANKL/OPG ratios in ser
170 pressed significantly higher RANKL and lower osteoprotegerin (OPG) mRNA and increased RANKL:OPG ratio
171 uclear factor kappaB ligand (RANKL) and RANK/osteoprotegerin (OPG) plays a dominant role in osteoclas
172 of nuclear factor kappaB ligand (RANKL) with osteoprotegerin (OPG) prevents the osteolytic activity o
173 or activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) production by ST2 cells, despite M
175 f nuclear factor kappaB ligand) promotes and osteoprotegerin (OPG) protects against vascular calcific
176 ce with established myeloma with recombinant osteoprotegerin (OPG) protein, the soluble decoy recepto
177 e dermatomyositis (DM), to compare the RANKL:osteoprotegerin (OPG) ratio in patients with juvenile DM
178 f nuclear factor kappa-B ligand (RANKL)-RANK-osteoprotegerin (OPG) signaling associated with bone res
179 or activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) signaling in osteocytes was not st
180 ctor-kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) signaling pathway (RANKL/RANK/OPG
181 r activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) that modulate bone homeostasis.
182 ivator of nuclear factor kappa-B (RANKL) and osteoprotegerin (OPG) to diagnose healthy peri-implant c
185 ctor kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also investigated by immunohi
186 tion of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitati
187 of nuclear factor-kappaB ligand (RANKL), and osteoprotegerin (OPG) were analyzed in the furcation are
188 of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) were assessed by enzyme-linked imm
189 of nuclear factor kappaB ligand (RANKL), and osteoprotegerin (OPG) were determined by immunohistochem
190 tor of nuclear factor-kappa B (RANKL) and of osteoprotegerin (OPG) were evaluated by immunofluorescen
191 or kappa B ligand (RANKL) and its antagonist osteoprotegerin (OPG) were measured prospectively before
192 onocyte chemoattractant protein (MCP)-1, and osteoprotegerin (OPG) were measured with qPCR and ELISA.
193 s, RvE1 significantly enhanced expression of osteoprotegerin (OPG) without inducing change in recepto
196 teoclastogenesis by inhibiting expression of osteoprotegerin (OPG), a decoy receptor for the receptor
201 or of nuclear factor-kappaB ligand (sRANKL), osteoprotegerin (OPG), a proliferation-inducing ligand (
202 t survival, in part through the induction of osteoprotegerin (OPG), a protein known to inhibit osteoc
204 hormones or cytokines, and is neutralized by osteoprotegerin (OPG), a soluble decoy receptor also cru
205 addition to its effects on bone metabolism, osteoprotegerin (OPG), a soluble member of the tumor nec
208 nd activation, we examined the expression of osteoprotegerin (OPG), an inhibitor of osteoclast format
212 ptor activator of NF-kappa B ligand (RANKL), osteoprotegerin (OPG), and monocyte chemotactic and stim
213 r factor-kappaB (RANK), RANK-ligand (RANKL), osteoprotegerin (OPG), and osteocalcin was performed.
214 he levels and relative ratios of sclerostin, osteoprotegerin (OPG), and receptor activator of nuclear
215 or of nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant acid phosp
216 tor of nuclear factor kappaB ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant acid phosp
217 ctivator of nuclear factor-kappaB (RANK) and osteoprotegerin (OPG), are known to be regulators of dev
218 r of nuclear factor-kappa B ligand (sRANKL), osteoprotegerin (OPG), B-cell activating factor (BAFF),
219 oclast numbers and activity are regulated by osteoprotegerin (OPG), bisphosphonates suppress osteocla
220 kappaB (RANK), soluble RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin-K, and sclerostin.
221 on index (ACI), fibroblast growth factor 23, osteoprotegerin (OPG), fetuin A, and clinical and bioche
222 of TRAIL, DR5 and the TRAIL decoy receptors osteoprotegerin (OPG), mDcTRAILR1, and mDcTRAILR2 were d
223 gate virus, we found that a soluble protein, osteoprotegerin (OPG), or an OPG/Fc chimeric protein inh
224 of Nuclear factor Kappa B Ligand (RANKL) and osteoprotegerin (OPG), positive and negative regulators
226 d soluble TNF receptor type I (pegTNFRI) and osteoprotegerin (OPG), respectively, affected bony spur
227 tor of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), tartrate-resistant acid phosphata
228 nce with RANKL by systemic administration of osteoprotegerin (OPG), the decoy receptor for (and inhib
229 ceptor activator of NF-kappaB ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alpha (TNF-
230 tor of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), wingless (WNT) 10b, dickkopf-rela
231 recent work showed that daily injections of osteoprotegerin (OPG)-immunoglobulin fragment complex (O
232 predictive markers of bone inflammation-the osteoprotegerin (OPG)-RANK-RANKL system or osteopontin (
245 of nuclear factor-kappa B ligand (RANKL); 2) osteoprotegerin (OPG); 3) interleukin (IL)-6; and 4) tum
246 eine chemokine receptor-5 (CCR5, 59653 C>T), osteoprotegerin (OPG, 245 T>G), and osteopontin (OPN, 70
247 osteopontin [OPN], bone sialoprotein [BSP], osteoprotegerin [OPG] and receptor activator of NF-KB li
248 mentation rate, and bone metabolism markers (osteoprotegerin [OPG], osteocalcin, procollagen type I N
249 hymic epithelial cells by using mice lacking osteoprotegerin or by adding TRANCE (RANKL, Tnfsf11).
250 this system with recombinant decoy receptor, osteoprotegerin, or soluble forms of the receptor activa
251 r for nuclear factor kappa-B ligand (RANKL), osteoprotegerin, osteocalcin, and osteopontin as potenti
253 steoblast markers bone alkaline phosphatase, osteoprotegerin, osteopontin, and matrix Gla protein.
254 e the molecular genetic interactions between osteoprotegerin, osteoprotegerin ligand, and RANK during
259 whereas no inhibition was observed by adding osteoprotegerin, RANK:Fc, TNFalpha, or interleukin-8 or
260 high receptor activator of NF-kappaB ligand/osteoprotegerin (RANKL/OPG) ratio as the primary determi
262 ppaB ligand (RANKL)), the deviation of RANKL/osteoprotegerin ratio in favor of antiosteoclastic activ
263 duced receptor activator of NF-kappaB ligand/osteoprotegerin ratio in Runx2-overexpressing osteoblast
264 kin-6, interleukin-1beta, bone sialoprotein, osteoprotegerin, receptor activator of nuclear factor ka
265 l analyses for the detection of osteocalcin, osteoprotegerin, receptor activator of nuclear factor ka
266 on-gamma, toll-like receptor (TLR)-2, TLR-4, osteoprotegerin, receptor activator of nuclear factor-ka
267 pha1, osteocalcin, alkaline phosphatase, and osteoprotegerin, representative bone-regulating proteins
268 osteoblast differentiation, also stimulates osteoprotegerin secretion to attenuate bone resorption b
270 This enhanced chemotaxis can be abrogated by osteoprotegerin (soluble decoy receptor of RANKL), MIK-G
272 uld explain juvenile Paget's disease because osteoprotegerin suppresses bone turnover by functioning
273 The map locations of 25 genes including osteoprotegerin, syndecan-2, and autotaxin have been ref
274 receptor activator of nuclear factor kappa B/osteoprotegerin system involved in osteoblast-osteoclast
276 ew, we provide an overview of the RANK/RANKL/osteoprotegerin system; we describe its interaction with
278 f receptor activator of NF-kappaB ligand and osteoprotegerin through both PTH-dependent and -independ
279 t's disease for defects in the gene encoding osteoprotegerin (TNFRSF11B) using polymerase-chain-react
280 rationally designed small molecule mimic of osteoprotegerin to inhibit osteoclast formation in vitro
281 lance stemmed from a switch in production of osteoprotegerin to that of receptor activator of NF-kapp
284 Gene expression levels of soluble RANKL, osteoprotegerin, tumor necrosis factor alpha, and M-CSF
285 ator of nuclear factor kappaB ligand (RANKL)/osteoprotegerin, tumor necrosis factor-alpha, and interl
286 eptor-activated nuclear factor-kappaB ligand/osteoprotegerin/tumor necrosis factor-related apoptosis-
289 sitive to the effects of the RANKL inhibitor osteoprotegerin was identified in the activated T cell-c
290 steocalcin, and osteopontin were higher, and osteoprotegerin was lower in females than in males.
291 ctivator of nuclear factor-kappaB ligand and osteoprotegerin) was observed in the ligature group on d
292 Alterations in BM plasma levels of RANKL/osteoprotegerin were confirmed in a mouse model of posti
294 scular cell adhesion molecule 1 (VCAM-1) and osteoprotegerin were significantly associated with incid
295 lasma levels of RANKL and of the ratio RANKL/osteoprotegerin were significantly elevated in patients
296 d macrophage inflammatory protein-1Delta and osteoprotegerin were significantly elevated in patients
298 hereas other genes, such as interleukin-5 or osteoprotegerin, were initially identified as having a r
299 or Tax and the osteoclast inhibitory factor, osteoprotegerin, were protected from osteolytic bone dis