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1 ressive signals that determine the extent of osteoclastogenesis.
2 enhanced Nfatc1 levels, conditions favoring osteoclastogenesis.
3 he periodontal bone loss via upregulation of osteoclastogenesis.
4 induces sustained changes in RANKL-mediated osteoclastogenesis.
5 as evident by reduction in all hallmarks of osteoclastogenesis.
6 regulate RANKL expression and contribute to osteoclastogenesis.
7 ssociated pathology by negatively regulating osteoclastogenesis.
8 r of activated T cells, c1 (NFATc1) to drive osteoclastogenesis.
9 matory osteolysis is governed by exacerbated osteoclastogenesis.
10 g their bioavailability in order to regulate osteoclastogenesis.
11 s unclear how Lrp4 deficiency in OBs impairs osteoclastogenesis.
12 RANKL-driven OC differentiation, also called osteoclastogenesis.
13 motif might counteract OC inhibitors during osteoclastogenesis.
14 lpha13 (Galpha13) is a negative regulator of osteoclastogenesis.
15 es targeting the receptor activation inhibit osteoclastogenesis.
16 evealed unique upregulation of KCa3.1 during osteoclastogenesis.
17 from monocytes and JNJ7777120 decreased the osteoclastogenesis.
18 mmatory and E2F1 target genes and downstream osteoclastogenesis.
19 elated receptor alpha (ERRalpha) to regulate osteoclastogenesis.
20 on as targets of Wnt signaling in regulating osteoclastogenesis.
21 tor of nuclear factor kappaB (RANK)-mediated osteoclastogenesis.
22 ently addressed, with focus on their role in osteoclastogenesis.
23 macrophage growth factors and regulators of osteoclastogenesis.
24 ed TNFalpha and RANKL signaling and enhanced osteoclastogenesis.
25 important role for epigenetic mechanisms in osteoclastogenesis.
26 lating gene pathways required for proficient osteoclastogenesis.
27 mportance of IRF8 as a negative regulator of osteoclastogenesis.
28 played significant expression changes during osteoclastogenesis.
29 role in regulating OPG-RANKL interaction and osteoclastogenesis.
30 on in vitro, while simultaneously inhibiting osteoclastogenesis.
31 on of the Th17/T-regulatory cell balance and osteoclastogenesis.
32 mic, calcineurin-dependent 1 (NFATC1) during osteoclastogenesis.
33 hy altered BMSC phenotype and influenced BMM osteoclastogenesis.
34 : increased osteoblastogenesis and decreased osteoclastogenesis.
35 gesting that M1 macrophages can downregulate osteoclastogenesis.
36 BM) cells to the osteoclast (OC) lineage for osteoclastogenesis.
37 tor activator of NF-kappaB ligand needed for osteoclastogenesis.
38 also abrogated M1-mediated downregulation of osteoclastogenesis.
39 -gamma or IL-12 in M1-mediated inhibition of osteoclastogenesis.
40 ers our understanding of how HS functions in osteoclastogenesis.
41 h in vitro and at H3NT cleavage sites during osteoclastogenesis.
42 ned a heat-labile factor that increased BMMs osteoclastogenesis.
43 ut not M0 or M2, was demonstrated to inhibit osteoclastogenesis.
44 is an intrinsic inhibitor for RANKL-mediated osteoclastogenesis.
45 ts of M1 and M2 macrophages on RANKL-induced osteoclastogenesis.
46 n stromal cell activation, angiogenesis, and osteoclastogenesis.
47 ma-KO) mice lost the ability to downregulate osteoclastogenesis.
48 tion of inflammatory monocytes as well as in osteoclastogenesis.
49 KL), which plays a central role in promoting osteoclastogenesis.
50 icantly, differentially expressed throughout osteoclastogenesis.
51 s gene expression by histone methylation, in osteoclastogenesis.
52 onality including the inhibititory effect on osteoclastogenesis.
53 ng ligand (TRAIL) has been shown to increase osteoclastogenesis.
54 d1 and Id2, which are negative regulators of osteoclastogenesis.
55 last-derived EVs are paracrine regulators of osteoclastogenesis.
56 n, interleukin (IL)-3 inhibits RANKL-induced osteoclastogenesis.
57 STAT5 overexpression inhibited RANKL-induced osteoclastogenesis.
58 eased by osteoclasts are novel regulators of osteoclastogenesis.
59 ss the effect of CFZ on PTH action to induce osteoclastogenesis.
60 uted, at least in part, by the inhibition of osteoclastogenesis.
61 mechanisms linked to reduced RANKL-mediated osteoclastogenesis.
62 imiting regulatory loop to prevent excessive osteoclastogenesis.
63 iminished CIA pathology and local markers of osteoclastogenesis.
64 he primary effect of Col6a2 deficiency is on osteoclastogenesis.
65 teopetrosis in mice as a result of defective osteoclastogenesis.
66 rsors in bone marrow, resulting in decreased osteoclastogenesis.
67 nchymal compartment of dental pulp attenuate osteoclastogenesis.
68 ly(ADP-ribose) polymerase 1, an inhibitor of osteoclastogenesis.
69 B and Ca(2+)/NFATc1 signaling pathway during osteoclastogenesis.
70 ion in human cells correlates with excessive osteoclastogenesis.
71 eas ABCs slightly but significantly promoted osteoclastogenesis.
72 er linking Dim1 to the dynamic regulation of osteoclastogenesis.
73 mechanisms governing gene expression during osteoclastogenesis.
74 ed cells exhibited a diminished capacity for osteoclastogenesis.
75 rats showed enhanced osteoblastogenesis and osteoclastogenesis.
76 sis identifies a MYC-NFAT axis important for osteoclastogenesis.
77 mild osteopetrosis due to the inhibition of osteoclastogenesis.
78 tes also produce IFN-beta as an inhibitor of osteoclastogenesis.
79 tabolic requirement and bioenergetics during osteoclastogenesis.
80 roduction and OXPHOS is necessary for normal osteoclastogenesis.
81 alleviating bone cancer pain by suppressing osteoclastogenesis.
82 BMM-OB cocultures diminishes the increase of osteoclastogenesis.
83 6 h of culture only was sufficient to reduce osteoclastogenesis.
84 vates, while osteoprotegerin (OPG) inhibits, osteoclastogenesis.
85 vitamin D(3) and parathyroid hormone-induced osteoclastogenesis.
86 ing to the actions of TNFalpha and NOTCH2 on osteoclastogenesis.
87 amplifying the NOTCH2-dependent induction of osteoclastogenesis.
88 ctivator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis.
89 tophagic mechanism underlying JNK1-regulated osteoclastogenesis.
90 hen oxygen is abundant, is also critical for osteoclastogenesis.
91 erentiation, suggesting ACVR1 is involved in osteoclastogenesis.
92 fects by suppressing NF-kappaB signaling and osteoclastogenesis.
93 lammatory pathways, phagocytic function, and osteoclastogenesis.
94 Th17) cells increased initially and promoted osteoclastogenesis.
95 n D(3) (D3) and parathyroid hormone (PTH) on osteoclastogenesis.
96 rough suppression of NF-kappaB signaling and osteoclastogenesis.
97 hondral bone formation, but notably enhanced osteoclastogenesis.
98 st-progenitor survival, leading to increased osteoclastogenesis.
99 ent subsequent alveolar bone destruction and osteoclastogenesis.
100 tor of nuclear factor-kappaB ligand-mediated osteoclastogenesis.
102 mplant-bone interface may indirectly control osteoclastogenesis and bone accrual around endosseous im
104 ligand (RANKL)-evoked signaling; its role in osteoclastogenesis and bone homeostasis, however, remain
105 PTHrP, 1,25-Dyhydroxyvitamin D (1,25(OH)2D), osteoclastogenesis and bone loss in response to the high
106 activation of mTORC1 corrected the enhanced osteoclastogenesis and bone loss in Slc7a5-deficient mic
108 indings identify galectins as new players in osteoclastogenesis and bone remodeling, and highlight a
109 osteoporosis, associated with an increase in osteoclastogenesis and bone resorption and an increase i
110 s and cytokines including RANKL and BMPs, in osteoclastogenesis and bone resorption by ablating p38al
111 dition of a PKCzeta pseudosubstrate restores osteoclastogenesis and bone resorption of Phlpp1-deficie
112 fore, our data demonstrated that XN inhibits osteoclastogenesis and bone resorption through RANK/TRAF
114 ficantly inhibited titanium particle-induced osteoclastogenesis and calvarial osteolysis in vitro, ex
115 mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinates osteoclastogenesis an
116 thus acts as an inhibitory switch to control osteoclastogenesis and cytokine production and may be a
117 hibited impaired fracture healing, disturbed osteoclastogenesis and delayed cartilage-to-bone transfo
118 ed the expression of different regulators of osteoclastogenesis and discovered that NEMO deletion lea
119 d human and mouse breast cancer cell-induced osteoclastogenesis and exacerbated osteolysis, and these
120 uced by TcREG is required for suppression of osteoclastogenesis and for degradation of TNFR-associate
121 d progenitor cell differentiation, promoting osteoclastogenesis and increasing adipogenesis while sup
122 diated by RBP-J/NFATc1-miR182 in TNF-induced osteoclastogenesis and inflammatory bone resorption.
123 suppression of alternative NF-kappaB-induced osteoclastogenesis and is down-modulated in response to
124 in macrophage/osteoclast lineage suppresses osteoclastogenesis and leads to the osteopetrotic phenot
125 y, C/EBPalpha knockdown drastically inhibits osteoclastogenesis and markedly abrogates the expression
128 roles in bone homeostasis by regulating both osteoclastogenesis and osteoblastogenesis, and they serv
131 ct of periodontal homeostasis as they affect osteoclastogenesis and osteoclast function, either by di
132 study the direct impact of live S. aureus on osteoclastogenesis and osteoclast resorption activity.
134 ), a potent inhibitor of osteoclast activity/osteoclastogenesis and promoter of osteogenic lineage, w
135 esis whereas its deletion partially restored osteoclastogenesis and reversed the phenotype of Tak1 de
136 ent studies show the involvement of Foxo3 in osteoclastogenesis and rheumatoid arthritis, which promp
137 ligand (RANKL) and sclerostin (SOST) levels, osteoclastogenesis and serum proteomics were also analyz
138 rived and de novo synthesized GSLs influence osteoclastogenesis and suggest that NB-DNJ may reduce pa
139 partment have an innate ability to attenuate osteoclastogenesis and that this innate ability may be r
140 , the HCS mutation enhances TNFalpha-induced osteoclastogenesis and the inflammatory bone-resorptive
143 fragments of type I collagen (CTX), elevated osteoclastogenesis, and increased osteoclasts in bone.
146 robiome, as shown by increased inflammation, osteoclastogenesis, and periodontal bone loss when trans
147 gain-of-function inhibits Akt activation and osteoclastogenesis, and protects mice from pathological
148 , IRE1alpha was transiently activated during osteoclastogenesis, and suppression of the IRE1alpha/XBP
150 ross talk between A2AR and RANK signaling in osteoclastogenesis, and uncover an unrecognized pathophy
151 IVVY(538) (IVVY) motif that is essential for osteoclastogenesis, and we found that mutation of the IV
156 vated osteoclast numbers and size in ex vivo osteoclastogenesis assays, accompanied by enhanced expre
157 eoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast
158 3 (CCR3) is dramatically upregulated during osteoclastogenesis, but the role of CCR3 in osteoclast f
159 ely, this study revealed that JNK1 regulated osteoclastogenesis by activating Bcl-2-Beclin1-autophagy
160 le IL-3-mediated inhibition of RANKL-induced osteoclastogenesis by activating Id genes and their asso
161 xpression in multiple myeloma cells promoted osteoclastogenesis by activating TRAF6-dependent signali
162 verexpression of RelB restores RANKL-induced osteoclastogenesis by activation of Akt/Cot/IKKalpha-ind
164 tly that NUMB-like (NUMBL) protein modulates osteoclastogenesis by down regulating NF-kappaB activati
165 Hypoxia augments inflammatory responses and osteoclastogenesis by incompletely understood mechanisms
167 ment in terms of macrophage polarization and osteoclastogenesis by modulating tumor necrosis factor (
168 , the complex I inhibitor Rotenone decreased osteoclastogenesis by promoting osteoclast progenitor ap
169 novel mechanism through which Shp2 regulates osteoclastogenesis by promoting preosteoclast fusion.
170 We found that TRAF3 limits RANKL-induced osteoclastogenesis by suppressing canonical and noncanon
171 ogenous regulator of NF-kappaB signaling and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis
173 hages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulated conditions
174 Most importantly, the proliferation and osteoclastogenesis defects observed in the absence of PL
175 K/TNFR signaling and allowing fine tuning of osteoclastogenesis during bone homeostasis and under inf
176 utions of BM-resident and circulating OCP to osteoclastogenesis during homeostasis and fracture repai
177 fine the role that circulating cells play in osteoclastogenesis during homeostasis, we parabiosed TRA
178 on and downstream gene transcription driving osteoclastogenesis during skeletal remodeling and pathol
179 more, the inhibitory effect of miR-142-3p on osteoclastogenesis extended to the conversion of a third
181 bone mass at three ages and greater in vitro osteoclastogenesis from Fndc5-transgenic bone marrow pro
182 ate miR-142-3p to be a negative regulator of osteoclastogenesis from the 3 main precursor cell types:
186 have functional implications in homeostasis, osteoclastogenesis, immune functions, tumor metastasis a
187 4c) that selectively inhibited RANKL-induced osteoclastogenesis in a dose-dependent manner, without a
192 oid deletion of Commd1 resulted in increased osteoclastogenesis in arthritis and inflammatory osteoly
193 uclear factor- kappab ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived macrophages (B
194 es, leading to the increase of RANKL-induced osteoclastogenesis in bone marrow-derived macrophages.
195 ctivator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis in both a contact-dependent and -inde
196 ctopic expression of rat C/EBPalpha restores osteoclastogenesis in C/EBPalpha-depleted MBM cells.
197 that C/EBPalpha overexpression might rescue osteoclastogenesis in cells expressing the mutated IVVY
198 e expression analyses supported up-regulated osteoclastogenesis in D2J mice and increased osteoclast
199 tch co-cultures demonstrated an induction of osteoclastogenesis in D2J osteoblasts co-cultured with o
205 ly, in vitro N2-NRR Ab reduced RANKL-induced osteoclastogenesis in PAR1 KO cells to WT levels without
206 We found that N2-NRR Ab reduced TNF-induced osteoclastogenesis in PAR1 KO mice to WT levels without
208 rsors from Sirt3-/- mice underwent increased osteoclastogenesis in response to receptor activator of
209 PAR1 KO myeloid cells demonstrated enhanced osteoclastogenesis in response to receptor activator of
211 ion of Hes1 prevented the TNFalpha effect on osteoclastogenesis in the context of the Notch2(tm1.1Eca
214 ein Beclin1 rescued autophagy deficiency and osteoclastogenesis in the presence of a JNK inhibitor (S
215 ession of RelB fails to rescue RANKL-induced osteoclastogenesis in the presence of p100DeltaGRR, whic
216 Additionally, ASCs inhibited RANKL-induced osteoclastogenesis in the presence of proinflammatory cy
218 pression via CaMKIV/CREB during inflammatory osteoclastogenesis in the presence of TNF, corroborating
221 g as K270A substitution results in exuberant osteoclastogenesis in vitro and murine inflammatory oste
222 atory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanis
227 fy LOX as a novel regulator of NFATc1-driven osteoclastogenesis, independent of RANK ligand, which di
229 /TAK1-deficient cells significantly restored osteoclastogenesis, indicating that activation of NF-kap
232 netic silencing of the negative regulator of osteoclastogenesis Irf8 by DNA methylation is required f
233 norhabditis elegans, the cell fusion step in osteoclastogenesis is controlled by phosphatidylserine-r
236 dherent bone marrow stromal cells (BMSCs) in osteoclastogenesis is influenced by surface topography.
237 scovered that the principal H3NT protease of osteoclastogenesis is matrix metalloproteinase 9 (MMP-9)
240 clear factor-kB (RANK), the key regulator of osteoclastogenesis, is frequently expressed in primary l
241 Because both isoforms are activated during osteoclastogenesis, it is plausible that PLCgamma1 modul
242 ceptor activator of NF-kappaB ligand-induced osteoclastogenesis, leading to enhanced resorption pit f
243 unoregulatory effects on osteoblastogenesis, osteoclastogenesis, marrow T-cell hematopoiesis, and ext
244 osteoclast-like cells in chemically defined osteoclastogenesis medium with 20 ng/mL of macrophage co
245 y reveals a metabolite-mediated mechanism of osteoclastogenesis modulation that contributes to bone d
246 of the gene encoding the master regulator of osteoclastogenesis nuclear factor of activated T cells c
248 , and subsequently RANKL and M-CSF-dependent osteoclastogenesis of murine bone marrow monocytes.
249 he STAT3 signaling pathway and restrains the osteoclastogenesis of rat bone-marrow macrophages (BMMs)
251 f uninfected mature osteoclasts and promoted osteoclastogenesis of the uninfected precursors at the s
253 vent osteoporosis and fractures by mediating osteoclastogenesis, osteoblastogenesis, and bone collage
254 abundant prenylflavonoid from hops plant, on osteoclastogenesis, osteoclast resorption, and RANKL-ind
255 steocytic RANKL is known to be important for osteoclastogenesis, our data suggest that osteocytes als
256 risingly, despite being expressed throughout osteoclastogenesis, PLCgamma1 did not compensate for PLC
258 s a results, XN suppressed the expression of osteoclastogenesis-related marker genes, including CtsK,
262 echanism by which osteoblastic Lrp4 controls osteoclastogenesis, reveal a cross talk between A2AR and
263 olved in periodontal tissue inflammation and osteoclastogenesis-such as interleukin 6, monocyte-chemo
264 ciency prevented IL-3-mediated inhibition of osteoclastogenesis, suggesting a key role of STAT5 in IL
266 echanism of epigenetic IRF8 silencing during osteoclastogenesis that likely works cooperatively with
267 her demonstrate that Hdac3 deficiency limits osteoclastogenesis, the number of nuclei per cell and bo
268 veolar bone surrounding teeth by influencing osteoclastogenesis through IL-17A and receptor activator
269 nvironment, and PD-L1 promoted RANKL-induced osteoclastogenesis through JNK activation and CCL2 secre
270 triggers skeletal colonization by activating osteoclastogenesis through osteoblast production of RANK
271 3 is a master endogenous negative switch for osteoclastogenesis through regulation of the RhoA/Akt/GS
272 cts as a proinflammatory mediator increasing osteoclastogenesis through the down-regulation of COX2.
273 ion 5 (STAT5) by IL-3 inhibits RANKL-induced osteoclastogenesis through the induction of the expressi
274 ing exerts protective effects by suppressing osteoclastogenesis through Wnt signaling, but little is
276 ear factor kappa-Beta ligand (RANKL) induced osteoclastogenesis to model MGC formation, here we repor
279 In this study, we examined the role of OA in osteoclastogenesis, using mice with a nonsense mutation
281 genes to RANKL stimulation and thus inhibits osteoclastogenesis via endogenous IFN-beta-mediated feed
282 demonstrated that Mincle activation triggers osteoclastogenesis via ITAM-based calcium signaling path
288 that corresponded to mouse AtoMs, and human osteoclastogenesis was inhibited by the FoxM1 inhibitor
289 ed to osteoclast formation in vitro, because osteoclastogenesis was markedly reduced by IL-8-specific
290 part, to be cell autonomous because enhanced osteoclastogenesis was seen in highly purified PAR1 KO o
291 t and less toxic inhibitors of RANKL-induced osteoclastogenesis, we synthesized a focused set of comp
293 dingly, forced expression of Numbl abrogated osteoclastogenesis whereas its deletion partially restor
294 expression of NFATc1, a master regulator of osteoclastogenesis, whereas IL-12 increased the apoptosi
295 ogenesis and pro-catabolic effects enhancing osteoclastogenesis, which drive bone loss in health.
296 s with D3 and PTH signaling, causing massive osteoclastogenesis, which may explain the rapid bone los
297 causes bone loss by enhancing Itch-mediated osteoclastogenesis, which was prevented by Zoledronic ac
298 he Notch2(tm1.1Ecan) mice displayed enhanced osteoclastogenesis, which was suppressed by Notch2 ASOs.
299 d (RANKL) constitutes the master mediator of osteoclastogenesis, while its pharmaceutical inhibition
300 RBP-J silencing in the mutant cells rescued osteoclastogenesis with C/EBPalpha or c-Fos overexpressi