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1 st-progenitor survival, leading to increased osteoclastogenesis.
2 is an intrinsic inhibitor for RANKL-mediated osteoclastogenesis.
3 ts of M1 and M2 macrophages on RANKL-induced osteoclastogenesis.
4 ma-KO) mice lost the ability to downregulate osteoclastogenesis.
5 tion of inflammatory monocytes as well as in osteoclastogenesis.
6 KL), which plays a central role in promoting osteoclastogenesis.
7 induces sustained changes in RANKL-mediated osteoclastogenesis.
8 icantly, differentially expressed throughout osteoclastogenesis.
9 s gene expression by histone methylation, in osteoclastogenesis.
10 onality including the inhibititory effect on osteoclastogenesis.
11 ng ligand (TRAIL) has been shown to increase osteoclastogenesis.
12 as evident by reduction in all hallmarks of osteoclastogenesis.
13 d1 and Id2, which are negative regulators of osteoclastogenesis.
14 last-derived EVs are paracrine regulators of osteoclastogenesis.
15 n, interleukin (IL)-3 inhibits RANKL-induced osteoclastogenesis.
16 STAT5 overexpression inhibited RANKL-induced osteoclastogenesis.
17 eased by osteoclasts are novel regulators of osteoclastogenesis.
18 ss the effect of CFZ on PTH action to induce osteoclastogenesis.
19 mechanisms linked to reduced RANKL-mediated osteoclastogenesis.
20 imiting regulatory loop to prevent excessive osteoclastogenesis.
21 iminished CIA pathology and local markers of osteoclastogenesis.
22 teopetrosis in mice as a result of defective osteoclastogenesis.
23 rsors in bone marrow, resulting in decreased osteoclastogenesis.
24 nchymal compartment of dental pulp attenuate osteoclastogenesis.
25 ly(ADP-ribose) polymerase 1, an inhibitor of osteoclastogenesis.
26 regulate RANKL expression and contribute to osteoclastogenesis.
27 B and Ca(2+)/NFATc1 signaling pathway during osteoclastogenesis.
28 ion in human cells correlates with excessive osteoclastogenesis.
29 eas ABCs slightly but significantly promoted osteoclastogenesis.
30 er linking Dim1 to the dynamic regulation of osteoclastogenesis.
31 mechanisms governing gene expression during osteoclastogenesis.
32 ed cells exhibited a diminished capacity for osteoclastogenesis.
33 ent subsequent alveolar bone destruction and osteoclastogenesis.
34 rats showed enhanced osteoblastogenesis and osteoclastogenesis.
35 sis identifies a MYC-NFAT axis important for osteoclastogenesis.
36 mild osteopetrosis due to the inhibition of osteoclastogenesis.
37 tes also produce IFN-beta as an inhibitor of osteoclastogenesis.
38 costimulation of RANKL or TNF-alpha-induced osteoclastogenesis.
39 ssociated pathology by negatively regulating osteoclastogenesis.
40 g to acetylated histones strongly suppresses osteoclastogenesis.
41 and the expression of molecules involved in osteoclastogenesis.
42 nd significantly impaired RANKL/CSF1-induced osteoclastogenesis.
43 osteoclast progenitors show no difference in osteoclastogenesis.
44 of Itch in Itch(-/-) cells rescued increased osteoclastogenesis.
45 that TAK1 is indispensable to RANKL-induced osteoclastogenesis.
46 uced interleukin-6, a molecule that promotes osteoclastogenesis.
47 r of activated T cells, c1 (NFATc1) to drive osteoclastogenesis.
48 with tetramethylsilane or proadifen reduced osteoclastogenesis.
49 activity, suggesting potential reduction of osteoclastogenesis.
50 new RANKL target gene that is induced during osteoclastogenesis.
51 g their bioavailability in order to regulate osteoclastogenesis.
52 explanation for AMPK-mediated inhibition of osteoclastogenesis.
53 nction antagonistically in the regulation of osteoclastogenesis.
54 nvolved in inflammation and is essential for osteoclastogenesis.
55 on, coinciding with a reduction in RANKL and osteoclastogenesis.
56 nsequence of TAK1 deletion in RANKL-mediated osteoclastogenesis.
57 No differences were seen with RANKL-induced osteoclastogenesis.
58 dynamic range of the CRAC channel regulating osteoclastogenesis.
59 ed inflammatory response of macrophages, and osteoclastogenesis.
60 s unclear how Lrp4 deficiency in OBs impairs osteoclastogenesis.
61 RANKL-driven OC differentiation, also called osteoclastogenesis.
62 motif might counteract OC inhibitors during osteoclastogenesis.
63 lpha13 (Galpha13) is a negative regulator of osteoclastogenesis.
64 tor of nuclear factor-kappaB ligand-mediated osteoclastogenesis.
65 es targeting the receptor activation inhibit osteoclastogenesis.
66 evealed unique upregulation of KCa3.1 during osteoclastogenesis.
67 from monocytes and JNJ7777120 decreased the osteoclastogenesis.
68 mmatory and E2F1 target genes and downstream osteoclastogenesis.
69 elated receptor alpha (ERRalpha) to regulate osteoclastogenesis.
70 on as targets of Wnt signaling in regulating osteoclastogenesis.
71 tor of nuclear factor kappaB (RANK)-mediated osteoclastogenesis.
72 ently addressed, with focus on their role in osteoclastogenesis.
73 macrophage growth factors and regulators of osteoclastogenesis.
74 ed TNFalpha and RANKL signaling and enhanced osteoclastogenesis.
75 important role for epigenetic mechanisms in osteoclastogenesis.
76 lating gene pathways required for proficient osteoclastogenesis.
77 mportance of IRF8 as a negative regulator of osteoclastogenesis.
78 played significant expression changes during osteoclastogenesis.
79 role in regulating OPG-RANKL interaction and osteoclastogenesis.
80 on of the Th17/T-regulatory cell balance and osteoclastogenesis.
81 enhanced Nfatc1 levels, conditions favoring osteoclastogenesis.
82 mic, calcineurin-dependent 1 (NFATC1) during osteoclastogenesis.
83 hy altered BMSC phenotype and influenced BMM osteoclastogenesis.
84 : increased osteoblastogenesis and decreased osteoclastogenesis.
85 gesting that M1 macrophages can downregulate osteoclastogenesis.
86 BM) cells to the osteoclast (OC) lineage for osteoclastogenesis.
87 he periodontal bone loss via upregulation of osteoclastogenesis.
88 tor activator of NF-kappaB ligand needed for osteoclastogenesis.
89 also abrogated M1-mediated downregulation of osteoclastogenesis.
90 -gamma or IL-12 in M1-mediated inhibition of osteoclastogenesis.
91 ers our understanding of how HS functions in osteoclastogenesis.
92 h in vitro and at H3NT cleavage sites during osteoclastogenesis.
93 ned a heat-labile factor that increased BMMs osteoclastogenesis.
94 ut not M0 or M2, was demonstrated to inhibit osteoclastogenesis.
95 of NF-kappaB (RANK) plays a critical role in osteoclastogenesis, an essential process for the initiat
96 ecular mechanisms mediating the up-regulated osteoclastogenesis and alveolar bone loss in SPF mice co
98 mplant-bone interface may indirectly control osteoclastogenesis and bone accrual around endosseous im
100 ligand (RANKL)-evoked signaling; its role in osteoclastogenesis and bone homeostasis, however, remain
102 indings identify galectins as new players in osteoclastogenesis and bone remodeling, and highlight a
103 osteoporosis, associated with an increase in osteoclastogenesis and bone resorption and an increase i
104 s and cytokines including RANKL and BMPs, in osteoclastogenesis and bone resorption by ablating p38al
105 fore, our data demonstrated that XN inhibits osteoclastogenesis and bone resorption through RANK/TRAF
108 ficantly inhibited titanium particle-induced osteoclastogenesis and calvarial osteolysis in vitro, ex
109 mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinates osteoclastogenesis an
110 thus acts as an inhibitory switch to control osteoclastogenesis and cytokine production and may be a
112 hibited impaired fracture healing, disturbed osteoclastogenesis and delayed cartilage-to-bone transfo
113 ed the expression of different regulators of osteoclastogenesis and discovered that NEMO deletion lea
114 demonstrated markedly higher propensity for osteoclastogenesis and enhanced bone degradation capacit
115 d human and mouse breast cancer cell-induced osteoclastogenesis and exacerbated osteolysis, and these
116 uced by TcREG is required for suppression of osteoclastogenesis and for degradation of TNFR-associate
118 d progenitor cell differentiation, promoting osteoclastogenesis and increasing adipogenesis while sup
119 suppression of alternative NF-kappaB-induced osteoclastogenesis and is down-modulated in response to
120 y, C/EBPalpha knockdown drastically inhibits osteoclastogenesis and markedly abrogates the expression
122 roles in bone homeostasis by regulating both osteoclastogenesis and osteoblastogenesis, and they serv
125 ct of periodontal homeostasis as they affect osteoclastogenesis and osteoclast function, either by di
126 study the direct impact of live S. aureus on osteoclastogenesis and osteoclast resorption activity.
127 ), a potent inhibitor of osteoclast activity/osteoclastogenesis and promoter of osteogenic lineage, w
128 esis whereas its deletion partially restored osteoclastogenesis and reversed the phenotype of Tak1 de
130 rived and de novo synthesized GSLs influence osteoclastogenesis and suggest that NB-DNJ may reduce pa
131 egulatory circuit of RANKL-RANK signaling in osteoclastogenesis and that the augmentation of Pax6 mig
132 partment have an innate ability to attenuate osteoclastogenesis and that this innate ability may be r
134 BPalpha(-/-) newborn mice exhibited impaired osteoclastogenesis, and a severe osteopetrotic phenotype
135 as a significant source of RANKL to support osteoclastogenesis, and in secreting the bone formation
137 fragments of type I collagen (CTX), elevated osteoclastogenesis, and increased osteoclasts in bone.
139 Expression of LPA1 was up-regulated during osteoclastogenesis, and LPA1 antagonists (Ki16425, Debio
141 teoclastogenesis-related marker genes during osteoclastogenesis, and prevented osteoclastic bone reso
142 gain-of-function inhibits Akt activation and osteoclastogenesis, and protects mice from pathological
143 ce of an I-BET151-inhibited MYC-NFAT axis in osteoclastogenesis, and suggest targeting epigenetic chr
144 , IRE1alpha was transiently activated during osteoclastogenesis, and suppression of the IRE1alpha/XBP
145 ross talk between A2AR and RANK signaling in osteoclastogenesis, and uncover an unrecognized pathophy
146 IVVY(538) (IVVY) motif that is essential for osteoclastogenesis, and we found that mutation of the IV
147 whom talin is deleted late in the course of osteoclastogenesis are substantially protected from ovar
149 9 (Mmp9) and Mmp13 and enhanced growth plate osteoclastogenesis, as well as increased sensitivity to
152 iR-34a as a novel and critical suppressor of osteoclastogenesis, bone resorption and the bone metasta
153 eoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast
156 infiltration and expression of molecules for osteoclastogenesis, but simvastatin significantly modula
157 FAT) are transcription factors that regulate osteoclastogenesis, but their function in osteoblasts is
158 changes in chromatin state are important for osteoclastogenesis, but these epigenetic mechanisms are
159 nia with normal bone formation and increased osteoclastogenesis, but this phenotype was not associate
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
163 tly that NUMB-like (NUMBL) protein modulates osteoclastogenesis by down regulating NF-kappaB activati
164 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 novel mechanism through which Shp2 regulates osteoclastogenesis by promoting preosteoclast fusion.
169 nally, constitutively activated Akt enhanced osteoclastogenesis by RelB-induced Cot, and a dominant-n
171 We found that TRAF3 limits RANKL-induced osteoclastogenesis by suppressing canonical and noncanon
172 monstrate that Dim1 attenuates RANKL-induced osteoclastogenesis by targeting NFATc1 signaling pathway
173 ogenous regulator of NF-kappaB signaling and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis
174 signaling in prostate cancer cells increases osteoclastogenesis by up-regulating osteoclastogenic gen
175 hages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulated conditions
177 Vps35 gene in mice promoted hyperresorptive osteoclastogenesis, decreased bone formation, and caused
178 Most importantly, the proliferation and osteoclastogenesis defects observed in the absence of PL
179 t their activity but rather causes increased osteoclastogenesis due to insufficient production of ost
180 K/TNFR signaling and allowing fine tuning of osteoclastogenesis during bone homeostasis and under inf
181 show how a discrete miRNA network regulates osteoclastogenesis during breast cancer bone metastasis.
182 on and downstream gene transcription driving osteoclastogenesis during skeletal remodeling and pathol
183 more, the inhibitory effect of miR-142-3p on osteoclastogenesis extended to the conversion of a third
185 ceptor activator of NF-kappaB ligand-induced osteoclastogenesis from mouse or human osteoclast precur
186 Their inhibitory effects on RANKL-induced osteoclastogenesis from RAW264.7 cells were evaluated by
187 ate miR-142-3p to be a negative regulator of osteoclastogenesis from the 3 main precursor cell types:
190 have functional implications in homeostasis, osteoclastogenesis, immune functions, tumor metastasis a
191 ese findings indicate that Tak1 functions in osteoclastogenesis in a cell-autonomous manner and in os
195 oid deletion of Commd1 resulted in increased osteoclastogenesis in arthritis and inflammatory osteoly
196 iators (e.g., IL-17 and RANKL) and decreased osteoclastogenesis in bone biopsy specimens, as compared
197 uclear factor- kappab ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived macrophages (B
198 es, leading to the increase of RANKL-induced osteoclastogenesis in bone marrow-derived macrophages.
199 ctivator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis in both a contact-dependent and -inde
201 ctopic expression of rat C/EBPalpha restores osteoclastogenesis in C/EBPalpha-depleted MBM cells.
202 t B-subunit and microfilaments and inhibited osteoclastogenesis in cell culture with IC50s of about 1
203 that C/EBPalpha overexpression might rescue osteoclastogenesis in cells expressing the mutated IVVY
204 e expression analyses supported up-regulated osteoclastogenesis in D2J mice and increased osteoclast
205 tch co-cultures demonstrated an induction of osteoclastogenesis in D2J osteoblasts co-cultured with o
209 rsors from Sirt3-/- mice underwent increased osteoclastogenesis in response to receptor activator of
213 ession of RelB fails to rescue RANKL-induced osteoclastogenesis in the presence of p100DeltaGRR, whic
214 Additionally, ASCs inhibited RANKL-induced osteoclastogenesis in the presence of proinflammatory cy
216 pression via CaMKIV/CREB during inflammatory osteoclastogenesis in the presence of TNF, corroborating
219 osumab to neutralize the effects of RANKL on osteoclastogenesis in vitro, but also potently stimulate
220 atory and others has shown that MYC promotes osteoclastogenesis in vitro, but the underlying mechanis
225 one morphogenetic protein (BMP) signaling in osteoclastogenesis in vivo, we eliminated BMPRII in oste
227 showed a markedly reduced ability to support osteoclastogenesis in wild-type bone marrow macrophages,
229 fy LOX as a novel regulator of NFATc1-driven osteoclastogenesis, independent of RANK ligand, which di
231 /TAK1-deficient cells significantly restored osteoclastogenesis, indicating that activation of NF-kap
232 The gel-embedded MLO-Y4 cells inhibited the osteoclastogenesis induced by 1,25(OH)2D3 without modula
236 netic silencing of the negative regulator of osteoclastogenesis Irf8 by DNA methylation is required f
238 norhabditis elegans, the cell fusion step in osteoclastogenesis is controlled by phosphatidylserine-r
241 dherent bone marrow stromal cells (BMSCs) in osteoclastogenesis is influenced by surface topography.
242 scovered that the principal H3NT protease of osteoclastogenesis is matrix metalloproteinase 9 (MMP-9)
245 clear factor-kB (RANK), the key regulator of osteoclastogenesis, is frequently expressed in primary l
246 Because both isoforms are activated during osteoclastogenesis, it is plausible that PLCgamma1 modul
247 ceptor activator of NF-kappaB ligand-induced osteoclastogenesis, leading to enhanced resorption pit f
248 unoregulatory effects on osteoblastogenesis, osteoclastogenesis, marrow T-cell hematopoiesis, and ext
249 osteoclast-like cells in chemically defined osteoclastogenesis medium with 20 ng/mL of macrophage co
250 y reveals a metabolite-mediated mechanism of osteoclastogenesis modulation that contributes to bone d
251 erentiation and mineralization and stimulate osteoclastogenesis more potently in the osteoblast-osteo
252 of the gene encoding the master regulator of osteoclastogenesis nuclear factor of activated T cells c
253 ed bone formation and increased OB-dependent osteoclastogenesis (OC-genesis), and deletion in hematop
257 f uninfected mature osteoclasts and promoted osteoclastogenesis of the uninfected precursors at the s
259 vent osteoporosis and fractures by mediating osteoclastogenesis, osteoblastogenesis, and bone collage
260 abundant prenylflavonoid from hops plant, on osteoclastogenesis, osteoclast resorption, and RANKL-ind
261 steocytic RANKL is known to be important for osteoclastogenesis, our data suggest that osteocytes als
262 risingly, despite being expressed throughout osteoclastogenesis, PLCgamma1 did not compensate for PLC
263 eukin-6 and -1beta) and proteins involved in osteoclastogenesis (receptor activator of nuclear factor
264 lopeptidase 13, etc.) and a key regulator of osteoclastogenesis (receptor activator of nuclear factor
265 esis is controlled by osteocytes; osteocytic osteoclastogenesis regulatory molecules are largely unkn
266 in the nucleus, suppressed the expression of osteoclastogenesis-related marker genes during osteoclas
267 s a results, XN suppressed the expression of osteoclastogenesis-related marker genes, including CtsK,
269 chymal stem cells (BMMSCs) and activation of osteoclastogenesis, resulting in increased bone mass.
270 echanism by which osteoblastic Lrp4 controls osteoclastogenesis, reveal a cross talk between A2AR and
271 olved in periodontal tissue inflammation and osteoclastogenesis-such as interleukin 6, monocyte-chemo
272 ciency prevented IL-3-mediated inhibition of osteoclastogenesis, suggesting a key role of STAT5 in IL
273 sion of multiple miRNAs downregulated during osteoclastogenesis suppresses osteoclast differentiation
275 echanism of epigenetic IRF8 silencing during osteoclastogenesis that likely works cooperatively with
276 veolar bone surrounding teeth by influencing osteoclastogenesis through IL-17A and receptor activator
277 ivator of NF-kappaB ligand (RANKL) regulates osteoclastogenesis through its receptor, RANK, and the s
278 triggers skeletal colonization by activating osteoclastogenesis through osteoblast production of RANK
280 3 is a master endogenous negative switch for osteoclastogenesis through regulation of the RhoA/Akt/GS
281 ion 5 (STAT5) by IL-3 inhibits RANKL-induced osteoclastogenesis through the induction of the expressi
286 In this study, we examined the role of OA in osteoclastogenesis, using mice with a nonsense mutation
289 tive influence of canonical Wnt signaling on osteoclastogenesis was confirmed in vitro and through th
290 ed to osteoclast formation in vitro, because osteoclastogenesis was markedly reduced by IL-8-specific
291 e demonstrated that bone marrow cell-induced osteoclastogenesis was reduced in Lpar1(-/-) mice but no
293 one-related protein (PTHrP), known to induce osteoclastogenesis, were also observed in alphavbeta6-ex
295 dingly, forced expression of Numbl abrogated osteoclastogenesis whereas its deletion partially restor
296 expression of NFATc1, a master regulator of osteoclastogenesis, whereas IL-12 increased the apoptosi
297 ogenesis and pro-catabolic effects enhancing osteoclastogenesis, which drive bone loss in health.
299 causes bone loss by enhancing Itch-mediated osteoclastogenesis, which was prevented by Zoledronic ac
300 RBP-J silencing in the mutant cells rescued osteoclastogenesis with C/EBPalpha or c-Fos overexpressi
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