ライフサイエンスコーパス: RANK ligand

1 teoclast differentiation factor (also called RANK ligand).

2 osteoclast formation through upregulation of RANK ligand.

3 f M-CSF and receptor activator of NF-kappaB (RANK) ligand.

4 de of the receptor activator of NF-kB (RANK)-RANK ligand and B cell-activating factor-APRIL (a prolif

5 the aegis of two critical cytokines, namely RANK ligand and M-CSF.

6 ted by macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin.

7 or activator of nuclear factor-kappaB (RANK)/RANK ligand, and TNF-related apoptosis-inducing ligand (

8 demonstrated the superiority of denosumab, a RANK-ligand antagonist, compared to zoledronic acid in t

9 aimed to investigate the effects of the anti-RANK ligand antibody denosumab in postmenopausal, aromat

10 genetically deficient in RANK or the cognate RANK ligand are profoundly osteopetrotic because of the

11 Moreover, the top-ranked ligands are strongly enriched in compounds with h

12 al cells during pregnancy and in response to RANK ligand but not TNFalpha.

13 receptor activator of nuclear factor kappaB (RANK) ligand but attach to substrate and migrate poorly,

14 RANK ligand can act to enhance the effects of other fact

15 receptor activator of nuclear factor kappab (RANK) ligand-expressing proT2-cells induce changes in bo

16 Enhanced RANK ligand expression also plays an important role in b

17 ested 15 compounds from among the top 50 top-ranked ligands from docking, and found 5 inhibitors with

18 receptor activator of nuclear factor kappaB (RANK) ligand, have been reported.

19 mediated by receptor activator of NF-kappaB (RANK)-ligand in the bone microenvironment.

20 FHL2 overexpression delays RANK ligand-induced (RANKL-induced) osteoclast formation

21 Although IKKalpha is required for RANK ligand-induced osteoclast formation in vitro, it is

22 Denosumab, an anti-RANK ligand monoclonal antibody, significantly increases

23 Bisphosphonate therapy and rank-ligand monoclonal antibody therapy are the most com

24 During chronic immune activation, RANK ligand on activated immune cells likewise drives pa

25 eceptor activator of nuclear factor kappa-B (RANK) ligand on osteoblasts drives OC differentiation by

26 L)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, parathyroid hormone-related protein (PTHrP

27 eptor activator of nuclear factor-kappaB and RANK ligand) pathway has been shown to be essential for

28 NF) receptor superfamily and is activated by RANK ligand (RANK-L), a homotrimeric, TNF-like cytokine.

29 mporally coordinated cross talks between the RANK ligand/RANK and IRF7/IFN-beta/IFNAR/STAT1 pathways

30 cted that regents such as AMG-162 that block RANK-ligand/RANK interaction will have activity in infla

31 tivator of nuclear factor-kappaB (RANK), and RANK ligand (RANKL) are mediators of various cellular in

32 from dendritic cells, and the isolation of a RANK ligand (RANKL) by direct expression screening.

33 ppa B (RANK), and by enhancing production of RANK ligand (RANKL) by osteoblasts.

34 ceptor family, is expressed on DCs, and that RANK ligand (RANKL) enhances DC survival and induces the

35 ppeared to result from reduced expression of RANK ligand (RANKL) in osteoblasts.

36 RANK Ligand (RANKL) is a critical osteoclastogenic facto

37 To examine these possibilities, we compared RANK ligand (RANKL) mRNA expression in a marrow stromal

38 olytic bone destruction independently of the RANK ligand (RANKL) pathway.

39 ates NF-kappaB and AP-1 activation following RANK ligand (RANKL) stimulation.

40 RANK ligand (RANKL), a TNF-related molecule, is essentia

41 r activator of nuclear factor-kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) signaling

42 r activator of nuclear factor kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also

43 treated with colony-stimulating factor 1 and RANK ligand (RANKL), as the cells failed to form large,

44 RANK ligand (RANKL), by mechanisms unknown, directly act

45 VPS35 loss of function altered RANK ligand (RANKL)-induced RANK distribution, enhanced

46 r activator of nuclear factor-kappa B (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) axis.

47 clear abundance is specifically increased by RANK ligand (RANKL).

48 inhibits TNF-alpha-induced activity bound to RANK ligand (RANKL).

49 osteoprotegerin ligand (OPGL), also known as RANK ligand (RANKL).

50 ivated by the secreted or cell surface-bound RANK ligand (RANKL).

51 the receptor activator for NF-kappaB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and expre

52 IKKalpha activation by RANK ligand (RANKL/TNFSF11) inhibits Maspin expression i

53 receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) and inhibited osteoclast formation.

54 Receptor activator of NF-kappaB (RANK) ligand (RANKL) and its receptor RANK play an essen

55 receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) and lymphotoxin.

56 is context, receptor activator of NF-kappaB (RANK) ligand (RANKL) plays a pivotal role in lymphoid ti

57 ntly of the receptor activator of NF-kappaB (RANK) ligand (RANKL), others demonstrated that TNF-media

58 equires the receptor activator of NF-kappaB (RANK) ligand (RANKL).

59 ic cytokine receptor activator of NF-kappaB (RANK) ligand (RANKL).

60 s implicated the TNF family members RANK and RANK-Ligand (RANKL) in the development of Aire-expressin

61 r activator of nuclear factor-kappaB (RANK), RANK-ligand (RANKL), osteoprotegerin (OPG), and osteocal

62 or with denosumab (a monoclonal antibody to RANK ligand) reduces risk for skeletal events in men wit

63 tor of nuclear factor-kappaB (RANK), soluble RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin-K

64 ,5) abundance and desensitizes precursors to RANK ligand-stimulated differentiation.

65 Receptor activator for NF-kappaB (RANK) ligand stimulation results in IFN-beta upregulatio

66 c1-driven osteoclastogenesis, independent of RANK ligand, which disrupts normal bone homeostasis lead

67 eceptor activator of nuclear factor kappa B (RANK) ligand, with zoledronic acid in delaying or preven