ライフサイエンスコーパス: bone marrow macrophage

1 fibroblasts, primary embryo fibroblasts, and bone marrow macrophages.

2 llino 2 in human 293-IL-1R cells and primary bone marrow macrophages.

3 bone marrow, where they are phagocytosed by bone marrow macrophages.

4 phosphorylation and STAT1 ubiquitination in bone marrow macrophages.

5 MSP-1 to inhibit nitric oxide production in bone marrow macrophages.

6 ke was examined in osteoclasts prepared from bone marrow macrophages.

7 ve stress but did not impair growth in mouse bone marrow macrophages.

8 ) sufficient for a locus control function in bone marrow macrophages.

9 CSF-1-derived bone marrow macrophages also synthesize this 25-kDa IGFB

10 Using a coculture system containing bone marrow macrophage and osteoblastic cells, here we r

11 ofiling of isogenic wild-type and cebpb(-/-) bone marrow macrophages and identified a number of IFN-g

12 ication was confirmed in vitro using primary bone marrow macrophages and in vivo for peritoneal macro

13 phavbeta3 integrin was observed in RAGE(-/-) bone marrow macrophages and precursors of OCs.

14 expression by over 40-fold in primary mouse bone marrow macrophages and Raw 264.7 cells.

15 osine receptor (A2bAR) is highly abundant in bone marrow macrophages and vascular smooth muscle cells

16 tify discrete DNA-binding factors in primary bone marrow macrophages as candidate transcriptional reg

17 Introduction of Pax6 retrovirally into bone marrow macrophages attenuates RANKL-induced osteocl

18 of NF-kappaB ligand (RANKL)-activated murine bone marrow macrophage (BMM) cultures revealed unique up

19 egulated the development of F4/80(+)VCAM1(+) bone marrow macrophages (BMM) and that Spic expression i

20 , we compared the CSF-1 responses of primary bone marrow macrophages (BMM) from wild-type and SHP-1-d

21 Wild-type (WT) bone marrow macrophages (BMM) that overexpress the tande

22 Phagocytosis of zymosan by bone marrow macrophages (BMM) was enhanced by opsonizati

23 Bone marrow macrophages (BMM) were generated by culturin

24 noparticles (NP, nanoART) loaded into murine bone marrow macrophages (BMM, IDV-NP-BMM) after ex vivo

25 okines is suppressed in mice with DIO and in bone marrow macrophages (BMMPhi) from mice with DIO expo

26 une evasion genes function in H-2(b) primary bone marrow macrophages (BMMphi) in the same way that th

27 associated peptide antigen by differentiated bone marrow macrophages (BMMphis) to a T cell hybridoma

28 To identify this inhibitor, we used bone marrow macrophages (BMMs) and primary osteoblasts (

29 Consistent with these observations, primary bone marrow macrophages (BMMs) derived from S100A4(-/-)

30 In vitro, bone marrow macrophages (BMMs) from MCP-1(-/-) and WT mi

31 Myr)-Akt or a dominant-negative CAAX-Akt and bone marrow macrophages (BMMs) from wild-type and transg

32 ear proteins from RAW264.7 cells and primary bone marrow macrophages (BMMs) in an electrophoretic mob

33 Bone marrow macrophages (BMMs) isolated from cKO mice ar

34 esence of permissive levels of RANKL or from bone marrow macrophages (BMMs) pretreated by RANKL.

35 Bone marrow macrophages (BMMs) share common progenitors

36 We find that LPS induces bone marrow macrophages (BMMs) to express c-src, a proto

37 decreases upon stimulation of wild type (WT) bone marrow macrophages (BMMs) with RANKL, TAK1 deficien

38 hat implant particles induce c-src in murine bone marrow macrophages (BMMs), a protein specifically e

39 we find TNF induction of NF-kappaB in murine bone marrow macrophages (BMMs), is mediated, by c-Src, i

40 id phosphatase, and carbonic anhydrase II in bone marrow macrophages (BMMs), RANKL renders these oste

41 in cultured mouse bone marrow cells (BMCs), bone marrow macrophages (BMMs), spleen cells, and RAW264

42 inhibits formation of osteoclasts (OCs) from bone marrow macrophages (BMMs), we examined the capacity

43 ntrast to other cell types, IkappaBalpha, in bone marrow macrophages (BMMs), which are osteoclast pre

44 iated signaling in osteoclast (OC) precursor bone marrow macrophages (BMMs).

45 socs3, and il10 expression in infected mouse bone marrow macrophages but did correlate with enhanced

46 urine alveolar macrophages as well as murine bone marrow macrophages, but not alveolar epithelial cel

47 how that expression of AnxA1 is required for bone marrow macrophages, but not peritoneal macrophages,

48 However, bone marrow macrophage cells from MAGP1Delta mice show a

49 umber of osteoclasts derived from MAGP1Delta bone marrow macrophage cells is increased relative to th

50 utant, we further show that in an osteoblast/bone marrow macrophage co-culture system, immobilization

51 Mice receiving 11 doses also had suppressed bone marrow macrophage colony formation.

52 lity by treatment with WT but not Porcn-null bone marrow macrophage-conditioned medium (CM).

53 ents of NOS2 and arginase activity in normal bone marrow macrophages confirm these findings.

54 Chromatin immunoprecipitation experiments in bone marrow macrophages confirmed that EWS, but not FUS/

55 y to support osteoclastogenesis in wild-type bone marrow macrophages, demonstrating that CD47-induced

56 for effector translocation were discerned in bone marrow macrophages derived from C57BL/6 mice, which

57 Bone marrow macrophages derived from IL-23p19(-/-) mice

58 ophages, LPS-induced events were compared in bone marrow macrophages derived from SHIP(+/+) and SHIP(

59 To this end, we used immortalized bone marrow macrophages derived from SHP-1-deficient mot

60 Bone marrow macrophages derived from these mutants diffe

61 P. gingivalis-stimulated macrophages induced bone marrow macrophage-derived osteoclastogenesis.

62 peripheral blood cells and the percentage of bone marrow macrophages did not differ between VDR KO an

63 First, deletion of Notch1-3 in bone marrow macrophages directly promotes their commitme

64 ern analysis of rat glioma C6 cells or mouse bone marrow macrophages exposed to crosslinking reagents

65 Stimulation of bone marrow macrophages from C3H/HeN mice with the B. bu

66 expression of the M-CSFR in M-CSF-dependent bone marrow macrophages from Dicer-deficient mice rescue

67 h RAW264.7 cells expressing SHP-1(C453S) and bone marrow macrophages from Me(v)/Me(v) mice.

68 0 synthesis and inhibited IL-12 synthesis by bone marrow macrophages from normal, but not gamma-chain

69 n comparable experiments employing activated bone marrow macrophages from wild-type and NO synthase 2

70 e II strain to enhance the capacity of mouse bone marrow macrophages (from primary cultures) and huma

71 We show that peritoneal and bone marrow macrophages generate peptide/MHC-I complexes

72 Similar observations were made with murine bone marrow macrophages infected ex vivo: growth of the

73 rovar Typhimurium-infected BALB/c mice lysed bone marrow macrophages infected with S. enterica serova

74 PKD activity is dispensable for induction of bone marrow macrophages into tartrate-resistant acid pho

75 tilized to monitor differential migration of bone marrow macrophages into viable and apoptotic MASIs

76 .01, 0.1, and 1.0) were incubated with mouse bone marrow macrophages isolated from C57BL/6J mice and

77 A sequencing to profile the transcriptome of bone marrow macrophages isolated from diabetic db/db mic

78 Furthermore, primary bone marrow macrophages isolated from mice deficient in

79 Primary bone marrow macrophages isolated from mice in which FAK

80 L. monocytogenes-infected B6.Tla(a)-derived bone marrow macrophages (Kb Qa-1a) are not lysed by BALB

81 We derived primary bone marrow macrophages lacking Arp2/3 complex (Arpc2(-/

82 RAW264.7 cells expressing SHP-1(C453S), the bone marrow macrophages of Me(v)/Me(v) mice generated mu

83 Here, we show that bone marrow macrophages of SHIP(-/-) animals have elevat

84 Committed bone marrow macrophage precursors and blood monocytes ex

85 s in the nuclei of osteoclasts but not their bone marrow macrophage precursors and that osteoclast in

86 ion in the capacity to form osteoclasts from bone marrow macrophage precursors in vitro in response t

87 eading to failure of the PLCgamma2-deficient bone marrow macrophage precursors to differentiate into

88 We report that primary SHIP-deficient bone marrow macrophages produce elevated levels of super

89 Finally, we show that bone marrow macrophages produce factors that support the

90 However, the loss of CapG in bone marrow macrophages profoundly inhibits macrophage c

91 L-13Ralpha2-deficient mice display increased bone marrow macrophage progenitor frequency and decrease

92 Lipopolysaccharide-activated bone marrow macrophages released molecules that induced

93 However, bone marrow macrophages showed only nonspecific uptake.

94 eoblast and chondrocyte lineages, as well as bone marrow macrophages, showed intense beta-gal histo-

95 Bone marrow macrophages stimulate skeletal wound repair

96 that the uptake of apoptotic neutrophils by bone marrow macrophages stimulates their production of G

97 L. monocytogenes-infected TAP-/- bone marrow macrophage targets are not lysed by MHC clas

98 Bone marrow macrophages that lacked IGTP or LRG-47 displ

99 Using primary bone marrow macrophages, these studies demonstrate that

100 and JAGGED1 blunts the capacity of wild-type bone marrow macrophages to become osteoclasts.

101 sequences and did not affect the capacity of bone marrow macrophages to form osteoclasts in vitro In

102 othesis, we found that C57BL/6 mouse-derived bone marrow macrophages treated with exosomes released f

103 eoclasts formed by differentiating CD47(-/-) bone marrow macrophages was decreased, high doses of RAN

104 d (RifK) M. tuberculosis in activated murine bone marrow macrophages was examined by using an I-A(b)-

105 Using primary murine bone marrow macrophages, we established that p38 and ext

106 In bone marrow macrophages, we show that E2f1-3 respond to

107 Splenocytes were isolated and bone marrow macrophages were derived from B27-transgenic

108 studied gene expression in RNAs from BALB/c bone marrow macrophages with and without Leishmania chag

109 te, increased after 2-3 days of treatment of bone marrow macrophages with M-CSF and RANKL, correspond

110 paired for intracellular growth within mouse bone marrow macrophages, with the defect absolute in tri