ライフサイエンスコーパス: bone marrow macrophage

1 matopoietic maintenance factor expression in bone marrow macrophages.

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

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

4 ive in C. elegans intestinal cells and mouse bone marrow macrophages.

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

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

7 phosphorylation and STAT1 ubiquitination in bone marrow macrophages.

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

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

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

11 rophage colony-stimulating factor (M-CSF) in bone marrow macrophages.

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

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

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

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

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

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

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

19 crosis factor alpha (TNF-alpha) release from bone marrow macrophages, and both were shown to activate

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

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

22 zed proteomes of cultured XOI-treated murine bone marrow macrophages (BMDMs).

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

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

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

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

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

28 Bone marrow macrophages (BMM) were generated by culturin

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

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

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

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

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

34 teoclasts, respectively, in the MC3T3-E1 and bone marrow macrophages (BMMs) cells.

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

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

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

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

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

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

41 Bone marrow macrophages (BMMs) share common progenitors

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

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

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

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

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

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

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

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

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

51 and restrains the osteoclastogenesis of rat bone-marrow macrophages (BMMs).

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

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

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

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

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

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

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

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

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

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

62 In vitro, addition of AC to bone marrow macrophage cultures decreased B. burgdorferi

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

64 Herein, we used bone marrow macrophages derived from adult male CCR3-pro

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

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

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

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

69 Bone marrow macrophages derived from these mutants diffe

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

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

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

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

74 e trait loci mapping of lysosome function in bone marrow macrophages from an AKR/J x DBA/2J strain in

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

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

77 Bone marrow macrophages from influenza-infected Apoe-/-

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

79 0 synthesis and inhibited IL-12 synthesis by bone marrow macrophages from normal, but not gamma-chain

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

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

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

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

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

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

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

87 .01, 0.1, and 1.0) were incubated with mouse bone marrow macrophages isolated from C57BL/6J mice and

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

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

90 Primary bone marrow macrophages isolated from mice in which FAK

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

92 n mediating RANKL-induced signaling in mouse bone marrow macrophages, known as osteoclast precursors.

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

94 ell compartment and enhances the response of bone marrow macrophages, monocytes, and splenocytes to s

95 oclast (OC) differentiation in cocultures of bone marrow macrophages/monocytes (BMMs) and OBs after t

96 We found that Sfrp4 is expressed during bone marrow macrophage OC differentiation and that Sfrp4

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

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

99 Committed bone marrow macrophage precursors and blood monocytes ex

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

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

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

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

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

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

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

107 Lipopolysaccharide-activated bone marrow macrophages released molecules that induced

108 However, bone marrow macrophages showed only nonspecific uptake.

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

110 riptional program, which was also present in bone marrow macrophages sorted from patients with sHLH.

111 Bone marrow macrophages stimulate skeletal wound repair

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

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

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

115 Using primary bone marrow macrophages, these studies demonstrate that

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

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

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

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

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

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

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

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

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

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

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