ライフサイエンスコーパス: G-CSF receptor

1 t BM HSC compartment by expression of CD114 (G-CSF receptor).

2 ine surface required for dimerization of the G-CSF receptor.

3 induction of gene transcription through the G-CSF receptor.

4 ical complex between alpha9beta1 and ligated G-CSF receptor.

5 f G-CSF signalling, we coexpressed exogenous G-CSF receptor.

6 ion containing the first tyrosine residue of G-CSF receptor.

7 G-CSF required the C-terminal region of the G-CSF receptor.

8 y active structures that could recognize the G-CSF receptor.

9 nd the association of these enzymes with the G-CSF receptor.

10 ny-stimulating factor (G-CSF) acting via the G-CSF receptors.

11 g the granulocyte colony-stimulating factor (G-CSF) receptor.

12 f the granulocyte colony-stimulating factor (G-CSF) receptor.

13 f the Granulocyte-Colony-Stimulating Factor (G-CSF) receptor activates non-receptor protein tyrosine

14 ural differences suggested that the IL-3 and G-CSF receptor agonist domains within the MPO chimera ma

15 IL-3 receptor agonists linked with a common G-CSF receptor agonist have been examined for their IL-3

16 sequences to engineer chimeric dual IL-3 and G-CSF receptor agonists in which the relative spatial or

17 ) and granulocyte colony-stimulating factor (G-CSF) receptor agonists that are superior in comparison

18 r and granulocyte colony-stimulating factor (G-CSF) receptor agonists.

19 ic mice carrying targeted mutations of their G-CSF receptor and displaying markedly different G-CSF-i

20 pheral sympathetic nerve neurons express the G-CSF receptor and ex vivo stimulation of peripheral sym

21 Oval cells were found to express G-CSF receptor and G-CSF was produced within the regener

22 aling, the data support the concept that the G-CSF receptor and gp130 are both structurally and funct

23 all of the G-CSF-expressing lines lacked the G-CSF receptor and injections of purified recombinant G-

24 w that resident spinal microglia express the G-CSF receptor and that G-CSF signaling mediates microgl

25 Since bone marrow myeloid cells express G-CSF receptors and G-CSF rapidly reduces CXCR4 expressi

26 e cell lines were transfected with the human G-CSF receptor, and stable transfectants were studied.

27 , the granulocyte colony-stimulating factor (G-CSF) receptor, and the granulocyte-macrophage colony-s

28 (Mpl, granulocyte-colony-stimulating factor [G-CSF] receptor, and Flt-3) were inserted into mouse pri

29 Truncating mutations of the G-CSF receptor are found during disease course in nearly

30 that two distinct cytoplasmic regions of the G-CSF receptor are involved in the regulation of the int

31 the membrane-proximal 55 amino acids of the G-CSF receptor are sufficient for activation of Stat5, t

32 Truncation of the carboxyl terminus of the G-CSF receptor, as seen in patients with acute myeloid l

33 (MCP-1), matrix metalloproteinase 9 (MMP-9), G-CSF receptor, beta2 integrins, or selectins responded

34 Importantly, G-CSF receptor blockade did not adversely affect viral c

35 we describe for the first time the effect of G-CSF receptor blockade in a therapeutic model of inflam

36 animals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflamma

37 in Shp2-deficient cells transfected with the G-CSF receptor but intact in cells expressing phosphatas

38 io of STAT1:STAT3:STAT5 activated by various G-CSF receptor C-terminal deletion mutants.

39 n the receptor by nearly 15 degrees C in the G-CSF/receptor complex.

40 mutations in the extracellular domain of the G-CSF receptor (CSF3R) have been reported only in severe

41 The membrane-proximal 55 amino acids of the G-CSF receptor cytoplasmic domain are sufficient for med

42 G-CSF receptor deficiency and CXCL1 blockade suppressed

43 but not flt-3 ligand is markedly impaired in G-CSF receptor-deficient (G-CSFR-deficient) mice.

44 G-CSF- and G-CSF receptor-deficient mice are profoundly protected i

45 or and IL-6 or by retroviral transduction of G-CSF receptors, demonstrating that loss of both of thes

46 hanism by which the carboxyl terminus of the G-CSF receptor down-regulates G-CSF-induced Stat activat

47 at Lyn-deficient DT40 cells that express the G-CSF receptor (DT40GR) do not demonstrate G-CSF-induced

48 t activation mediated by a carboxy truncated G-CSF receptor, expressed in patients with acute myeloid

49 correlate with the reduction in bone marrow G-CSF receptor expression.

50 to liver repopulation, as well as the G-CSF/G-CSF-receptor expression levels were evaluated.

51 emia (AML) associated with a mutation of the G-CSF receptor (G-CSF-R) developed in a patient with SCN

52 The G-CSF receptor (G-CSFR) activates the Jak/STAT pathway,

53 Truncation mutations of the G-CSF receptor (G-CSFR) are associated with the developm

54 the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this r

55 The G-CSF receptor (G-CSFR) belongs to the superfamily of th

56 ns that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.

57 Mutations in the G-CSF receptor (G-CSFR) in patients with severe congenit

58 in the expression of truncated forms of the G-CSF receptor (G-CSFR) protein.

59 CD11b(+) myeloid cells, is known to regulate G-CSF receptor (G-CSFR) signaling, we hypothesized that

60 y, we describe a system to study the role of G-CSF receptor (G-CSFR) signals in granulocytic differen

61 rated mice with a targeted mutation of their G-CSF receptor (G-CSFR) such that the cytoplasmic (signa

62 cation mutations of CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic prog

63 We use mixed G-CSF receptor (G-CSFR)-deficient bone marrow chimeras t

64 Because G-CSF receptor (G-CSFR)-deficient mice do not have the e

65 n progenitor mobilization was examined using G-CSF receptor (G-CSFR)-deficient mice.

66 a is known to be marked by expression of the G-CSF receptor (G-CSFR).

67 human fibrosarcoma cell line expressing the G-CSF receptor, G-CSF induces the tyrosine phosphorylati

68 onstrate elevated risk with mutations in the G-CSF receptor gene and a specific mutation in the ELANE

69 SCN patients with mutations in the G-CSF receptor gene are predisposed to acute myeloid leu

70 N) has been shown to harbor mutations in the G-CSF receptor gene that resulted in the truncation of t

71 , and granulocyte colony-stimulating factor (G-CSF) receptor genes by 2.5-, 1.8-, and 1.6-fold, respe

72 Because patients with a truncated G-CSF receptor have a high risk of developing acute myel

73 ctivated by G-CSF in cells expressing the wt G-CSF receptor, in addition to the previously reported S

74 dy used a retroviral vector to transduce the G-CSF receptor into MO7e cells, which are known to expre

75 The transduced G-CSF receptor is functionally active, and the resultant

76 However, the G-CSF receptor is not expressed on osteoblasts; accordin

77 emonstrate that the carboxyl terminus of the G-CSF receptor is required for SHP-1 down-regulation of

78 The granulocyte colony-stimulating factor (G-CSF) receptor is expressed exclusively in myeloid cell

79 model of hematopoietic deficiency, T(-) and G-CSF-receptor knock-out (GR(-)) mice were crossed, and

80 ing a granulocyte-colony stimulating factor (G-CSF) receptor knockout mouse model in combination with

81 w cells of wild-type mice, activation of the G-CSF receptor leads to upregulation of cyclin D3.

82 omains, domains with the L1 linker had lower G-CSF receptor-mediated proliferative activities and con

83 for functional importance and redundancy of G-CSF receptor-mediated signaling in human granulopoiesi

84 To investigate the role Gab2 plays in G-CSF receptor-mediated signaling, we have analyzed its

85 This phenotype is distinct from that of G-CSF receptor-/- mice, suggesting that other genes are

86 Bone marrow G-CSF receptor mRNA levels and G-CSF-stimulated prolifer

87 ion was associated with the up-regulation of G-CSF receptor mRNA, and the combination of GM-CSF and G

88 that granulocyte colony-stimulating factor (G-CSF) receptor mRNA was undetectable and granulocyte ma

89 ion of the myeloperoxidase, lactoferrin, and G-CSF receptor mRNAs.

90 g the granulocyte-colony-stimulating factor (G-CSF) receptor, neutrophil elastase, and myeloperoxidas

91 olecules that bind and activate the IL-3 and G-CSF receptors on hematopoietic cells.

92 This may reflect the presence of functional G-CSF receptors on other cell types and tissues, as well

93 ells stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutant

94 G-CSF receptor positive (aka G-CSFr(+) or CD114(+)) cell

95 Cells expressing the truncated G-CSF receptor produced more ROSs than those with the fu

96 lso found two regions that are important for G-CSF receptor promoter activity.

97 A 1,391-bp fragment of the G-CSF receptor promoter is both active in myeloid cell l

98 e other functionally important region of the G-CSF receptor promoter is in the 5' untranslated region

99 Anti-G-CSF receptor rapidly halted the progression of establi

100 hap30 repressed expression of the endogenous G-CSF receptor several-fold.

101 er investigate the actions of blocking G-CSF/G-CSF receptor signaling in inflammatory disease, and as

102 nulopoiesis-specific mechanism downstream of G-CSF receptor signaling that leads to LEF-1 downregulat

103 d thereby inhibits STAT3 phosphorylation and G-CSF receptor signaling.

104 intact STAT3 upregulation, characteristic of G-CSF receptor signaling.

105 nd correlated that with wild-type and mutant G-CSF receptors stably expressed in the murine factor-de

106 atterns by Gr-1 antigen expression and their G-CSF receptor status.

107 e, blocking neutrophil trafficking with anti-G-CSF receptor suppressed local production of proinflamm

108 genic mice with a targeted mutation of their G-CSF receptor (termed d715F) that abolishes G-CSF-depen

109 rom an inflammatory phenotype following anti-G-CSF receptor therapy in collagen Ab-induced arthritis.

110 We show here that the G-CSF receptor transcription start site is identical in

111 We established a G-CSF receptor-transduced promyelocytic cell line, EPRO-

112 The G-CSF receptor transduces signals that regulate the prol

113 ls in the blood and arthritic joints of anti-G-CSF receptor-treated mice showed alterations in cell a

114 le in granulocyte colony-stimulating factor (G-CSF) receptor-triggered granulopoiesis, is downregulat

115 The extracellular domain of the murine G-CSF receptor was required for the activity of SB 24746

116 Dcl3 cells and FDCP1 cells expressing mutant G-CSF receptors was examined and it was found that G-CSF

117 s; instead, mutations of CSF3R, encoding the G-CSF receptor, were common.

118 e developed a neutralizing mAb to the murine G-CSF receptor, which potently antagonizes binding of mu

119 s expressing a carboxyl-terminally truncated G-CSF receptor, which supports proliferation but not dif

120 kinetics, the MPOs were found to bind to the G-CSF receptor with low nanomolar affinities, similar to