ライフサイエンスコーパス: chemokine CXCL1

1 timulating factor (G-CSF) and the ELR(+) CXC chemokine CXCL1.

2 inflammatory cytokines IL1beta, IL6, and the chemokine CXCL1.

3 opoietic tissue of the neutrophil-recruiting chemokine CXCL1.

4 t through seed-derived factors including the chemokine CXCL1.

5 on in response to both retinoic acid and the chemokine CXCL1.

6 ack of crossover reactivity with the related chemokine CXCL1.

7 and consequent secretion of pro-inflammatory chemokine, CXCL1.

8 bility through secreted products such as the chemokines CXCL1, 2, 3, and 8, through adhesion-dependen

9 ast, cathepsins specifically process ELR CXC chemokines CXCL1, -2, -3, -5, and -8 N-terminally to the

10 arding the binding ability of the other ELR+ chemokines (CXCL1-3 and CXCL5-8).

11 n-coupled receptor (GPCR) that binds the CXC chemokines, CXCL1-3 and CXCL5-8, and induces intracellul

12 lm infection led to significant increases in chemokine (CXCL1 and CCL2) and proinflammatory cytokine

13 Here we demonstrate a role for the chemokine CXCL1 and its receptor CXCR2 in patterning the

14 ptor family, induced potent secretion of the chemokines CXCL1 and CCL2 as well as expression of induc

15 ated with marked astrocytic synthesis of the chemokines CXCL1 and CCL2 in response to both cytokine c

16 teria has higher levels of mRNA encoding the chemokines CXCL1 and CCL2 than does tissue isolated from

17 optosis, and expression of mRNA encoding the chemokines CXCL1 and CXCL10.

18 ed the secretion of VEGF and proinflammatory chemokines CXCL1 and CXCL16, leading to increased myeloi

19 ts demonstrated diminished production of the chemokines CXCL1 and CXCL2 and delayed neutrophil and T

20 The ELR(+) CXC chemokines CXCL1 and CXCL2 are up-regulated in the centr

21 eased mRNA expression of neutrophil-specific chemokines CXCL1 and CXCL2 in the lungs of C57BL/6 and I

22 peritonitis, we show in this study that the chemokines Cxcl1 and Cxcl2 play distinctive roles in enh

23 he melanoma growth and migration stimulatory chemokines CXCL1 and CXCL2 were significantly up-regulat

24 d T cells, whereas the neutrophil-attracting chemokines CXCL1 and CXCL2 were up-regulated in the CNS

25 -protein-coupled receptor CXCR2 (recognizing chemokines CXCL1 and CXCL2) as another arm feeding into

26 steoblasts constitutively expressed the ELR+ chemokines CXCL1 and CXCL2, and CXCL2 expression was ind

27 okines, as well as the neutrophil-attracting chemokines Cxcl1 and Cxcl2, were increased.

28 uced expression of the neutrophil-attracting chemokines CXCL1 and CXCL5 in kidney cells.

29 3 has been shown to have a high affinity for chemokines CXCL1 and CXCL8 and to diminish inflammation

30 Here we demonstrate that chemokines CXCL1 and CXCL8 chemoattract ASC by signallin

31 es expression of Bcl-2 and the proangiogenic chemokines CXCL1 and CXCL8 in HNSCC cells.

32 lock the post-translational secretion of the chemokines CXCL1 and CXCL8 independent of transcription

33 ammatory cytokines and chemokines, including chemokines CXCL1 and CXCL8, which are both agonists of t

34 stinctly different compared with the related chemokines CXCL1 and CXCL8.

35 we found that expression of 2 PMN-attracting chemokines, Cxcl1 and Cxcl2, was rapidly and dramaticall

36 st rapidly (1 hour) expressed genes were the chemokines, Cxcl1 and Cxcl2.

37 ogenous luminal restoration of IL-17-related chemokines, CXCL1 and CXCL5, improves host defenses agai

38 actions of two related neutrophil-activating chemokines, CXCL1 and CXCL5, with HS, CS, and DS.

39 motactic chemokines KC (keratinocyte-derived chemokine) (CXCL1) and MIP-2 (macrophage inflammatory pr

40 es, TNF-alpha elicited marked release of the chemokine CXCL1, and the release was blocked by carbenox

41 hich revealed the neutrophil chemoattractant chemokine CXCL1 as one of the top genes upregulated.

42 In rodents, the chemokine CXCL1 both induces the proliferation and inhib

43 nflammatory cytokines (sICAM-1 and IL-6) and chemokines (CXCL1, CCL1, CCL2 and CCL5) that are hallmar

44 ng showed many up-regulated genes, including chemokines (Cxcl1, Ccl7), cytokines (tumor necrosis fact

45 g infection, included upregulation of innate chemokines (Cxcl1, Cxcl10, and Cxcl16) that were also ex

46 TNF-alpha, IL1-b, IFN-gamma, and IL-12), and chemokines (CXCL1, CXCL2, CCL2, CCL3, CCL4, and CXCL10).

47 tory molecules (CD80, CD86, CD40, and CD70), chemokines (CXCL1, CXCL2, CXCL3, CCL12, CCL17), as well

48 ted in the generation of neutrophil-specific chemokines CXCL1, CXCL2 as well as TNFalpha.

49 6, IL-23, IL-1beta, as well as IL-17 and the chemokines CXCL1, CXCL2, and CCL2, whereas similarly tre

50 d endothelial expression of the neutrophilic chemokines CXCL1, CXCL2, and CXCL5 and led to a function

51 Substantial induction of the chemokines CXCL1, CXCL2, and S100A8; the acute-phase pro

52 d deficit in their capability to release the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-alpha in

53 We found that the mRNA expression of chemokines CXCL1, CXCL2, CXCL3 and CCL2 was significantl

54 These cytokine genes included chemokines (Cxcl1, Cxcl3, Cxcl5, Ccl2, and Ccl3), ILs (I

55 F], interleukin-17 [IL-17], and IL-1beta) or chemokine (CXCL1, CXCL5, CXCL9, and CXCL10) induction.

56 gories: proangiogenic factors (MMP9, VEGFA), chemokines (CXCL1, CXCL5, IL8, CCL2), cytokines (IL1B, I

57 ce proteins, CD80 and CD38, and cytokines or chemokines (CXCL1, CXCL5, RANTES) released by activated

58 In addition, the chemokines CXCL1, CXCL5, CXCL6, and complement C3, known

59 Serum CXC chemokines (CXCL1, CXCL8, CXCL9, CXCL10, CXCL12, CXCL13

60 differentially elicited a further downstream chemokine (CXCL1/CXCL8) autocrine loop, with the two loo

61 were expressed at adult levels, whereas the chemokines CXCL1, CXCL9, and CCL2 remained at baseline l

62 onuclear cells (PMNs) through binding of the chemokines CXCL1 (CXCR1) and CXCL8 (CXCR1 and CXCR2).

63 al colony forming units, and by elevation of chemokine CXCL1, cytokine IL-6, and endogenous G-CSF pro

64 okines, as well as a prolonged half-life for chemokine CXCL1-encoding mRNA after treatment with IL-17

65 instead reduced secretion of the angiogenic chemokine CXCL1 from head and neck cancer cells in vitro

66 s was governed by enhanced production of the chemokine CXCL1 from mast cells that localized at endoth

67 ncer Genome Atlas showed that the neutrophil chemokine CXCL1 gene was highly upregulated in colon tum

68 , HNP 1-3, elafin, and LL-37) and neutrophil chemokines (CXCL1/GRO-alpha, CXCL2/GRO-beta, CXCL5/ENA-7

69 and correspondingly had lower levels of the chemokine CXCL1 in bronchoalveolar lavage fluid and lung

70 The functional role of the ELR(+) chemokine CXCL1 in host defense and disease following in

71 Although the chemokine CXCL1 induces neutrophil influx during bacteri

72 anoma cells, the basal expression of the CXC chemokine, CXCL1, is constitutively up-regulated.

73 previous studies have revealed that the CXC chemokine, CXCL1, is overexpressed in human malignant me

74 Using the mouse chemokine CXCL1 (KC) gene as a model, we have examined t

75 f intron content on the rate of decay of the chemokine CXCL1 (KC) mRNA.

76 i) DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in r

77 appin-2-treated PA01 up-regulated the murine chemokine CXCL1/KC after 2 hours with a corresponding in

78 cytes but with elevated levels of the ELR(+) chemokines (CXCL1/keratinocyte-derived chemokine and CXC

79 inflammatory cytokines (Il-6, Tnf-alpha) and chemokines (Cxcl1, Mcp-1, Mif-1alpha) and Nos2 in the in

80 In humans, the chemokine CXCL1/MGSA (hCXCL1) plays fundamental and dive

81 The chemokine CXCL1/MGSA plays a pivotal role in the host im

82 Levels of the angiogenic chemokine CXCL1 (mouse functional homologue of human IL-

83 ow here that IL-17 enhanced the stability of chemokine CXCL1 mRNA and other mRNAs through a pathway t

84 The ELR-CXC chemokine, CXCL1 or MGSA/GROalpha, is traditionally cons

85 The CXC chemokine CXCL1, or MGSA/GROalpha, is traditionally cons

86 on E-selectin (slowly) or by exposure to the chemokine CXCL1 (rapidly).

87 e data reveal a novel mechanism by which the chemokine CXCL1, through neutrophil recruitment, alters

88 r alpha (TNF-alpha), IL-10, and IL-6 and the chemokine CXCL1 were upregulated in cocultured HT-29 cel

89 and VCAM-1), and enhanced the release of CXC chemokine CXCL1 when incubated with primary cultures of

90 lso had higher levels of the proinflammatory chemokine CXCL1, which CD T cells produce, in the kidney

91 In addition, expression of the chemokine CXCL1, which is associated with developmental

92 fungal immunity by driving production of the chemokine CXCL1, which recruited neutrophils expressing