ライフサイエンスコーパス: eotaxin-3

1 nd activation-regulated chemokine [TARC] and eotaxin-3).

2 ing decreased IL-13-induced transcription of eotaxin-3.

3 38.2% to -51.5% (placebo +8.3% to -0.16%) in eotaxin-3; -24.8% to -76.7% (placebo +8.3% to -4.4%) in

4 for the change from baseline) vs placebo for eotaxin-3 (-30.06 vs -0.86 pg/mL; P = 0.0008) and total

5 Acidic pH increased cellular release of eotaxin-3 (4.6 +/- 1.98 ng/ml versus 12.46 +/- 2.90 ng/m

6 ding the eosinophil-specific chemoattractant eotaxin-3 (also known as CCL26) was the most highly indu

7 tment can be regulated by chemokines such as eotaxin-3 and CCL17.

8 um IgE levels, blood eosinophil count, TARC, eotaxin-3 and FeNO in patients both with and without FS

9 childhood central nervous system vasculitis; eotaxin-3 and other markers related to eosinophils or Th

10 A comparison between the structures of eotaxin-3 and related chemokines suggests that the elect

11 Reductions in serum TARC, plasma eotaxin-3 and serum periostin occurred rapidly, whereas

12 ed P-selectin, thymic stromal lymphopoietin, eotaxin-3, and thrombopoietin receptor to the RNA-induce

13 -1), galectin-10 (CLC/GAL-10), Eotaxin-2 and Eotaxin-3, and urine osteopontin (OPN) and matrix metall

14 These results implicate eotaxin-3 as a critical effector molecule for EE and pro

15 ted, markers (CCL13/MCP-4, CCL18/PARC, CCL26/eotaxin-3, CCL24/Eotaxin-2), coupled with significant up

16 cluding the genes for eosinophil chemotaxis (eotaxin 3, CCL26), barrier molecules (desmoglein 1, DSG1

17 okines eotaxin-1/CCL11, eotaxin-2/CCL24, and eotaxin-3/CCL26 are expressed.

18 including eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26, RANTES/CCL5, and MEC/CCL28.

19 rt the 3D structure and backbone dynamics of eotaxin-3 determined by NMR spectroscopy.

20 A panel comprising CLC/GAL-10, Eotaxin-3, ECP, EDN, MBP-1, and AEC was superior to AEC

21 thelial inflammatory pathways (production of eotaxin-3 [encoded by CCL26]), impaired barrier function

22 In contrast to eotaxin, eotaxin-3 exhibits no substantial mobility on the micros

23 he presence of an EoE-like (characterized by eotaxin-3 expression), non-specific, and lymphocytic var

24 sely correlated with basal and IL-13-induced eotaxin-3 gene expression.

25 single-nucleotide polymorphism in the human eotaxin-3 gene was associated with disease susceptibilit

26 es induced strong up-regulation of chemokine eotaxin-3, Il8, Mip1b, and Groa gene expression.

27 tween epigenetic regulation and IL-13-driven eotaxin-3 in the pathogenesis of chronic allergic inflam

28 d production of the chemoattractant cytokine eotaxin-3 in the tissue of patients with allergic diseas

29 1beta, IL-6, IL-10, IL-12/IL-23p40, eotaxin, eotaxin-3, Interferon gamma-induced Protein (IP-10), Mon

30 terleukin-8, interleukin-10, interleukin-15, eotaxin-3, interferon gamma-induced protein 10, macropha

31 , endoscopic, and molecular characteristics [eotaxin-3, interleukin (IL-5), and IL-13 expression].

32 Eotaxin-3 is monomeric under the conditions in this stud

33 Eotaxin-3 is one of three related chemokines that specif

34 and chemokines (eg, interleukin-8 [IL-8] and eotaxin-3), it is generally assumed that WPB exocytosis

35 Additionally, other biomarkers (Eotaxin-3, Leptin, PYY) exhibited altered levels in AD p

36 Plasma eotaxin-3 levels strongly associated with gastric CCL26

37 EST-captured eotaxin-3, major basic protein 1, EDN, eosinophil peroxi

38 Plasma (CLC/GAL-10, ECP, EDN, Eotaxin-3, MBP-1) and urine (OPN) biomarkers were increa

39 Esophageal eotaxin-3 mRNA and protein levels strongly correlated wi

40 In contrast to EoE, eotaxin-3 mRNA and protein were markedly reduced in EoE-

41 pression levels of three selected EoE genes (eotaxin-3, MUC4, and CDH26) allowed to discriminate betw

42 nds CCL11/eotaxin, CCL24/eotaxin-2, or CCL26/eotaxin-3 on 1) wound repair, using an established wound

43 ted with marked gene dysregulation including eotaxin-3 overproduction.

44 .003), and epithelial CLCA1 (P < .0001) and eotaxin-3 (P = .001) mRNA expression.

45 protein (P = 0.008), eotaxin-2 (P = 0.008), eotaxin-3 (P = 0.031), pulmonary and activation-regulate

46 E-relevant esophageal transcripts, including eotaxin-3, periostin, and markers of mast cells and barr

47 leptin augmented IL-13-induced eotaxin-1 and eotaxin-3 production and IL13RA2 expression.

48 n of methylation with 5-azacytidine promoted eotaxin-3 production in association with decreasing CpG

49 utory role for DNA methylation in regulating eotaxin-3 production in human allergic inflammation.

50 istone deacetylation increased IL-13-induced eotaxin-3 production.

51 ed to IL-13 at similar levels as assessed by eotaxin-3 production.

52 the eotaxin-3 promoter affects IL-13-induced eotaxin-3 promoter activity.

53 sferase, induced base-line and IL-13-induced eotaxin-3 promoter activity.

54 he cAMP-responsive element (CRE) site in the eotaxin-3 promoter affects IL-13-induced eotaxin-3 promo

55 Regions of the human eotaxin-3 promoter were found to be hypomethylated in pr

56 e subsequent acetylation of histone 3 at the eotaxin-3 promoter.

57 sion level of the eosinophil chemoattractant eotaxin-3, respectively.

58 ng intracellular calcium that contributes to eotaxin-3 secretion by EoE cells.

59 and explored molecular pathways involved in eotaxin-3 secretion by IL-4 receptor-a signaling.

60 ole and verapamil suppressed IL-4-stimulated eotaxin-3 secretion more than either agent alone.

61 L-4) receptor-a have been shown to stimulate eotaxin-3 secretion via a nongastric proton pump (ngH(+)

62 ular calcium transients, and IL-4-stimulated eotaxin-3 secretion was blocked by ethylene glycol-bis(B

63 IL-4-stimulated eotaxin-3 secretion was measured by enzyme-linked immuno

64 ibitors block T helper 2 cytokine-stimulated eotaxin-3 secretion, suggesting a potential role for the

65 that mediates T helper 2 cytokine-stimulated eotaxin-3 secretion.

66 zole and SCH 28080 decreased IL-4-stimulated eotaxin-3 secretion.

67 ctivation-regulated chemokine (TARC), plasma eotaxin-3, serum total immunoglobulin E (IgE), serum per

68 PARC, periostin, and IL-22), eotaxin-1, and eotaxin-3 significantly decreased.

69 CL22/macrophage-derived chemokine, and CCL26/eotaxin-3), T(H)17/T(H)22 (lipocalins, PI3/elafin, CCL20

70 udies have identified genetic perturbations (eotaxin-3, thymic stromal lymphopoietin, IL-13, and fila

71 For blood-based platforms, eotaxin-3, thymus and activation-regulated chemokine, IL

72 In addition, the basal and IL-13-induced eotaxin-3 transcriptional activity was suppressed by pro

73 K cells/muL had higher Th2 markers (eotaxin, eotaxin-3, TSLP, MCP-4/CCL13), and African American PN p

74 Involvement of the eotaxin 3' untranslated region in the mRNA-stabilizing e

75 inducible beta-globin reporter linked to the eotaxin 3' untranslated region.

76 patients had lower eosinophils, eotaxin, and eotaxin-3 versus Caucasian and Asian PN patients (p < 0.

77 IL-13-stimulated expression of CCL26 (eotaxin-3) was inhibited in a dose-dependent manner, dem

78 The backbone dynamics of eotaxin-3 were determined from 15N NMR relaxation data u

79 els of eosinophil cationic protein (ECP) and eotaxin-3 were observed.

80 (BECs) produce CC chemokines, notably CCL26 (eotaxin-3), which recruits and activates eosinophils fro