ライフサイエンスコーパス: eotaxin-3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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