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Validated All-in-One™ qPCR Primer for CCL11(NM_002986.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene is one of several Cys-Cys (CC) cytokine genes clustered on the q-arm of chromosome 17. Cytokines are a family of secreted proteins involved in immunoregulatory and inflammatory processes. The CC cytokines are proteins characterized by two adjacent cysteines. The cytokine encoded by this gene displays chemotactic activity for eosinophils, but not mononuclear cells or neutrophils. This eosinophil specific chemokine assumed to be involved in eosinophilic inflammatory diseases such as atopic dermatitis, allergic rhinitis, asthma and parasitic infections.
Gene References into function
- Eotaxin/CCL11 may down-regulate production of the neutrophil chemoattractant IL-8/CXCL8 by vascular endothelial cells in vivo, acting as a negative regulator of neutrophil recruitment.
- Expression of eotaxin parallels eosinophil accumulation in the vesiculobullous stage of incontinentia pigmenti
- bronchial expression increased in exacerbated chronic bronchitis
- Histamine and serotonin stimulate eotaxin and augment the expression of eotaxin mRNA production by a human lung fibroblast cell line.
- Pretreatment or co-treatment with each of the eotaxins augmented PMAtate-induced superoxide generation, concentration-dependent degranulation of eosinophil peroxidase, & potentiation of A23187-induced degranulation.
- Intradermal injection of CCL11 induces recruitment of eosinophils, basophils, neutrophils, and macrophages as well as features of early- and late-phase allergic reactions in atopic and nonatopic volunteers.
- Eotaxin-1 protein and mRNA are synergistically up-regulated in airway fibroblasts from asthmatic and normal subjects by TGF-beta 1 and IL-13 in combination.
- Infiltrating eosinophils that express eotaxin and the changes of blood eotaxin levels during steroid therapy suggest that eotaxin may be associated with idiopathic eosinohilic esophagitis
- results suggest that expression of chemokine receptor 3(CCR3) and its ligand eotaxin/CCL11 plays a role in the recruitment and retention of CD30(+) malignant T cells to the skin
- eosinophil responses mediated by chemokines acting at CCR3 may be regulated by two distinct mechanisms: the antagonistic effects of CXCR3 ligands and the sequestration of CCL11 by CXCR3-expressing cells
- IL-5 and eotaxin are associated with acute exacerbation of asthma.
- Production of Eotaxin by eosinophils already within nasal polyps is likely an important mecahanism by which even more eosinophils may be recruited into the polyp tissue.
- High local levels of eotaxin as present in the blister fluid correspond to the high state of activation of the infiltrated eosinophils in tissue eosinophilia in pemphigoid gestationis
- the two N-terminal motifs of eotaxin must cooperate with other regions to successfully bind and activate CCR3
- Our results suggest that the polymorphisms of the eotaxin gene family are associated with the susceptibility of asthma and Eotaxin-3 might play the critical role for the recruitment of eosinophils and the maintenance of IgE levels.
- Asthmatics who were vaccinated with a single dose of influenza subunit vaccine showed elevated eotaxin seum levesls.
- Results show that human chondrocytes express eotaxin-1, that its expression is induced by treatment with interleukin-1beta and TNF-alpha, and suggest that it plays an important role in cartilage degradation in osteoarthritis.
- However, In the presence of TNF-alpha, melatonin promoted RANTES melatonin, respectively) expression in a dose dependent manner in A549 cells).
- Cigarette smoke may directly cause the release of IL-8 from HASMC, an effect enhanced by TNF-alpha which is overexpressed in COPD
- Single nucleotide polymorphisms at the CCL11 locus is an important determinant of serum total IgE levels among patients with asthma.
- Eotaxin (CCL11) is a CC chemokine, whose systemic levels might be associated with coronary artery disease (CAD) and genetic variants predispose to the myocardial infarction (MI).
- mast cell beta-tryptase selectively cleaves asthmatic airway smooth muscle (ASM)-derived eotaxin and RANTES and abrogates their chemotactic activities, thus providing an explanation for the eosinophil paucity in asthmatic ASM bundles
- serum expression of eotaxin & IL-5 were significantly increased in patients with strongyloidiasis compared with controls; this rise suggests that selective mediators of the eosinophil can have a role in immunity against S. stercoralis in human infection
- A highly significant association of the newly studied (GAAGGA)(n) hexanucleotide repeat with asthma (p = 3x10(-6)), log(10)TsIgE (p = 0.006) and eotaxin levels (p = 0.004) was observed.
- The Th2 cytokine IL-4 preferentially stimulated eotaxin expression. IL-4 activated the eotaxin promoter and STAT6 binding to it.
- A significant correlation exists between bronchoalveolar lavage concentration of CCL11 and eosinophils in veterans with sulfur mustard gas-induced pulmonary fibrosis.
- There were significantly greater concentrations of the chemokines CCL3 and CCL11 in plasma of leprosy patients than in non-infected individuals
- This study finding provide a strong evidence that Eotaxin 1 Thr23Thr homozygote has a protective effect on asthma and significantly decreases plasma Eotaxin 1 concentrations in asthmatics in Taiwan.
- Developing lung expresses the eotaxins and functional CCR3 receptor.
- Results suggest that dexamethasone, depending on the exposure duration, can either inhibit or enhance IL-4-induced expression and production of eotaxin in lung fibroblasts.
- the eotaxin gene may play a crucial role in the development of extrinsic Atopic Dermatitis, probably with other genetic factors.
- This study raises the hypothesis that high serum levels of eotaxin predict less radiographic progression in early RA patients.
- Gram-negative bacteria inhibited the release of eotaxin-1 from human airway smooth muscle cells.
- except for IL-6 and eotaxin, CLL B-cells and their normal counterparts produce and secrete similar amounts of cytokines and cytokine receptors in vitro.
- There are elevated concentrations of the chemokines MDC, eotaxin, I-TAC, and MCP-1 in malignant pleural effusions.
- In a collagen matrix three-dimensional model, CCL11-induced eosinophil migration is fully dependent on both RhoA GTP-binding protein and Rho-associated protein kinase (ROCK).
- CCL11 mediates airway smooth muscle migration
- Eotaxin-1, Eotaxin-2 and Eotaxin-3 gene polymorphisms and gene-gene interactions among them are associated with the development of asthma.
- protein kinase C betaII augments NF-kappaB-mediated TNF-alpha-induced transcription of the target gene CCL11, promoting p65 association with the CCL11 promoter, in human airway smooth muscle cells by phosphorylating p300/CBP-associated factor
- Gene expression of eotaxin-1/CCL11 showed relevant downregulation in four cases and a modest twofold decrease in three of the patients studied with EE treated with topical steroids.
- activation of prostanoid thromboxane A(2) receptors in a Th2-dominant microenvironment might exacerbate the eosinophilic inflammation of the airways by synthesis and release of CCL11 from bronchial smooth muscle cells
- CCL11 induces SOCS1 and SOCS3 expression in murine macrophages, human monocytes, and dendritic cells and inhibits GM-CSF-mediated STAT5 activation and IL-4-induced STAT6 activation in a range of hematopoietic cells.
- intestinal macrophage and epithelial cell-derived eotaxin-1 plays a critical role in the regulation of eosinophil recruitment in colonic eosinophilic disease such as pediatric ulcerative colitis
