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results revealed that melatonin attenuated chemokine CCL24 levels through inhibition of the JNK pathway to hinder human osteosarcoma cell invasion, thereby highlighting the therapeutic potential of melatonin for osteosarcoma metastasis.
Study showed that CCL24 was upregulated in hepatocellular carcinoma (HCC) tissues and correlated with poor prognosis in HCC patients . Also, CCL24 was associated with the metastatic potential of HCC cell lines and promoted proliferation, migration, and invasion.
Mean eotaxin 2 concentrations in nasal fluid in patients with perennial allergic rhinitis and nonallergic and allergic chronic rhinosinusitis with nasal polyps patients were significantly higher in comparison to control subjects.
Review: eotaxins (CCL11, CCL24, and CCL26) play key role(s) during symptomatic inflammatory responses raised in response to allergic crisis of allergic asthma and atopic dermatitis
HMGB1 did not elicit chemotaxis of human eosinophils alone and had no effect in combination with the eosinophil chemotactic agent, eotaxin-2 (CCL24).
these data suggest that CCL26 and CCL24 are likely involved in the pathogenesis of chronic nasal hypereosinophilia, with a complex cooperation and different involvement of the various members of eotaxin family.
CCL11, CCL24, and CCL26 are increased in TB patients; hence, it seems that TB suppresses Th1 and the classic function of macrophages subsequently by inducing the chemokines' expression
CCL11, CCL24, and CCL26 has a role in the recruitment of extravillous trophoblast into decidual tissue and vessels.
Pregnancy associated environments increased local CCL24/CCR3, supporting the process of decidualization in human early pregnancy.
Phosphodiesterase 4 inhibitors, rolipram and RO-20-1724 have no effect on CCL24 expression in human primary bronchial epithelial cells.
The level of eotaxin expression and inflammatory cell count were measured in the material from nasal brushing in healthy controls and in patients with allergic rhinitis, asthma, and chronic obstructive pulmonary disease.
Study shows that CCL24 levels were significantly increased in age-related macular degeneration (AMD) patients despite Avastin treatment as compared with normal controls and those without Avastin.
After corticosteroid therapy, the expressions of Eotaxin and Eotaxin-2 in mucosal epithelia of nasal polyps were significantly decreased.
The expression of Eotaxin-1 and -2 in nasal polyposis and polyps was dramatically higher than in controls.
Serum CCL11 was increased in ulcerative colitis (UC) and less in Crohn's disease (CD), whereas CCL24 and CCL26 were increased only in UC. Colon expression of the CCL's was higher in UC vs. CD, and was induced by Th2 cytokines in colon epithelial cells.
CCR3 is differentially expressed on inflammatory cells in rheumatoid arthritis, while eotaxin-2, a potent CCR3 agonist, is differentially expressed in active disease.
The mean gene expression level for CCL11, CCL24, CCL26 was higher in skin changes of atopic dermatitis patients than in uninvolved skin.
stimulates lung fibroblast proliferation and collagen synthesis
Data show that induction of CCL2 and CCL24 was directly mediated by ligand-activated retinoic acid receptors.
alters eosinophil integrin function via mitogen-activated protein kinases
the increased airway eosinophils and mucous cell metaplasia in house dust mite-challenged Cd163-/- mice are mediated by augmented CCL24 production
TPL-2-regulated Ccl24 in CD11c+CD11b+ cells prevents accelerated type-2 mediated immunity to H. polygyrus.
this study shows that TPL-2 inhibits Ccl24 expression in lung dendritic cells, and blockade of Ccl24 prevents the exaggerated airway eosinophilia and lung inflammation in mice given house dust mites-pulsed Map3k8-/- dendritic cells
production in M-CSF-induced bone marrow-derived macrophages is synergistically induced by IL-4 and IL-10
Autologous transfer of peritoneal macrophages in to the airways of asthmatic mice reduces eotaxin production.
Data indicate that eotaxin 2 (CCL-24), which is known to influence eosinophil migration, was highly up-regulated in broncho-alveolar macrophages (BAMs).
The oesophageal production of CCL24 upon IL-13 stimulation is sufficient to promote eosinophil migration.
Results demonstrate a cooperative mechanism between interleukin-13 and eotaxin-2, where IL-13 mediates allergen-induced eotaxin-2 expression, and eotaxin-2 mediates IL-13-induced airway eosinophilia.
Distinct acidic and basic residues within CCR3 determine both receptor expression and activation by the eotaxins.
The eotaxin-2 pathway plays a fundamental role in eosinophil recruitment during ovalbumin-induced experimental asthma.
eosinophils via chemokine (C-C) receptor 3 have a central role in chronic allergic airway disease
CCL24 seems important for recruitment of eosinophils into BAL.
This gene belongs to the subfamily of small cytokine CC genes. 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 on resting T lymphocytes, a minimal activity on neutrophils, and is negative on monocytes and activated T lymphocytes. The protein is also a strong suppressor of colony formation by a multipotential hematopoietic progenitor cell line.
C-C motif chemokine 24
, eosinophil chemotactic protein 2
, myeloid progenitor inhibitory factor 2
, small inducible cytokine subfamily A (Cys-Cys), member 24
, small-inducible cytokine A24
, CC chemokine CCL24
, small inducible cytokine A24
, eotaxin-2-like protein
, eosinophil chemotactic protein-2
, small chemokine ligand 24