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Human IL-13 Kit ELISA pour Sandwich ELISA - ABIN625011
Zurawski, de Vries: Interleukin 13, an interleukin 4-like cytokine that acts on monocytes and B cells, but not on T cells. dans Immunology today 1994
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Rat (Rattus) IL-13 Kit ELISA pour Sandwich ELISA - ABIN416369
Fang, Li, Liang, Xue, Liu, Yang, Gao, Jiang: Downregulation of SUMF2 gene in ovalbumin-induced rat model of allergic inflammation. dans International journal of clinical and experimental pathology 2016
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Pig (Porcine) IL-13 Kit ELISA pour Sandwich ELISA - ABIN415833
Baker, Romero, Bach, Strom, Gamelli, Majetschak: Systemic release of cytokines and heat shock proteins in porcine models of polytrauma and hemorrhage*. dans Critical care medicine 2012
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Guinea Pig IL-13 Kit ELISA pour Sandwich ELISA - ABIN364909
Maarsingh, Dekkers, Zuidhof, Bos, Menzen, Klein, Flik, Zaagsma, Meurs: Increased arginase activity contributes to airway remodelling in chronic allergic asthma. dans The European respiratory journal 2011
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Mouse (Murine) IL-13 Kit ELISA pour Sandwich ELISA - ABIN415504
Fang, Shi, Wu, Zhang, Zhong, Deng, Zhang, Xie: Targeted inhibition of GATA-6 attenuates airway inflammation and remodeling by regulating caveolin-1 through TLR2/MyD88/NF-κB in murine model of asthma. dans Molecular immunology 2016
investigated the role of six potentially functional variants of the IL4 (Montrer IL4 Kits ELISA), IL13, and IL4R (Montrer IL4R Kits ELISA) genes in gastrointestinal cancer; both IL13 rs20541 and rs1800925 were not associated with gastrointestinal cancer risk for any of the genetic models and subgroup analyses [meta-analysis]
IL13 in bronchial epithelial cells and bronchial alveolar lavage fluid, rather than RAD50 (Montrer RAD50 Kits ELISA), IL4 (Montrer IL4 Kits ELISA), or IL5 (Montrer IL5 Kits ELISA), is more likely to be the asthma susceptibility gene.
We also found that the activation of H4R (Montrer HRH4 Kits ELISA) caused the release of IL-13 and RANTES (Montrer CCL5 Kits ELISA) on human mast cells.these data demonstrate that the H4R (Montrer HRH4 Kits ELISA) activates divergent signaling pathways to induce cytokine and chemokine (Montrer CCL1 Kits ELISA) production in human mast cells
IL13 Arg130Gln genotypes can play a role in genetic susceptibility to allergy via regulation of serum total IgE levels and affecting IFN-gamma (Montrer IFNG Kits ELISA) gene expression.
The GG genotype of IL-13 130A/G cytokine gene might be involved in the induced production of total IgE and IL-13 cytokine serum levels suggesting IL-13 may be important in the signalling of asthma.
STAT6 (Montrer STAT6 Kits ELISA)-TMEM16A (Montrer ANO1 Kits ELISA)-ERK1/2 (Montrer MAPK1/3 Kits ELISA) signal pathway and TMEM16A (Montrer ANO1 Kits ELISA) channel activity are required for the IL-13-induced TMEM16A (Montrer ANO1 Kits ELISA) mediated mucus production
TGF-beta (Montrer TGFB1 Kits ELISA)- and IL-13-producing mast cells might be key players in the development of bone marrow fibrosis.
this study shows that low expression of tristetraprolin (Montrer ZFP36 Kits ELISA) is associated with glioma growth and metastasis by targeting IL-13
this study shows that IL-13 gene polymorphism is associated with allergic rhinitis and/or allergic conjunctivitis in Finnish asthma patients
The role of Th2 cytokines (IL-4 (Montrer IL4 Kits ELISA), IL-13) and STAT6 (Montrer STAT6 Kits ELISA) in Th1 (Montrer TH1L Kits ELISA)/Th2 imbalance.
These data demonstrate that multiple pathogenic strains of RSV induce IL-13-producing group 2 innate lymphoid cell proliferation and activation through a TSLP (Montrer TSLP Kits ELISA)-dependent mechanism in a murine model and suggest the potential therapeutic targeting of TSLP (Montrer TSLP Kits ELISA) during severe RSV infection.
The soluble antigen from A. cantonensis could promote the Chil3 expression in macrophage and microglial cell lines induced by interleukin-13.
The reduction in fibrosis observed when IL-13 signalling is suppressed is not dependent on increased IFN-gamma (Montrer IFNG Kits ELISA) activity. Instead, by reducing compensatory increases in type 1-associated inflammation, therapeutic strategies that block IFN-gamma (Montrer IFNG Kits ELISA) and IL-13 activity simultaneously can confer greater protection from progressive fibrosis than IL-13 blockade alone.
Ellagic acid treatment augmented specific IL-10 (Montrer IL10 Kits ELISA) production in response to S. mansoni antigenic stimulation. However, specific IL-1beta (Montrer IL1B Kits ELISA), IL-4 (Montrer IL4 Kits ELISA), IL-12 (Montrer IL12A Kits ELISA), IL-13, IL-17A (Montrer IL17A Kits ELISA), TNF-alpha (Montrer TNF Kits ELISA) and IFN-gamma (Montrer IFNG Kits ELISA) production were significantly reduced with ex vivo and in vivo ellagic acid treatment.
The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL-13 secreted by CD11b(+)Ly6C(lo) monocytes may be associated with recovery from liver damage.
PLD1 activation enhanced binding of ROCK1 (Montrer ROCK1 Kits ELISA) to ATF-2 (Montrer ATF2 Kits ELISA) and leads to increased expression of IL-13
Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis.
IL-25 and CD4(+) TH2 cells enhance type 2 innate lymphoid cell-derived IL-13 production, which promotes IgE-mediated experimental food allergy.
Placenta growth factor (Montrer PGF Kits ELISA) augments airway hyperresponsiveness via leukotrienes and IL-13.
Natural helper cells contribute to pulmonary eosinophilia by producing IL-13 via IL-33/ST2 pathway in a murine model of respiratory syncytial virus infection
T helper (Th) type 2 cell cytokine IL-13 modulates airway contraction by secreting matrix metalloproteinase-1 (Montrer MMP1 Kits ELISA) from the smooth muscle cells via phosphatidylinositol 3-kinase activation and changing cell-to-matrix interactions.
This gene encodes an immunoregulatory cytokine produced primarily by activated Th2 cells. This cytokine is involved in several stages of B-cell maturation and differentiation. It up-regulates CD23 and MHC class II expression, and promotes IgE isotype switching of B cells. This cytokine down-regulates macrophage activity, thereby inhibits the production of pro-inflammatory cytokines and chemokines. This cytokine is found to be critical to the pathogenesis of allergen-induced asthma but operates through mechanisms independent of IgE and eosinophils. This gene, IL3, IL5, IL4, and CSF2 form a cytokine gene cluster on chromosome 5q, with this gene particularly close to IL4.
, T-cell activation protein P600