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Mouse (Murine) IL-13 Protein expressed in Escherichia coli (E. coli) - ABIN1305069
Doherty, Kastelein, Menon, Andrade, Coffman: Modulation of murine macrophage function by IL-13. in Journal of immunology (Baltimore, Md. : 1950) 1994
Show all 3 Pubmed References
the intracellular interaction of IL-32theta;, PKCdelta, and STAT3 to regulate IL-13 and IL-13Ralpha2 synthesis, supporting the role of IL-32theta; as an inflammatory modulator.
Our present findings demonstrate the significance of the IL-13/periostin/IL-24 pathway in the pathogenesis of skin allergic inflammation and help to explain and support the utility of the inhibitors of this pathway such as dupilumab and tofacitinib.
Targeted interventions against IL-13 should be evaluated to decrease severity of human rhinovirus illness in infancy and early childhood.
Results suggest that inflammation provoked by obesity, notably by increased expression of the cytokine IL-13, could play an important role in the carcinogenesis of obesity-related colorectal cancer.
These data highlight an essential mechanism in asthma pathogenesis by demonstrating that ILC2s are responsible for bronchial epithelial TJ barrier leakiness through IL-13.
miR-98-5p may affect the occurrence and development of bronchial asthma in children via affecting expression of IL-13
IL-13/IL-13Ralpha2 axis can mediate signal transduction in situ via AP-1 pathway in Glioblastoma multiforme.
The current studies demonstrate that the proinflammatory IL-13 induces Bcl-2 in airway epithelial cells. Because IL-13 also induces the proapoptotic Bik, targeted blocking of Bcl-2 function switches IL-13 into a cell death inducer.
These findings provide a potential pathophysiologic link between increased IL-13 expression found among patients with chronic rhinosinusitis (CRS) and the subsequent neo-osteogenesis observed in certain CRS subsets.
This study demonstrated that the G allele at the rs20541 locus of IL-13 gene was not risk factors for severe Hand, Foot, and Mouth Disease (HFMD) in either male or female patients.
C allele of IL-13 is a risk factor for glioma susceptibility
Because of the link of IL-13 to allergy, we looked for IgE and found it decorating the surface of mast cells and antigen-presenting follicular dendritic cells in capsules and lymph nodes infiltrated by anaplastic lymphoma cells
rs20541 CT/TT genotypes may be a risk factor for systemic lupus erythematosus, probably by increasing the level of IL-13.
findings concluded that IL-13 inhibited chemotherapy sensitivity of NK/T-cell lymphoma cells by regulating ABCC4, disrupting which may effectively improve the therapy protocols against resistant NK/T-cell lymphoma.
IL-13 serum levels correlated with a favorable outcome in polytraumatic patients with bacteremia
These findings suggest that CISH plays a key role in the eosinophilic inflammation associated with bronchial asthma by regulating IL-13-induced CCL26 production.
The concentration of Th2-related cytokines (IL-5 and IL-13) in asthmatic children with Rhinovirus(+) was significantly higher than those with Rhinovirus(-).
results suggest that SOX11 acts as a trans-acting transcriptional factor downstream of STAT6 and that in lung fibroblasts the IL-13 signals are hierarchically controlled by STAT6 and SOX11
miR-21 levels positively correlated with IL-13 levels and eosinophil percentage in asthmatic children
This study indicated that high arginase activity and IL-13 concentration in the serum and ARG1 rs2781666 G/T genotype might increase the risk of asthma in susceptible population.
this paper shows involvement of IL-13 signaling via a STAT6 independent mechanism during murine IgG2a development following viral vaccination
Nod1(+/+) mice with chronic H. pylori infection exhibited significantly increased gastric IL-33 and splenic IL-13 responses, but decreased IFN-gamma responses, when compared with Nod1(-/-) animals. Collectively, our data identify NOD1 as an important regulator of mucosal IL-33 responses in H. pylori infection. We suggest that NOD1 may play a role in protection against excessive inflammation.
these results indicate that multiple signaling pathways downstream of IL-13Ralpha1 activation play a role in the toxic effects of IL-13 in dopaminergic neurons in the presence of mild oxidative stress and suggest that any of these pathways might provide potential targets for the treatment of Parkinson's disease.
S1PR2 facilitates lung fibrosis through the mechanisms involving augmentation of IL-13 expression and its signaling in BALF cells.
Combined blockade of the IL-13 and IL-33 pathways leads to a greater inhibition of type 2 inflammation over inhibition of either pathway alone.
Both pre- and post-transcriptional processes may be involved in the AR modulation of ILC2 IL-5 and IL-13 production.
the endothelial barrier was preserved in respiratory epithelium isolated from MCU-/- mice after exposure to IL-13. In the ovalbumin-model of allergic airway disease, MCU deficiency resulted in decreased apoptosis within the large airway epithelial cells. Concordantly, expression of the tight junction protein ZO-1 was preserved, indicative of maintenance of epithelial barrier function
controls the rate of epithelial cell movement through the epidermis and acts as a molecular bridge between intraepithelial lymphocytes and epithelial cells
results demonstrate that IL-13 is a major regulator of radiation-induced lung injury and demonstrates that strategies focusing on IL-13 may be useful in screening for timely delivery of anti-IL-13 therapeutics.
Using a mouse model of Th2-mediated inflammation induced by OVA-allergen, this study observed elevated lung amounts of IL-13 and IL-4 accompanied by increased autophagosome levels, determined by LC3BII protein levels and immunostaining.
Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages.
IL-13 is able to signal independent of the IL-4Ra chain in AD (atopic dermatitis), which may lead to the identification of molecular pathways downstream of IL-13 signaling that could be targeted in future therapies for AD.
the presence of interleukin-13 (IL-13), which can convert inflammatory into Ym1+ alternatively activated macrophages, at (acinar-to-ductal metaplasia [ADM]), which then gives rise to pancreatic intraepithelial neoplasia lesions, is reported.
Data indicate that interleukin-33 (IL-33)-induced Interleukin-13 (IL-13) production by type-2 helper T cells (Th2 cells) Is dependent on epidermal growth factor receptor (EGFR) expression.
this study shows that environmental IL-13 plays a role in conditioning early thymic progenitors lineage choice, which would impact T cell development
IL-4 and IL-13 are required to effectively polarize macrophages/dendritic cells to an M2a phenotype and to promote recovery from acute kidney injury.
this study shows that ST2 regulates early IL-13 production in fungus-induced allergic airway inflammation
These observations suggest that IL-4 and IL-13 likely operate through the Heteroreceptor and influence Th17 cells to convert to Th1 cells and to acquire increased sensitivity to suppression, leading to control of immune-mediated CNS inflammation.
MIF-deficient mice have reduced Nippostrongylus brasiliensis burden and mounted an enhanced type 2 immune response, including increased Gata3 expression and IL-13 production in the mesenteric lymph nodes
T helper (Th) type 2 cell cytokine IL-13 modulates airway contraction by secreting matrix metalloproteinase-1 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