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IL31, which is made principally by activated Th2-type T cells, interacts with a heterodimeric receptor consisting of IL31RA (MIM 609510) and OSMR (MIM 601743) that is constitutively expressed on epithelial cells and keratinocytes. Additionally we are shipping Interleukin 31 Antibodies (115) and Interleukin 31 Proteins (41) and many more products for this protein.
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Human IL31 ELISA Kit for Sandwich ELISA - ABIN1672880
Ip, Wong, Li, Li, Cheung, Lam et al.: Interleukin-31 induces cytokine and chemokine production from human bronchial epithelial cells through activation of mitogen-activated protein kinase signalling pathways: implications for the ... in Immunology 2007
Show all 2 references for ABIN1672880
Mouse (Murine) IL31 ELISA Kit for Sandwich ELISA - ABIN1672895
Dillon, Sprecher, Hammond, Bilsborough, Rosenfeld-Franklin, Presnell, Haugen, Maurer, Harder, Johnston, Bort, Mudri, Kuijper, Bukowski, Shea, Dong, Dasovich, Grant, Lockwood, Levin, LeCiel, Waggie et al.: Interleukin 31, a cytokine produced by activated T cells, induces dermatitis in mice. ... in Nature immunology 2004
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Suggest that IL-31 gene may play a role in the development of systemic lupus erythematosus.
High IL31 expression is associated with Endometrial Cancer.
In a CML (show BCR ELISA Kits) patient with pruritus receiving imatinib mesylate, IL-31 and IL-33 (show IL33 ELISA Kits) serum levels were significantly higher than controls. Imatinib could cause keratinocyte injury, the release of IL-33 (show IL33 ELISA Kits), and the consequent interaction with its receptor on mast cells, inducing IL-31 secretion. The IL-31/IL-33 (show IL33 ELISA Kits) axis may be involved in the pathogenesis of skin side effects related to imatinib mesylate treatment.
Distinct polymorphic variants of the IL-31 gene may be involved in the patho-genesis of mastocytosis, and IL-31 may be involved in the induction of pruritus in patients with mastocytosis.
Serum/pleural fluid IL-31 levels are elevated in tuberculous pleural effusion.
both SCF (show KITLG ELISA Kits) and IL-31 play an important role in mediating inflammation and enhancing severity of atopic asthma.
IL-31 affects keratinocyte differentiation in multiple ways and the IL-1 (show IL1A ELISA Kits) cytokine network is a major downstream effector of IL-31 signaling in deregulating the physical skin barrier.
Oncostatin M (show OSM ELISA Kits) and interleukin-31: Cytokines, receptors, signal transduction and physiology.
The results of our analyses regarding serum levels and receptor expression do not suggest a central role of IL-31 in Mycosis fungoides/Sezary syndrome pathogenesis.
In summary, TGF-beta1 (show TGFB1 ELISA Kits) and IL-31 were linked to progression from chronic hepatitis B to liver cirrhosis, and correlated well with the severity of disease.
IL-31 upregulates IL-31RA (show IL31RA ELISA Kits) expression in DRG neuron cell bodies, and cutaneous-injected IL-31-induced itching is enhanced by DRG IL-31RA (show IL31RA ELISA Kits) expression in mice
our results suggest a functional cooperation between NFAT1 (show NFAT1 ELISA Kits) and JunB (show JUNB ELISA Kits) in mediating IL-31 gene expression in CD4 (show CD4 ELISA Kits)(+) T cells
Data not only illustrate various functions that cysteines perform during IL-31 biosynthesis and secretion, but also highlight their potential roles in cytokine effector functions.
IL-31 may be involved in promoting the dermatitis and epithelial responses that characterize allergic and non-allergic diseases
IL-31 interaction with IL-31 receptor (IL-31R) is identified in an acute model of T helper cell type 2 inflammation in the lung.
these data provide the first evidence of a function for IL-31-IL-31R interactions in limiting the magnitude of type 2 inflammatory responses within the intestine.
IL31, which is made principally by activated Th2-type T cells, interacts with a heterodimeric receptor consisting of IL31RA (MIM 609510) and OSMR (MIM 601743) that is constitutively expressed on epithelial cells and keratinocytes. IL31 may be involved in the promotion of allergic skin disorders and in regulating other allergic diseases, such as asthma (Dillon et al., 2004