|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_062564, 9665234|
|Calculated MW||Predicted: 19 kDa |
Observed: 22 kDa
|Application Notes||IL-36G antibody can be used for detection of IL-36G by Western blot at 1 - 2 µg/ml.|
|Target/Specificity||IL36G; IL-36G antibody is human specific. IL-36G antibody will not cross-react with IL-36A or IL-36B.|
|Reconstitution & Storage||IL-36G antibody can be stored at 4℃ for three months and -20℃, stable for up to one year.|
|Precautions||IL-36G Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||IL1E, IL1F9, IL1H1, IL1RP2|
|Function||Cytokine that binds to and signals through the IL1RL2/IL-36R receptor which in turn activates NF-kappa-B and MAPK signaling pathways in target cells. Part of the IL-36 signaling system that is thought to be present in epithelial barriers and to take part in local inflammatory response; similar to the IL-1 system with which it shares the coreceptor IL1RAP. Seems to be involved in skin inflammatory response by acting on keratinocytes, dendritic cells and indirectly on T-cells to drive tissue infiltration, cell maturation and cell proliferation. In cultured keratinocytes induces the expression of macrophage, T-cell, and neutrophil chemokines, such as CCL3, CCL4, CCL5, CCL2, CCL17, CCL22, CL20, CCL5, CCL2, CCL17, CCL22, CXCL8, CCL20 and CXCL1; also stimulates its own expression and that of the prototypic cutaneous proinflammatory parameters TNF-alpha, S100A7/psoriasin and inducible NOS. May play a role in proinflammatory responses during particular neutrophilic airway inflammation: activates mitogen-activated protein kinases and NF-kappa B in primary lung fibroblasts, and stimulates the expression of IL-8 and CXCL3 and Th17 chemokine CCL20 in lung fibroblasts. May be involved in the innate immune response to fungal pathogens, such as Aspergillus fumigatus.|
|Tissue Location||Highly expressed in tissues containing epithelial cells: skin, lung, stomach and esophagus. Expressed in bronchial epithelial. In skin is expressed only in keratinocytes but not in fibroblasts, endothelial cells or melanocytes. Up- regulated in lesional psoriasis skin. Expressed in monocyte- derived dendritic cells and M1 macrophages|
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Provided below are standard protocols that you may find useful for product applications.
IL-36G is is a member of the interleukin 1 cytokine family whose gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2 (1). IL-36G is thought to activate the NF-kappaB pathway through IL-1 receptor family members IL-1RL2 and IL-1RAcP (2). Like the related proteins IL-36A and IL-36B, IL-36G requires post-translational processing for full agonist activity, but the cleavage mechanism is currently unknown (3). IL-36G expression is stimulated by interferon-gamma, tumor necrosis factor-alpha and interleukin 1 (4). The IL-36 cytokines have been suggested to amplify Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells (5).
Smith DE, Renshaw BR, Ketchem RR, et al. Four new members expand the interleukin-1 superfamily. J. Biol. Chem. 2000; 275:1169-75.
Towne JE, Garka KE, Renshaw BR, et al. Interleukin (IL)-1F6, IL-1F8, and IL-1F9 signal through IL-1Rrp2 and IL-1RAcP to activate the pathway leading to NF-kappaB and MAPKs. J. Biol. Chem. 2004; 279:13677-88.
Towne JE, Renshaw BR, Douangpanya J, et al. Interleukin-36 (IL-36) ligands require processing for full agonist agonist (IL-36a, IL-36b, and IL-36g) or antagonist (IL-36Ra) activity. J. Biol. Chem. 2011; 286:42594-602.
Chustz RT, Nagarkar DR, Popowski JA, et al. Regulation and function of the IL-1 family cytokine IL-1F9 in human bronchial epithelial cells. Am. J. Respir. Cell Mol. Biol. 2011; 45:145-53.
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