|Other Names||Toll-interacting protein, TOLLIP|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP2163b was selected from the C-term region of human TOLLIP . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Component of the signaling pathway of IL-1 and Toll-like receptors. Inhibits cell activation by microbial products. Recruits IRAK1 to the IL-1 receptor complex. Inhibits IRAK1 phosphorylation and kinase activity (PubMed:11751856). Connects the ubiquitin pathway to autophagy by functioning as a ubiquitin- ATG8 family adapter and thus mediating autophagic clearance of ubiquitin conjugates. The TOLLIP-dependent selective autophagy pathway plays an important role in clearance of cytotoxic polyQ proteins aggregates (PubMed:25042851).|
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Provided below are standard protocols that you may find useful for product applications.
Toll like protein is a component of the signaling pathway of IL1 and Toll like receptors. It inhibits cell activation by microbial products. Tollip recruits IRAK1 to the IL1 receptor complex and inhibits IRAK1 phosphorylation and kinase activity. It oligomerizes and binds to TLR2 and the TLR4-MD2 complex via its C terminus. It exists as a complex with IRAK1 in unstimulated cells. Upon IL1 signaling, Tollip binds to the activated IL1 receptor complex containing IL-1RI, IL-1RacP and the adapter protein MyD88, where it interacts with the TIR domain of IL-1RacP. MyD88 then triggers IRAK1 autophosphorylation, which in turn leads to the dissociation of IRAK1 from Tollip and IL-1RAcP. TOLLIP also interacts with TLR2 and TLR4; TOLLIP overexpression inhibits nuclear factor kappa-B (NFKB) activation in response to lipopolysaccharide and IL1B.
Zhang, G., et al., J. Biol. Chem. 277(9):7059-7065 (2002).Bulut, Y., et al., J. Immunol. 167(2):987-994 (2001).Burns, K., et al., Nat. Cell Biol. 2(6):346-351 (2000).Volpe, F., et al., FEBS Lett. 419(1):41-44 (1997).
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