|Other Names||Toll-interacting protein, TOLLIP|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1521a was selected from the N-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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Toll-interacting protein (Tollip) was initially identified as an important constituent of the IL-1R signaling pathway. Recently it was showed that this adapter protein is also involved in TLR2 and TLR4 signaling pathways. Tollip coimmunoprecipitates with TLR2 and TLR4 and overexpression of Tollip was shown to inhibit NF-kB activation in response to TLR2 and TLR4 signaling. Human TOLLIP protein is 274-amino acid, which is 97% identical to the mouse sequence. Structurally, Tollip contains a type II C2 motif. Immunoblot analysis showed expression of a 30-kD protein in numerous tissues and cell lines. Functionally, Tollip inhibits cell activation by microbial products, recruits IRAK1 to the IL-1 receptor complex and inhibits IRAK1 phosphorylation and kinase activity. Since the inhibition by Tollip is mediated through its ability to suppress the activity of IRAK, Tollip may act as moderator of the inflammatory response following TLR activation.
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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