|Application ||WB, ICC, E|
|Other Accession||AAH18272, 17390641|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||30282 Da|
|Application Notes||TOLLIP antibody can be used for the detection of TOLLIP by Western blot at 0.5 - 2 µg/mL. Antibody can also be used for immunocytochemistry starting at 2 µg/mL.|
|Other Names||TOLLIP Antibody: IL-1RAcPIP, Toll-interacting protein, toll interacting protein|
|Reconstitution & Storage||TOLLIP antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||TOLLIP Antibody is for research use only and 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.
TOLLIP Antibody: Toll-like receptors (TLRs) are evolutionarily conserved pattern-recognition molecules resembling the toll proteins that mediate antimicrobial responses in Drosophila. These proteins recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. The TLRs act through adaptor molecules to activate various kinases and transcription factors so the organism can respond to potential infection. These adaptor molecules include TOLLIP, MyD88, and TRIF. TOLLIP associates directly with TLR2 and TLR 4, acting as an inhibitor to TLR activation. This negative regulation of TLR signaling may serve to limit the production of proinflammatory mediators during infection and inflammation.
Takeda K, Kaisho T, and Akira S. Toll-like receptors. Annu. Rev. Immunol.2003; 21:335-76.
Janeway CA Jr. and Medzhitov R. Innate immune recognition. Annu. Rev. Immunol.2002; 20:197-216.
McGettrick AF and O’Neill LAJ. The expanding family of MyD88-like adaptors in Toll-like receptor signal transduction. Mol. Imm.2004; 41:577-82.
Zhang G and Ghosh S. Negative regulation of Toll-like receptor-mediated signaling by Tollip. J. Biol. Chem.2002; 277:7059-65.
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