Tollip Antibody #4748
- WB
Supporting Data
| REACTIVITY | H Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 33 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Tollip Antibody detects endogenous levels of total Tollip protein.
Species Reactivity:
Human, Monkey
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding cysteine 229 of human Tollip. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses (1-4). TLRs recognize conserved motifs found in various pathogens and mediate defense responses (5-7). Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes (4). The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the Toll/Interleukin-1 receptor (TIR) domain (1). Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adaptor-like/TIR-associated protein (MAL/TIRAP), Toll-receptor-associated activator of interferon (TRIF), and Toll-receptor-associated molecule (TRAM) (8-10). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK (8,11-14). Activation of IKK leads to the degradation of IκB, which normally maintains NF-κB in an inactive state by sequestering it in the cytoplasm.
Tollip (Toll interacting protein) is an adaptor protein discovered to be associated with the IRAK complex and recruited to IL1-R following IL-1 stimulation (4). Overexpression of Tollip results in impaired NF-κB signaling (4). Tollip also associates directly with TLR2 and TLR4 and inhibits TLR-mediated signaling through inhibition of IRAK (5). Studies of Tollip deficient mice suggest that it plays a role in the regulation of inflammatory cytokines in response to IL-1 and LPS (6).
Limited Uses
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