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Details on Person TIRAP/Mal-deficient mice showed normal responses to the TLR3...
| Class:Id | Summation:937057 |
|---|---|
| _displayName | TIRAP/Mal-deficient mice showed normal responses to the TLR3... |
| _timestamp | 2012-11-15 22:18:04 |
| created | [InstanceEdit:937065] Shamovsky, V, 2010-08-25 |
| modified | [InstanceEdit:937292] Shamovsky, V, 2010-08-25 [InstanceEdit:975197] Shamovsky, V, 2010-09-22 [InstanceEdit:975771] Shamovsky, V, 2010-10-04 [InstanceEdit:977264] D'Eustachio, P, 2010-10-15 [InstanceEdit:2201356] Shamovsky, V, 2012-04-19 [InstanceEdit:2206275] Shamovsky, V, 2012-04-26 [InstanceEdit:2272817] D'Eustachio, P, 2012-05-25 [InstanceEdit:2559481] Shamovsky, V, 2012-11-02 [InstanceEdit:2586589] Shamovsky, V, 2012-11-15 |
| text | TIRAP/Mal-deficient mice showed normal responses to the TLR3, TLR5, TLR7, and TLR9 ligands, but were defective in TLR4 and TLR2 ligand-induced proinflammatory cytokine production (Horng et al. 2002,Yamamoto et al. 2002). In contrast, TLR4 ligand-induced activation of IRF-3 and expression of IFN-inducible genes were not impaired in TIRAP/Mal knockout macrophages or in mice lacking both MyD88 and TIRAP/Mal (Horng et al. 2002,Yamamoto et al. 2002). Thus, TIRAP/Mal is an essential adapter that is involved in the MyD88-dependent pathway via TLR4 and TLR2, but not in the MyD88-independent pathway. Mal contains a phosphatidylinositol 4,5-bisphosphate-binding domain required for retention in the plasma membrane. The intracellular TIR domains of TLR2 or 4 associate with Mal at the cytoplasmic side of the plasma membrane, which in turn facilitates the binding of MyD88 to the activated TLR, leading to NF-kB and MAPK activation [Nunez Miguel et al 2007]. |
| (summation) | [Reaction:2201316] Activated TLR2/4 interacts with MAL (TIRAP) [Homo sapiens] |
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