A Dimer of the Toll-Like Receptor 4 Cytoplasmic Domain Provides a Specific Scaffold for the Recruitment of Signalling Adaptor Proteins
Figure 5
Modelling suggests a molecular explanation for the caspase 1 dependence of Mal and the malfunctional human polymorphism Ser180Leu.
The models are shown as van der Waal surface representations. (A) Side view showing the position of the BB loop (green) and the phosphorylated tyrosine, Tyr86. In the complex this part of Mal forms the interface with TLR4. The position of the α-E helix (red) which is cleaved out by caspase 1 is shown on the opposite surface to the BB loop. (B) Back view of Mal (rotated 90° to the right relative to (A)). (C), (D) Mal with the α-E helix removed highlighting the deep groove created and the exposed position of the otherwise buried Ser180 residue (yellow).