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Figure 1

LPS-induced TLR4 activation induces the transcription of pro-inflammatory mediators, via the recruitment of adaptor molecules such as MyD88 and TRIF. LPS is mainly sensed through the activation of TLR4 by the LBP–LPS trigger complex. CD14 and MD-2 are critical elements in this receptor complex giving it responsiveness to LPS. TLR4 activation provokes the recruitment of four adaptor molecules, including MyD88 and TRIF. MyD88 activates the IKK complex via IRAK kinases/TRAF recruitment, lately leading to NFκB diffusion to the nucleus. TRAF6 activation also promotes MAPK activation and nuclear translocation, also inducing the transcription of pro-inflammatory cytokines. NFκB transcription also occurs in a MyD88-dependent pathway, via TRIF-mediated activation of the kinases TBK1 and RIP1. Full color version of this figure available via http://dx.doi.org/10.1530/JME-13-0079

This Article

  1. J Mol Endocrinol vol. 51 no. 2 R51-R64