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Platelets contain all of the proteins (e.g., MyD88 and interferon regulatory factor 3 (IRF3)) that are required for signal transduction through TLR4 and so at first glance it would appear that platelets utilise the same mechanisms as in nucleated cells [2,25].
Alternatively, it has been described that TLR stimulation can activate a MyD88-independent alternative pathway mediated by TIR-domain-containing adapter-inducing interferon-[beta] (TRIF) and IRF3. TRIF, one of the TIR domaincontaining adaptors, is a MyD88 homologous protein, which is specifically implicated in the TLR3- and TLR4-mediated MyD88-independent pathway .
MAVS and TRIF then trigger signaling cascades leading to the activation of different cytosolic kinases (I[kappa]B kinases (IKK) and TANK-binding kinase 1 (TBK1)), which in turn induce activation of the key transcription factors NF-[kappa]B and IRF3 [79, 80].
Tian et al., "Endoplasmic reticulum stress regulates the innate immunity critical transcription factor IRF3," Journal of Immunology, vol.
Expression of the IFN[beta] gene is controlled by cooperative activation of NF-[kappa]B, ATF2/c-Jun, IRF3, and IRF7.
First, we aimed to describe the regulation of NF-[kappa]B, IRF3, and indirectly AP-1 through TLR4 signaling Pathway activation in PBMC in response to an acute bout of eccentric exercise in young female subjects.
This coordinated response is dependent on TBK-1 and IRF3 but occurs independently of STAT1 and STAT2 .
RLRs mediate type I and type IIIIFN expression through an adapter molecule, IFN-[beta] promoter stimulator-1 (IPS-1), and subsequent activation of IRF3 and NF-[kappa]B signal transduction pathways.
Inborn errors underlying herpes simplex encephalitis: From TLR3 to IRF3. J Exp Med 2015; 212:1342-3
MAPK (mitogen associated protein kinase); NF[kappa]B (nuclear factor kappa light chain enhancer of activated B-cells); IRF3 (interferon regulatory factor 3); AP-1 (activator protein 1).
MyD88-independent pathway involves TRIF and TRAM adaptor proteins, the activation of TRAF3, and downstream induction of TBK1 and IKK[epsilon], which are responsible for the recruitment and activation of the transcription factor, IFN regulatory factor 3 (IRF3).
TRIF plays a pivotal role following the activation of Toll-like receptor (TLR) 3 and 4 signaling, leading to the production of inflammatory mediators through the activation of several transcription factors, including NF-[kappa]B, IRF3, and AP-1 [8-11].
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