IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway.

By Katherine A. Fitzgerald, S. McWhirter, K. Faia, D. C. Rowe, E. Latz, D. Golenbock, A. Coyle, S. Liao, T. Maniatis. Nature Immunology, 2003

1,192 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ef4ccd0a32b13a33fc0b51e33ff7ae36d43d3f88

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Citations in the corpus

Hepatitis C virus protease NS3/4A cleaves mitochondrial antiviral signaling protein off the mitochondria to evade innate immunity. (2005, background): “In response to a viral challenge, IRF3 is phosphorylated by the IKK-like kinases TBK-1 and IKKe [ 7 , 8]. Phosphorylation of IRF3 leads to its dimerization and translocation into the nucleus.”
Direct activation of STING in the tumor microenvironment leads to potent and systemic tumor regression and immunity (2015, methodology): “Luciferase Assay 10(4) HEK293T cells were seeded in 96-well plates and transiently transfected (Lipofectamine 2000) with human IFN-b firefly reporter plasmid (Fitzgerald et al., 2003) and TK-Renilla luciferase reporter for normalization.”
Lipopolysaccharide signaling in endothelial cells (2006, background): “111 In a parallel pathway, TRAF family member-associated NF- κ B activator (TANK) binding kinase 1 (TBK1) and IKK e (also known as IKKi) interact with TRIF and mediate activation of IRF3, leading to the induction of IFN β”
The PINK1-PARKIN mitochondrial ubiquitylation pathway drives a program of TBK1 activation and recruitment of OPTN and NDP52 to promote mitophagy (2015, background): “As expected (Fitzgerald et al., 2003), Poly(I:C) treatment resulted in robust IRF3 phosphorylation, but interestingly, AO treatment did not induce IRF3 phosphorylation (Figures 1D and 1E).”
NF-κB activation as a pathological mechanism of septic shock and inflammation (2006, unknown): “IKK⑀/ IKKi plays a pivotal role in integrating inflammatory signals into a coordinated activation of IRF-3 and NF-␬B (94) as well as coordinated activation of NF-␬B and C/EBP␤ or C/EBP␦ (73), augmenting the inflammatory response.”
Cyclic GMP-AMP Synthase is Activated by Double-stranded DNA-Induced Oligomerization (2013, background): “Phosphorylation of IRF-3 by TBK1 at the signaling complex on STING promotes the oligomerization of IRF-3 and its translocation into the nucleus, where it activates the transcription of the IFN-b gene together with the transcription factor NF-kB (Fitzgerald et al., 2003; Tanaka and Chen, 2012).”
Integrative genomic approaches identify IKBKE as a breast cancer oncogene. (2007, background): “The following antibodies were used: anti-IKK3 K-14 (Santa Cruz, CA) (Figure 3) or anti-IKK3 c-terminal (Sigma) (Figures 3–6), anti-IkBa C-15 (Santa Cruz, CA), anti-NF-kB H-119 (Santa Cruz, CA), anti-MEK1/2 (Cell Signaling), anti-Cyclin D1 (Neomarkers), or anti-IRF3 (Santa Cruz, CA).”
Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. (2006, background): “Activation of IRF3 leads to expression of interferon and interferon inducible genes through activation of TANK-binding kinase and IKKε (32).”
Pathogen recognition and innate immunity. (2006, unknown): “TRAM, another TIR-domain-containing adaptor, is specifically involved in TLR4 signaling (Fitzgerald et al., 2003b; Yamamoto et al., 2003b).”
LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF (2003, methodology): “IKK (38, 39) and TANK-binding kinase (TBK)1 (40–42) are key regulators of the IRF-3 and IRF-7 activation pathways in cells that have been exposed to some viruses and/or activated by dsRNA via TLR3 (43, 44).”
The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation. (2008, background): “Consistently, overexpression of MITA caused translocation of IRF3 into the nucleus (Figure 2C), whereas MITA-mediated IRF-E activation was inhibited by dominant-negative mutants of IRF3 and IRF7 (Figure 2D).”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “CBP and p300, bind to target sequences in DNA, such as IFN-stimulated response elements (89, 330).”