Signaling Pathways to the Assembly of an Interferon-β Enhanceosome

Kim, Taeil; Kim, Tae Young; Lee, Woo Ghil; Yim, Jeongbin; Kim, Tae Kook

doi:10.1074/jbc.m000524200

Cited by 44 publications

(47 citation statements)

References 40 publications

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“…The necessity for cooperation between NF-B and IRF-3 has been outlined in other studies (14,28,29). Interestingly, p65 is redundant for induction of the IFN␤ promoter after poly(I-C) data stimulation but is absolutely essential for LPS-stimulated IFN␤ expression (30).…”

Section: Discussionmentioning

confidence: 69%

Interferon Regulatory Factor-3-mediated Activation of the Interferon-sensitive Response Element by Toll-like receptor (TLR) 4 but Not TLR3 Requires the p65 Subunit of NF-κ

Wietek

Miggin

Jefferies

et al. 2003

Journal of Biological Chemistry

104

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Interferon regulatory factor (IRF) 3 is a transcription factor that binds the interferon-sensitive response element (ISRE) and is activated by Toll-like receptor 3 (TLR3) and TLR4. We have found that a dominant negative form of IB kinase 2 and a mutant form of IB, which acts as a super-repressor of NF-B, blocked activation of the ISRE by the TLR4 ligand lipopolysaccharide but not the TLR3 ligand poly(I-C). TLR4 failed to activate the ISRE in mouse embryonic fibroblasts bearing a targeted deletion of p65, whereas the response to TLR3 in these cells was normal. The p65 subunit of NF-B was detected in the lipopolysaccharide-activated but not poly(I-C)-activated ISRE-binding complex. Finally, p65 promoted transactivation of gene expression by IRF-3. These results therefore indicate that IRF-3-mediated activation of the ISRE by TLR4 but not TLR3 requires the p65 subunit of NF-B.

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Section: Discussionmentioning

confidence: 69%

Interferon Regulatory Factor-3-mediated Activation of the Interferon-sensitive Response Element by Toll-like receptor (TLR) 4 but Not TLR3 Requires the p65 Subunit of NF-κ

Wietek

Miggin

Jefferies

et al. 2003

Journal of Biological Chemistry

104

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“…We show a critical role of MEKK1 in IFN-␥-induced and C͞EBP-␤-dependent pathways. Previously this kinase has been implicated in the regulation of I B-kinase-dependent NF-B activation (49,50) including the activation of the IFN-␤ gene enhancer (51). Thus, MEKK1 plays a critical role in IFN synthesis and IFN action.…”

Section: Discussionmentioning

confidence: 99%

MEKK1 plays a critical role in activating the transcription factor C/EBP-β-dependent gene expression in response to IFN-γ

Roy

Meng

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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IFN-γ induces a number of genes to up-regulate cellular responses by using specific transcription factors and the cognate elements. We recently discovered that CCAAT/enhancer-binding protein-β (C/EBP-β) induces gene transcription through an IFN-response element called γ-IFN-activated transcriptional element (GATE). Using mutant cells, chemical inhibitors, and specific dominant negative inhibitors, we show that induction of GATE-driven gene expression depends on MEK1 (mitogen-activated protein kinase kinase/extracellular signal-regulated protein kinase kinase) and ERKs (extracellular signal-regulated protein kinases) but is independent of Raf-1. Interestingly in cells lacking the MEKK1 gene or expressing the dominant negative MEKK1, ERK activation, and GATE dependent gene expression is inhibited. A dominant negative MEKK1 blocks C/EBP-β-driven gene expression stimulated by IFN-γ. These studies describe an IFN-γ-stimulated pathway that involves MEKK1-MEK1-ERK1/2 kinases to regulate C/EBP-β-dependent gene expression.

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“…These two TRIF-mediated pathways are triggered by TLR3 (through its direct interaction with TRIF), and TLR4 by its indirect association with TRIF (through the bridging adaptor TRAM) [42,43]. The concomitant activation of NF-kB and IRF3 by TRIF is of biological significance because the activation of the promoters of some genes, such as IFN-b, requires the functional cooperation of these two transcription factors [44].…”

Section: Tbk1 and Ikk-i Activate Irf3 And Irf7mentioning

confidence: 99%

TLR signalling and activation of IRFs: revisiting old friends from the NF-κB pathway

Moynagh

2005

Trends in Immunology

290

215

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Signaling Pathways to the Assembly of an Interferon-β Enhanceosome

Cited by 44 publications

References 40 publications

Interferon Regulatory Factor-3-mediated Activation of the Interferon-sensitive Response Element by Toll-like receptor (TLR) 4 but Not TLR3 Requires the p65 Subunit of NF-κ

Interferon Regulatory Factor-3-mediated Activation of the Interferon-sensitive Response Element by Toll-like receptor (TLR) 4 but Not TLR3 Requires the p65 Subunit of NF-κ

MEKK1 plays a critical role in activating the transcription factor C/EBP-β-dependent gene expression in response to IFN-γ

TLR signalling and activation of IRFs: revisiting old friends from the NF-κB pathway

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