Structure and Function of the Interferon-  Enhanceosome

Maniatis, Tom; Falvo, James V.; Kim, T.H.; Kim, T.K.; Lin, Charles; Parekh, Bhavin S.; Wathelet, Marc

doi:10.1101/sqb.1998.63.609

Cited by 340 publications

(339 citation statements)

References 44 publications

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“…This may indicate that the interaction is too weak or transient to be observed by this method or that the lower activation potential of GLI1 on the JUN promoter is due to differences in the activation complex. JUN has been shown to interact with many other transcription factors and is a member of the wellcharacterized enhanceosome complex at the IFN-b promoter (Maniatis et al, 1998) where ATF-2/JUN, IRF-3 and IRF-7, and NF-kB (p50/RelA) are necessary for promoter activation. Several members of the complex including JUN are able to interact with CBP or p300.…”

Section: Discussionmentioning

confidence: 99%

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes

et al. 2009

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Sustained Hedgehog (HH) signaling is implicated in basal cell carcinoma of the skin and other types of cancer. Here we show that GLI1 and GLI2, the main transcriptional activators of the HH pathway, directly regulate expression of the activator protein 1 (AP-1) family member JUN, a transcription factor controlling keratinocyte proliferation and skin homeostasis. Activation of the JUN promoter by GLI is dependent on a GLI-binding site and the AP-1 sites known to be involved in self-activation of JUN. Transcription of JUN is greatly enhanced in the presence of GLI and requires activated JUN protein.GLI2act is a more potent activator than GLI1 in these experiments and physical interaction with phosphorylated JUN was only detected for GLI2act. The synergistic effect of GLI and JUN extends to the activation of further GLI target genes as shown by shRNA-mediated knockdown of JUN in human keratinocytes. Some of these cooperatively activated genes are involved in cell-cycle progression, which is consistent with a significant reduction of the proliferative potential of GLI in the absence of JUN. These results suggest a novel connection between HH/GLI pathway activity and JUN, which may contribute to the oncogenic activity of HH/GLI signaling in skin.

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Section: Discussionmentioning

confidence: 99%

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes

et al. 2009

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“…This model may best describe the case of the b-interferon enhancer, in which gene expression is dependent on the simultaneous presence of all required transcription factors on the enhancer (Maniatis et al, 1998). A less complex but apparently widespread phenomenon is the synergistic function of IRF-3 and RelA dimers.…”

Section: Coincident Functions Of Nf-kb and Cooperating Transcription mentioning

confidence: 99%

Transcriptional regulation via the NF-κB signaling module

2006

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Stimulus-induced nuclear factor-jB (NF-jB) activity, the central mediator of inflammatory responses and immune function, comprises a family of dimeric transcription factors that regulate diverse gene expression programs consisting of hundreds of genes. A family of inhibitor of jB (IjB) proteins controls NF-jB DNA-binding activity and nuclear localization. IjB protein metabolism is intricately regulated through stimulus-induced degradation and feedback re-synthesis, which allows for dynamic control of NF-jB activity. This network of interactions has been termed the NF-jB signaling module. Here, we summarize the current understanding of the molecular structures and biochemical mechanisms that determine NF-jB dimer formation and the signal-processing characteristics of the signaling module. We identify NF-jB-jB site interaction specificities and dynamic control of NF-jB activity as mechanisms that generate specificity in transcriptional regulation. We discuss examples of gene regulation that illustrate how these mechanisms may interface with other transcription regulators and promoter-associated events, and how these mechanisms suggest regulatory principles for NF-jB-mediated gene activation.

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“…The promoter region of IFN-b has been shown to bind several DNAbinding transcription factors that cooperate in an enhanceosome complex including IRF-3, NF-kB and AP-1 (c-jun:ATF2). [49][50][51] In this case, IRF-3 is required for IFN-b expression, but IRF-3 is not sufficient for its transcriptional induction.…”

Section: Irf-3 Target Genesmentioning

confidence: 99%

IRF-3-dependent and augmented target genes during viral infection

et al. 2007

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Activation of the transcription factor interferon regulatory factor-3 (IRF-3) is an essential event in the innate immune response to viral infection. To understand the contribution of IRF-3 to host defense, we used a systems biology approach to analyze global gene expression dependent on IRF-3. Comparison of expression profiles in cells from IRF-3 knockout animals or wild-type siblings following viral infection revealed three sets of induced genes, those that are strictly dependent on IRF-3, augmented with IRF-3, or not responsive to IRF-3. Products of identified IRF-3 target genes are involved in innate or acquired immunity, or in the regulation of cell cycle, apoptosis and proliferation. These results reveal the global effects of one transcription factor in the immune response and provide information to evaluate the integrated response to viral infection.

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Structure and Function of the Interferon- Enhanceosome

Cited by 340 publications

References 44 publications

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes

Transcriptional regulation via the NF-κB signaling module

IRF-3-dependent and augmented target genes during viral infection

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