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Journal ArticleDOI

Return to homeostasis: downregulation of NF-κB responses

Jürgen Ruland
- 01 Aug 2011 - 
- Vol. 12, Iss: 8, pp 709-714
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TLDR
This review highlights key negative regulatory principles that affect the amount, localization or conformational properties of NF-κB-activating proteins to attenuate the NF-kB response to prevent inflammation, autoimmune disease and oncogenesis.
Abstract
Activation of NF-κB transcription factors by receptors of the innate or adaptive immune system is essential for host defense. However, after danger is eliminated, NF-κB signaling needs to be tightly downregulated for the maintenance of tissue homeostasis. This review highlights key negative regulatory principles that affect the amount, localization or conformational properties of NF-κB-activating proteins to attenuate the NF-κB response. These mechanisms are needed to prevent inflammation, autoimmune disease and oncogenesis.

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Citations
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NF-κB, inflammation, immunity and cancer: coming of age

TL;DR: How the initial discovery of a role for NF-κB in linking inflammation and cancer led to an improved understanding of tumour-elicited inflammation and its effects on anticancer immunity is discussed.
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Inflammation meets cancer, with NF-κB as the matchmaker

TL;DR: Although it seems to fulfill a distinctly tumor-promoting role in many types of cancer, NF-κB has a confounding role in certain tumors.
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A Cytoplasmic NF-κB Interacting Long Noncoding RNA Blocks IκB Phosphorylation and Suppresses Breast Cancer Metastasis

TL;DR: This work identifies an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-κB, binds to NF-σκB/IκBs, and directly masks phosphorylation motifs of IKKB, thereby inhibiting IKK-induced IκBosphorylation and NF-kkB activation.
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Regulation of NF-κB by TNF family cytokines.

TL;DR: The authors explored general mechanisms of TNF cytokine signaling, with a focus on the upstream signaling events leading to activation of the so-called canonical and non-canonical NF-κB pathways by TNFR1 and CD40, respectively.
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Curcumin—From Molecule to Biological Function

TL;DR: This Review describes the development of curcumin from a "traditional" spice and food coloring to a "modern" biological regulator.
References
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Journal ArticleDOI

Degradation of Bcl10 Induced by T-Cell Activation Negatively Regulates NF-κB Signaling

TL;DR: It is shown that PKC or T-cell receptor (TCR)/CD28 signaling results in downregulation of Bcl10 protein levels, thereby attenuating NF-κB transcriptional activity, suggesting a new mechanism of negative signaling in which TCR/PKC signaling initially activates B cl10 but later promotes its degradation.
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Negative Regulation of NF-κB Signaling by PIAS1

TL;DR: It is reported here that PIAS1 (protein inhibitor of activated STAT1) is an important negative regulator of NF-κB, and microarray analysis indicates that the removal ofPIAS1 results in an increased expression of a subset of NF -κB-mediated genes in response to tumor necrosis factor alpha and lipopolysaccharide.
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Essential role for IκB kinase β in remodeling carma1-bcl10-malt1 complexes upon T cell activation

TL;DR: The data provide evidence that IKKbeta serves a dual role upstream of its classical substrates, the IkappaB proteins, while being essential for triggering initial CBM complex formation, IKK beta-dependent phosphorylation of Bcl10 exhibits a negative regulatory role in T cell activation.
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