Journal ArticleDOI
Return to homeostasis: downregulation of NF-κB responses
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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.read more
Citations
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NF-κB, inflammation, immunity and cancer: coming of age
Koji Taniguchi,Michael Karin +1 more
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.
Journal ArticleDOI
Inflammation meets cancer, with NF-κB as the matchmaker
Yinon Ben-Neriah,Michael Karin +1 more
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
Bodu Liu,Lijuan Sun,Qiang Liu,Chang Gong,Yandan Yao,Xiao-Bin Lv,Ling Lin,Herui Yao,Fengxi Su,Dangsheng Li,Mu Sheng Zeng,Erwei Song +11 more
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.
Journal ArticleDOI
Regulation of NF-κB by TNF family cytokines.
Matthew S. Hayden,Sankar Ghosh +1 more
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
The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses.
David L. Boone,Emre E. Turer,Eric Lee,Regina Celeste Ahmad,Matthew T. Wheeler,Colleen Tsui,Paula J. Hurley,Marcia Chien,Sophia Chai,Osamu Hitotsumatsu,Elizabeth M. McNally,Cecile M. Pickart,Averil Ma +12 more
TL;DR: A20 was required for the termination of Toll-like receptor–induced activity of the transcription factor NF-κB and proinflammatory gene expression in macrophages, and this function protected mice from endotoxic shock, indicating that A20 is also critical for the regulation of TNF-independent signals in vivo.
Journal ArticleDOI
MicroRNAs: new regulators of immune cell development and function.
David Baltimore,Mark Boldin,Ryan M. O'Connell,Dinesh S. Rao,Dinesh S. Rao,Konstantin Taganov +5 more
TL;DR: Much of the work which has so far only scratched the surface of this very fertile field of investigation is brought together, and the results illuminate many historic questions about hematopoiesis and immune function.
Journal ArticleDOI
Mutations of multiple genes cause deregulation of NF-κB in diffuse large B-cell lymphoma
Mara Compagno,Wei Keat Lim,Adina Grunn,Subhadra V. Nandula,Manisha Brahmachary,Qiong Shen,Francesco Bertoni,Maurilio Ponzoni,Marta Scandurra,Andrea Califano,Govind Bhagat,Amy Chadburn,Riccardo Dalla-Favera,Laura Pasqualucci +13 more
TL;DR: The results demonstrate that NF-κB activation in DLBCL is caused by genetic lesions affecting multiple genes, the loss or activation of which may promote lymphomagenesis by leading to abnormally prolonged NF-σκB responses.
Journal ArticleDOI
Promiscuous Mutations Activate the Noncanonical NF-κB Pathway in Multiple Myeloma
Jonathan J Keats,Rafael Fonseca,Marta Chesi,Roelandt F.J. Schop,Angela Baker,Wee Joo Chng,Scott Van Wier,Rodger E. Tiedemann,Chang Xin Shi,Michael Sebag,Esteban Braggio,Travis J. Henry,Yuan Xiao Zhu,Homer Fogle,Tammy Price-Troska,Gregory J. Ahmann,Catherine Mancini,Leslie A. Brents,Shaji Kumar,Philip R. Greipp,Angela Dispenzieri,Barb Bryant,George Mulligan,Laurakay Bruhn,Michael T. Barrett,Riccardo Valdez,Jeff Trent,A. Keith Stewart,John D. Carpten,P. Leif Bergsagel +29 more
TL;DR: In this paper, an integrated analysis of high-density oligonucleotide array CGH and gene expression profiling data from 155 multiple myeloma samples identified a promiscuous array of abnormalities contributing to the dysregulation of NF-kappaB in approximately 20% of patients.
Journal ArticleDOI
The tumour suppressor CYLD negatively regulates NF-kappaB signalling by deubiquitination.
Andrew Kovalenko,Christine Chable-Bessia,Giuseppina Cantarella,Giuseppina Cantarella,Alain Israël,David Wallach,Gilles Courtois +6 more
TL;DR: CYLD, a tumour suppressor that is mutated in familial cylindromatosis, interacts with NEMO, the regulatory subunit of IKK, strengthening the notion that ubiquitination is involved in IKK activation by TRAFs and suggesting that CYLD functions in this process.
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