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We are analyzing https://www.nature.com/articles/sigtrans201723.

Title:
NF-κB signaling in inflammation | Signal Transduction and Targeted Therapy
Description:
The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition. Targeting a critical signaling pathway involved in innate and adaptive immunity could help treat a range of inflammatory diseases. In a review article, Shao-Cong Sun and colleagues from the University of Texas MD Anderson Cancer Center in Houston, USA, discuss how the family of transcription factors that make up the nuclear factor-κB (NF-κB) pathway mediate the expression of many genes implicated in different processes of the body’s immune and inflammatory responses. The authors first describe the function of NF-κB in different types of immune cells. They then detail how NF-κB signaling goes awry in various inflammatory diseases, including rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease. Drugs that block different steps of the NF-κB pathway could help treat these diseases, although broadly inhibiting NF-κB function often brings unwanted side effects.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

Content Management System {📝}

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Custom-built

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What is the average monthly size of nature.com audience?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 42,554,915 visitors per month in the current month.

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The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

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Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {💰}


Display Ads {🎯}

$536,300 per month
According to our algorithms, Nature.com's monthly online income from display advertising ranges from $357,503 to $983,134.

Keywords {🔍}

pubmed, nfκb, google, scholar, cas, cells, activation, central, inflammatory, immune, cell, signaling, nfkappab, immunol, inflammation, pathway, inflammasome, function, role, induction, innate, responses, differentiation, diseases, nlrp, expression, mice, transcription, factor, including, cytokines, regulation, noncanonical, ikk, iκbα, tcell, kinase, macrophages, disease, arthritis, nature, proinflammatory, sun, genes, canonical, nat, regulates, development, inhibition, nuclear,

Topics {✒️}

nature portfolio privacy policy research & therapy research institute donghyun joo & shao-cong sun advertising hyperactivity-nf-kappab illuminates autoimmunity nf-kappab-inducing kinase regulates social media nature 2011 nature 2007 nature 1998 nature nf-κb member c-rel t-cell-specific ikkβ deletion 0/ reprints nf-kappab-inducing kinase plays nf-κb-stimulating immune receptors author information authors astroglial nf-kappab protects constitutively express pro-il-1β t-cell intrinsic factors anti-cd3/anti-cd28 apoe-deficient mice fed noncanonical nf-kappab pathway t-cell intrinsic effect myeloid cell-specific deficiency promotes t-cell activation transcription factor nf-kappab noncanonical nf-κb pathway mouse collagen-induced arthritis myeloid cell-specific deletion prevent nf-κb subunits author correspondence long-lasting tissue damages c-terminal potion resembles noncanonical nf-κb pathways nf-κb regulates eae t-cell-specific deletion murine collagen-induced arthritis attenuating nlrp3-mediated neurotoxicity nuclear factor-kappab activation iκbα super-repressor nf-kappab transcription factors active nf-κb promotes multi-subunit iκb kinase naive t-cell activation canonical nf-κb pathway processing-defective p100 mutant myd88-dependent tlr pathway

Questions {❓}

  • Anti-TNF alpha therapy of rheumatoid arthritis: what have we learned?

Schema {🗺️}

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         description:The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition. Targeting a critical signaling pathway involved in innate and adaptive immunity could help treat a range of inflammatory diseases. In a review article, Shao-Cong Sun and colleagues from the University of Texas MD Anderson Cancer Center in Houston, USA, discuss how the family of transcription factors that make up the nuclear factor-κB (NF-κB) pathway mediate the expression of many genes implicated in different processes of the body’s immune and inflammatory responses. The authors first describe the function of NF-κB in different types of immune cells. They then detail how NF-κB signaling goes awry in various inflammatory diseases, including rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease. Drugs that block different steps of the NF-κB pathway could help treat these diseases, although broadly inhibiting NF-κB function often brings unwanted side effects.
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External Links {🔗}(362)

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CDN Services {📦}

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