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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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Traffic Estimate {📈}

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

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Nature.com Make Money? {💸}


Display Ads {🎯}


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

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Direct Advertisers (10)
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Reseller Advertisers (38)
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How Much Does Nature.com Make? {💰}


Display Ads {🎯}

$63,100 per month
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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)

Analytics and Tracking {📊}

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Libraries {📚}

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Emails and Hosting {✉️}

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CDN Services {📦}

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