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We are analyzing https://www.nature.com/articles/nature14191.

Title:
Necroptosis and its role in inflammation | Nature
Description:
Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {๐Ÿ“š}

  • Education
  • Telecommunications
  • Science

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What CMS is nature.com built with?

Custom-built

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Traffic Estimate {๐Ÿ“ˆ}

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

๐ŸŒ  Phenomenal Traffic: 5M - 10M visitors per month


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How Does Nature.com Make Money? {๐Ÿ’ธ}


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Direct Advertisers (10)
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How Much Does Nature.com Make? {๐Ÿ’ฐ}


Display Ads {๐ŸŽฏ}

$63,100 per month
According to our algorithms, Nature.com's monthly online income from display advertising ranges from $42,042 to $115,616.

Keywords {๐Ÿ”}

pubmed, article, google, scholar, cas, cell, central, nature, necroptosis, death, ripk, apoptosis, rip, kinase, caspase, necrosis, ads, inflammation, protein, signaling, immunol, sci, immunity, mice, vandenabeele, access, biol, proc, natl, acad, usa, mlkl, mol, cells, tnfinduced, showed, activation, research, homeostasis, inflammatory, regulates, receptor, wang, role, regulated, development, rev, cellular, necrotic, activity,

Topics {โœ’๏ธ}

nature portfolio privacy policy receptor-interacting kinase-3-mediated pathway author information authors advertising tnf-induced nf-ฮบb signal rip1โ€“rip3-drp1 signaling pathway permissions reprints social media european research council german research foundation research foundation flanders induce tnfฮฑ-dependent apoptosis ripk3-dependent necroptosis mediated rip3-mediated macrophage necrosis necrotic mem-brane disruption tnf-induced keratinocyte apoptosis dsrna-induced retinal degeneration smac-mimetic-induced apoptosis pka/creb/ripk1 axis caspase-independent apoptosis pathway rip3-rip3 homo-interaction pro-necrotic kinase activity dai/zbp1/dlm-1 complexes nf-ฮบb activation liver ischemia/reperfusion rip1/rip3 necrosome forms receptor 3-mediated necrosis tnf-ฮฑ feedforward signaling nature cell biol tnfr1-induced inflammatory mediates noncanonical il-1ฮฒ human inflammatory diseases fas/cd95-induced chemokines diverse cell-death patterns personal data early postnatal lethality tnfฮฑ-dependent apoptosis research virus-induced inflammation springerlink instant access innate immune defense intestinal epithelial cells data protection reduces allograft survival canonical nf-ฮบb tnf-induced necrosis prevents skin inflammation important kinase-dependent specific cellular target

Schema {๐Ÿ—บ๏ธ}

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         headline:Necroptosis and its role in inflammation
         description:Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.
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      headline:Necroptosis and its role in inflammation
      description:Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.
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