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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Schema
  9. Social Networks
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  14. CDN Services

We began analyzing https://www.nature.com/articles/nature14191, but it redirected us to https://www.nature.com/articles/nature14191. The analysis below is for the second page.

Title[redir]:
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.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

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


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

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 {✒️}

nature portfolio privacy policy receptor-interacting kinase-3-mediated pathway author information authors advertising tnf-induced nf-κb signal rip1–rip3-drp1 signaling pathway permissions reprints social media european research council german research foundation research foundation flanders induce tnfα-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-κb activation liver ischemia/reperfusion rip1/rip3 necrosome forms receptor 3-mediated necrosis tnf-α feedforward signaling nature cell biol tnfr1-induced inflammatory mediates noncanonical il-1β human inflammatory diseases fas/cd95-induced chemokines diverse cell-death patterns personal data early postnatal lethality tnfα-dependent apoptosis research virus-induced inflammation springerlink instant access innate immune defense intestinal epithelial cells data protection reduces allograft survival canonical nf-κb tnf-induced necrosis prevents skin inflammation important kinase-dependent specific cellular target

Schema {🗺️}

WebPage:
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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.
         datePublished:2015-01-14T00:00:00Z
         dateModified:2015-01-14T00:00:00Z
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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.
      datePublished:2015-01-14T00:00:00Z
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         name:Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
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               name:Institute for Genetics, Centre for Molecular Medicine and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, Cologne, Germany
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               name:VIB Inflammation Research Center, Ghent University, UGhent-VIB Research Building FSVM, Ghent, Belgium
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Social Networks {👍}(2)

External Links {🔗}(547)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

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Name Servers:

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CDN Services {📦}

  • Crossref

4.94s.