Here's how NATURE.COM makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

NATURE . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Nature.com Make Money
  6. How Much Does Nature.com Make
  7. Keywords
  8. Topics
  9. Questions
  10. Schema
  11. Social Networks
  12. External Links
  13. Analytics And Tracking
  14. Libraries
  15. Hosting Providers
  16. CDN Services

We are analyzing https://www.nature.com/articles/nrmicro2070.

Title:
Pyroptosis: host cell death and inflammation | Nature Reviews Microbiology
Description:
Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is nature.com built with?

Custom-built

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

Traffic Estimate {📈}

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 42,556,742 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

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
Our estimates place Nature.com's monthly online earnings from display ads at $357,519 to $983,176.

Keywords {🔍}

pubmed, article, google, scholar, cas, cell, caspase, activation, central, death, nature, inflammasome, immunol, infection, pyroptosis, apoptosis, host, macrophages, microbiol, cells, inflammatory, biol, protein, cookson, interleukin, salmonella, usa, dependent, immunity, inflammation, interleukinβ, ilβ, release, access, macrophage, sci, chem, proc, natl, acad, secretion, response, role, infect, immun, caspasedependent, exp, med, ipaf, content,

Topics {✒️}

nature portfolio permissions reprints privacy policy key pyroptosis-related genes advertising anaplasma phagocytophilum infection author information authors social media candida albicans conserved carboxy-terminal domain leucine-rich repeat domain human monocyte-derived macrophages inflammasome components cias1/cryopyrin/nlrp3 author correspondence alarm-ringing inflammatory recruitment caspase-1-dependent pore formation nigericin-induced interleukin-1β release il-1β-converting enzyme interleukin 1β-converting enzyme n-end rule pathway endolysosome-related vesicles murine phospho-mlkl-s345 nature rev il-1β-loaded microvesicles nature genet pro-inflammatory il-1β pathogen-induced cell death dye uptake-independent pathway naip5-mediated macrophage immunity salmonella-induced caspase-2 activation personal data il-18/ifn-γ axis nature immunol shigella flexneri-induced apoptosis shigella flexneri-induced inflammation outcome dictates life springerlink instant access inflammatory cytokines interleukin-1β data protection nature nature 440 nature 452 nature 430 nature 399 nature 425 nature 453 human dendritic cells pseudomonas aeruginosa mediated nf-κb activation anthrax lethal toxin

Questions {❓}

  • Apoptosis: who was first?
  • Death-defying immunity: do apoptotic cells influence antigen processing and presentation?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Pyroptosis: host cell death and inflammation
         description: Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
         datePublished:
         dateModified:
         pageStart:99
         pageEnd:109
         sameAs:https://doi.org/10.1038/nrmicro2070
         keywords:
            Life Sciences
            general
            Microbiology
            Medical Microbiology
            Parasitology
            Infectious Diseases
            Virology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig4_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig5_HTML.jpg
         isPartOf:
            name:Nature Reviews Microbiology
            issn:
               1740-1534
               1740-1526
            volumeNumber:7
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Nature Publishing Group UK
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Tessa Bergsbaken
               affiliation:
                     name:University of Washington
                     address:
                        name:Department of Microbiology, University of Washington, Seattle, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Susan L. Fink
               affiliation:
                     name:University of Washington
                     address:
                        name:Departments of Molecular and Cellular Biology, University of Washington, Seattle, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Brad T. Cookson
               affiliation:
                     name:University of Washington
                     address:
                        name:Department of Microbiology, University of Washington, Seattle, USA
                        type:PostalAddress
                     type:Organization
                     name:Laboratory Medicine, University of Washington
                     address:
                        name:Laboratory Medicine, University of Washington, Seattle, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Pyroptosis: host cell death and inflammation
      description: Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
      datePublished:
      dateModified:
      pageStart:99
      pageEnd:109
      sameAs:https://doi.org/10.1038/nrmicro2070
      keywords:
         Life Sciences
         general
         Microbiology
         Medical Microbiology
         Parasitology
         Infectious Diseases
         Virology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig4_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fnrmicro2070/MediaObjects/41579_2009_Article_BFnrmicro2070_Fig5_HTML.jpg
      isPartOf:
         name:Nature Reviews Microbiology
         issn:
            1740-1534
            1740-1526
         volumeNumber:7
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Nature Publishing Group UK
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Tessa Bergsbaken
            affiliation:
                  name:University of Washington
                  address:
                     name:Department of Microbiology, University of Washington, Seattle, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Susan L. Fink
            affiliation:
                  name:University of Washington
                  address:
                     name:Departments of Molecular and Cellular Biology, University of Washington, Seattle, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Brad T. Cookson
            affiliation:
                  name:University of Washington
                  address:
                     name:Department of Microbiology, University of Washington, Seattle, USA
                     type:PostalAddress
                  type:Organization
                  name:Laboratory Medicine, University of Washington
                  address:
                     name:Laboratory Medicine, University of Washington, Seattle, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Nature Reviews Microbiology
      issn:
         1740-1534
         1740-1526
      volumeNumber:7
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Washington
      address:
         name:Department of Microbiology, University of Washington, Seattle, USA
         type:PostalAddress
      name:University of Washington
      address:
         name:Departments of Molecular and Cellular Biology, University of Washington, Seattle, USA
         type:PostalAddress
      name:University of Washington
      address:
         name:Department of Microbiology, University of Washington, Seattle, USA
         type:PostalAddress
      name:Laboratory Medicine, University of Washington
      address:
         name:Laboratory Medicine, University of Washington, Seattle, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Tessa Bergsbaken
      affiliation:
            name:University of Washington
            address:
               name:Department of Microbiology, University of Washington, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Susan L. Fink
      affiliation:
            name:University of Washington
            address:
               name:Departments of Molecular and Cellular Biology, University of Washington, Seattle, USA
               type:PostalAddress
            type:Organization
      name:Brad T. Cookson
      affiliation:
            name:University of Washington
            address:
               name:Department of Microbiology, University of Washington, Seattle, USA
               type:PostalAddress
            type:Organization
            name:Laboratory Medicine, University of Washington
            address:
               name:Laboratory Medicine, University of Washington, Seattle, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Microbiology, University of Washington, Seattle, USA
      name:Departments of Molecular and Cellular Biology, University of Washington, Seattle, USA
      name:Department of Microbiology, University of Washington, Seattle, USA
      name:Laboratory Medicine, University of Washington, Seattle, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

Social Networks {👍}(1)

External Links {🔗}(426)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mxa-002c5801.gslb.pphosted.com
  • mxb-002c5801.gslb.pphosted.com

Name Servers:

  • pdns1.ultradns.net
  • pdns2.ultradns.net
  • pdns3.ultradns.org
  • pdns4.ultradns.org
  • pdns5.ultradns.info
  • pdns6.ultradns.co.uk

CDN Services {📦}

  • Crossref

5.79s.