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/s41583-018-0093-1.

Title:
Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases | Nature Reviews Neuroscience
Description:
Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death. However, under pathological conditions, upregulation of death receptor family ligands, such as tumour necrosis factor (TNF), can sensitize cells in the CNS to apoptosis and a form of regulated necrotic cell death known as necroptosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL). Necroptosis promotes further cell death and neuroinflammation in the pathogenesis of several neurodegenerative diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disease. In this Review, we outline the evidence implicating necroptosis in these neurological diseases and suggest that targeting RIPK1 might help to inhibit multiple cell death pathways and ameliorate neuroinflammation. Necroptosis is a form of cell death mediated by receptor-interacting protein kinase 1 (RIPK1), and is observed in several CNS disorders. Here, Yuan, Amin and Ofengeim give an overview of necroptosis in the CNS and explain its relationship with inflammation in CNS disorders.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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?

🌠 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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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 {🎯}

$63,100 per month
Our analysis indicates Nature.com generates between $42,042 and $115,616 monthly online from display ads.

Keywords {🔍}

pubmed, google, scholar, cas, cell, central, death, necroptosis, ripk, disease, apoptosis, kinase, nature, rip, nat, activation, signaling, sclerosis, biol, protein, inflammation, mol, necrosis, neurosci, alzheimers, development, rev, mice, article, diseases, yuan, receptor, access, caspase, paper, nfκb, cells, amyotrophic, lateral, inhibitor, science, differ, med, degeneration, factor, tnf, multiple, injury, role, regulation,

Topics {✒️}

nature portfolio journals permissions reprints tumour-necrosis-factor-related apoptosis-inducing ligand nature portfolio privacy policy ischemia–reperfusion-induced retinal damage advertising mammalian interleukin-1β-converting enzyme tnf-related apoptosis-inducing ligand tnf-related apoptosis-inducing ligands tnf receptor i-mediated apoptosis death-domain dimerization-mediated activation social media genome-wide sirna screen author information authors cytochrome c-mediated caspase activation death receptor-ligand systems tumor necrosis factor-α dsrna-induced retinal degeneration nf-κb signals induce author correspondence nature+ nature 407 nature 384 nature 424 nature 430 nature 513 nature c-myc governs age systemic inflammatory response experimental retinal detachment nf-κb essential modulator data protection age-related neurodegenerative disorders microglia-targeted candidates push tumor necrosis factor personal data cell death-independent activities apoptosis-regulatory proteins bid protein kinase rip ubiquitin-binding protein implicated tumour necrosis factor mediate cell death rip1 kinase signalling nf-κb-dependent rip1/rip3 necrosome forms nf-κb-independent role permissions caspase-independent cell death multiple sclerosis induced

Questions {❓}

  • Multiple sclerosis: an immune or neurodegenerative disorder?
  • Why is Wallerian degeneration in the CNS so slow?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases
         description:Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death. However, under pathological conditions, upregulation of death receptor family ligands, such as tumour necrosis factor (TNF), can sensitize cells in the CNS to apoptosis and a form of regulated necrotic cell death known as necroptosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL). Necroptosis promotes further cell death and neuroinflammation in the pathogenesis of several neurodegenerative diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disease. In this Review, we outline the evidence implicating necroptosis in these neurological diseases and suggest that targeting RIPK1 might help to inhibit multiple cell death pathways and ameliorate neuroinflammation. Necroptosis is a form of cell death mediated by receptor-interacting protein kinase 1 (RIPK1), and is observed in several CNS disorders. Here, Yuan, Amin and Ofengeim give an overview of necroptosis in the CNS and explain its relationship with inflammation in CNS disorders.
         datePublished:2018-11-22T00:00:00Z
         dateModified:2018-11-22T00:00:00Z
         pageStart:19
         pageEnd:33
         sameAs:https://doi.org/10.1038/s41583-018-0093-1
         keywords:
            Apoptosis
            Necroptosis
            Neurodegenerative diseases
            Neuroimmunology
            Biomedicine
            general
            Neurosciences
            Behavioral Sciences
            Biological Techniques
            Neurobiology
            Animal Genetics and Genomics
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig2_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig3_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig4_HTML.png
         isPartOf:
            name:Nature Reviews Neuroscience
            issn:
               1471-0048
               1471-003X
            volumeNumber:20
            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:Junying Yuan
               affiliation:
                     name:Harvard Medical School
                     address:
                        name:Department of Cell Biology, Harvard Medical School, Boston, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Palak Amin
               affiliation:
                     name:Harvard Medical School
                     address:
                        name:Department of Cell Biology, Harvard Medical School, Boston, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Dimitry Ofengeim
               affiliation:
                     name:Neuroscience Research, Sanofi
                     address:
                        name:Neuroscience Research, Sanofi, Framingham, USA
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases
      description:Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death. However, under pathological conditions, upregulation of death receptor family ligands, such as tumour necrosis factor (TNF), can sensitize cells in the CNS to apoptosis and a form of regulated necrotic cell death known as necroptosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL). Necroptosis promotes further cell death and neuroinflammation in the pathogenesis of several neurodegenerative diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Parkinson disease and Alzheimer disease. In this Review, we outline the evidence implicating necroptosis in these neurological diseases and suggest that targeting RIPK1 might help to inhibit multiple cell death pathways and ameliorate neuroinflammation. Necroptosis is a form of cell death mediated by receptor-interacting protein kinase 1 (RIPK1), and is observed in several CNS disorders. Here, Yuan, Amin and Ofengeim give an overview of necroptosis in the CNS and explain its relationship with inflammation in CNS disorders.
      datePublished:2018-11-22T00:00:00Z
      dateModified:2018-11-22T00:00:00Z
      pageStart:19
      pageEnd:33
      sameAs:https://doi.org/10.1038/s41583-018-0093-1
      keywords:
         Apoptosis
         Necroptosis
         Neurodegenerative diseases
         Neuroimmunology
         Biomedicine
         general
         Neurosciences
         Behavioral Sciences
         Biological Techniques
         Neurobiology
         Animal Genetics and Genomics
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig2_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig3_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fs41583-018-0093-1/MediaObjects/41583_2018_93_Fig4_HTML.png
      isPartOf:
         name:Nature Reviews Neuroscience
         issn:
            1471-0048
            1471-003X
         volumeNumber:20
         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:Junying Yuan
            affiliation:
                  name:Harvard Medical School
                  address:
                     name:Department of Cell Biology, Harvard Medical School, Boston, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Palak Amin
            affiliation:
                  name:Harvard Medical School
                  address:
                     name:Department of Cell Biology, Harvard Medical School, Boston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Dimitry Ofengeim
            affiliation:
                  name:Neuroscience Research, Sanofi
                  address:
                     name:Neuroscience Research, Sanofi, Framingham, USA
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Nature Reviews Neuroscience
      issn:
         1471-0048
         1471-003X
      volumeNumber:20
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Harvard Medical School
      address:
         name:Department of Cell Biology, Harvard Medical School, Boston, USA
         type:PostalAddress
      name:Harvard Medical School
      address:
         name:Department of Cell Biology, Harvard Medical School, Boston, USA
         type:PostalAddress
      name:Neuroscience Research, Sanofi
      address:
         name:Neuroscience Research, Sanofi, Framingham, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Junying Yuan
      affiliation:
            name:Harvard Medical School
            address:
               name:Department of Cell Biology, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Palak Amin
      affiliation:
            name:Harvard Medical School
            address:
               name:Department of Cell Biology, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Dimitry Ofengeim
      affiliation:
            name:Neuroscience Research, Sanofi
            address:
               name:Neuroscience Research, Sanofi, Framingham, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Cell Biology, Harvard Medical School, Boston, USA
      name:Department of Cell Biology, Harvard Medical School, Boston, USA
      name:Neuroscience Research, Sanofi, Framingham, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

Social Networks {👍}(2)

External Links {🔗}(441)

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

5.21s.