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/4401179.

Title:
Signaling and transcriptional control of Fas ligand gene expression | Cell Death & Differentiation
Description:
Fas ligand (FasL), a member of the tumor necrosis factor family, initiates apoptosis by binding to its surface receptor Fas. As a consequence, there is sequential activation of caspases and the release of cytochrome c from the mitochondria, with additional caspase activation followed by cellular degradation and death. Recent studies have shed important insight into the molecular mechanisms controlling FasL gene expression at the level of transcription. Nuclear factors such as nuclear factor in activated T cells, nuclear factor-kappa B, specificity protein-1, early growth response factor, interferon regulatory factor, c-Myc and the forkhead transcriptional regulator, alone or cooperatively, activate FasL expression. These factors are often coexpressed with FasL in pathophysiologic settings including human atherosclerotic lesions. Here, we review these important advances in our understanding of the signaling and transcriptional mechanisms controlling FasL gene expression.
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?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 42,798,980 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 {🎯}

$539,300 per month
Our analysis indicates Nature.com generates between $359,553 and $988,772 monthly online from display ads.

Keywords {🔍}

fasl, pubmed, google, scholar, article, cas, apoptosis, cell, fas, expression, cells, death, ligand, promoter, egr, factor, demonstrated, activation, transcription, gene, mice, role, nfat, human, transcriptional, binding, immune, immunol, regulation, activated, tcell, vascular, biol, nature, cmyc, sites, activity, factors, protein, identified, lymphocytes, activationinduced, central, response, type, pathway, nfκb, signaling, faslfas, green,

Topics {✒️}

nature portfolio permissions reprints privacy policy principal research fellow medical research council advertising il-2-induced fasl-promoter-dependent expression vascular research inhibit anti-cd3-induced apoptosis social media t-cell activation-induced expression nature 373 nature 376 nature 377 nature author information authors teniposide-treated jurkat t-cells tcr/cd3-mediated fasl induction cyclosporin a-insensitive manner fasl-dependent t-cell function anti-cd3-induced expression extracellular fasl–fas engagement potential n-glycosylation sites activation-induced fas ligand inhibits fas-mediated apoptosis inhibitory protein i-κb vascular development author correspondence t-cell hybridoma line uncontrolled t-cell activation activation-induced cell death death-inducing signaling complex fas ligand-induced apoptosis fas–fc fusion protein cyclin-dependent kinase activity egr-1-mediated gene transcription fasl/fas-induced death t-cell-mediated cytotoxicity death-receptor initiated pathway anti-fas monoclonal antibody aberrant double-negative 1pr curcumin c3 complex®/bioperine® fasl/fas- dependent pathway c-myc-induced apoptosis enhances egr-dependent transactivation inducible-binding complexes formed stable/unstable angina pectoris protein–protein combinatorial interactions tcr-mediated fasl expression tunel-positive vascular smcs

Questions {❓}

  • Chappell DB and Restifo NP (1998) T cell-tumor cell: a fatal interaction?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Signaling and transcriptional control of Fas ligand gene expression
         description:Fas ligand (FasL), a member of the tumor necrosis factor family, initiates apoptosis by binding to its surface receptor Fas. As a consequence, there is sequential activation of caspases and the release of cytochrome c from the mitochondria, with additional caspase activation followed by cellular degradation and death. Recent studies have shed important insight into the molecular mechanisms controlling FasL gene expression at the level of transcription. Nuclear factors such as nuclear factor in activated T cells, nuclear factor-kappa B, specificity protein-1, early growth response factor, interferon regulatory factor, c-Myc and the forkhead transcriptional regulator, alone or cooperatively, activate FasL expression. These factors are often coexpressed with FasL in pathophysiologic settings including human atherosclerotic lesions. Here, we review these important advances in our understanding of the signaling and transcriptional mechanisms controlling FasL gene expression.
         datePublished:2003-03-25T00:00:00Z
         dateModified:2003-03-25T00:00:00Z
         pageStart:36
         pageEnd:44
         sameAs:https://doi.org/10.1038/sj.cdd.4401179
         keywords:
            Fas ligand
            apoptosis
            gene expression
            transcription factor
            Life Sciences
            general
            Biochemistry
            Cell Biology
            Stem Cells
            Apoptosis
            Cell Cycle Analysis
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.cdd.4401179/MediaObjects/41418_2003_Article_BF4401179_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.cdd.4401179/MediaObjects/41418_2003_Article_BF4401179_Fig2_HTML.jpg
         isPartOf:
            name:Cell Death & Differentiation
            issn:
               1476-5403
               1350-9047
            volumeNumber:10
            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:M M Kavurma
               affiliation:
                     name:Centre for Thrombosis and Vascular Research, The University of New South Wales
                     address:
                        name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
                        type:PostalAddress
                     type:Organization
                     name:The Prince of Wales Hospital
                     address:
                        name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
                        type:PostalAddress
                     type:Organization
               type:Person
               name:L M Khachigian
               affiliation:
                     name:Centre for Thrombosis and Vascular Research, The University of New South Wales
                     address:
                        name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
                        type:PostalAddress
                     type:Organization
                     name:The Prince of Wales Hospital
                     address:
                        name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Signaling and transcriptional control of Fas ligand gene expression
      description:Fas ligand (FasL), a member of the tumor necrosis factor family, initiates apoptosis by binding to its surface receptor Fas. As a consequence, there is sequential activation of caspases and the release of cytochrome c from the mitochondria, with additional caspase activation followed by cellular degradation and death. Recent studies have shed important insight into the molecular mechanisms controlling FasL gene expression at the level of transcription. Nuclear factors such as nuclear factor in activated T cells, nuclear factor-kappa B, specificity protein-1, early growth response factor, interferon regulatory factor, c-Myc and the forkhead transcriptional regulator, alone or cooperatively, activate FasL expression. These factors are often coexpressed with FasL in pathophysiologic settings including human atherosclerotic lesions. Here, we review these important advances in our understanding of the signaling and transcriptional mechanisms controlling FasL gene expression.
      datePublished:2003-03-25T00:00:00Z
      dateModified:2003-03-25T00:00:00Z
      pageStart:36
      pageEnd:44
      sameAs:https://doi.org/10.1038/sj.cdd.4401179
      keywords:
         Fas ligand
         apoptosis
         gene expression
         transcription factor
         Life Sciences
         general
         Biochemistry
         Cell Biology
         Stem Cells
         Apoptosis
         Cell Cycle Analysis
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.cdd.4401179/MediaObjects/41418_2003_Article_BF4401179_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.cdd.4401179/MediaObjects/41418_2003_Article_BF4401179_Fig2_HTML.jpg
      isPartOf:
         name:Cell Death & Differentiation
         issn:
            1476-5403
            1350-9047
         volumeNumber:10
         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:M M Kavurma
            affiliation:
                  name:Centre for Thrombosis and Vascular Research, The University of New South Wales
                  address:
                     name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
                     type:PostalAddress
                  type:Organization
                  name:The Prince of Wales Hospital
                  address:
                     name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
                     type:PostalAddress
                  type:Organization
            type:Person
            name:L M Khachigian
            affiliation:
                  name:Centre for Thrombosis and Vascular Research, The University of New South Wales
                  address:
                     name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
                     type:PostalAddress
                  type:Organization
                  name:The Prince of Wales Hospital
                  address:
                     name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Cell Death & Differentiation
      issn:
         1476-5403
         1350-9047
      volumeNumber:10
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Centre for Thrombosis and Vascular Research, The University of New South Wales
      address:
         name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
         type:PostalAddress
      name:The Prince of Wales Hospital
      address:
         name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
         type:PostalAddress
      name:Centre for Thrombosis and Vascular Research, The University of New South Wales
      address:
         name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
         type:PostalAddress
      name:The Prince of Wales Hospital
      address:
         name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:M M Kavurma
      affiliation:
            name:Centre for Thrombosis and Vascular Research, The University of New South Wales
            address:
               name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
            name:The Prince of Wales Hospital
            address:
               name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:L M Khachigian
      affiliation:
            name:Centre for Thrombosis and Vascular Research, The University of New South Wales
            address:
               name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
            name:The Prince of Wales Hospital
            address:
               name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
      name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia
      name:Department of Pathology, Centre for Thrombosis and Vascular Research, The University of New South Wales, Sydney, Australia
      name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia

Social Networks {👍}(1)

External Links {🔗}(307)

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

6.1s.