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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. Questions
  9. Schema
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  15. CDN Services

We began analyzing https://www.nature.com/articles/4401179, but it redirected us to https://www.nature.com/articles/4401179. The analysis below is for the second page.

Title[redir]:
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.

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 80,479,999 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We don't see any clear sign of profit-making.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Doi.org might be cashing in, but we can't detect the method they're using.

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
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            Life Sciences
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            Cell Biology
            Stem Cells
            Apoptosis
            Cell Cycle Analysis
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      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
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         gene expression
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         Life Sciences
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         Stem Cells
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         Cell Cycle Analysis
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fsj.cdd.4401179/MediaObjects/41418_2003_Article_BF4401179_Fig2_HTML.jpg
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      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
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      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 {🔗}(500)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

4.97s.