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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

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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.

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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:

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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 calculations suggest that Nature.com earns between $357,519 and $983,176 monthly online from display advertisements.

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 {🗺️}

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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.
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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
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      name:Department of Haematology, The Prince of Wales Hospital, Sydney, Australia

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