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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. Schema
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://www.nature.com/articles/1203222, but it redirected us to https://www.nature.com/articles/1203222. The analysis below is for the second page.

Title[redir]:
Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel | Oncogene
Description:
The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-κB transcription factor family. v-Rel induces a rapidly fatal lymphoma/leukemia in young birds, and v-Rel can transform and immortalize a variety of avian cell types in vitro. Although Rel/NF-κB transcription factors have been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly oncogenic in animal model systems. The potent oncogenicity of v-Rel is the consequence of a number of mutations that have altered its activity and regulation: for example, certain mutations decrease its ability to be regulated by IκBα, change its DNA-binding site specificity, and endow it with new transactivation properties. The study of v-Rel will continue to increase our knowledge of how cellular Rel proteins contribute to oncogenesis by affecting cell growth, altering cell-cycle regulation, and blocking apoptosis. This review will discuss biological and molecular activities of v-Rel, with particular attention to how these activities relate to structure – function aspects of the Rel/NF-κB transcription factors.

Matching Content Categories {📚}

  • Telecommunications
  • Science
  • Education

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 96,105,781 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't figure out the monetization strategy.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Doi.org has a revenue plan, but it's either invisible or we haven't found it.

Keywords {🔍}

oncogene, virol, bose, cell, gilmore, biol, mol, enrietto, virology, temin, nature, gélinas, avian, vrel, access, natl, usa, dis, article, hannink, humphries, cancer, proc, acad, sci, chen, hrdlicková, rice, content, nfκb, kabrun, olson, zhang, bargmann, white, research, cookies, nehyba, res, witter, privacy, open, walker, capobianco, mosialos, gilden, lim, press, genes, data,

Topics {✒️}

nature portfolio permissions reprints rel/nf-κb transcription factors privacy policy 1981 nature 294 nature author information authors advertising scientific legacy social media retroviral oncoprotein v-rel literature research tobacco research research nf-κb pathway personal data rapidly fatal lymphoma/leukemia springerlink instant access nf-κb data protection permissions v-rel oncoprotein dna-binding site specificity altering cell-cycle regulation v-rel induces privacy multiple mutations contribute explore content subscription content 1999 gene expression li c-ch european economic area animal model systems institutional subscriptions read antigen receptor-activated bose jr hr min-min wan noori-daloii mr hr bose jr accepting optional cookies journals search log affecting cell growth v-rel article purchase manage preferences structure – function aspects elsevier science publishers b-cell lymphoma content article gilmore

Schema {🗺️}

WebPage:
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         headline:Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel
         description:The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-κB transcription factor family. v-Rel induces a rapidly fatal lymphoma/leukemia in young birds, and v-Rel can transform and immortalize a variety of avian cell types in vitro. Although Rel/NF-κB transcription factors have been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly oncogenic in animal model systems. The potent oncogenicity of v-Rel is the consequence of a number of mutations that have altered its activity and regulation: for example, certain mutations decrease its ability to be regulated by IκBα, change its DNA-binding site specificity, and endow it with new transactivation properties. The study of v-Rel will continue to increase our knowledge of how cellular Rel proteins contribute to oncogenesis by affecting cell growth, altering cell-cycle regulation, and blocking apoptosis. This review will discuss biological and molecular activities of v-Rel, with particular attention to how these activities relate to structure – function aspects of the Rel/NF-κB transcription factors.
         datePublished:1999-11-22T00:00:00Z
         dateModified:1999-11-22T00:00:00Z
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            Cell Biology
            Human Genetics
            Oncology
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      headline:Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel
      description:The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-κB transcription factor family. v-Rel induces a rapidly fatal lymphoma/leukemia in young birds, and v-Rel can transform and immortalize a variety of avian cell types in vitro. Although Rel/NF-κB transcription factors have been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly oncogenic in animal model systems. The potent oncogenicity of v-Rel is the consequence of a number of mutations that have altered its activity and regulation: for example, certain mutations decrease its ability to be regulated by IκBα, change its DNA-binding site specificity, and endow it with new transactivation properties. The study of v-Rel will continue to increase our knowledge of how cellular Rel proteins contribute to oncogenesis by affecting cell growth, altering cell-cycle regulation, and blocking apoptosis. This review will discuss biological and molecular activities of v-Rel, with particular attention to how these activities relate to structure – function aspects of the Rel/NF-κB transcription factors.
      datePublished:1999-11-22T00:00:00Z
      dateModified:1999-11-22T00:00:00Z
      pageStart:6925
      pageEnd:6937
      sameAs:https://doi.org/10.1038/sj.onc.1203222
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         transcription factor
         retroviral oncogene
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         general
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         Cell Biology
         Human Genetics
         Oncology
         Apoptosis
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Social Networks {👍}(1)

External Links {🔗}(99)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
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Name Servers:

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

CDN Services {📦}

  • Crossref

3.9s.