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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
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We began analyzing https://www.nature.com/articles/ni.3440, but it redirected us to https://www.nature.com/articles/ni.3440. The analysis below is for the second page.

Title[redir]:
Interferon-induced guanylate-binding proteins in inflammasome activation and host defense | Nature Immunology
Description:
In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their effects on immunity to a wide variety of microbial pathogens. Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to

Matching Content Categories {📚}

  • Education
  • Science
  • Business & Finance

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?

🌠 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.
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How Does Doi.org Make Money? {💸}

We don’t know how the website earns money.

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 could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

pubmed, article, google, scholar, cas, central, inflammasome, nature, immunol, activation, cell, guanylatebinding, proteins, nat, host, protein, caspase, macmicking, immunity, human, access, science, defense, toxoplasma, infection, usa, gondii, gtpases, inflammasomes, rev, guanylate, binding, content, kim, sci, nlrp, noncanonical, role, biol, cookies, interferon, gbp, proc, natl, acad, aim, intracellular, plos, privacy, data,

Topics {✒️}

nature portfolio permissions reprints privacy policy ifn-γ-activated human cells ifn-γ-induced cell-autonomous responses interferon-induced guanylate-binding proteins advertising ifn-γ-induced macrophage immunity social media zebrafish guanylate-binding protein murine guanylate-binding protein sqstm1/p62/a170 regulates author information authors tnf-α mediates sensitization development ifn-induced gtpases mgbp1 ifn-γ-inducible lrg-47 interferon-γ-induced presentation caspase-1-deficient mice infected inflammasome-activating molecular component human autophagy proteins c-terminal α-helices host-virus arms races hsv-1-induced inflammasome activation author correspondence inflammatory diseases lps-induced inos production guanylate-binding proteins guanylate binding proteins ifn-γ primes keratinocytes personal data interferon-inducible effector mechanisms mouse p47-resistance gtpases tlr4-independent endotoxic shock nature 509 nature 526 nature 479 nature 514 nature 490 nature 458 nature 488 nature 440 nature pathogen-induced cell death guanylate-binding protein 1 data protection springerlink instant access cell-autonomous immunity protects ifn-inducible gtpases ifn-induced gtpases

Schema {🗺️}

WebPage:
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         headline:Interferon-induced guanylate-binding proteins in inflammasome activation and host defense
         description:In this Perspective, MacMicking and colleagues discuss the roles of interferon-induced guanylate-binding proteins in directing inflammasome responses and their effects on immunity to a wide variety of microbial pathogens. Traditional views of the inflammasome highlight the assembly of pre-existing core components shortly after infection or tissue damage. Emerging work, however, suggests that the inflammasome machinery is also subject to 'tunable' or inducible signals that might accelerate its autocatalytic properties and dictate where inflammasome assembly takes place in the cell. Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators, including a new family of interferon-induced GTPases called 'guanylate-binding proteins' (GBPs). Here we investigate the critical roles of interferon-induced GBPs in directing inflammasome subtype–specific responses and their consequences for cell-autonomous immunity to a wide variety of microbial pathogens. We discuss emerging mechanisms of action and the potential effect of these GBPs on predisposition to sepsis and other infectious or inflammatory diseases.
         datePublished:2016-04-19T00:00:00Z
         dateModified:2016-04-19T00:00:00Z
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      headline:Interferon-induced guanylate-binding proteins in inflammasome activation and host defense
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Social Networks {👍}(1)

External Links {🔗}(454)

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

4.99s.