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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. External Links
  10. Analytics And Tracking
  11. Libraries
  12. Hosting Providers

We began analyzing https://link.springer.com/chapter/10.1007/978-981-10-5987-2_8, but it redirected us to https://link.springer.com/chapter/10.1007/978-981-10-5987-2_8. The analysis below is for the second page.

Title[redir]:
cGAS-STING Activation in the Tumor Microenvironment and Its Role in Cancer Immunity | SpringerLink
Description:
Stimulator of interferon (IFN) genes (STING) is a key mediator in the immune response to cytoplasmic DNA sensed by cyclic GMP-AMP (cGAMP) synthase (cGAS). After synthesis by cGAS, cGAMP acts as a second messenger activating STING in the cell harboring cytoplasmic DNA...

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

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 80,911,460 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 every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Doi.org could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, central, sting, dna, cells, chen, immunity, immune, cell, innate, activation, tumor, pathway, type, zhang, res, cytosolic, immunol, huang, signaling, cgassting, cyclic, barber, tumors, gap, nature, stingdependent, connexin, chapter, response, sun, wang, sci, activates, doijimmuni, science, human, rep, antitumor, microenvironment, role, ifn, cgas, disease, gantier,

Topics {✒️}

s-phase-specific dna damage cgas-sting dna-sensing pathway dmba-induced mouse model sting/irf3-dependent manner cgas-dependent antiviral responses biochemical recurrence-free survival interferon-dependent autoimmune disease trex1-deficient mouse model interferon-dependent innate immunity cd8{alpha}+ dendritic cells cytosolic dna sensor small-cell lung cancer c-di-amp secreted sting-targeting oligonucleotides results early-stage colorectal cancer cyclic gmp-amp synthase mediates innate resistance interferon-dependent rejection cells predict outcome cgas-sting signaling axis endogenous high-affinity ligand interferon-dependent antitumor immunity cell-inflamed tumors rejected cytoplasmic dna sensed dna damage primes cytosolic dna activates innate immune signaling sting-dependent sensors sting-dependent pathway annotated interferon-regulated genes human papillomavirus dna endoplasmic reticulum adaptor innate immune system sting induces apoptosis privacy choices/manage cookies activates human sting agonist-mediated activation gray ee cyclic gmp-amp damaged nuclear dna cgas-sting axis heterologous gap junctions impaired gap junctions maintaining genome stability dna confers resistance lethal autoimmune disease gap junction composed cytosolic surveillance pathway sting pathway ligand dna hybrids activate

Schema {🗺️}

ScholarlyArticle:
      headline:cGAS-STING Activation in the Tumor Microenvironment and Its Role in Cancer Immunity
      pageEnd:194
      pageStart:175
      image:https://media.springernature.com/w153/springer-static/cover/book/978-981-10-5987-2.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Regulation of Inflammatory Signaling in Health and Disease
         isbn:
            978-981-10-5987-2
            978-981-10-5986-5
         type:Book
      publisher:
         name:Springer Singapore
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Geneviève Pépin
            affiliation:
                  name:Hudson Institute of Medical Research
                  address:
                     name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
                     type:PostalAddress
                  type:Organization
                  name:Monash University
                  address:
                     name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Michael P. Gantier
            affiliation:
                  name:Hudson Institute of Medical Research
                  address:
                     name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
                     type:PostalAddress
                  type:Organization
                  name:Monash University
                  address:
                     name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
                     type:PostalAddress
                  type:Organization
            type:Person
      keywords:cGAS, cGAMP, STING, Interferon, Connexin, Cancer
      description:Stimulator of interferon (IFN) genes (STING) is a key mediator in the immune response to cytoplasmic DNA sensed by cyclic GMP-AMP (cGAMP) synthase (cGAS). After synthesis by cGAS, cGAMP acts as a second messenger activating STING in the cell harboring cytoplasmic DNA but also in adjacent cells through gap junction transfer. While the role of the cGAS-STING pathway in pathogen detection is now well established, its importance in cancer immunity has only recently started to emerge. Nonetheless, STING appears to be an essential component in the recruitment of immune cells to the tumor microenvironment, which is paramount to immune clearance of the tumor. This review presents an overview of the growing literature around the role of the cGAS-STING pathway in the tumor microenvironment, with a specific focus on the role that cancer cells may play in the direct activation of this pathway, and its amplification through cell-cell transfer of cGAMP.
      datePublished:2017
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
      context:https://schema.org
Book:
      name:Regulation of Inflammatory Signaling in Health and Disease
      isbn:
         978-981-10-5987-2
         978-981-10-5986-5
Organization:
      name:Springer Singapore
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Hudson Institute of Medical Research
      address:
         name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
         type:PostalAddress
      name:Monash University
      address:
         name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
         type:PostalAddress
      name:Hudson Institute of Medical Research
      address:
         name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
         type:PostalAddress
      name:Monash University
      address:
         name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Geneviève Pépin
      affiliation:
            name:Hudson Institute of Medical Research
            address:
               name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
               type:PostalAddress
            type:Organization
            name:Monash University
            address:
               name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Michael P. Gantier
      affiliation:
            name:Hudson Institute of Medical Research
            address:
               name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
               type:PostalAddress
            type:Organization
            name:Monash University
            address:
               name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
      name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
      name:Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Australia
      name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(393)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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  • mx3.zoho.eu

Name Servers:

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