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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
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We began analyzing https://link.springer.com/chapter/10.1007/978-3-319-41171-2_8, but it redirected us to https://link.springer.com/chapter/10.1007/978-3-319-41171-2_8. The analysis below is for the second page.

Title[redir]:
Inflammasome Recognition and Regulation of the Legionella Flagellum | SpringerLink
Description:
The Gram-negative bacterium Legionella pneumophila colonizes extracellular environmental niches and infects free-living protozoa. Upon inhalation into the human lung, the opportunistic pathogen grows in macrophages and causes a fulminant pneumonia termed...

Matching Content Categories {📚}

  • Education
  • Business & Finance
  • Science

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 8,445,319 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

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Topics {✒️}

dot/icm secretion system iqgap1-cdc42-arhgef9-dependent pathway leta-rsmyz-csra regulatory cascade icm/dot-dependent inhibition month download article/chapter rab5-activated phospholipase a1 sigma54 promoter-specificity factor α-hydroxyketone signaling molecule conserved carboxy-terminal domain irg1-derived itaconic acid rapid pathogen-induced apoptosis distinct membrane-bound compartment legionella pneumophila-translocated substrate prr-signaling pathways—learning naip5-mediated macrophage immunity naip5/ipaf signalling pathways thioglycolate-elicited peritoneal macrophages infects free-living protozoa case cl gram-negative bacteria targeting pro-death members infect-era project eugenpath lqs-dependent phosphorylation signaling response regulator lqsr tracked nf-kappab activation stationary-phase legionella pneumophila legionella quorum sensing machner mp secreted bacterial effectors bacterial pathogen-occupied vacuoles translocated pathogen effectors forsbach-birk autoinducer synthase lqsa german research foundation legionella effector functioning legionella pneumophila csra called effector proteins privacy choices/manage cookies pathogen–host interactions pathogen-host interactions host-pathogen interactions nlrc4 inflammasome contributes device instant download nf-κb pathway α-hydroxyketone signaling host cell death alveolar epithelial cells rab gtpases identified signaling compound lai-1 chapter inflammasome signaling

Schema {🗺️}

ScholarlyArticle:
      headline:Inflammasome Recognition and Regulation of the Legionella Flagellum
      pageEnd:181
      pageStart:161
      image:https://media.springernature.com/w153/springer-static/cover/book/978-3-319-41171-2.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Inflammasome Signaling and Bacterial Infections
         isbn:
            978-3-319-41171-2
            978-3-319-41170-5
         type:Book
      publisher:
         name:Springer International Publishing
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Ursula Schell
            affiliation:
                  name:Ludwig-Maximilians University
                  address:
                     name:Max von Pettenkofer Institute, Ludwig-Maximilians University, Munich, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Sylvia Simon
            affiliation:
                  name:University of Zürich
                  address:
                     name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Hubert Hilbi
            affiliation:
                  name:University of Zürich
                  address:
                     name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      keywords:Amoeba, Autoinducer, Dictyostelium , Effector protein, Flagellin, Macrophage, NAIP5/NLRC4 inflammasome, Pathogen vacuole, Phosphoinositide, Small GTPase, Type IV secretion, Quorum sensing
      description:The Gram-negative bacterium Legionella pneumophila colonizes extracellular environmental niches and infects free-living protozoa. Upon inhalation into the human lung, the opportunistic pathogen grows in macrophages and causes a fulminant pneumonia termed Legionnaires’ disease. L. pneumophila employs a biphasic life cycle, comprising a replicative, non-virulent, and a stationary, virulent form. In the latter phase, the pathogen produces a plethora of so-called effector proteins, which are injected into host cells, where they subvert pivotal processes and promote the formation of a distinct membrane-bound compartment, the Legionella-containing vacuole. In the stationary phase, the bacteria also produce a single monopolar flagellum and become motile. L. pneumophila flagellin is recognized by and triggers the host’s NAIP5 (Birc1e)/NLRC4 (Ipaf) inflammasome, which leads to caspase-1 activation, pore formation, and pyroptosis. The production of L. pneumophila flagellin and pathogen–host interactions are controlled by a complex stationary phase regulatory network, detecting nutrient availability as well as the Legionella quorum sensing (Lqs) signaling compound LAI-1 (3-hydroxypentadecane-4-one). Thus, the small molecule LAI-1 coordinates L. pneumophila flagellin production and motility, inflammasome activation, and virulence.
      datePublished:2016
      isAccessibleForFree:
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         type:WebPageElement
      context:https://schema.org
Book:
      name:Inflammasome Signaling and Bacterial Infections
      isbn:
         978-3-319-41171-2
         978-3-319-41170-5
Organization:
      name:Springer International Publishing
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Ludwig-Maximilians University
      address:
         name:Max von Pettenkofer Institute, Ludwig-Maximilians University, Munich, Germany
         type:PostalAddress
      name:University of Zürich
      address:
         name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
         type:PostalAddress
      name:University of Zürich
      address:
         name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Ursula Schell
      affiliation:
            name:Ludwig-Maximilians University
            address:
               name:Max von Pettenkofer Institute, Ludwig-Maximilians University, Munich, Germany
               type:PostalAddress
            type:Organization
      name:Sylvia Simon
      affiliation:
            name:University of Zürich
            address:
               name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
               type:PostalAddress
            type:Organization
      name:Hubert Hilbi
      affiliation:
            name:University of Zürich
            address:
               name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Max von Pettenkofer Institute, Ludwig-Maximilians University, Munich, Germany
      name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
      name:Institute of Medical Microbiology, University of Zürich, Zürich, Switzerland
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

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