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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
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We began analyzing https://www.nature.com/articles/nrmicro2070, but it redirected us to https://www.nature.com/articles/nrmicro2070. The analysis below is for the second page.

Title[redir]:
Pyroptosis: host cell death and inflammation | Nature Reviews Microbiology
Description:
Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • 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 5,000,019 visitors per month in the current month.
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How Does Doi.org Make Money? {💸}

We see no obvious way the site makes money.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, article, google, scholar, cas, cell, caspase, activation, central, death, nature, inflammasome, immunol, infection, pyroptosis, apoptosis, host, macrophages, microbiol, cells, inflammatory, biol, protein, cookson, interleukin, salmonella, usa, dependent, immunity, inflammation, interleukinβ, ilβ, release, access, macrophage, sci, chem, proc, natl, acad, secretion, response, role, infect, immun, caspasedependent, exp, med, ipaf, content,

Topics {✒️}

permissions reprints nature portfolio privacy policy key pyroptosis-related genes advertising anaplasma phagocytophilum infection social media author information authors candida albicans conserved carboxy-terminal domain leucine-rich repeat domain human monocyte-derived macrophages inflammasome components cias1/cryopyrin/nlrp3 alarm-ringing inflammatory recruitment caspase-1-dependent pore formation nigericin-induced interleukin-1β release il-1β-converting enzyme author correspondence interleukin 1β-converting enzyme n-end rule pathway murine phospho-mlkl-s345 nature rev il-1β-loaded microvesicles nature genet pro-inflammatory il-1β pathogen-induced cell death dye uptake-independent pathway naip5-mediated macrophage immunity salmonella-induced caspase-2 activation personal data il-18/ifn-γ axis endolysosome-related vesicles nature immunol shigella flexneri-induced apoptosis shigella flexneri-induced inflammation outcome dictates life springerlink instant access inflammatory cytokines interleukin-1β data protection permissions nature nature 440 nature 452 nature 430 nature 399 nature 425 nature 453 human dendritic cells pseudomonas aeruginosa mediated nf-κb activation

Questions {❓}

  • Apoptosis: who was first?
  • Death-defying immunity: do apoptotic cells influence antigen processing and presentation?

Schema {🗺️}

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         headline:Pyroptosis: host cell death and inflammation
         description: Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
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      headline:Pyroptosis: host cell death and inflammation
      description: Microorganism- and host-derived signals can stimulate formation of a multiprotein complex called the inflammasome, which activates the cysteine protease caspase 1. In turn, caspase 1 triggers an inflammatory programmed cell death pathway known as pyroptosis. Numerous pathogens have evolved a mechanism to subvert pyroptosis and persist within infected cells. Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
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Social Networks {👍}(1)

External Links {🔗}(520)

Analytics and Tracking {📊}

  • Google Tag Manager

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Mail Servers:

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CDN Services {📦}

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