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

We began analyzing https://link.springer.com/chapter/10.1007/978-3-319-39406-0_1, but it redirected us to https://link.springer.com/chapter/10.1007/978-3-319-39406-0_1. The analysis below is for the second page.

Title[redir]:
Molecular Cell Biology of Apoptosis and Necroptosis in Cancer | SpringerLink
Description:
Cell death is a major mechanism to eliminate cells in which DNA is damaged, organelles are stressed, or oncogenes are overexpressed, all events that would otherwise predispose cells to oncogenic transformation. The pathways that initiate and execute cell death are...

Matching Content Categories {šŸ“š}

  • Education
  • Telecommunications
  • Business & Finance

Content Management System {šŸ“}

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 {šŸ“ˆ}

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 5,000,420 visitors per month in the current month.

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How Does Doi.org Make Money? {šŸ’ø}

We can't tell how the site generates income.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org could be secretly minting cash, but we can't detect the process.

Keywords {šŸ”}

pubmed, google, scholar, cas, article, central, cell, death, caspase, cancer, apoptosis, biol, bcl, necroptosis, cells, mol, differ, mice, mcl, nature, necrosis, chapter, family, sci, rip, ripk, tumor, apoptotic, nat, res, activation, signaling, dev, role, proc, natl, acad, essential, green, response, abt, chem, pathways, therapeutic, med, protein, deficiency, leukemia, clin, caspases,

Topics {āœ’ļø}

tlr3/rip3-dependent necroptosis backs strain-dependent neurodevelopmental abnormalities tnf-induced nf-kappab signal month download article/chapter heat shock-induced death kainic acid-induced excitotoxicity cancer-type-specific crosstalk hydrocarbon-stapled bh3 helix heat shock-induced apoptosis nanog/nanogp8 downregulates mcl-1 somatic copy-number alteration myc-induced myeloid leukemogenesis p53-mediated apoptotic response nucleotide insertion-deletion polymorphism nucleotide deletion/insertion variant peri-implantation embryonic lethality dna-damage-induced apoptosis p53-defective cells triggered bcl-x-deficient mice tnfalpha-induced necroptotic signaling death receptor-induced apoptosis hematopoietic stem/progenitor cells death receptor-mediated apoptosis targeted high-affinity inhibitor small-cell lung cancer normal nf-kappa bs tumor necrosis factor il-1alpha release nuclear caspase-2-activating complex selective small molecule chronic lymphocytic leukemia receptor 3-mediated necrosis phosphorylation-driven assembly anti-cancer therapy christopher cullen sp ripk-dependent necrosis tumor suppressor function specific cellular target p53-induced protein acute myeloid leukemia piddosome-independent tumor suppression outer membrane permeabilization hydrocarbon-stapled peptides privacy choices/manage cookies caspase-8 mediate priming virus-induced inflammation necrotic cell death rudin cm ischemic brain injury programmed cell death

Questions {ā“}

  • Bcl-2 family proteins in breast development and cancer: could Mcl-1 targeting overcome therapeutic resistance?

Schema {šŸ—ŗļø}

ScholarlyArticle:
      headline:Molecular Cell Biology of Apoptosis and Necroptosis in Cancer
      pageEnd:23
      pageStart:1
      image:https://media.springernature.com/w153/springer-static/cover/book/978-3-319-39406-0.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy
         isbn:
            978-3-319-39406-0
            978-3-319-39404-6
         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:Christopher P. Dillon
            affiliation:
                  name:St. Jude Children’s Research Hospital
                  address:
                     name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Douglas R. Green
            affiliation:
                  name:St. Jude Children’s Research Hospital
                  address:
                     name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      keywords:Cell death, Apoptosis, Necroptosis, RIPK3, BCL-2, Caspases, Cancer, Inflammation, Immunogenic
      description:Cell death is a major mechanism to eliminate cells in which DNA is damaged, organelles are stressed, or oncogenes are overexpressed, all events that would otherwise predispose cells to oncogenic transformation. The pathways that initiate and execute cell death are complex, genetically encoded, and subject to significant regulation. Consequently, while these pathways are often mutated in malignancy, there is considerable interest in inducing cell death in tumor cells as therapy. This chapter addresses our current understanding of molecular mechanisms contributing to two cell death pathways, apoptotic cell death and necroptosis, a regulated form of necrotic cell death. Apoptosis can be induced by a wide variety of signals, leading to protease activation that dismantles the cell. We discuss the physiological importance of each apoptosis pathway and summarize their known roles in cancer suppression and the current efforts at targeting each pathway therapeutically. The intricate mechanistic link between death receptor-mediated apoptosis and necroptosis is described, as well as the potential opportunities for utilizing necroptosis in the treatment of malignancy.
      datePublished:2016
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      name:Apoptosis in Cancer Pathogenesis and Anti-cancer Therapy
      isbn:
         978-3-319-39406-0
         978-3-319-39404-6
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      name:Springer International Publishing
      logo:
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         type:ImageObject
      name:St. Jude Children’s Research Hospital
      address:
         name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
         type:PostalAddress
      name:St. Jude Children’s Research Hospital
      address:
         name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
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      affiliation:
            name:St. Jude Children’s Research Hospital
            address:
               name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Douglas R. Green
      affiliation:
            name:St. Jude Children’s Research Hospital
            address:
               name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
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      name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
      name:Department of Immunology, St. Jude Children’s Research Hospital, Memphis, USA
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External Links {šŸ”—}(718)

Analytics and Tracking {šŸ“Š}

  • Google Tag Manager

Libraries {šŸ“š}

  • Clipboard.js

Emails and Hosting {āœ‰ļø}

Mail Servers:

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CDN Services {šŸ“¦}

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