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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/article/10.1007/s10911-008-9084-6, but it redirected us to https://link.springer.com/article/10.1007/s10911-008-9084-6. The analysis below is for the second page.

Title[redir]:
The ADAM17–amphiregulin–EGFR Axis in Mammary Development and Cancer | Journal of Mammary Gland Biology and Neoplasia
Description:
In order to fulfill its function of producing and delivering sufficient milk to newborn mammalian offspring, the mammary gland first has to form an extensive ductal network. As in all phases of mammary development, hormonal cues elicit local intra- and inter-cellular signaling cascades that regulate ductal growth and differentiation. Among other things, ductal development requires the epidermal growth factor receptor (EGFR), its ligand amphiregulin (AREG), and the transmembrane metalloproteinase ADAM17, which can cleave and release AREG from the cell surface so that it may interact with its receptor. Tissue recombination and transplantation studies demonstrate that EGFR phosphorylation and ductal development proceed only when ADAM17 and AREG are expressed on mammary epithelial cells and EGFR is present on stromal cells, and that local administration of soluble AREG can rescue the development of ADAM17-deficient transplants. Thus proper mammary morphogenesis requires the ADAM17-mediated release of AREG from ductal epithelial cells, the subsequent activation of EGFR on stromal cells, and EGFR-dependent stromal responses that in return elicit a new set of epithelial responses, all culminating in the formation of a fully functional ductal tree. This, however, raises new issues concerning what may act upstream, downstream or in parallel with the ADAM17–AREG–EGFR axis, how it may become hijacked or corrupted during the onset and evolution of cancer, and how such ill effects may be confronted.

Matching Content Categories {📚}

  • Education
  • Science
  • News & Politics

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

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How Does Doi.org Make Money? {💸}

We can't tell how the site generates income.

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 might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

google, scholar, cas, pubmed, article, mammary, growth, gland, factor, receptor, development, cell, cancer, biol, epidermal, morphogenesis, breast, epithelial, mice, ductal, amphiregulin, cells, branching, mouse, tumor, res, expression, egfr, proliferation, estrogen, necrosis, activation, werb, dev, sci, signaling, adam, egf, human, proc, natl, acad, erbb, chem, sternlicht, sunnarborg, metalloproteinase, stromal, enzyme, lee,

Topics {✒️}

stromal–epithelial interactions regulating mt1-mmp-mediated activation month download article/chapter estrogen receptor-alpha knockout tnf alpha-deficient mice mouse strain-specific patterns epidermal growth factor strain-dependent epithelial defects inter-cellular signaling cascades epithelial growth factor egfr-dependent stromal responses egfr signalling protein-coupled receptors related subjects full article pdf adam17–amphiregulin–egfr axis mammary epithelial cells mammary gland growth lung branching morphogenesis ductal epithelial cells cultured mammary gland adam17–areg–egfr axis tgf alpha gene regulate ductal growth mammary branching morphogenesis lung bud morphogenesis human breast cancer mammary gland morphogenesis mammary end bud matrix metalloproteinase expression mouse egf receptor transgenic mice reveals egf receptor ligands jackson-fisher privacy choices/manage cookies transmembrane metalloproteinase adam17 estrogen receptor expression fgfr2b signaling regulates mouse mammary gland estrogen receptor transcription mesenchyme-dependent morphogenesis 17 beta-estradiol dominant-negative erbb2 cell growth differ human mammary fibroblasts persistent parity-induced remodeling epithelial tissues mammary gland biology embryonic mammary gland rodent mammary gland

Questions {❓}

  • Do different branching epithelia use a conserved developmental mechanism?

Schema {🗺️}

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         headline:The ADAM17–amphiregulin–EGFR Axis in Mammary Development and Cancer
         description:In order to fulfill its function of producing and delivering sufficient milk to newborn mammalian offspring, the mammary gland first has to form an extensive ductal network. As in all phases of mammary development, hormonal cues elicit local intra- and inter-cellular signaling cascades that regulate ductal growth and differentiation. Among other things, ductal development requires the epidermal growth factor receptor (EGFR), its ligand amphiregulin (AREG), and the transmembrane metalloproteinase ADAM17, which can cleave and release AREG from the cell surface so that it may interact with its receptor. Tissue recombination and transplantation studies demonstrate that EGFR phosphorylation and ductal development proceed only when ADAM17 and AREG are expressed on mammary epithelial cells and EGFR is present on stromal cells, and that local administration of soluble AREG can rescue the development of ADAM17-deficient transplants. Thus proper mammary morphogenesis requires the ADAM17-mediated release of AREG from ductal epithelial cells, the subsequent activation of EGFR on stromal cells, and EGFR-dependent stromal responses that in return elicit a new set of epithelial responses, all culminating in the formation of a fully functional ductal tree. This, however, raises new issues concerning what may act upstream, downstream or in parallel with the ADAM17–AREG–EGFR axis, how it may become hijacked or corrupted during the onset and evolution of cancer, and how such ill effects may be confronted.
         datePublished:2008-05-10T00:00:00Z
         dateModified:2008-05-10T00:00:00Z
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            Branching morphogenesis
            Metalloproteinase
            ADAMs
            TNFα converting enzyme
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            Stromal–epithelial interactions
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            Oncology
            Cancer Research
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      headline:The ADAM17–amphiregulin–EGFR Axis in Mammary Development and Cancer
      description:In order to fulfill its function of producing and delivering sufficient milk to newborn mammalian offspring, the mammary gland first has to form an extensive ductal network. As in all phases of mammary development, hormonal cues elicit local intra- and inter-cellular signaling cascades that regulate ductal growth and differentiation. Among other things, ductal development requires the epidermal growth factor receptor (EGFR), its ligand amphiregulin (AREG), and the transmembrane metalloproteinase ADAM17, which can cleave and release AREG from the cell surface so that it may interact with its receptor. Tissue recombination and transplantation studies demonstrate that EGFR phosphorylation and ductal development proceed only when ADAM17 and AREG are expressed on mammary epithelial cells and EGFR is present on stromal cells, and that local administration of soluble AREG can rescue the development of ADAM17-deficient transplants. Thus proper mammary morphogenesis requires the ADAM17-mediated release of AREG from ductal epithelial cells, the subsequent activation of EGFR on stromal cells, and EGFR-dependent stromal responses that in return elicit a new set of epithelial responses, all culminating in the formation of a fully functional ductal tree. This, however, raises new issues concerning what may act upstream, downstream or in parallel with the ADAM17–AREG–EGFR axis, how it may become hijacked or corrupted during the onset and evolution of cancer, and how such ill effects may be confronted.
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         Branching morphogenesis
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         TNFα converting enzyme
         ErbB
         Stromal–epithelial interactions
         Epidermal growth factor receptor
         Oncology
         Cancer Research
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External Links {🔗}(382)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.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

5.75s.