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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s11427-017-9173-5.

Title:
Interplay between TGF-β signaling and receptor tyrosine kinases in tumor development | Science China Life Sciences
Description:
Transforming growth factor-β (TGF-β) signaling regulates cell proliferation, differentiation, migration and death, and plays a critical role in embryogenesis and tissue homeostasis. Its deregulation results in various diseases including tumor formation. Receptor tyrosine kinases (RTKs), such as epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR), also play key roles in the development and progression of many types of tumors. It has been realized that TGF-β signaling and RTK pathways interact with each other and their interplay is important for cancer development. They are mutually regulated and cooperatively modulate cell survival and migration, epithelial-mesenchymal transition, and tumor microenvironment to accelerate tumorigenesis and tumor metastasis. RTKs can modulate Smad-dependent transcription or cooperate with TGF-β to potentiate its oncogenic activity, while TGF-β signaling can in turn control RTK signaling by regulating their activities or expression. This review summarizes current understandings of the interplay between TGF-β signaling and RTKs and its influence on tumor development.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • News & Politics

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com 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 Link.springer.com Make Money? {💸}

We can't tell how the site generates income.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, tgfβ, cell, growth, central, signaling, factor, transforming, biol, cells, receptor, signalling, wang, transition, smad, res, nat, tumor, breast, rev, epithelial, development, chen, mammary, sci, mol, access, massagué, factorβ, progression, epithelialmesenchymal, expression, emt, zhang, nature, lung, privacy, cookies, content, life, tyrosine, pathways, metastasis, therapy, mesenchymal,

Topics {✒️}

mediate tgf-beta-induced transcription tgf-β-induced epithelial-mesenchymal transition transforming growth factor-beta tgf-β signal transduction transforming growth factor-β month download article/chapter phosphatidylinositol 3-kinase/akt-dependent suppression tgf-β family signalling integrin avβ3 induced tgf-β-induced epithelial tgf-β-induced apoptosis tgf-beta signalling extracellular signal-regulated kinase tgf-β-mediated cancer progression activate phosphatidylinositol-3 kinase/akt tgf-β1 involves mapk tgf-β signalling mitogen-activated protein kinase tgf-beta receptor activity tumour-induced systemic environment targeting fgfr signalling extracellular tgf-β signaling tgf-β family signaling tgf-β superfamily signaling wild-type p53 protein ye-guang chen smad tgf-β signals c-jun/c-fos erbb2-overexpressing breast cancer elicit epithelial-mesenchymal transition ap-1 signalling pathways modulate smad-dependent transcription rescues bmpr-ii expression china life sci inhibiting akt1-mediated phosphorylation full article pdf mammary epithelial cells article shi tgf-β signaling mammary gland development related subjects growth factor tgfβ signalling context-dependent bidirectional regulation promoting pulmonary metastasis smad2-mediated signaling akt interacts directly privacy choices/manage cookies receptor tyrosine kinases epithelial-mesenchymal transition

Questions {❓}

  • Gastric cancer and angiogenesis: is VEGF a useful biomarker to assess progression and remission?

Schema {🗺️}

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         headline:Interplay between TGF-β signaling and receptor tyrosine kinases in tumor development
         description:Transforming growth factor-β (TGF-β) signaling regulates cell proliferation, differentiation, migration and death, and plays a critical role in embryogenesis and tissue homeostasis. Its deregulation results in various diseases including tumor formation. Receptor tyrosine kinases (RTKs), such as epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR), also play key roles in the development and progression of many types of tumors. It has been realized that TGF-β signaling and RTK pathways interact with each other and their interplay is important for cancer development. They are mutually regulated and cooperatively modulate cell survival and migration, epithelial-mesenchymal transition, and tumor microenvironment to accelerate tumorigenesis and tumor metastasis. RTKs can modulate Smad-dependent transcription or cooperate with TGF-β to potentiate its oncogenic activity, while TGF-β signaling can in turn control RTK signaling by regulating their activities or expression. This review summarizes current understandings of the interplay between TGF-β signaling and RTKs and its influence on tumor development.
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      headline:Interplay between TGF-β signaling and receptor tyrosine kinases in tumor development
      description:Transforming growth factor-β (TGF-β) signaling regulates cell proliferation, differentiation, migration and death, and plays a critical role in embryogenesis and tissue homeostasis. Its deregulation results in various diseases including tumor formation. Receptor tyrosine kinases (RTKs), such as epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR), also play key roles in the development and progression of many types of tumors. It has been realized that TGF-β signaling and RTK pathways interact with each other and their interplay is important for cancer development. They are mutually regulated and cooperatively modulate cell survival and migration, epithelial-mesenchymal transition, and tumor microenvironment to accelerate tumorigenesis and tumor metastasis. RTKs can modulate Smad-dependent transcription or cooperate with TGF-β to potentiate its oncogenic activity, while TGF-β signaling can in turn control RTK signaling by regulating their activities or expression. This review summarizes current understandings of the interplay between TGF-β signaling and RTKs and its influence on tumor development.
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External Links {🔗}(256)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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