4.8 Article

The aryl hydrocarbon receptor regulates focal adhesion sites through a non-genomic FAK/Src pathway

期刊

ONCOGENE
卷 32, 期 14, 页码 1811-1820

出版社

NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2012.197

关键词

AhR; cell plasticity; FAK; integrin; Src

资金

  1. ANSES (Agence Nationale de SEcurite Sanitaire de l'alimentation, de l'environnement et du travail)
  2. ANR (Agence Nationale de la Recherche) [06SEST26]
  3. ARC (Association pour la Recherche sur le Cancer) [3927, SFI20101201842]
  4. CNRS (Center Nationale de la recherche scientifique)
  5. Fondation pour la Recherche Medicale
  6. Ecole Doctorale du Medicament
  7. Hospitals Europeen Georges Pompidou and Necker Enfants Malade
  8. INSERM (Institut National de la Sante et de la Recherche Medicale)
  9. Ligue contre le Cancer
  10. Ministere de l'enseignement superieur et de la recherche
  11. Region Ile de France
  12. Universite Paris Descartes, Paris Sorbonne Cite

向作者/读者索取更多资源

The aryl hydrocarbon receptor (AhR) is commonly described as a transcription factor, which regulates xenobiotic-metabolizing enzymes. Recent studies have suggested that the binding of ligands to the AhR also activates the Src kinase. In this manuscript, we show that the AhR, through the activation of Src, activates focal adhesion kinase (FAK) and promotes integrin clustering. These effects contribute to cell migration. Further, we show that the activation of the AhR increases the interaction of FAK with the metastatic marker, HEF1/NEDD9/CAS-L, and the expression of several integrins. Xenobiotic exposure, thus, may contribute to novel cell-migratory programs. Oncogene (2013) 32, 1811-1820; doi: 10.1038/onc.2012.197; published online 4 June 2012

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