Activation of Ras and Rho GTPases and MAPKs by G protein coupled receptors (Articolo in rivista)

Type
Label
  • Activation of Ras and Rho GTPases and MAPKs by G protein coupled receptors (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Chiariello M.; Vaqué J. P.; Crespo P.; Gutkind S. J. (2010)
    Activation of Ras and Rho GTPases and MAPKs by G protein coupled receptors
    in Methods in molecular biology (Clifton N.J.)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Chiariello M.; Vaqué J. P.; Crespo P.; Gutkind S. J. (literal)
Pagina inizio
  • 137 (literal)
Pagina fine
  • 150 (literal)
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  • 661 (literal)
Rivista
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  • In: Methods in Molecular Biology, vol. 661 pp. 137 - 150. SpringerLink, 2010. (literal)
Note
  • PubMe (literal)
  • Scopu (literal)
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  • CNR-IFC, Siena, NIDCR, National Institutes of Health (NIH), Bethesda, USA, Consejo Superior de Investigaciones Científicas, Instituto de Investigaciones Biomédicas, Madrid, Spain (literal)
Titolo
  • Activation of Ras and Rho GTPases and MAPKs by G protein coupled receptors (literal)
Abstract
  • A complex intracellular signaling network mediates the multiple biological activities of G-protein-coupled receptors (GPCRs). Among them, monomeric GTPases and a family of closely related proline-targeted serine-threonine kinases, collectively known as Mitogen-Activated Protein Kinases (MAPKs), appears to play central roles in orchestrating the proliferative responses to multiple mitogens that act on GPCRs. Upon GDP/GTP exchange, monomeric GTPases control the phosphorylation of conserved threonine and tyrosine residues in MAPKs by their immediate upstream kinases, increasing their enzymatic activity and inducing their translocation to the nucleus where they phosphorylate transcription factors, thereby regulating the expression of genes playing a key role in normal and aberrant cell growth. Recently, a number of GPCRs have been engineered to provide exclusive activation by synthetic drug-like compounds while becoming insensitive to endogenous ligands. These engineered receptors, named Receptors Activated Solely by Synthetic Ligands (RASSLs), promise better understanding of GPCRs signaling in vitro and in vivo, thus representing ideal tools to selectively modulate MAPK signaling routes controlling a wide range of biological functions, from proliferation to differentiation, migration, invasion, and cell survival or death by apoptosis. (literal)
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