Role of G protein-coupled receptor kinases in cell migration
Entidad
UAM. Departamento de Biología MolecularEditor
Elsevier Inc.Fecha de edición
2014-04-01Cita
10.1016/j.ceb.2013.10.005
Current Opinion In Cell Biology 27.1 (2014): 10-17
ISSN
0955-0674 (print); 1879-0410 (online)DOI
10.1016/j.ceb.2013.10.005Financiado por
Our laboratory is funded by grants from Ministerio de Educación y Ciencia (SAF2011-23800), Fundación Ramón Areces, The Cardiovascular Network (RECAVA) of Ministerio Sanidad y Consumo-Instituto Carlos III (RD12/0042/0012), Comunidad de Madrid Indisnet Network (S2011/BMD-2332) to F.M, and Fundación Eugenio Rodriguez Pascual, Fundación Ramón Areces and Instituto de Salud Carlos III (PI11/00859) to P.P.Proyecto
Comunidad de Madrid. S2010/BMD-2332/INDISNETVersión del editor
http://dx.doi.org/10.1016/j.ceb.2013.10.005Materias
Cells; Cell differentiation; Biología y Biomedicina / BiologíaDerechos
© 2014 Elselvier Inc.Esta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional.
Resumen
G protein-coupled receptor kinases (GRKs) are emerging as important integrative nodes in cell migration processes. Recent evidence links GRKs (particularly the GRK2 isoform) to the complex modulation of diverse aspects of cell motility. In addition to its well-established role in the desensitization of G protein-coupled receptors involved in chemotaxis, GRK2 can play a effector role in the organization of actin and microtubule networks and in adhesion dynamics, by means of novel substrates and transient interacting partners, such as the GIT-1 scaffold or the cytoplasmic α-tubulin deacetylase histone deacetylase 6 (HDAC6). The overall effect of altering GRK levels or activity on chemotaxis would depend on how such different roles are integrated in a
given cell type and physiological context, and may have relevant implications in inflammatory diseases or cancer progression
Lista de ficheros
Google Scholar:Penela Márquez, Petronila
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Nogués, Laura
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Mayor Menéndez, Federico
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