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Role of the PI3K regulatory subunit in the control of actin organization and cell migration

AuthorsJiménez, Concepción; Armas Portela, Rosario; Mellado, Mario; Rodríguez Frade, José M.; Collard, John; Serrano, Antonio; Martínez-Alonso, Carlos; Ávila, Jesús ; Carrera, Ana C.
Phosphatidylinositol 3-kinase
Actin cytoskeleton
Issue DateOct-2000
PublisherRockefeller University Press
CitationThe Journal of Cell Biology, volume 151, number 2, october 16, 2000, pp. 249–261
AbstractCell migration represents an important cellular response that utilizes cytoskeletal reorganization as its driving force. Here, we describe a new signaling cascade linking PDGF receptor stimulation to actin rearrangements and cell migration. We demonstrate that PDGF activates Cdc42 and its downstream effector N-WASP to mediate filopodia formation, actin stress fiber disassembly, and a reduction in focal adhesion complexes. Induction of the Cdc42 pathway is independent of phosphoinositide 3-kinase (PI3K) enzymatic activity, but it is dependent on the p85 a regulatory subunit of PI3K. Finally, data are provided showing that activation of this pathway is required for PDGF-induced cell migration on collagen. These observations show the essential role of the PI3K regulatory subunit p85 a in controlling PDGF receptor–induced cytoskeletal changes and cell migration, illustrating a novel signaling pathway that links receptor stimulation at the cell membrane with actin dynamics
DescriptionCopyright © by The Rockefeller University Press
Appears in Collections:(CNB) Artículos
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