| First Author | Jiménez C | Year | 2000 |
| Journal | J Cell Biol | Volume | 151 |
| Issue | 2 | Pages | 249-62 |
| PubMed ID | 11038173 | Mgi Jnum | J:292595 |
| Mgi Id | MGI:6450670 | Doi | 10.1083/jcb.151.2.249 |
| Citation | Jimenez C, et al. (2000) Role of the PI3K regulatory subunit in the control of actin organization and cell migration. J Cell Biol 151(2):249-62 |
| abstractText | Cell 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 p85alpha 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 p85alpha 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. |
