Epidermal growth factor receptor‐mediated motility in fibroblasts
Identifieur interne : 000A27 ( Istex/Curation ); précédent : 000A26; suivant : 000A28Epidermal growth factor receptor‐mediated motility in fibroblasts
Auteurs : Alan Wells [États-Unis] ; Kiran Gupta [États-Unis] ; Philip Chang [États-Unis] ; Scott Swindle [États-Unis] ; Angela Glading [États-Unis] ; Hidenori Shiraha [États-Unis]Source :
- Microscopy Research and Technique [ 1059-910X ] ; 1998-12-01.
English descriptors
- KwdEn :
- Teeft :
- Actin, Actin cytoskeleton, Actin polymerization, Adhesion, Adhesiveness, Biol, Biophysical processes, Broblast, Broblast cell motility, Broblast motility, Broblasts, Calpain, Cell adhesion, Cell biol, Cell body, Cell motility, Chem, Chemokinesis, Chemokinetic, Chemotaxis, Cytoskeletal, Cytoskeleton, Disassembly, Dominant lamellipod, Egfr, Egfr activation, Egfrmediated, Egfrmediated motility, Epidermal, Epidermal growth factor, Epithelial, Epithelial cells, Extracellular, Extracellular matrix, Focal adhesion disassembly, Focal adhesions, Focal contacts, Gelsolin, Growth cell motility, Growth factor, Growth factor receptors, Growth factors, Growth motility, Gupta, Haptokinesis, Haptokinetic, Haptokinetic motility, Horwitz, Integrin, Integrins, Intracellular, Kinase, Klemke, Kundra, Lamellipod, Lamellipodia, Lauffenburger, Ligand, Locomotion, Matrix, Membrane ruffling, Mitogenesis, Motility, Myosin, Pathway, Pdgf, Phospholipase, Phosphorylation, Physiol, Pip2, Protein kinase, Receptor, Ridley, Ruffling, Stossel, Substratum, Transduction, Wound healing.
Abstract
Cell motility is induced by many growth factors acting through cognate receptors with intrinsic tyrosine kinase activity (RPTK). However, most of the links between receptor activation and the biophysical processes of cell motility remain undeciphered. We have focused on the mechanisms by which the EGF receptor (EGFR) actuates fibroblast cell motility in an attempt to define this integrated process in one system. Our working model is that divergent, but interconnected pathways lead to the biophysical processes necessary for cell motility: cytoskeleton reorganization, membrane extension, formation of new adhesions to substratum, cell contraction, and release of adhesions at the rear. We postulate that for any given growth factor some of the pathways/processes will be actively signaled and rate‐limiting, while others will be permissive due to background low‐level activation. Certain couplings have been defined, such as PLCγ and actin modifying proteins being involved in cytoskeletal reorganization and lamellipod extension and MEK being implicated in detachment from substratum. Others are suggested by complementary investigations in integrin‐mediated motility, including rac in membrane protrusion, rho in new adhesions, myosin II motors in contraction, and calpain in detachment, but have yet to be placed in growth factor‐induced motility. Our model postulates that many biochemical pathways will be shared between chemokinetic and haptokinetic motility but that select pathways will be activated only during RPTK‐enhanced motility. Microsc. Res. Tech. 43:395–411, 1998. © 1998 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1097-0029(19981201)43:5<395::AID-JEMT6>3.0.CO;2-T
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Res. Tech.</title><idno type="ISSN">1059-910X</idno><idno type="eISSN">1097-0029</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-12-01">1998-12-01</date><biblScope unit="volume">43</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="395">395</biblScope><biblScope unit="page" to="411">411</biblScope></imprint><idno type="ISSN">1059-910X</idno></series><idno type="istex">66B2E1F8812D8F4C3934B1B8E4ADC13A38EC3223</idno><idno type="DOI">10.1002/(SICI)1097-0029(19981201)43:5<395::AID-JEMT6>3.0.CO;2-T</idno><idno type="ArticleID">JEMT6</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1059-910X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>EGF receptor</term><term>cell migration</term><term>chemokinesis</term><term>signal transduction</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Actin</term><term>Actin cytoskeleton</term><term>Actin polymerization</term><term>Adhesion</term><term>Adhesiveness</term><term>Biol</term><term>Biophysical processes</term><term>Broblast</term><term>Broblast cell motility</term><term>Broblast motility</term><term>Broblasts</term><term>Calpain</term><term>Cell adhesion</term><term>Cell biol</term><term>Cell body</term><term>Cell motility</term><term>Chem</term><term>Chemokinesis</term><term>Chemokinetic</term><term>Chemotaxis</term><term>Cytoskeletal</term><term>Cytoskeleton</term><term>Disassembly</term><term>Dominant lamellipod</term><term>Egfr</term><term>Egfr activation</term><term>Egfrmediated</term><term>Egfrmediated motility</term><term>Epidermal</term><term>Epidermal growth factor</term><term>Epithelial</term><term>Epithelial cells</term><term>Extracellular</term><term>Extracellular matrix</term><term>Focal adhesion disassembly</term><term>Focal adhesions</term><term>Focal contacts</term><term>Gelsolin</term><term>Growth cell motility</term><term>Growth factor</term><term>Growth factor receptors</term><term>Growth factors</term><term>Growth motility</term><term>Gupta</term><term>Haptokinesis</term><term>Haptokinetic</term><term>Haptokinetic motility</term><term>Horwitz</term><term>Integrin</term><term>Integrins</term><term>Intracellular</term><term>Kinase</term><term>Klemke</term><term>Kundra</term><term>Lamellipod</term><term>Lamellipodia</term><term>Lauffenburger</term><term>Ligand</term><term>Locomotion</term><term>Matrix</term><term>Membrane ruffling</term><term>Mitogenesis</term><term>Motility</term><term>Myosin</term><term>Pathway</term><term>Pdgf</term><term>Phospholipase</term><term>Phosphorylation</term><term>Physiol</term><term>Pip2</term><term>Protein kinase</term><term>Receptor</term><term>Ridley</term><term>Ruffling</term><term>Stossel</term><term>Substratum</term><term>Transduction</term><term>Wound healing</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cell motility is induced by many growth factors acting through cognate receptors with intrinsic tyrosine kinase activity (RPTK). However, most of the links between receptor activation and the biophysical processes of cell motility remain undeciphered. We have focused on the mechanisms by which the EGF receptor (EGFR) actuates fibroblast cell motility in an attempt to define this integrated process in one system. Our working model is that divergent, but interconnected pathways lead to the biophysical processes necessary for cell motility: cytoskeleton reorganization, membrane extension, formation of new adhesions to substratum, cell contraction, and release of adhesions at the rear. We postulate that for any given growth factor some of the pathways/processes will be actively signaled and rate‐limiting, while others will be permissive due to background low‐level activation. Certain couplings have been defined, such as PLCγ and actin modifying proteins being involved in cytoskeletal reorganization and lamellipod extension and MEK being implicated in detachment from substratum. Others are suggested by complementary investigations in integrin‐mediated motility, including rac in membrane protrusion, rho in new adhesions, myosin II motors in contraction, and calpain in detachment, but have yet to be placed in growth factor‐induced motility. Our model postulates that many biochemical pathways will be shared between chemokinetic and haptokinetic motility but that select pathways will be activated only during RPTK‐enhanced motility. Microsc. Res. Tech. 43:395–411, 1998. © 1998 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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