FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly
Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite t...
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| Veröffentlicht in: | Nature cell biology 2004-02, Vol.6 (2), p.154-161 |
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| creator | Webb, Donna J. Donais, Karen Whitmore, Leanna A. Thomas, Sheila M. Turner, Christopher E. Parsons, J. Thomas Horwitz, Alan F. |
| description | Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration. |
| doi_str_mv | 10.1038/ncb1094 |
| format | Article |
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Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.</description><identifier>ISSN: 1465-7392</identifier><identifier>EISSN: 1476-4679</identifier><identifier>DOI: 10.1038/ncb1094</identifier><identifier>PMID: 14743221</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adaptor Proteins, Vesicular Transport - metabolism ; Adhesion ; Animals ; Biomedical and Life Sciences ; Cancer Research ; Cell Adhesion - physiology ; Cell adhesion molecules ; Cell Biology ; Cell Movement - physiology ; Cellular signal transduction ; Crk-Associated Substrate Protein ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Developmental Biology ; Fibroblasts - cytology ; Fibroblasts - physiology ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Genetic aspects ; letter ; Life Sciences ; Mice ; Mitogen-Activated Protein Kinases - genetics ; Mitogen-Activated Protein Kinases - metabolism ; Myosin-Light-Chain Kinase - genetics ; Myosin-Light-Chain Kinase - metabolism ; Paxillin ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Physiological aspects ; Protein kinases ; Protein-Tyrosine Kinases - genetics ; Protein-Tyrosine Kinases - metabolism ; Proteins ; Recombinant Fusion Proteins - genetics ; Recombinant Fusion Proteins - metabolism ; Retinoblastoma-Like Protein p130 ; Signal Transduction - physiology ; src-Family Kinases - genetics ; src-Family Kinases - metabolism ; Stem Cells</subject><ispartof>Nature cell biology, 2004-02, Vol.6 (2), p.154-161</ispartof><rights>Springer Nature Limited 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Feb 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-3f8096befc18832bc1c2537c580f918006ddbf0c720ce55747e471638c3a99ea3</citedby><cites>FETCH-LOGICAL-c438t-3f8096befc18832bc1c2537c580f918006ddbf0c720ce55747e471638c3a99ea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ncb1094$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ncb1094$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14743221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Webb, Donna J.</creatorcontrib><creatorcontrib>Donais, Karen</creatorcontrib><creatorcontrib>Whitmore, Leanna A.</creatorcontrib><creatorcontrib>Thomas, Sheila M.</creatorcontrib><creatorcontrib>Turner, Christopher E.</creatorcontrib><creatorcontrib>Parsons, J. Thomas</creatorcontrib><creatorcontrib>Horwitz, Alan F.</creatorcontrib><title>FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly</title><title>Nature cell biology</title><addtitle>Nat Cell Biol</addtitle><addtitle>Nat Cell Biol</addtitle><description>Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. 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Thomas</au><au>Horwitz, Alan F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly</atitle><jtitle>Nature cell biology</jtitle><stitle>Nat Cell Biol</stitle><addtitle>Nat Cell Biol</addtitle><date>2004-02-01</date><risdate>2004</risdate><volume>6</volume><issue>2</issue><spage>154</spage><epage>161</epage><pages>154-161</pages><issn>1465-7392</issn><eissn>1476-4679</eissn><abstract>Cell migration is a complex, highly regulated process that involves the continuous formation and disassembly of adhesions (adhesion turnover). Adhesion formation takes place at the leading edge of protrusions, whereas disassembly occurs both at the cell rear and at the base of protrusions. Despite the importance of these processes in migration, the mechanisms that regulate adhesion formation and disassembly remain largely unknown. Here we develop quantitative assays to measure the rate of incorporation of molecules into adhesions and the departure of these proteins from adhesions. Using these assays, we show that kinases and adaptor molecules, including focal adhesion kinase (FAK), Src, p130CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are critical for adhesion turnover at the cell front, a process central to migration.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>14743221</pmid><doi>10.1038/ncb1094</doi><tpages>8</tpages></addata></record> |
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| ispartof | Nature cell biology, 2004-02, Vol.6 (2), p.154-161 |
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| language | eng |
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| subjects | Adaptor Proteins, Vesicular Transport - metabolism Adhesion Animals Biomedical and Life Sciences Cancer Research Cell Adhesion - physiology Cell adhesion molecules Cell Biology Cell Movement - physiology Cellular signal transduction Crk-Associated Substrate Protein Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Developmental Biology Fibroblasts - cytology Fibroblasts - physiology Focal Adhesion Kinase 1 Focal Adhesion Protein-Tyrosine Kinases Genetic aspects letter Life Sciences Mice Mitogen-Activated Protein Kinases - genetics Mitogen-Activated Protein Kinases - metabolism Myosin-Light-Chain Kinase - genetics Myosin-Light-Chain Kinase - metabolism Paxillin Phosphoproteins - genetics Phosphoproteins - metabolism Physiological aspects Protein kinases Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Proteins Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Retinoblastoma-Like Protein p130 Signal Transduction - physiology src-Family Kinases - genetics src-Family Kinases - metabolism Stem Cells |
| title | FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly |
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