FAK–Src signalling through paxillin, ERK and MLCK regulates adhesion disassembly

By D. Webb, K. Donais, Leanna A. Whitmore, Sheila M. Thomas, C. Turner, J. Parsons, A. Horwitz. Nature Cell Biology, 2004

1,442 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology and Allergy, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9a8c39adfa88db85190c9f9384f8d81fc2e96974

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Citations in the corpus

Mechanical Integration of Actin and Adhesion Dynamics in Cell Migration (2010, background): “…within 10–20 minutes (Gupton & Waterman-Storer 2006, Laukaitis et al. 2001, Webb et al. 2004, Zaidel-Bar et al. 2003) or mature further into stable fibrillar adhesions that do not promote migration but are involved in ECM remodeling (Laukaitis et al. 2001, Webb et al. 2004, Zaidel-Bar et al. 2003).”
Analysis of the myosinII-responsive focal adhesion proteome reveals a role for β-Pix in negative regulation of focal adhesion maturation (2011, background): “These may be undiscovered, weakly associated or transient focal adhesion proteins, or cytosolic and/or cytoskeletal contaminants, and were classified according to biological function: endomembrane systems/trafficking (129), uncharacterized (84), cytoskeleton (81), metabolism (70), plasma membrane ch”
The role of focal-adhesion kinase in cancer — a new therapeutic opportunity (2005, background): “, although maintenance of focal adhesions does not generally require FA”
Spatiotemporal feedback between actomyosin and focal-adhesion systems optimizes rapid cell migration. (2006, methodology): “FA formation may immobilize the local actin network via connection to the ECM.”
Cellular functions of FAK kinases: insight into molecular mechanisms and novel functions (2010, background): “One established FAK-dependent mechanism controlling cell migration is regulation of the disassembly of focal adhesions (Ren et al., 2000; Webb et al., 2004).”
Calpain-mediated proteolysis of talin regulates adhesion dynamics (2004, background): “Recent progress has been made in defining some of the molecular mechanisms by which adhesion disassembly is regulated, including the contributions of adhesion adaptor proteins and tyrosine kinase”
A renaissance for SRC (2004, background): “Recently, using quantitative assays to determine levels of kinase and adaptor molecules in focal adhesions, it has been demonstrated that the FAK–c-SRC complex, CAS, paxillin, extracellular signal-regulated kinase (ERK) and myosin light-chain kinase (MLCK) are crucial for adhesion turnover at the ce”
Actin and α-actinin orchestrate the assembly and maturation of nascent adhesions in a myosin II motor-independent manner (2008, neutral): “Stationary spatial distribution of the barbed ends near the leading edge follows easily from (1): ( ) s x b ! = .”
Microtubule-induced focal adhesion disassembly is mediated by dynamin and focal adhesion kinase (2005, background): “In contrast, few factors other than components of the focal adhesion or factors that affect Rho activity have been implicated in regulating focal adhesion disassembl”
Adhesion signaling – crosstalk between integrins, Src and Rho (2009, background): “Finally, the recruitment of paxillin to the FAKSrc complex can further modulate cell motility; this occurs through the effects of paxillin on signaling pathways that lead to an increase in Rac1-GTP and Cdc42-GTP levels, or through the activation of a signaling pathway [involving paxillin, extracellu”
Genetic and cell biological analysis of integrin outside-in signaling. (2009, background): “ERK2 phosphorylation downstream from integrins modulates both FA dynamics through myosin light chain kinase, as well as cell proliferation, cell cycle progression, and survival through regulating cyclin D1 and PI-3-kinase activity (Chen et al. 1996; Webb et al. 2004; Walker et al. 2005).”
The LIM domain: from the cytoskeleton to the nucleus (2004, neutral): “Tyrosine phosphorylation of paxillin by complexes of focal adhesion kinase (FAK) and Src promotes the disassembly of these structures, perhaps by changing the complement of proteins that bind to the modified paxilli”