Focal adhesions are foci for tyrosine-based signal transduction via GIV/Girdin and G proteins

GIV is a guanine-nucleotide exchange factor and a bona fide metastasis-related protein. It is found, unexpectedly, that focal adhesions are the major foci for GIV-dependent signaling and that GIV modulates integrin-FAK signaling via activation of G proteins. It is also shown how this phenomenon is altered during cancer progression.

[1]  Utku Horzum,et al.  Differentiation of Normal and Cancer Cell Adhesion on Custom Designed Protein Nanopatterns. , 2015, Nano letters.

[2]  P. Ghosh G protein coupled growth factor receptor tyrosine kinase: no longer an oxymoron , 2015, Cell cycle.

[3]  A. Newton,et al.  Multimodular biosensors reveal a novel platform for activation of G proteins by growth factor receptors , 2015, Proceedings of the National Academy of Sciences.

[4]  A. Eguchi,et al.  GIV/girdin links vascular endothelial growth factor signaling to Akt survival signaling in podocytes independent of nephrin. , 2015, Journal of the American Society of Nephrology : JASN.

[5]  M. Farquhar,et al.  GIV/Girdin Transmits Signals from Multiple Receptors by Triggering Trimeric G Protein Activation* , 2015, The Journal of Biological Chemistry.

[6]  R. Abagyan,et al.  Structural basis for activation of trimeric Gi proteins by multiple growth factor receptors via GIV/Girdin , 2014, Molecular biology of the cell.

[7]  D. Schlaepfer,et al.  FAK in cancer: mechanistic findings and clinical applications , 2014, Nature Reviews Cancer.

[8]  D. Brenner,et al.  GIV/Girdin is a central hub for pro-fibrogenic signalling networks during liver fibrosis , 2014, Nature Communications.

[9]  M. Kris,et al.  Serpins Promote Cancer Cell Survival and Vascular Co-Option in Brain Metastasis , 2014, Cell.

[10]  H. Häring,et al.  The Akt substrate Girdin is a regulator of insulin signaling in myoblast cells. , 2013, Biochimica et biophysica acta.

[11]  M. Farquhar,et al.  Protein kinase C-theta (PKCθ) phosphorylates and inhibits the guanine exchange factor, GIV/Girdin , 2013, Proceedings of the National Academy of Sciences.

[12]  B. Giepmans,et al.  Immunolabeling artifacts and the need for live-cell imaging , 2012, Nature Methods.

[13]  M. Frame,et al.  FAK and talin: Who is taking whom to the integrin engagement party? , 2012, The Journal of cell biology.

[14]  D. Mehta,et al.  Heterotrimeric G proteins, focal adhesion kinase, and endothelial barrier function. , 2012, Microvascular research.

[15]  R. Abagyan,et al.  Tyrosine Phosphorylation of the Gα-Interacting Protein GIV Promotes Activation of Phosphoinositide 3-Kinase During Cell Migration , 2011, Science Signaling.

[16]  M. Farquhar,et al.  GIV/Girdin is a rheostat that fine-tunes growth factor signals during tumor progression , 2011, Cell adhesion & migration.

[17]  J. Carethers,et al.  A Gαi–GIV Molecular Complex Binds Epidermal Growth Factor Receptor and Determines Whether Cells Migrate or Proliferate , 2010, Molecular biology of the cell.

[18]  D. Dhanasekaran Faculty Opinions recommendation of A structural determinant that renders G alpha(i) sensitive to activation by GIV/girdin is required to promote cell migration. , 2010 .

[19]  M. Farquhar,et al.  A Structural Determinant That Renders Gαi Sensitive to Activation by GIV/Girdin Is Required to Promote Cell Migration* , 2010, The Journal of Biological Chemistry.

[20]  T. Voyno-Yasenetskaya,et al.  G Protein Subunit Gα13 Binds to Integrin αIIbβ3 and Mediates Integrin “Outside-In” Signaling , 2010, Science.

[21]  Marc Ladanyi,et al.  WNT/TCF Signaling through LEF1 and HOXB9 Mediates Lung Adenocarcinoma Metastasis , 2009, Cell.

[22]  M. Farquhar,et al.  GIV is a Non-Receptor GEF for G{alpha}i with a Unique Motif that Regulates Akt Signaling , 2009 .

[23]  M. Farquhar,et al.  GIV is a nonreceptor GEF for Gαi with a unique motif that regulates Akt signaling , 2009, Proceedings of the National Academy of Sciences.

[24]  R. Fässler,et al.  Mechanisms that regulate adaptor binding to β-integrin cytoplasmic tails , 2009, Journal of Cell Science.

[25]  M. Farquhar,et al.  Activation of Gαi3 triggers cell migration via regulation of GIV , 2008, The Journal of cell biology.

[26]  U. Landegren,et al.  Direct observation of individual endogenous protein complexes in situ by proximity ligation , 2006, Nature Methods.

[27]  Y. Murakumo,et al.  Akt/PKB regulates actin organization and cell motility via Girdin/APE. , 2005, Developmental cell.

[28]  Jyrki Heino,et al.  Integrin-mediated Cell Adhesion to Type I Collagen Fibrils* , 2004, Journal of Biological Chemistry.

[29]  M. Lohse,et al.  Gi protein activation in intact cells involves subunit rearrangement rather than dissociation , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[30]  S. Saga,et al.  Association of the gamma12 subunit of G proteins with actin filaments. , 1997, Journal of cell science.

[31]  J. Guan,et al.  Phosphorylation of Tyrosine 397 in Focal Adhesion Kinase Is Required for Binding Phosphatidylinositol 3-Kinase* , 1996, The Journal of Biological Chemistry.

[32]  G. Johnson,et al.  Gα12 and Gα13 Stimulate Rho-dependent Stress Fiber Formation and Focal Adhesion Assembly (*) , 1995, The Journal of Biological Chemistry.

[33]  G L Johnson,et al.  G alpha 12 and G alpha 13 stimulate Rho-dependent stress fiber formation and focal adhesion assembly. , 1995, The Journal of biological chemistry.

[34]  D. Carey,et al.  Localization of a heterotrimeric G protein gamma subunit to focal adhesions and associated stress fibers , 1994, The Journal of cell biology.