The Non-transmembrane Form of Delta1, but Not of Jagged1, Induces Normal Migratory Behavior Accompanied by Fibroblast Growth Factor Receptor 1-dependent Transformation
Autor: | Dimitry Kovalenko, Raffaella Soldi, Vihren Kolev, Deena Small, Radianna Trifonova, Anna Mandinova, Lucy Liaw, Doreen Kacer, Thomas Maciag, Igor Prudovsky |
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Rok vydání: | 2004 |
Předmět: |
Notch signaling pathway
Biology Transfection Fibroblast growth factor Biochemistry 3T3 cells Mice Cell Movement Stress Fibers medicine Animals Humans Serrate-Jagged Proteins Receptor Fibroblast Growth Factor Type 1 Molecular Biology Focal Adhesions Receptors Notch Fibroblast growth factor receptor 1 Calcium-Binding Proteins Intracellular Signaling Peptides and Proteins Membrane Proteins Proteins Receptor Protein-Tyrosine Kinases Cell Biology Fibroblast growth factor receptor 4 Fibroblast growth factor receptor 3 FGF1 Receptors Fibroblast Growth Factor Cell biology Phenotype medicine.anatomical_structure NIH 3T3 Cells Intercellular Signaling Peptides and Proteins Signal transduction Jagged-1 Protein Signal Transduction |
Zdroj: | Journal of Biological Chemistry. 279:13285-13288 |
ISSN: | 0021-9258 6405-1641 |
Popis: | The interactions between Notch (N) receptors and their transmembrane ligands, Jagged1 (JI) and Delta1 (Dl1), mediate signaling events between neighboring cells that are crucial during embryonal development and in adults. Since the non-transmembrane extracellular form of J1 acts as an antagonist of N activation in NIH 3T3 mouse fibroblast cells and induces fibroblast growth factor 1 (FGF1)-dependent transformation (Small, D., Kovalenko, D., Soldi, R., Mandinova, A., Kolev, V., Trifonova, R., Bagala, C., Kacer, D., Battelli, C., Liaw, L., Prudovsky, I., and Maciag, T. (2003) J. Biol. Chem. 278, 16405-16413), we examined the potential redundant functions of the two subfamilies of Notch ligands and report that while the soluble (s) forms of both Dl1 and J1 act as N signaling antagonists in NIH 3T3 cells, they do display disparate functions. While sJ1 induced an attenuation of cell motility which is accompanied by a decrease in actin stress fibers and an increase in adherence junctions, sDl1 does not. However, sJ1, like sDl1, induces a NIH 3T3 cell tranformed phenotype mediated by FGF signaling. Because the inhibition of N signaling by sJ1 and sDl1 is rescued by dominant-negative Src expression, we suggest that there may be cooperation between the Notch and Src signaling pathways. |
Databáze: | OpenAIRE |
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