Requirement of Stat3 signaling for HGF/SF-Met mediated tumorigenesis
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R. Jove | G. Woude | Ling-mei Wang | Richard Jove | Yu-Wen Zhang | Ling-Mei Wang | George F Vande Woude | Yu-Wen Zhang
[1] A. Bardelli,et al. A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor family , 1994, Cell.
[2] J. Lammers,et al. STAT3β, a Splice Variant of Transcription Factor STAT3, Is a Dominant Negative Regulator of Transcription* , 1996, The Journal of Biological Chemistry.
[3] P. Comoglio,et al. Evidence for autocrine activation of a tyrosine kinase in a human gastric carcinoma cell line , 1988, Journal of cellular biochemistry.
[4] E. Rosen,et al. Hepatocyte growth factor/scatter factor effects on epithelia. Regulation of intercellular junctions in transformed and nontransformed cell lines, basolateral polarization of c-met receptor in transformed and natural intestinal epithelia, and induction of rapid wound repair in a transformed model epi , 1994, The Journal of clinical investigation.
[5] P. Comoglio,et al. Constitutive activation of the RON gene promotes invasive growth but not transformation , 1996, Molecular and cellular biology.
[6] J. Darnell,et al. A Single Amino Acid Substitution in the v-Eyk Intracellular Domain Results in Activation of Stat3 and Enhances Cellular Transformation , 1999, Molecular and Cellular Biology.
[7] S. Akira,et al. Keratinocyte‐specific ablation of Stat3 exhibits impaired skin remodeling, but does not affect skin morphogenesis , 1999, The EMBO journal.
[8] Pavel Kovarik,et al. Serine phosphorylation of STATs , 2000, Oncogene.
[9] M. Fiscella,et al. The mutationally activated Met receptor mediates motility and metastasis. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[10] C. Birchmeier,et al. Scatter factor/hepatocyte growth factor and its receptor, the c-met tyrosine kinase, can mediate a signal exchange between mesenchyme and epithelia during mouse development , 1993, The Journal of cell biology.
[11] G. G. Stokes. "J." , 1890, The New Yale Book of Quotations.
[12] J. Downward,et al. Phosphoinositide 3-Kinase Induces Scattering and Tubulogenesis in Epithelial Cells through a Novel Pathway* , 1998, The Journal of Biological Chemistry.
[13] T. Nakamura,et al. Tumorigenicity of the met proto-oncogene and the gene for hepatocyte growth factor , 1992, Molecular and cellular biology.
[14] H. Kleinman,et al. Scatter factor induces blood vessel formation in vivo. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[15] E. Rosen,et al. The cytokine hepatocyte growth factor/scatter factor inhibits apoptosis and enhances DNA repair by a common mechanism involving signaling through phosphatidyl inositol 3′ kinase , 2000, Oncogene.
[16] N. Rahimi,et al. c-Src Kinase Activity Is Required for Hepatocyte Growth Factor-induced Motility and Anchorage-independent Growth of Mammary Carcinoma Cells* , 1998, The Journal of Biological Chemistry.
[17] C. S. Zong,et al. Stat3 Plays an Important Role in Oncogenic Ros- and Insulin-like Growth Factor I Receptor-induced Anchorage-independent Growth* , 1998, The Journal of Biological Chemistry.
[18] Tetsuo Noda,et al. Placental defect and embryonic lethality in mice lacking hepatocyte growth factor/scatter factor , 1995, Nature.
[19] G. V. Vande Woude,et al. Enhanced tumorigenicity and invasion-metastasis by hepatocyte growth factor/scatter factor-met signalling in human cells concomitant with induction of the urokinase proteolysis network , 1996, Molecular and cellular biology.
[20] W. Birchmeier,et al. Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis , 1996, Nature.
[21] M. Sharpe,et al. Scatter factor/hepatocyte growth factor is essential for liver development , 1995, Nature.
[22] L. Ferrell,et al. Activation of the Met Receptor by Cell Attachment Induces and Sustains Hepatocellular Carcinomas in Transgenic Mice , 2001, The Journal of cell biology.
[23] A. Davies,et al. Met receptor signaling is required for sensory nerve development and HGF promotes axonal growth and survival of sensory neurons. , 1997, Genes & development.
[24] J. Rubin,et al. Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. , 1991, Science.
[25] P. Comoglio,et al. Somatic mutations of the MET oncogene are selected during metastatic spread of human HNSC carcinomas , 2000, Oncogene.
[26] P. Comoglio,et al. Regulation of scatter factor/hepatocyte growth factor responses by Ras, Rac, and Rho in MDCK cells , 1995, Molecular and cellular biology.
[27] M. Jaroszeski,et al. Gene therapy with dominant-negative Stat3 suppresses growth of the murine melanoma B16 tumor in vivo. , 1999, Cancer research.
[28] S. Rane,et al. IL-3 signaling and the role of Src kinases, JAKs and STATs: a covert liaison unveiled , 2000, Oncogene.
[29] A. Bardelli,et al. Induction of epithelial tubules by growth factor HGF depends on the STAT pathway , 1998, Nature.
[30] G. V. Vande Woude,et al. Invasiveness and metastasis of NIH 3T3 cells induced by Met-hepatocyte growth factor/scatter factor autocrine stimulation. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[31] K. Kaibuchi,et al. Activation of cdc42, rac, PAK, and rho-kinase in response to hepatocyte growth factor differentially regulates epithelial cell colony spreading and dissociation. , 2000, Molecular biology of the cell.
[32] Carmen Birchmeier,et al. Essential role for the c-met receptor in the migration of myogenic precursor cells into the limb bud , 1995, Nature.
[33] J. Darnell,et al. The role of STATs in transcriptional control and their impact on cellular function , 2000, Oncogene.
[34] J. Darnell,et al. Stat3 Activation Is Required for Cellular Transformation by v-src , 1998, Molecular and Cellular Biology.
[35] J. Schlessinger,et al. Activation of the JNK pathway is essential for transformation by the Met oncogene , 1997, The EMBO journal.
[36] J. Turkson,et al. Stat3 Activation by Src Induces Specific Gene Regulation and Is Required for Cell Transformation , 1998, Molecular and Cellular Biology.
[37] D. Kamikura,et al. Pathways Downstream of Shc and Grb2 Are Required for Cell Transformation by the Tpr-Met Oncoprotein* , 1996, The Journal of Biological Chemistry.
[38] W. Birchmeier,et al. The Met receptor tyrosine kinase transduces motility, proliferation, and morphogenic signals of scatter factor/hepatocyte growth factor in epithelial cells , 1993, The Journal of cell biology.
[39] E. Hudson,et al. Met and hepatocyte growth factor/scatter factor expression in human gliomas. , 1997, Cancer research.
[40] J. Turkson,et al. Requirement for Ras/Rac1-Mediated p38 and c-Jun N-Terminal Kinase Signaling in Stat3 Transcriptional Activity Induced by the Src Oncoprotein , 1999, Molecular and Cellular Biology.
[41] R. Sharp,et al. Diverse tumorigenesis associated with aberrant development in mice overexpressing hepatocyte growth factor/scatter factor. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[42] L. Naldini,et al. Hepatocyte growth factor is a potent angiogenic factor which stimulates endothelial cell motility and growth , 1992, The Journal of cell biology.
[43] Roy Garcia,et al. STATs in oncogenesis , 2000, Oncogene.
[44] Michael Stoker,et al. Scatter factor is a fibroblast-derived modulator of epithelial cell mobility , 1987, Nature.
[45] L. Schmidt,et al. A novel germ line juxtamembrane Met mutation in human gastric cancer , 2000, Oncogene.
[46] G. V. Vande Woude,et al. Met expression and sarcoma tumorigenicity. , 1993, Cancer research.
[47] G. Merlino,et al. NK1, a Natural Splice Variant of Hepatocyte Growth Factor/Scatter Factor, Is a Partial Agonist In Vivo , 1998, Molecular and Cellular Biology.
[48] G. V. Vande Woude,et al. Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. , 2001, Proceedings of the National Academy of Sciences of the United States of America.