Analysis of the transcriptional program induced by Raf in epithelial cells
暂无分享,去创建一个
[1] H. Lehrach,et al. Induction of putative tumor-suppressing genes in Rat-1 fibroblasts by oncogenic Raf-1 as evidenced by robot-assisted complex hybridization , 2000, Journal of Molecular Medicine.
[2] C. Der,et al. Understanding Ras: 'it ain't over 'til it's over'. , 2000, Trends in cell biology.
[3] J. Pouysségur,et al. The p42/p44 MAP kinase pathway prevents apoptosis induced by anchorage and serum removal. , 2000, Molecular biology of the cell.
[4] S. Yonehara,et al. Oncogenic K-Ras and Basic Fibroblast Growth Factor Prevent FAS-Mediated Apoptosis in Fibroblasts through Activation of Mitogen-Activated Protein Kinase , 2000, The Journal of cell biology.
[5] J. Blenis,et al. Rsk1 mediates a MEK–MAP kinase cell survival signal , 2000, Current Biology.
[6] L. Coussens,et al. Extrinsic regulators of epithelial tumor progression: metalloproteinases. , 2000, Current opinion in genetics & development.
[7] Johannes Zuber,et al. A genome-wide survey of RAS transformation targets , 2000, Nature Genetics.
[8] J. Folkman,et al. The Hemostatic System as a Regulator of Angiogenesis* , 2000, The Journal of Biological Chemistry.
[9] H. Ruan,et al. p90RSK Blocks Bad-mediated Cell Death via a Protein Kinase C-dependent Pathway* , 1999, The Journal of Biological Chemistry.
[10] Y. Sun,et al. Essential role of biliary glycoprotein (CD66a) in morphogenesis of the human mammary epithelial cell line MCF10F. , 1999, Journal of cell science.
[11] S. R. Datta,et al. Cellular survival: a play in three Akts. , 1999, Genes & development.
[12] S. R. Datta,et al. Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms. , 1999, Science.
[13] J. Downward,et al. Involvement of FADD and caspase-8 signalling in detachment-induced apoptosis , 1999, Current Biology.
[14] G. Cooper,et al. B-Raf Inhibits Programmed Cell Death Downstream of Cytochrome c Release from Mitochondria by Activating the MEK/Erk Pathway , 1999, Molecular and Cellular Biology.
[15] Andrius Kazlauskas,et al. Diverse Signaling Pathways Activated by Growth Factor Receptors Induce Broadly Overlapping, Rather Than Independent, Sets of Genes , 1999, Cell.
[16] J. Downward. How BAD phosphorylation is good for survival , 1999, Nature Cell Biology.
[17] R. Montesano,et al. Constitutively Active Mitogen-activated Protein Kinase Kinase Mek1 Disrupts Morphogenesis and Induces an Invasive Phenotype in Madin-darby Canine Kidney Epithelial Cells 1 , 1999 .
[18] S. Cook,et al. The Repertoire of Fos and Jun Proteins Expressed during the G1 Phase of the Cell Cycle Is Determined by the Duration of Mitogen-Activated Protein Kinase Activation , 1999, Molecular and Cellular Biology.
[19] M. Roussel,et al. Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization. , 1998, Genes & development.
[20] A. Klippel,et al. Activation of Phosphatidylinositol 3-Kinase Is Sufficient for Cell Cycle Entry and Promotes Cellular Changes Characteristic of Oncogenic Transformation , 1998, Molecular and Cellular Biology.
[21] R. Bicknell,et al. Thymidine phosphorylase, 2-deoxy-D-ribose and angiogenesis. , 1998, The Biochemical journal.
[22] J. Downward,et al. Phosphoinositide 3-Kinase Induces Scattering and Tubulogenesis in Epithelial Cells through a Novel Pathway* , 1998, The Journal of Biological Chemistry.
[23] J Downward,et al. Ras signalling and apoptosis. , 1998, Current opinion in genetics & development.
[24] L. Wodicka,et al. Genome-wide expression monitoring in Saccharomyces cerevisiae , 1997, Nature Biotechnology.
[25] M. Schwartz,et al. Growth factor activation of MAP kinase requires cell adhesion , 1997, The EMBO journal.
[26] A Sewing,et al. High-intensity Raf signal causes cell cycle arrest mediated by p21Cip1 , 1997, Molecular and cellular biology.
[27] M. McMahon,et al. Mutations of critical amino acids affect the biological and biochemical properties of oncogenic A-Raf and Raf-1 , 1997, Oncogene.
[28] Asim Khwaja,et al. Matrix adhesion and Ras transformation both activate a phosphoinositide 3‐OH kinase and protein kinase B/Akt cellular survival pathway , 1997, The EMBO journal.
[29] U. Rodeck,et al. Regulation of Bcl-xL expression in human keratinocytes by cell-substratum adhesion and the epidermal growth factor receptor. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[30] P. Warne,et al. Role of Phosphoinositide 3-OH Kinase in Cell Transformation and Control of the Actin Cytoskeleton by Ras , 1997, Cell.
[31] Michael C. Ostrowski,et al. Rapid phosphorylation of Ets-2 accompanies mitogen-activated protein kinase activation and the induction of heparin-binding epidermal growth factor gene expression by oncogenic Raf-1 , 1997, Molecular and cellular biology.
[32] D. Hanahan,et al. Patterns and Emerging Mechanisms of the Angiogenic Switch during Tumorigenesis , 1996, Cell.
[33] R. Treisman,et al. Regulation of transcription by MAP kinase cascades. , 1996, Current opinion in cell biology.
[34] C. Albanese,et al. Transforming p21ras Mutants and c-Ets-2 Activate the Cyclin D1 Promoter through Distinguishable Regions (*) , 1995, The Journal of Biological Chemistry.
[35] J. Abraham,et al. Rapid induction of heparin-binding epidermal growth factor/diphtheria toxin receptor expression by Raf and Ras oncogenes. , 1995, Genes & development.
[36] S. Krajewski,et al. Apoptosis regulation by interaction of Bcl-2 protein and Raf-1 kinase. , 1994, Oncogene.
[37] R. Hipskind,et al. Transient activation of RAF-1, MEK, and ERK2 coincides kinetically with ternary complex factor phosphorylation and immediate-early gene promoter activity in vivo , 1994, Molecular and cellular biology.
[38] S. Frisch,et al. Disruption of epithelial cell-matrix interactions induces apoptosis , 1994, The Journal of cell biology.
[39] J. Russo,et al. Isolation and characterization of a spontaneously immortalized human breast epithelial cell line, MCF-10. , 1990, Cancer research.
[40] Masui,et al. Transforming growth factor-alpha expression is enhanced in human mammary epithelial cells transformed by an activated c-Ha-ras protooncogene but not by the c-neu protooncogene, and overexpression of the transforming growth factor-alpha complementary DNA leads to transformation. , 1990, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[41] J. L. Bos,et al. ras oncogenes in human cancer: a review. , 1989, Cancer research.
[42] G. Todaro,et al. Growth factors from murine sarcoma virus-transformed cells. , 1978, Proceedings of the National Academy of Sciences of the United States of America.
[43] S. Yonehara,et al. Oncogenic KRas and Basic Fibroblast Growth Factor Prevent Fas-mediated Apoptosis in Fibroblasts through Activation of Mitogen-activated Protein Kinase , 2000 .
[44] S. P. Fodor,et al. High density synthetic oligonucleotide arrays , 1999, Nature Genetics.
[45] D. Botstein,et al. The transcriptional program in the response of human fibroblasts to serum. , 1999, Science.
[46] D. Lockhart,et al. Expression monitoring by hybridization to high-density oligonucleotide arrays , 1996, Nature Biotechnology.
[47] C. Marshall. Ras effectors. , 1996, Current opinion in cell biology.
[48] I. Rabinovitz,et al. The integrin alpha 6 beta 4 and the biology of carcinoma. , 1996, Biochemistry and cell biology = Biochimie et biologie cellulaire.