Antitumor effect of E1A in ovarian cancer by cytoplasmic sequestration of activated ERK by PEA15

[1]  E. Schaefer,et al.  Phosphorylation of phosphoprotein enriched in astrocytes (PEA-15) regulates extracellular signal-regulated kinase-dependent transcription and cell proliferation. , 2005, Molecular biology of the cell.

[2]  G. Ferbeyre,et al.  PEA-15 Is Inhibited by Adenovirus E1A and Plays a Role in ERK Nuclear Export and Ras-induced Senescence* , 2004, Journal of Biological Chemistry.

[3]  S. Frisch.  E1A as a Tumor Suppressor Gene , 2004, Clinical Cancer Research.

[4]  M. Cobb,et al.  The Death Effector Domain Protein PEA-15 Prevents Nuclear Entry of ERK2 by Inhibiting Required Interactions* , 2004, Journal of Biological Chemistry.

[5]  Isabelle Callebaut,et al.  The multifunctional protein PEA-15 is involved in the control of apoptosis and cell cycle in astrocytes. , 2003, Biochemical pharmacology.

[6]  G. Condorelli,et al.  Protein Kinase B/Akt Binds and Phosphorylates PED/PEA-15, Stabilizing Its Antiapoptotic Action , 2003, Molecular and Cellular Biology.

[7]  G. Hannon,et al.  Transformation of normal human cells in the absence of telomerase activation. , 2002, Cancer cell.

[8]  S. Frisch,et al.  Adenovirus-5 E1A: paradox and paradigm , 2002, Nature Reviews Molecular Cell Biology.

[9]  A. Musti,et al.  Multiple Members of the Mitogen-activated Protein Kinase Family Are Necessary for PED/PEA-15 Anti-apoptotic Function* , 2002, The Journal of Biological Chemistry.

[10]  E. Formstecher,et al.  PEA-15 mediates cytoplasmic sequestration of ERK MAP kinase. , 2001, Developmental cell.

[11]  G. Hortobagyi,et al.  Cationic liposome-mediated E1A gene transfer to human breast and ovarian cancer cells and its biologic effects: a phase I clinical trial. , 2001, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[12]  H. Qin,et al.  Adenovirus 5 E1a-mediated gene therapy for human ovarian cancer cells in vitro and in vivo , 2000, International Journal of Gynecologic Cancer.

[13]  E. Formstecher,et al.  Death effector domain protein PEA-15 potentiates Ras activation of extracellular signal receptor-activated kinase by an adhesion-independent mechanism. , 2000, Molecular biology of the cell.

[14]  H. Blau,et al.  The phosphoprotein protein PEA-15 inhibits Fas- but increases TNF-R1-mediated caspase-8 activity and apoptosis. , 1999, Developmental biology.

[15]  M. Hung,et al.  Axl-Gas6 Interaction Counteracts E1A-Mediated Cell Growth Suppression and Proapoptotic Activity , 1999, Molecular and Cellular Biology.

[16]  J. Pouysségur,et al.  Defective thymocyte maturation in p44 MAP kinase (Erk 1) knockout mice. , 1999, Science.

[17]  G. Condorelli,et al.  PED/PEA-15: an anti-apoptotic molecule that regulates FAS/TNFR1-induced apoptosis , 1999, Oncogene.

[18]  Alan R. Saltiel,et al.  Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo , 1999, Nature Medicine.

[19]  M. Hung,et al.  Adenovirus 5 E1A-mediated tumor suppression associated with E1A-mediated apoptosis in vivo , 1998, Oncogene.

[20]  J. Girault,et al.  Endothelin Induces a Calcium‐Dependent Phosphorylation of PEA‐15 in Intact Astrocytes: Identification of Ser104 and Ser116 Phosphorylated, Respectively, by Protein Kinase C and Calcium/Calmodulin Kinase II In Vitro , 1998, Journal of neurochemistry.

[21]  F. Andreozzi,et al.  PED/PEA‐15 gene controls glucose transport and is overexpressed in type 2 diabetes mellitus , 1998, The EMBO journal.

[22]  M. Hung,et al.  Inhibition of Nuclear Factor-κB Activity Is Involved in E1A-mediated Sensitization of Radiation-induced Apoptosis* , 1997, The Journal of Biological Chemistry.

[23]  M. Hung,et al.  Chemosensitization of HER-2/neu-overexpressing human breast cancer cells to paclitaxel (Taxol) by adenovirus type 5 E1A , 1997, Oncogene.

[24]  W. Kuo,et al.  Assignment of HMAT1, the human homolog of the murine mammary transforming gene (MAT1) associated with tumorigenesis, to 1q21.1, a region frequently gained in human breast cancers. , 1997, Genomics.

[25]  Joe Y. Chang,et al.  The tumor suppression activity of E1A in HER-2/neu-overexpressing breast cancer* , 1997, Oncogene.

[26]  R. Long.  WHAT RESEARCH TRAINING OPPORTUNITIES ARE SPONSORED BY NIGMS AT THE NIH? HOW CAN I GET INFORMATION ABOUT THIS AND OTHER POSTDOCTORAL PROGRAMS AT THE NIH? , 1996, Pharmaceutical Research.

[27]  J. Glowinski,et al.  The Major Astrocytic Phosphoprotein PEA-15 Is Encoded by Two mRNAs Conserved on Their Full Length in Mouse and Human* , 1996, The Journal of Biological Chemistry.

[28]  E. Lengyel,et al.  Stimulation of 92-kDa Gelatinase B Promoter Activity by ras Is Mitogen-activated Protein Kinase Kinase 1-independent and Requires Multiple Transcription Factor Binding Sites Including Closely Spaced PEA3/ets and AP-1 Sequences (*) , 1996, The Journal of Biological Chemistry.

[29]  J. Glowinski,et al.  Cellular Expression, Developmental Regulation, and Phylogenic Conservation of PEA‐15, the Astrocytic Major Phosphoprotein and Protein Kinase C Substrate , 1995, Journal of neurochemistry.

[30]  S. Frisch,et al.  E1a induces the expression of epithelial characteristics , 1994, The Journal of cell biology.

[31]  S. Miyamoto,et al.  Identification of a mammary transforming gene (MAT1) associated with mouse mammary carcinogenesis. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[32]  J. Pouysségur,et al.  Mitogen-activated protein kinases p42mapk and p44mapk are required for fibroblast proliferation. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[33]  E. White,et al.  Wild-type p53 mediates apoptosis by E1A, which is inhibited by E1B. , 1993, Genes & development.

[34]  S. Korsmeyer,et al.  The adenovirus E1A proteins induce apoptosis, which is inhibited by the E1B 19-kDa and Bcl-2 proteins. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[35]  S. Frisch.  Antioncogenic effect of adenovirus E1A in human tumor cells. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[36]  M. Hung,et al.  Adenovirus type 5 E1A gene products act as transformation suppressors of the neu oncogene , 1991, Molecular and cellular biology.

[37]  C. Nelson,et al.  E1a-dependent expression of adenovirus genes in OTF963 embryonal carcinoma cells: role of E1a-induced differentiation. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[38]  M. Hung,et al.  Transcriptional repression of the neu protooncogene by the adenovirus 5 E1A gene products. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[39]  J. Nevins,et al.  Adenovirus E1A-mediated negative control of genes activated during F9 differentiation , 1989, Molecular and cellular biology.

[40]  H. Ruley.  Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture , 1983, Nature.

[41]  Robert A. Weinberg,et al.  Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes , 1983, Nature.

[42]  V. Freedman,et al.  Cellular tumorigenicity in nude mice: correlation with cell growth in semi-solid medium. , 1974, Cell.

[43]  A. Jemal,et al.  Cancer Statistics, 2004 , 2004, CA: a cancer journal for clinicians.