Downregulation of Ras C-terminal processing by JNK inhibition.

[1]  A. Cox,et al.  Geranylgeranyltransferase I as a target for anti-cancer drugs. , 2007, The Journal of clinical investigation.

[2]  C. Cordon-Cardo,et al.  Hyperactivation of Ha-ras oncogene, but not Ink4a/Arf deficiency, triggers bladder tumorigenesis. , 2007, The Journal of clinical investigation.

[3]  L. Heasley,et al.  JNK regulation of oncogenesis. , 2006, Molecules and cells.

[4]  G. K. Bilter,et al.  Inhibition of Tumor Growth, Angiogenesis, and Tumor Cell Proliferation by a Small Molecule Inhibitor of c-Jun N-terminal Kinase , 2005, Journal of Pharmacology and Experimental Therapeutics.

[5]  Jean-Pierre Gotteland,et al.  AS601245 (1,3-Benzothiazol-2-yl (2-{[2-(3-pyridinyl) ethyl] amino}-4 pyrimidinyl) Acetonitrile): A c-Jun NH2-Terminal Protein Kinase Inhibitor with Neuroprotective Properties , 2004, Journal of Pharmacology and Experimental Therapeutics.

[6]  J. Hancock,et al.  Ras proteins: different signals from different locations , 2003, Nature Reviews Molecular Cell Biology.

[7]  S. Yokoyama,et al.  Increased Ras expression and caspase-independent neuroblastoma cell death: possible mechanism of spontaneous neuroblastoma regression. , 2002, Journal of the National Cancer Institute.

[8]  M. Quon,et al.  Inhibition of Phosphatidylinositol 3-Kinase Enhances Mitogenic Actions of Insulin in Endothelial Cells* , 2002, The Journal of Biological Chemistry.

[9]  S. Yokoyama,et al.  Oncogenic Ras triggers cell suicide through the activation of a caspase-independent cell death program in human cancer cells , 1999, Oncogene.

[10]  M. Goalstone,et al.  Insulin stimulates the phosphorylation and activity of farnesyltransferase via the Ras-mitogen-activated protein kinase pathway. , 1997, Endocrinology.

[11]  J. Downward.  Regulatory mechanisms for ras proteins , 1992, BioEssays : news and reviews in molecular, cellular and developmental biology.

[12]  C. Marshall,et al.  All ras proteins are polyisoprenylated but only some are palmitoylated , 1989, Cell.

[13]  J. Hancock,et al.  Post‐translational processing of p21ras is two‐step and involves carboxyl‐methylation and carboxy‐terminal proteolysis. , 1989, The EMBO journal.

[14]  E. Scolnick,et al.  Identification of a precursor in the biosynthesis of the p21 transforming protein of harvey murine sarcoma virus , 1982, Journal of virology.

[15]  J. Downward.  Targeting RAS signalling pathways in cancer therapy , 2003, Nature Reviews Cancer.

[16]  C. Kitanaka,et al.  Caspase-independent programmed cell death with necrotic morphology. , 1999, Cell death and differentiation.

[17]  加藤 聖子.  Isoprenoid addition to Ras protein is the critical modification for its membrane association and transforming activity , 1995 .