Identification of a Novel Ras-Regulated Proapoptotic Pathway

[1]  J. Avruch,et al.  The putative tumor suppressor RASSF1A homodimerizes and heterodimerizes with the Ras-GTP binding protein Nore1 , 2002, Oncogene.

[2]  A. Protopopov,et al.  The candidate tumor suppressor gene, RASSF1A, from human chromosome 3p21.3 is involved in kidney tumorigenesis , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[3]  E. Krebs,et al.  Both Phosphorylation and Caspase-mediated Cleavage Contribute to Regulation of the Ste20-like Protein Kinase Mst1 during CD95/Fas-induced Apoptosis* , 2001, The Journal of Biological Chemistry.

[4]  J. Minna,et al.  Epigenetic inactivation of RASSF1A in lung and breast cancers and malignant phenotype suppression. , 2001, Journal of the National Cancer Institute.

[5]  Norinobu M. Watanabe,et al.  The Ste20 group kinases as regulators of MAP kinase cascades. , 2001, Trends in cell biology.

[6]  G. Yang,et al.  Hypermethylation of the cpG island of Ras association domain family 1A (RASSF1A), a putative tumor suppressor gene from the 3p21.3 locus, occurs in a large percentage of human breast cancers. , 2001, Cancer research.

[7]  X. F. Zhang,et al.  Ras activation of the Raf kinase: tyrosine kinase recruitment of the MAP kinase cascade. , 2001, Recent progress in hormone research.

[8]  D. Bredesen,et al.  An alternative, nonapoptotic form of programmed cell death. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[9]  D. Faller,et al.  Oncogenic Ras Mediates Apoptosis in Response to Protein Kinase C Inhibition through the Generation of Reactive Oxygen Species* , 2000, The Journal of Biological Chemistry.

[10]  A. Bell,et al.  Ras Uses the Novel Tumor Suppressor RASSF1 as an Effector to Mediate Apoptosis* , 2000, The Journal of Biological Chemistry.

[11]  J. Minna,et al.  The 630-kb lung cancer homozygous deletion region on human chromosome 3p21.3: identification and evaluation of the resident candidate tumor suppressor genes. The International Lung Cancer Chromosome 3p21.3 Tumor Suppressor Gene Consortium. , 2000, Cancer research.

[12]  C. Reutelingsperger,et al.  Flow cytometry of apoptotic cell death. , 2000, Journal of immunological methods.

[13]  H. Sheng,et al.  Oncogenic Ras-mediated Cell Growth Arrest and Apoptosis are Associated with Increased Ubiquitin-dependent Cyclin D1 Degradation* , 2000, The Journal of Biological Chemistry.

[14]  G. Clark,et al.  The importance of being K-Ras. , 2000, Cellular signalling.

[15]  Chun Xing Li,et al.  Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3 , 2000, Nature Genetics.

[16]  C. Der,et al.  Understanding Ras: 'it ain't over 'til it's over'. , 2000, Trends in cell biology.

[17]  S. Chandra,et al.  A second cytotoxic proteolytic peptide derived from amyloid β-protein precursor , 2000, Nature Medicine.

[18]  A. Balmain,et al.  Integration of positive and negative growth signals during ras pathway activation in vivo. , 2000, Current opinion in genetics & development.

[19]  C. Der,et al.  Analysis of function and regulation of proteins that mediate signal transduction by use of lipid-modified plasma membrane-targeting sequences. , 2000, Methods in enzymology.

[20]  S. Chandra,et al.  A second cytotoxic proteolytic peptide derived from amyloid beta-protein precursor. , 2000, Nature medicine.

[21]  J. Minna,et al.  The 630-kb Lung Cancer Homozygous Deletion Region on Human Chromosome 3 p 21 . 3 : Identification and Evaluation of the Resident Candidate Tumor Suppressor Genes 1 , 2000 .

[22]  S. Rabizadeh,et al.  Neurotrophin dependence mediated by p75NTR: contrast between rescue by BDNF and NGF , 1999, Cell Death and Differentiation.

[23]  D. Bar-Sagi,et al.  Suppression of Ras-Induced Apoptosis by the Rac GTPase , 1999, Molecular and Cellular Biology.

[24]  R. Klemke,et al.  Four Human Ras Homologs Differ in Their Abilities to Activate Raf-1, Induce Transformation, and Stimulate Cell Motility* , 1999, The Journal of Biological Chemistry.

[25]  R. Wolthuis,et al.  Ras caught in another affair: the exchange factors for Ral. , 1999, Current opinion in genetics & development.

[26]  J. Hancock,et al.  Ras Isoforms Vary in Their Ability to Activate Raf-1 and Phosphoinositide 3-Kinase* , 1998, The Journal of Biological Chemistry.

[27]  Karen H. Vousden,et al.  p14ARF links the tumour suppressors RB and p53 , 1998, Nature.

[28]  M. Serrano,et al.  p19ARF links the tumour suppressor p53 to Ras , 1998, Nature.

[29]  E. Nishida,et al.  Proteolytic activation of MST/Krs, STE20-related protein kinase, by caspase during apoptosis , 1998, Oncogene.

[30]  E. Krebs,et al.  Caspase‐mediated activation and induction of apoptosis by the mammalian Ste20‐like kinase Mst1 , 1998, The EMBO journal.

[31]  J. Avruch,et al.  Identification of Nore1 as a Potential Ras Effector* , 1998, The Journal of Biological Chemistry.

[32]  A. Lloyd Ras versus cyclin-dependent kinase inhibitors. , 1998, Current opinion in genetics & development.

[33]  C. Y. Wang,et al.  Requirement of NF-kappaB activation to suppress p53-independent apoptosis induced by oncogenic Ras. , 1997, Science.

[34]  C. Martínez-A,et al.  Ras activation leads to cell proliferation or apoptotic cell death upon interleukin‐2 stimulation or lymphokine deprivation, respectively , 1997, European journal of immunology.

[35]  S. Eliason,et al.  Regulation of CD95 (Fas) ligand expression by TCR-mediated signaling events. , 1997, Journal of immunology.

[36]  S. Lowe,et al.  Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a , 1997, Cell.

[37]  G. V. Vande Woude,et al.  Synergy between the Mos/mitogen-activated protein kinase pathway and loss of p53 function in transformation and chromosome instability , 1997, Molecular and cellular biology.

[38]  D. Shalloway,et al.  Cell cycle-dependent activation of Ras , 1996, Current Biology.

[39]  R. Erikson,et al.  Newly identified stress-responsive protein kinases, Krs-1 and Krs-2. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[40]  D. McConkey,et al.  Ras signaling in tumor necrosis factor‐induced apoptosis. , 1996, The EMBO journal.

[41]  S. Oldham,et al.  Activation of the Raf-1/MAP kinase cascade is not sufficient for Ras transformation of RIE-1 epithelial cells. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[42]  C. Reutelingsperger,et al.  A novel assay to measure loss of plasma membrane asymmetry during apoptosis of adherent cells in culture. , 1996, Cytometry.

[43]  J. Downward,et al.  Activation of phosphoinositide 3‐kinase by interaction with Ras and by point mutation. , 1996, The EMBO journal.

[44]  M. Wigler,et al.  Stimulation of Membrane Ruffling and MAP Kinase Activation by Distinct Effectors of RAS , 1996, Science.

[45]  M. Nakafuku,et al.  Identification of AF-6 and Canoe as Putative Targets for Ras (*) , 1996, The Journal of Biological Chemistry.

[46]  J. Chernoff,et al.  Cloning and Characterization of a Human Protein Kinase with Homology to Ste20 (*) , 1995, The Journal of Biological Chemistry.

[47]  J. Colicelli,et al.  A human protein selected for interference with Ras function interacts directly with Ras and competes with Raf1 , 1995, Molecular and cellular biology.

[48]  M. Wigler,et al.  Multiple ras functions can contribute to mammalian cell transformation , 1995, Cell.

[49]  L. Greene,et al.  Proliferative inhibition by dominant‐negative Ras rescues naive and neuronally differentiated PC12 cells from apoptotic death. , 1994, The EMBO journal.

[50]  M. Marshall,et al.  The effector interactions of p21ras. , 1993, Trends in biochemical sciences.

[51]  J. Walker,et al.  Isolation, characterization and localization of annexin V from chicken liver. , 1993, The Biochemical journal.

[52]  D. Lane,et al.  ras-Induced hyperplasia occurs with mutation of p53, but activated ras and myc together can induce carcinoma without p53 mutation , 1992, Cell.

[53]  E. Meyerowitz,et al.  Plant genome studies: restriction fragment length polymorphism and chromosome mapping information. , 1991, Current opinion in genetics & development.

[54]  J. L. Bos,et al.  ras oncogenes in human cancer: a review. , 1989, Cancer research.

[55]  M. Noble,et al.  Ras‐mediated cell cycle arrest is altered by nuclear oncogenes to induce Schwann cell transformation. , 1988, The EMBO journal.

[56]  H. Ruley,et al.  Rescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[57]  J. Sambrook,et al.  Molecular Cloning: A Laboratory Manual , 2001 .

[58]  R. Newbold,et al.  Fibroblast immortality is a prerequisite for transformation by EJ c-Ha-ras oncogene , 1983, Nature.