Skip to main content

Suppression of ras oncogene-mediated transformation

  • Chapter
  • First Online:
Reviews of Physiology, Biochemistry and Pharmacology, Volume 124

Part of the book series: Reviews of Physiology, Biochemistry and Pharmacology ((REVIEWS,volume 124))

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  • Aaltonen LA, Peltomäki P, Leach FS, Sistonen P, Pylkkänen L, Mecklin J-P, Järvinen H, Powell SM, Jen J, Hamilton SR, Petersen GM, Kinzler KW, Vogelstein B, De la Chapelle A (1993) Clues to the pathogenesis of familial colorectal cancer. Science 260:812–816

    Google Scholar 

  • Andersen LB, Ballester R, Marchuk DA, Chang E, Gutmann DH, Saulino AM, Camonis J, Wigler M, Collins FS (1993a) A conserved alternative splice in the Vonrecklinghausen neurofibromatosis (NF1) gene produces 2 neurofibromin isoforms, both of which have GTPase-activating protein activity. Mol Cell Biol 13:487–495

    Google Scholar 

  • Andersen LB, Fountain JW, Gutmann DH, Tarlé SA, Glover TW, Dracopoli NC, Housman DE, Collins FS (1993b) Mutations in the neurofibromatosis 1 gene in sporadic malignant melanoma cell lines. Nature Genet 3:118–121

    Google Scholar 

  • Argiolas A, Pisano JJ (1983) Facilitation of phospholipase A2 activity by mastoparans, a new class of mast cell degranulating peptides from wasp venom. J Biol Chem 258:13697–13702

    Google Scholar 

  • Baker SJ, Fearon ER, Nigro JM, Hamilton SR, Preisinger AC, Jessup JM, Van Tuinen P, Ledbetter DH, Barker DF, Nakamura Y, White R, Vogelstein B (1989) Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science 244:217–221

    Google Scholar 

  • Baker SJ, Markowitz S, Fearon ER, Willson JKV, Vogelstein B (1990) Suppression of human colorectal carcinoma cell growth by wild-type p53. Science 249:912–915

    Google Scholar 

  • Ballester R, Marchuk D, Boguski M, Saulino A, Letcher R, Wigler M, Collins F (1990) The NF1 locus encodes a protein functionally related to mammalian GAP and yeast IRA proteins. Cell 63:851–859

    Google Scholar 

  • Balmain A, Ramsden M, Bowden GT, Smith J (1984) Activation of the mouse cellular Harvey-ras gene in chemically induced benign skin papillomas. Nature 307:658–660

    Google Scholar 

  • Bar-Sagi D, Feramisco JR (1985) Microinjection of the ras oncogene protein into PC12 cells induces morphological differentiation. Cell 42:841–848

    Google Scholar 

  • Barbacid M (1987) ras genes. Annu Rev Biochem 56:779–827

    Google Scholar 

  • Barker D, Wright E, Nguyen K, Cannon L, Fain P, Goldgar D, Bishop DT, Carey J, Baty B, Kivlin J, Willard H, Waye JS, Greig G, Leinwand L, Nakamura Y, O'Connell P, Leppert M, Lalouel J-M, White R, Skolnick M (1987) Gene for von Recklinghausen neurofibromatosis is in the pericentric region of chromosome 17. Science 236:1100–1102

    Google Scholar 

  • Baron HM, Bobrisheva IV, Varshaver NB (1992) The activated human c-Ha-ras-1 oncogene as a mutagen. Cancer Genet Cytogenet 62:15–20

    Google Scholar 

  • Bassin RH, Noda M (1987) Oncogene inhibition by cellular genes. Adv Viral Oncol 6:103–127

    Google Scholar 

  • Basu TN, Gutmann DH, Fletcher JA, Glover TW, Collins FS, Downward J (1992) Aberrant regulation of ras proteins in malignant tumour cells from type-1 neurofibromatosis patients. Nature 356:713–715

    Google Scholar 

  • Benade LE, Talbot N, Tagliaferri P, Hardy C, Card J, Noda M, Najam N, Bassin RH (1986) Ouabain sensitivity is linked to ras-transformation in human HOS cells. Biochem Biophys Res Comm 136:807–814

    Google Scholar 

  • Benito M, Porras A, Nebreda AR, Santos E (1991) Differentiation of 3T3-L1 fibroblasts to adipocytes induced by transfection of ras oncogenes. Science 253:565–568

    Google Scholar 

  • Birchmeier C, Broek D, Wigler M (1985) RAS proteins can induce meiosis in Xenopus oocytes. Cell 43:615–621

    Google Scholar 

  • Bokoch GM, Parkos CA, Mumby SM (1988) Purification and characterization of the 22,000-dalton GTP-binding protein substrate for ADP-ribosylation by botulinum toxin G22 K. J Biol Chem 263:16744–16749

    Google Scholar 

  • Bokoch GM, Quilliam LA, Bohl BP, Jesaitis AJ, Quinn MT (1991) Inhibition of Rap1A binding to cytochrome-b558 of NADPH oxidase by phosphorylation of Rap1A. Science 254:1794–1796

    Google Scholar 

  • Bokoch GM (1993) Biology of the Rap proteins, members of the ras superfamily of GTP-binding proteins. Biochem J 289:17–24

    Google Scholar 

  • Bollag G, McCormick F (1991) Differential regulation of rasGAP and neurofibromatosis gene product activities. Nature 351:576–579

    Google Scholar 

  • Bollag G, McCormick F (1992) RAS regulation-NF is enough of GAP. Nature 356:663–664

    Google Scholar 

  • Bos JL, Verlaan-de Vries M, Jansen AM, Veeneman GH, van Boom JH, Van der Eb AJ (1984) Three different mutations in codon 61 of the human N-ras gene detected by synthetic oligonucleotide hybridization. Nucleic Acids Res 12:9155–9163

    Google Scholar 

  • Bos JL (1989) Ras oncogenes in human cancer: a review. Cancer Res 49:4682–4689

    Google Scholar 

  • Bourne HR, Sanders DA, McCormick F (1991) The GTPase superfamily: Conserved structure and molecular mechanism. Nature 349:117–127

    Google Scholar 

  • Brancolini C, Bottega S, Schneider C (1992) Gas2, a growth arrest-specific protein, is a component of the microfilament network system. J Cell Biochem 117:1251–1261

    Google Scholar 

  • Buchberg AM, Cleveland LS, Jenkins NA, Copeland NG (1990) Sequence homology shared by neurofibromatosis type-1 gene and IRA-1 and IRA-2 negative regulators of the RAS cyclic AMP pathway. Nature 347:291–294

    Google Scholar 

  • Buss JE, Quilliam LA, Kato K, Casey PJ, Solski PA, Wong G, Clark R, McCormick F, Bokoch GM, Der CJ (1991) The COOH-terminal domain of the Rap1A (Krev-1) protein is isoprenylated and supports transformation by an H-Ras:Rap1A chimeric protein. Mol Cell Biol 11:1523–1530

    Google Scholar 

  • Bèranger F, Goud B, Tavitian A, de Gunzburg J (1991) Association of the Ras-antagonistic Rap1/Krev-1 proteins with the Golgi complex. Proc Natl Acad Sci USA 88:1606–1610

    Google Scholar 

  • Cai H, Szeberenyi J, Cooper GM (1990) Effect of a dominant inhibitory Ha-ras mutation on mitogenic signal transduction in NIH 3T3 cells. Mol Cell Biol 10:5314–5323

    Google Scholar 

  • Cairo G, Ferrero M, Biondi G, Colombo MP (1992) Expression of a growth arrest specific gene (gas-1) in transformed cells. Br J Cancer 66:27–31

    Google Scholar 

  • Campa MJ, Chang K-J, yVedia LM, Reep BR, Lapentina EG (1991) Inhibition of ras-induced germinal vesicle breakdown in Xenopus oocytes by rap-1B. Biochem Biophys Res Comm 174:1–5

    Google Scholar 

  • Cantley LC, Auger KR, Carpenter C, Duckworth B, Graziani A, Kapeller R, Soltoff S (1991) Oncogenes and signal transduction. Cell 64:281–302

    Google Scholar 

  • Capon DJ, Chen EY, Levinson AD, Seeburg PH, Goeddel DV (1983a) Complete nucleotide sequences of T24 human bladder carcinoma oncogene and its normal homologue. Nature 302:33–37

    Google Scholar 

  • Capon DJ, Seeburg PH, McGrath JP, Hayflick JS, Edman U, Levinson AD, Goeddel DV (1983b) Activation of Ki-ras2 gene in human colon and lung carcinomas by two different point mutations. Nature 304:507–513

    Google Scholar 

  • Cardiff RD, Sinn E, Muller W, Leder P (1991) Transgenic oncogene mice. Tumor phenotype predicts genotype. Am J Pathol 139:495–501

    Google Scholar 

  • Cawthon RM, Weiss R, Xu G, Viskochil D, Culver M, Stevens J, Robertson M, Dunn D, Gesteland R, O'Connell P, White R (1990a) A major segment of the neurofibromatosis type 1 gene: cDNA sequence, genomic structure, and point mutations. Cell 62:193–201

    Google Scholar 

  • Cawthon RM, O'Connell P, Buchberg AM, Viskochil D, Weiss RB, Culver M, Stevens J, Jenkins NA, Copeland NG, White R (1990b) Identification and characterization of transcripts from the neurofibromatosis 1 region: The sequence and genomic structure of EVI2 and mapping of other transcripts. Genomics 7:555–565

    Google Scholar 

  • Cawthon RM, Andersen LB, Buchberg AM, Xu G, O'Connell P, Viskochil D, Weiss RB, Wallace MR, Marchuk DA, Culver M, Stevens J, Jenkins NA, Copeland NG, Collins FS, White R (1991) cDNA sequence and genomic structure of EV12B, a gene lying within an intron of the neurofibromatosis type 1 gene. Genomics 9:446–460

    Google Scholar 

  • Chang EH, Furth ME, Scolnick EM, Lowy DR (1982) Tumorigenic transformation of mammalian cells induced by a normal human gene homologus to the oncogene of Harvey murine sarcoma virus. Nature 297:479–483

    Google Scholar 

  • Chang EH, Miller PS, Cushman C, Devadas K, Pirollo KF, Ts'o POP, Yu ZP (1991) Antisense inhibition of ras p21 expression that is sensitive to a point mutation. Biochemistry 30:8283–8296

    Google Scholar 

  • Chen C, Okayama H (1987) High-efficiency transformation of mammalian cells by plasmid DNA. Mol Cell Biol 7:2745–2752

    Google Scholar 

  • Chen S, Botteri F, van der Putten H, Landel CP, Evans GA (1987) A lymphoproliferative abnormality associated with inappropriate expression of the Thy-1 antigen in transgenic mice. Cell 51:7–19

    Google Scholar 

  • Chen TM, Defendi V (1992) Functional interaction of p53 with HPV18 E6, c-myc and H-ras in 3T3 Cells. Oncogene 7:1541–1547

    Google Scholar 

  • Chiao PJ, Kannan P, Yim SO, Krizman DB, Wu T-A, Gallick GE, Tainsky MA (1991) Susceptibility to ras oncogene transformation is coregulated with signal transduction through growth factor receptors. Oncogene 6:713–720

    Google Scholar 

  • Cho HY, Cutchins EC, Rhim JS, Huebner RJ (1976) Revertants of human cells transformed by murine sarcoma virus. Science 194:951–953

    Google Scholar 

  • Ciardiello F, Sanfilippo B, Yanagihara K, Kim N, Tortora G, Bassin RH, Kidwell WR, Salomon DS (1988) Differential growth sensitivity to 4-cis-hydroxy-L-proline of transformed rodent cell lines. Cancer Res 48:2483–2491

    Google Scholar 

  • Colicelli J, Field J, Ballester R, Chester N, Young D, Wigler M (1990) Mutational mapping of RAS-responsive domains of the Saccharomyces cerevisiae adenylyl cyclase. Mol Cell Biol 10:2539–2543

    Google Scholar 

  • Compere SJ, Baldacci P, Sharpe AH, Thompson T, Land H, Jaenisch R (1989) The ras and myc oncogenes cooperate in tumor induction in many tissues when introduced into midgestation mouse embryos by retroviral vectors. Proc Natl Acad Sci USA 86:2224–2228

    Google Scholar 

  • Contente S, Kenyon K, Rimoldi D, Friedman RM (1990) Expression of gene rrg is associated with reversion of NIH 3T3 transformed by LTR-c-Ha-ras. Science 249:796–798

    Google Scholar 

  • Cooper GM, Okenquist S, Silverman L (1980) Transforming activity of DNA of chemically transformed and normal cells. Nature 284:418–421

    Google Scholar 

  • Cox AD, Hisaka MM, Buss JE, Der CJ (1992) Specific isoprenoid modification is required for function of normal, but not oncogenic, ras protein. Mol Cell Biol 12:2606–2615

    Google Scholar 

  • Craig RW, Sager R (1985) Suppression of tumorigenicity in hybrids of normal and oncogene-transformed CHEF cells. Proc Natl Acad Sci USA 82:2062–2066

    Google Scholar 

  • Culine S, Olofsson B, Gosselin S, Honore N, Tavitian A (1989) Expression of the ras-related rap genes in human tumors. Int J Cancer 44:990–994

    Google Scholar 

  • Cutler ML, Bassin RH, Zanoni L, Talbot N (1992) Isolation of rsp-1, a novel cDNA capable of suppressing v-Ras transformation. Mol Cell Biol 12:3750–3756

    Google Scholar 

  • Daston MM, Scrable H, Nordlund M, Sturbaum AK, Nissen LM, Ratner N (1992) The protein product of the neurofibromatosis type 1 gene is expressed at highest abundance in neurons, Schwann cells, and oligodendrocytes. Neuron 8:415–428

    Google Scholar 

  • DeClue JE, Cohen BD, Lowy DR (1991) Identification and characterization of the neurofibromatosis type 1 protein product. Proc Natl Acad Sci USA 88:9914–9918

    Google Scholar 

  • DeClue JE, Papageorge AG, Fletcher JA, Diehl SR, Ratner N, Vass WC, Lowy DR (1992) Abnormal regulation of mammalian p21(ras) contributes to malignant tumor growth in Vonrecklinghausen (type-1) neurofibromatosis. Cell 69:265–273

    Google Scholar 

  • Declue JE, Zhang K, Redford P, Vass WC, Lowy DR (1991) Suppression of src transformation by overexpression of full-length GTPase-activating protein (GAP) or of the GAP terminus. Mol Cell Biol 11:2819–2825

    Google Scholar 

  • Delsal G, Ruaro ME, Philipson L, Schneider C (1992) The growth arrest-specific gene, gas1, is involved in growth suppression. Cell 70:595–607

    Google Scholar 

  • Diamantis ID, Nair APK, Hirsch HH, Moroni C (1989) Tumor suppression involves down-regulation of interleukin 3 expression in hybrids between autocrine mastocytoma and interleukin 3-dependent parental mast cells. Proc Natl Acad Sci USA 86:9299–9302

    Google Scholar 

  • Dibattiste D, Golubic M, Stacey D, Wolfman A (1993) Differences in the interaction of p21(c-Ha-ras)-GMP-PNP with full-length neurofibromin and GTPase-activating protein. Oncogene 8:637–643

    Google Scholar 

  • Downward J, Graves JD, Warne PH, Rayter S, Cantrell DA (1990) Stimulation of p21ras upon T-cell activation. Nature 346:719–723

    Google Scholar 

  • Downward J (1992) Regulatory mechanisms for ras proteins. Bioessays 14:177–184

    Google Scholar 

  • Duronio V, Welham MJ, Abraham S, Dryden P, Schrader JW (1992) P21ras activation via hemopoietin receptors and c-kit requires tyrosine kinase activity but not tyrosine phosphorylation of p21ras GTPase activating protein. Proc Natl Acad Sci USA 89:1587–1591

    Google Scholar 

  • Eliyahu D, Michalovitz D, Eliyahu S, Pinhasi-Kimhi O, Oren M (1989) Wild-type p53 can inhibit oncogene-mediated focus formation. Proc Natl Acad Sci USA 86:8763–8767

    Google Scholar 

  • Ellis C, Moran M, McCormick F, Pawson T (1990) Phosphorylation of GAP and GAP-associated proteins by transforming and mitogenic tyrosine kinases. Nature 343:377–381

    Google Scholar 

  • Farrell FX, Ohmstede C-A, Reep BR, Lapentina EG (1990) cDNA sequence of a new ras-related gene (rap2b) isolated from human platelets with sequence homology to rap2. Nucleic Acids Res 18:4281

    Google Scholar 

  • Farrell PJ, Allan GJ, Shanahan F, Vousden KH, Crook T (1991) p53 is frequently mutated in Burkitt's lymphoma cell lines. EMBO J 10:2879–2887

    Google Scholar 

  • Farrell RE, Greene JJ (1992) Regulation of c-myc and c-Ha-ras oncogene expression by cell shape. J Cell Physiol 153:429–435

    Google Scholar 

  • Fearon ER, Vogelstein B (1990) A genetic model for colorectal tumorigenesis. Cell 61:759–767

    Google Scholar 

  • Fearon ER, Cho KR, Nigro JM, Kern SE, Simons JW, Ruppert JM, Hamilton SR, Preisinger AC, Thomas G, Kinzler KW, Vogelstein B (1990) Identification of a chromosome 18q gene that is altered in colorectal cancers. Science 247:49–56

    Google Scholar 

  • Feinberg AP, Vogelstein B, Droller MJ, Baylin SB, Nelkin BD (1983) Mutation affecting the 12th amino acid of the c-Ha-ras oncogene product occurs infrequently in human cancer. Science 220:1175–1177

    Google Scholar 

  • Fernandez JLR, Geiger B, Salomon D, Sabanay I, Zoller M, Benzeev A (1992) Suppression of tumorigenicity in transformed cells after transfection with vinculin cDNA. J Cell Biol 119:427–438

    Google Scholar 

  • Field J, Xu H-P, Michaeli T, Ballester R, Sass P, Wigler M, Colicelli J (1990) Mutations of the adenylate cyclase gene that block RAS function in Saccharomyces cervisiae. Science 247:464–467

    Google Scholar 

  • Finlay CA, Hinds PW, Levine AJ (1989) The p53 proto-oncogene can act as a suppressor of transformation. Cell 57:1083–1093

    Google Scholar 

  • Finney RE, Bishop JM (1993) Predisposition to neoplastic transformation caused by gene replacement of H-rasl. Science 260:1524–1527

    Google Scholar 

  • Fischer TH, White II GC (1987) Partial purification and characterization of thrombolamban, a 22,000 dalton cAMP-dependent protein kinase substrate in platelets. Biochem Biophys Res Comm 149:700–706

    Google Scholar 

  • Folkman J, Moscona A (1978) Role of cell shape in growth control. Nature 273:345349

    Google Scholar 

  • Fountain JW, Wallace MR, Bruce MA, Seizinger BR, Menon AG, Gusella JF, Michels VV, Schmidt MA, Dewald GW, Collins FS (1989) Physical mapping of a translocation break-point in neurofibromatosis. Science 244:1085–1087

    Google Scholar 

  • Franza BR jr, Maruyama K, Garrels JI, Ruley HE (1986) In vitro establishment is not a sufficient prerequisite for transformation by activated ras oncogenes. Cell 44:409–418

    Google Scholar 

  • Frech M, John J, Pizon V, Chardin P, Tavitian A, Clark R, McCormick F, Wittinghofer A (1990) Inhibition of GTPase activating protein stimulation of Ras-p21 GTPase by the Krev-1 gene product. Science 249:169–171

    Google Scholar 

  • Fry DG, Milam LD, Dillberger JE, Maher VM, McCormick JJ (1990) Malignant transformation of an infinite life span human fibroblast cell strain by transfection with v-Ki-ras. Oncogene 5:1415–1418

    Google Scholar 

  • Fujita H, Suzuki H, Kuzumaki N, Müllauer L, Ogiso Y, Oda A, Ebisawa K, Sakurai T, Nonomura Y, Kijimoto-Ochiai S (1990) A specific protein, p92, detected in flat revertants derived from NIH/3T3 transformed by human activated c-Ha-ras oncogene. Exp Cell Res 186:115–121

    Google Scholar 

  • Geiser AG, Anderson MJ, Stanbridge EJ (1989) Suppression of tumorigenicity in human cell hybrids derived from cell lines expressing different activated ras oncogenes. Cancer Res 49:1572–1577

    Google Scholar 

  • Geiser AW, Der CJ, Marshall CJ, Stanbridge EJ (1986) Suppression of tumorigenicity with continued expression of the c-Ha-ras oncogene in EJ bladder carcinoma-human fibroblast hybrid cells. Proc Natl Acad Sci USA 83:5209–5213

    Google Scholar 

  • Gerfaux J, Sergiescu D, Hamelin R, Joret A-M, Lallemand C (1990) A common cellular pathway for v-mos and v-Ki-ras is not required for v-Ki-ras-induced tumorigenicity in a nonmalignant, v-mos-expressing revertant cell. Mol Carcinog 3:103–113

    Google Scholar 

  • Gerwin BI, Spillare E, Forrester K, Lehman TA, Kispert J, Welsh JA, Pfeifer AMA, Lechner JF, Baker SJ, Vogelstein B, Harris CC (1992) Mutant-p53 can induce tumorigenic conversion of human bronchial epithelial cells and reduce their responsiveness to a negative growth factor, transforming growth factor-beta(1). Proc Natl Acad Sci USA 89:2759–2763

    Google Scholar 

  • Giancotti FG, Ruoslahti E (1990) Elevated levels of the alpha5/beta1 fibronection receptor suppress the transformed phenotype of Chinese hamster ovary cells. Cell 60:849–859

    Google Scholar 

  • Gibbs JB, Marshall MS, Scolnick EM, Dixon RAF, Vogel US (1990) Modulation of guanine nucleotides bound to Ras in NIH 3T3 cells by oncogenes, growth factors, and the GTPase activating protein. J Biol Chem 265:20437–20442

    Google Scholar 

  • Goldgar DE, Green P, Parry DM, Mulvihill JJ (1989) Multipoint linkage analysis in neurofibromatosis type I: An international collaboration. Am J Hum Genet 44:6–12

    Google Scholar 

  • Golubic M, Tanaka K, Dobrowolski S, Wood D, Tsai MH, Marshall M, Tamanoi F, Stacey DW (1991) The GTPase stimulatory activities of the neurofibromatosis type 1 and the yeast IRA2 proteins are inhibited by arachidonic acid. EMBO J 10:2897–2903

    Google Scholar 

  • Golubic M, Roudebush M, Dobrowolski S, Wolfman A, Stacey DW (1992) Catalytic properties, tissue and intracellular distribution of neurofibromin. Oncogene 7:2151–2159

    Google Scholar 

  • Goyette MC, Cho K, Fasching CL, Levy DB, Kinzler KW, Paraskeva C, Vogelstein B, Stanbridge EJ (1992) Progression of colorectal cancer is associated with multiple tumor suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer. Mol Cell Biol 12:1387–1395

    Google Scholar 

  • Grand RJA, Owen D (1991) The biochemistry of ras p21. Biochem J 279:609–631

    Google Scholar 

  • Graves JD, Downward J, Rayter S, Warne P, Turr AL, Glennie M, Cantrell DA (1991) CD2 antigen mediated activation of the guanine nucleotide binding proteins p21ras in human T lymphocytes. J Immunol 146:3709–3712

    Google Scholar 

  • Graves JD, Downward J, Izquierdo M, Rayter S, Warne PH, Cantrell DA (1992) The growth factor IL-2 activates p21ras proteins in normal human T lymphocytes. J Immunol 148:2417–2422

    Google Scholar 

  • Greenberger JS, Aaaronson SA (1974) Morphologic revertants of murine sarcoma virus transformed nonproducer BALB/3T3: Selective techniques for isolation and biologic properties in vitro and in vivo. Virology 57:339–346

    Google Scholar 

  • Griegel S, Traub O, Willecke K, Schäfer R (1986) Suppression and re-expression of transformed phenotype in hybrids of Ha-ras1 transformed Rat-1 cells and early passage rat embryo fibroblasts. Int J Cancer 38:697–705

    Google Scholar 

  • Guerrero I, Villasante A, Corces V, Pellicer A (1984a) Activation of a c-K-ras oncogene by somatic mutation in mouse lymphomas induced by gamma irradiation. Science 225:1159–1161

    Google Scholar 

  • Guerrero I, Villasante A, D'Eustachio P, Pellicer A (1984b) Isolation, characterization, anmd chromosome assignment of mouse N-ras gene from carcinogen-induced thymic lymphoma. Science 225:1041–1044

    Google Scholar 

  • Hafen E, Basler K, Edstroem J-E, Rubin GM (1987) Sevenless, a cell-specific homeotic gene of Drosophila, encodes a putative transmembrane receptor with a tyrosine kinase domain. Science 236:55–63

    Google Scholar 

  • Hajnal A, Klemenz R, Schäfer R (1993a) Suppression of ras-mediated transformation. Differential expression of genes encoding extracellular matrix proteins in normal, transformed and revertant cells. Adv Enzyme Regul 33:267–280

    Google Scholar 

  • Hajnal A, Klemenz R, Schäfer R (1993b) Upregulation of lysyl oxidase in spontaneous revertants of H-ras transformed rat fibroblasts.

    Google Scholar 

  • Hajnal A, Klemenz R, Schäfer R (1994) Subtraction cloning of H-Rev107, a gene specifically expressed in H-ras resistant fibroblasts. Cancer Res 53:4670–4675

    Google Scholar 

  • Hall A, Marshall CJ, Spurr NK, Weiss RA (1983) Identification of transforming gene in two human sarcoma cell lines as a new member of the ras gene family located on chromosome 1. Nature 303:396–400

    Google Scholar 

  • Hall A (1990) ras and GAP — Who's controlling whom? Cell 61:921–923

    Google Scholar 

  • Hall A (1992) Signal transduction through small GTPases — A tale of 2 GAPs. Cell 69:389–391

    Google Scholar 

  • Hanahan D (1988) Dissecting multistep tumorigenesis in transgenic mice. Annu Rev Genet 22:479–519

    Google Scholar 

  • Hariharan IK, Carthew RW, Rubin GM (1991) The Drosophila roughened mutation: activation of a rap homolog disrupts eye development and interferes with cell determination. Cell 67:717–722

    Google Scholar 

  • Hart PA, Marshall CJ (1990) Amino acid 61 is a determinant of sensitivity of rap proteins to ras GTPase activating protein. Oncogene 5:1099–1101

    Google Scholar 

  • Hata Y, Kikuchi A, Sasaki T, Schaber MD, Gibbs JB, Takai Y (1990) Inhibition of the ras p21 GTPase-activating protein-stimulated GTPase activity of c-Ha-ras p21 by smg p21 having the same effector domain as ras p21s. J Biol Chem 265:7104–7107

    Google Scholar 

  • Hattori S, Maekawa M, Nakamura S (1992) Identification of neurofibromatosis type-I gene product as an insoluble GTPase-activating protein toward ras p21. Oncogene 7:481–485

    Google Scholar 

  • Haynes JR, Downing JR (1988) A recessive cellular mutation in v-fes-transformed mink cells restores contact inhibition and anchorage-dependent growth. Mol Cell Biol 8:2419–2427

    Google Scholar 

  • Heidaran MA, Molloy CJ, Pangelinan M, Choudhury GG, Wang L, Fleming TP, Sakaguchi AY, Pierce JH (1992) Activation of the colony-stimulating factor 1 receptor leads to the rapid tyrosine phosphorylation of GTPase-activating protein and activation of cellular p21ras. Oncogene 7:147–152

    Google Scholar 

  • Higgins PJ, Ryan MP (1989) Biochemical localization of the transformation-sensitive 52 kDA (p52) protein to the substratum contact regions of cultured rat fibroblasts. Biochem J 257:173–182

    Google Scholar 

  • Higgins PJ, Ryan MP (1991) p52 (PAI-1) and actin expression in butyrate-induced flat revertants of v-ras-transformed rat kidney cells. Biochem J 279:883–890

    Google Scholar 

  • Hirakawa T, Ruley HE (1988) Rescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene. Proc Natl Acad Sci USA 85:1519–1523

    Google Scholar 

  • Hoemann CD, Zarbl H (1990) Use of revertant cell lines to identify targets of v-fos transformation-specific alterations in gene expression. Cell Growth Diff 1:581–590

    Google Scholar 

  • Hollstein M, Sidransky D, Vogelstein B, Harris CC (1991) p53 mutations in human cancers. Science 253:49–53

    Google Scholar 

  • Hong HJ, Hsu L-C, Gould MN (1990) Molecular cloning of rat Krev-1 cDNA and analysis of the mRNA levels in normal and NMU-induced mammary carcinomas. Carcinogenesis 11:1245–1247

    Google Scholar 

  • Hsu L-C, Gould MN (1991) Molecular cloning of Copenhagen rat Krev-1 and rap1B cDNAs and study of their association with mammary tumor resistance in the Copenhagen rat. Carcinogenesis 12:533–536

    Google Scholar 

  • Huang DCS, Marshall CJ, Hancock JF (1993) Plasma membrane-targeted ras GTPase-activating protein is a potent suppressor of p21ras function. Mol Cell Biol 13:2420–2431

    Google Scholar 

  • Huang S, Axelrod DE (1991) Altered post-translational processing of p21ras oncoprotein in a transformation-suppressed cell line. Oncogene 6:1211–1218

    Google Scholar 

  • Hurlin PJ, Maher VM, McCormick JJ (1989) Malignant transformation of human fibroblasts caused by expression of a transfected T24 HRAS oncogene. Proc Natl Acad Sci USA 86:187–191

    Google Scholar 

  • Ichikawa T, Ichikawa Y, Isaacs JT (1992) Genetic factors and suppression of metastatic ability of v-Ha-ras-transfected rat mammary cancer cells. Proc Natl Acad Sci USA 89:1607–1610

    Google Scholar 

  • Itoh O, Kuroiwa S, Atsumi S, Umezawa K, Takeuchi T, Hori M (1989) Induction by the guanosine analogue oxanosine of reversion toward the normal phenotype of K-ras transformed rat kidney cells. Cancer Res 49:996–1000

    Google Scholar 

  • Jelinek MA, Hassell JA (1992) Reversion of middle T antigen-transformed rat-2 cells by Krev-1: Implications for the role of p21c-ras in polyomavirus-mediated transformation. Oncogene 7:1687–1698

    Google Scholar 

  • Jimenez B, Pizon V, Lerosey I, Bèranger F, Tavitian A, deGunzburg J (1991) Effects of the ras-related rap2 protein on cellular proliferation. Int J Cancer 49:471–479

    Google Scholar 

  • Kaibuchi K, Mizuno T, Fuijoka H, Yamamoto T, Kishi K, Fukumoto Y, Hori Y, Takai Y (1991) Molecular cloning of the cDNA for stimulatory GDP/GTP exchange protein for smg p21s (ras-like small GTP-binding proteins) and characterization of stimulatory GDP/GTP exchange protein. Mol Cell Biol 11:2873–2880

    Google Scholar 

  • Kaneko M, Horikoshi J (1989) Reversible suppression by nalidixic acid of anchorage-independent growth of mouse cells transformed by 3-methylcholanthrene or an activated c-Ha-ras gene. Br J Cancer 60:880–886

    Google Scholar 

  • Katz E, Carter BJ (1986) A mutant cell line derived from NIH/3T3 cells: Two oncogenes required for in vitro transformation. J Natl Cancer Inst 77:909–914

    Google Scholar 

  • Katz E, Samid D (1989) Transfection of EK-3, a subline of NIH 3T3, with the oncogene Ha-ras does not abolish its anchorage dependence. Europ J Cell Biol 49:221–224

    Google Scholar 

  • Kawata M, Matsui Y, Kondo J, Hishida T, Teranishi Y, Takai Y (1988) A novel small molecular weight GTP-binding protein with the same putative effector domain as the ras proteins in bovine brain membranes. J Biol Chem 263:18965–18971

    Google Scholar 

  • Kawata M, Kikuchi A, Hoshijima M, Yamamoto K, Hashimoto E, Yamamura H, Takai Y (1989a) Phosphorylation of smg p21, a ras p21-like GTP-binding protein, by cyclic AMP-dependent protein kinase in a cell-free system and in response to prostaglandin E1 in intact human platelets. J Biol Chem 264:15688–15695

    Google Scholar 

  • Kawata M, Kikuchi A, Hoshijima M, Yamamoto K, Hashimoto E, Yamamura H, Takai Y (1989b) Phosphorylation of smg p21, a ras p21-like GTP-binding protein, by cyclic AMP-dependent protein kinase in a cell-free system and in response to prostaglandin E1 in intact human platelets. J Biol Chem 264:15688–15695

    Google Scholar 

  • Kawata M, Kawahara Y, Sunako M, Araki S, Koide M, Tsuda T, Fukuzaki H, Takai Y (1991) The molecular heterogeneity of the smg-21/Krev-1/rap1 proteins, a GTP-Binding protein having the same effector domain as ras p21s, in bovine aortic smooth muscle membranes. Oncogene 6:841–848

    Google Scholar 

  • Kenyon K, Contente S, Trackman PC, Tang J, Kagan HM, Friedman RM (1991) Lysyl oxidase and rrg messenger RNA. Science 253:802

    Google Scholar 

  • Kikuchi A, Sasaki T, Araki S, Hata Y, Takai Y (1989) Purification and characterization from bovine brain cytosol of two GTPase-activating proteins specific for smg p21, a GTP-binding protein having the same effector domains as c-ras p21s. J Biol Chem 264:9133–9136

    Google Scholar 

  • Kikuchi A, Kaibuchi K, Hori Y, Nonaka H, Sakoda T, Kawamura M, Mizuno T, Takai Y (1992) Molecular cloning of the human cDNA for a stimulatory GDP/GTP exchange protein for c-Ki-ras p21 and smg p21. Oncogene 7:289–293

    Google Scholar 

  • Kim S, Mizoguchi A, Kikuchi A, Takai Y (1990) Tissue and subcellular distributions of the smg-21/rap1/Krev-1 proteins which are partly distinct from those of c-ras p21s. Mol Cell Biol 10:2645–2652

    Google Scholar 

  • Kinzler KW, Nilbert MC, Su L-K, Vogelstein B, Bryan TM, Levy DB, Smith KJ, Preisinger AC, Hedge P, McKechnie D, Finniear R, Markham A, Groffen J, Boguski MS, Altschul SF, Horii A, Ando H, Miyoshi Y, Miki Y, Nishisho I, Nakamura Y (1991) Identification of FAP locus genes from chromosome 5q21. Science 253:661–664

    Google Scholar 

  • Kitayama H, Sugimoto Y, Matsuzaki T, Ikawa Y, Noda M (1989) A ras-related gene with transformation suppressor activity. Cell 56:77–84

    Google Scholar 

  • Kitayama H, Matsuzaki T, Ikawa Y, Noda M (1990) Genetic analysis of the Kirsten-rasrevertant 1 gene: Potentiation of its tumor suppressor activity by specific point mutations. Proc Natl Acad Sci USA 87:4284–4288

    Google Scholar 

  • Kizaka S, Hakura A (1989) A cell mutant that exhibits temperature-dependent sensitivity to transformation by various oncogenes. Mol Cell Biol 9:5669–5675

    Google Scholar 

  • Koi M, Johnson LA, Kalikin LM, Little PFR, Nakamura Y, Feinberg AP (1993) Tumor cell growth arrest caused by subchromosomal transferable DNA fragments from chromosome 11. Science 260:361–364

    Google Scholar 

  • Koizumi M, Kamiya H, Ohtsuka E (1992) Ribozymes designed to inhibit transformation of NIH3T3 cells by the activated c-Ha-ras gene. Gene 117:179–184

    Google Scholar 

  • Kollias G, Evens DJ, Ritter M, Beech J, Morris R, Grosveldt F (1987) Ectopic expression of Thy-1 in the kidneys of transgenic mice induces functional and proliferative abnormalities. Cell 51:21–31

    Google Scholar 

  • Korn LJ, Siebel CW, McCormick F, Roth RA (1987) Ras p21 as a potential mediator of insulin action in Xenopus oocytes. Science 236:840–843

    Google Scholar 

  • Kotani K, Kikuchi A, Doi K, Kishida S, Sakoda T, Kishi K, Takai Y (1992) The functional domain of the stimulatory GDP/GTP exchange protein (smg GDS) which interacts with the C-terminal geranylgeranylated region of rap-1/Krev-1/smg-p21. Oncogene 7:1699–1704

    Google Scholar 

  • Krauss RS, Guadagno SN, Weinstein IB (1992) Novel revertants of H-ras oncogene-transformed R6-PKC3 cells. Mol Cell Biol 12:3117–3129

    Google Scholar 

  • Krizman DB, Giovanella BC, Tainsky MA (1990) Susceptibility for N-ras-mediated transformation requires loss of tumor suppressor activity. Somat Cell Mol Genet 16:15–27

    Google Scholar 

  • Krzyzosiak WJ, Shindookada N, Teshima H, Nakajima K, Nishimura S (1992) Isolation of genes specifically expressed in flat revertant cells derived from activated ras-transformed NIH-3T3 cells by treatment with azatyrosine. Proc Natl Acad Sci USA 89:4879–4883

    Google Scholar 

  • Kulesh DA, Greene JJ (1986) Shape-dependent regulation of proliferation in normal and malignant human cells and its alteration by interferon. Cancer Res 46:2793–2797

    Google Scholar 

  • Kuzumaki N, Ogiso Y, Oda A, Fujita H, Suzuki H, Sato C, Müllauer L (1989) Resistance to oncogenic transformation in revertant R1 of human ras-transformed NIH 3T3 cells. Mol Cell Biol 9:2258–2263

    Google Scholar 

  • Kyprianou N, Taylor-Papadimitriou J (1992) Isolation of azatyrosine-induced revertants from ras-transformed human mammary epithelial cells. Oncogene 7:57–63

    Google Scholar 

  • Land H, Parada LF, Weinberg RA (1983) Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes. Nature 304:596–602

    Google Scholar 

  • Land H, Chen AC, Morgenstern JP, Parada LF, Weinberg RA (1986) Behavior of myc and ras oncogenes in transformation of rat embryo fibroblasts. Mol Cell Biol 6:1917–1925

    Google Scholar 

  • Lane DP (1992) p53, Guardian of the genome. Nature 358:15–16

    Google Scholar 

  • Lapetina EG, Lacal JC, Reep BR, yVedia LM (1989) A ras-related protein is phosphorylated and translocated by agonists that increase cAMP levels in human platelets. Proc Natl Acad Sci USA 86:3131–3134

    Google Scholar 

  • Lazariskaratzas A, Smith MR, Frederickson RM, Jaramillo ML, Liu YL, Kung HF, Sonenberg N (1992) Ras mediates translation initiation factor-4E-induced malignant transformation. Gene Dev 6:1631–1642

    Google Scholar 

  • Ledwith BJ, Manam S, Kraynack AR, Nichols WW, Bradley MO (1990) Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene. Mol Cell Biol 10:1545–1555

    Google Scholar 

  • Lee SW, Tomasetto C, Sager R (1991) Positive selection of candidate tumor-suppressor genes by subtractive hybridization. Proc Natl Acad Sci USA 88:2825–2829

    Google Scholar 

  • Legius E, Marchuk DA, Collins FS, Glover TW (1993) Somatic deletion of the neurofibromatosis type 1 gene in a neurofibrosarcoma supports a tumour suppressor gene hypothesis. Nature Genet 3:122–126

    Google Scholar 

  • Lerosey I, Chardin P, deGunzburg J, Tavitian A (1991) The product of the rap2 gene, member of the ras superfamily. J Biol Chem 266:4315–4321

    Google Scholar 

  • Lerosey I, Polakis P, Tavitian A, de Gunzburg J (1992) Regulation of the GTPase activity of the ras-related rap2 proptein. Biochem Biophys Res Comm 189:455–464

    Google Scholar 

  • Levine AJ, Momand J, Finlay CA (1991) The p53 tumour suppressor gene. Nature 351:453–456

    Google Scholar 

  • Li Y, Bollag G, Clark R, Stevens J, Conroy L, Fults D, Ward K, Friedman E, Samowitz W, Robertson M, Bradley P, McCormick F, White R, Cawthon R (1992) Somatic mutations in the neurofibromatosis-1 gene in human tumors. Cell 69:275–281

    Google Scholar 

  • Low MG, Kincade PW (1985) Phosphatidylinositol is the membrane-anchoring domain of the Thy-1 glycoprotein. Nature 318:62–64

    Google Scholar 

  • Lu X, Park SH, Thompson TC, Lane DP (1992) ras-induced hyperplasia occurs with mutation of p53, but activated ras and myc together can induce carcinoma without p53 mutation. Cell 70:153–161

    Google Scholar 

  • Manfioletti G, Ruaro ME, Del Sal G, Philipson L, Schneider C (1990) A growth arrest-specific (gas) gene codes for a membrane protein. Mol Cell Biol 10:2924–2930

    Google Scholar 

  • Marchuck DA, Saulino AM, Tavakkol R, Swaroop M, Wallace MR, Andersen LB, Mitchell AL, Gutmann DH, Boguski M, Collins FS (1991) cDNA cloning of the type 1 neurofibromatosis gene: complete sequence of the NFl gene product. Genomics 11:931–940

    Google Scholar 

  • Maridonneau-Parini I, de Gunzburg J (1992) Association of rap1 and rap2 proteins with the specific granules of human neutrophils. J Biol Chem 267:6396–6402

    Google Scholar 

  • Marshall CJ (1993) Protein prenylation: a mediator of protein-protein interactions. Science 259:1865–1866

    Google Scholar 

  • Marshall MS, Davis LJ, Keys RD, Mosser SD, Hill WS, Scolnick EM, Gibbs JB (1991) Identification of amino acid residues required for ras p21 target activation. Mol Cell Biol 11:3997–4004

    Google Scholar 

  • Martin GA, Viskochil D, Bollag G, MyCabe PC, Crosier WJ, Haubruck H, Conroy L, Clark R, O'Connell P, Cawthon RM, Innis MA, McCormick F (1990) The GAP-related domain of the neurofibromatosis type 1 gene product interacts with ras p21. Cell 63:843–849

    Google Scholar 

  • Martin GA, Yatani A, Clark R, Conroy L, Polakis P, Brown AM, McCormick F (1992) GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents. Science 255:192–194

    Google Scholar 

  • Matsui Y, Kikuchi A, Kawata M, Kondo J, Teranishi Y, Takai Y (1990) Molecular cloning of smg p21B and identification of smg p21 purified from bovine brain and human platelets as smg p21B. Biochem Biophys Res Comm 166:1010–1016

    Google Scholar 

  • Matsumoto M, Matsutani S, Sugita K, Yoshida H, Hayashi F, Terui Y, Nakai H, Uotani N, Kawamura Y, Matsumoto K, Shoji J, Yoshida T (1992) Depudecin: A novel compound inducing the flat phenotype of NIH3T3 cells doubly transformed by ras-oncogene and srconcogene, produced by Alternaria-Brassicicola. J Antibiot 45:879–885

    Google Scholar 

  • McCormick F (1989) ras GTPase activating protein: Signal transmitter and signal terminator. Cell 56:5–8

    Google Scholar 

  • McCormick F (1993) How receptors turn Ras on. Nature 363:15–16

    Google Scholar 

  • Medema RH, Wubbolts R, Bos JL (1991) Two dominant inhbitory mutants of p21ras interfere with insulin-induced gene expression. Mol Cell Biol 11:5963–5967

    Google Scholar 

  • Michalovitz D, Halevy O, Oren M (1991) p53 mutations: Gains or losses? J Cell Biochem 45:22–29

    Google Scholar 

  • Mitelman F, Heim S (1990) Chromosome abnormalities in cancer. Cancer Detect Prevention 14:527–537

    Google Scholar 

  • Mizuno T, Kaibuchi K, Yamamoto T, Kawamura M, Sakoda T, Fujioka H, Matsuura Y, Takai Y (1991) A stimulatory GDP/GTP-exchange protein for smg p21 is active on the posttranslationally processed form of c-Ki-ras p21 and rho A p21. Proc Natl Acad Sci USA 88:6442–6446

    Google Scholar 

  • Molloy CJ, Bottaro DP, Fleming TP, Marshall MS, Gibbs JB, Aaronson SA (1989) PDGF induction of tyrosine phosphorylation of GTPase activating protein. Nature 342:711–714

    Google Scholar 

  • Molloy CJ, Fleming TP, Bottaro DP, Cuadrado A, Aaronson SA (1992) Platelet-derived growth factor stimulation of GTPase-activating protein tyrosine phosphorylation in control and c-H-ras-expressing NIH 3T3 cells correlates with p21(ras) activation. Mol Cell Biol 12:3903–3909

    Google Scholar 

  • Monia BP, Johnston JF, Ecker DJ, Zounes MA, Lima WF, Freier SM (1992) Selective inhibition of mutant Ha-ras messenger RNA expression by antisense oligonucleotides. J Biol Chem 267:19954–19962

    Google Scholar 

  • Morris A, Clegg C, Jones J, Rodgers B, Avery RJ (1980) The isolation and characterization of a clonally related series of murine retrovirus-infected mouse cells. J Gen Virol 49:105–113

    Google Scholar 

  • Morris RJ (1985) Thy-1 in developing nervous tissue. Dev Neurosci 7:133–160

    Google Scholar 

  • Mulcahy LS, Smith MR, Stacey DW (1985) Requirement for ras proto-oncogene function during serum-stimulated growth of NIH 3T3 cells. Nature 313:241–243

    Google Scholar 

  • Mulder KM, Morris SL (1992) Activation of p21ras by transforming growth factor-beta in epithelial cells. J Biol Chem 267:5029–5031

    Google Scholar 

  • Muleris M, Delattre O, Olschwang S, Dutrillaux A, Remvikos Y, Salmon R, Thomas G, Dutrillaux B (1990) Cytogenetic and molecular approaches of polyploidization in colorectal adenocarcinomas. Cancer Genet Cytogenet 44:107–118

    Google Scholar 

  • Müllauer L, Suzuki H, Fujita H, Katabami M, Kuzumaki N (1991) Identification of genes that exhibit increased expression after flat reversion of NIH/3T3 cells transformed by human activated Ha-ras oncogene. Cancer Lett 59:37–43

    Google Scholar 

  • Nakayasu M, Shima H, Aonuma S, Nakagama H, Nagao M, Sugimura T (1988) Deletion of transfected oncogenes from NIH 3T3 transformants by inhibitors of poly(ADP-ribose) polymerase. Proc Natl Acad Sci USA 85:9066–9070

    Google Scholar 

  • Narayanan R, Lawlor KG, Schaapveld RQJ, Cho KR, Vogelstein B, Tran PBV, Osborne MP, Telang NT (1992) Antisense RNA to the putative tumor-suppressor gene DCC transforms rat-1 fibroblasts. Oncogene 7:553–561

    Google Scholar 

  • Niles RM, Wilhelm SA, Thomas P, Zamcheck N (1988) The effect of sodium butyrate and retinoic acid on growth and CEA production in a series of human colorectal tumor cell lines representing different states of differentiation. Cancer Invest 6:39–45

    Google Scholar 

  • Nishi T, Lee PSY, Oka K, Levin VA, Tanase S, Morino Y, Saya H (1991) Differential expression of two types of the neurofibromatosis type 1 (NF1) gene transcripts related to neuronal differentiation. Oncogene 6:1555–1559

    Google Scholar 

  • Noda M, Selinger Z, Scolnick EM, Bassin RH (1983) Flat revertants isolated from Kirsten sarcoma virus-transformed cells are resistant to the action of specific oncogenes. Proc Natl Acad Sci USA 80:5602–5606

    Google Scholar 

  • Noda M, Ko M, Ogura A, Liu D, Amano T, Takano T, Ikawa Y (1985) Sarcoma viruses carrying ras oncogenes induce differentiation-associated properties in a neuronal cell line. Nature 318:73–75

    Google Scholar 

  • Noda M, Kitayama H, Matsuzaki T, Sugimoto Y, Okayama H, Bassin RH, Ikawa Y (1989) Detection of genes with a potential for suppressing the transformed phenotype associated with activated ras genes. Proc Natl Acad Sci USA 86:162–166

    Google Scholar 

  • Noda M (1990) Expression cloning of tumor suppressor genes: a guide for optimists. Mol Carcinog 3:251–253

    Google Scholar 

  • Nomura T, Ryoyama K, Okada G, Matano S, Nakamura S, Kameyama T (1992) Non-transformed, but not ras/myc-transformed, serum-free mouse embryo cells recover from growth suppression by azatyrosine. Jpn J Cancer Res 83:851–858

    Google Scholar 

  • Nori M, Vogel US, Gibbs JB, Weber MJ (1991) Inhibition of v-src-induced transformation by a GTPase-activating protein. Mol Cell Biol 11:2812–2818

    Google Scholar 

  • Norton JD, Cook F, Roberts PC, Clewley JP, Avery RJ (1984) Expression of Kirsten murine sarcoma virus in transformed nonproducer and revertant NIH/3T3 cells: Evidence for cell-mediated resistance to a viral oncogene in phenotypic reversion. J Virol 50:439–444

    Google Scholar 

  • Nur-E-Kamal MSA, Sizeland A, D'Abaco G, Maruta H (1992) Aparagine 26, glutamic acid 31, valine 45, and tyrosine 64 of ras proteins are required for their oncogenicity. J Biol Chem 267:1415–1418

    Google Scholar 

  • Nur-E-Kamal MSA, Varga M, Maruta H (1993) The GTPase-activating NF1 fragment of 91 amino acids reverses v-Ha-ras-induced malignant phenotype. J Biol Chem 268:22331–22337

    Google Scholar 

  • O'Connell P, Leach R, Cawthon RM, Culver M, Stevens J, Viskochil D, Fournier REK, Rich DC, Ledbetter DH, White R (1989) Two NF1 translocations map within a 600-kilobase segment of 17q11.2. Science 244:1087–1090

    Google Scholar 

  • Ohmori T, Kikuchi A, Yamamoto K, Kim S, Takai Y (1989) Small molecular weight GTP-binding proteins in human platelet membranes. J Biol Chem 264:1877–1881

    Google Scholar 

  • Ohmstede C-A, Farrell FX, Reep BR, Clemetson KJ, Lapetina EG (1990) RAP2B: A RAS-related GTP-binding protein from platelets. Proc Natl Acad Sci USA 87:6527–6531

    Google Scholar 

  • Oshimura M, Gilmer TM, Barrett JC (1985) Nonrandom loss of chromosome 15 in Syrian hamster tumours induced by the v-Ha-ras plus v-myc oncogenes. Nature 316:636–639

    Google Scholar 

  • Ozanne B, Vogel A (1974) Selection of revertants of Kirsten sarcoma virus transformed nonproducer BALB/3T3 cells. J Virol 14:239–248

    Google Scholar 

  • Pan J, Roskelley CD, Luu-The V, Rojiani M, Auersperg N (1992) Reversal of divergent differentiation by ras oncogene-mediated transformation. Cancer Res 52:4269–4272

    Google Scholar 

  • Paterson H, Reeves B, Brown R, Hall A, Furth M, Bos J, Jones P, Marshall C (1987) Activated N-ras controls the transformed phenotype of HT1080 human fibrosarcoma cells. Cell 51:803–812

    Google Scholar 

  • Paterson HF, Self AJ, Garrett MD, Just I, Aktories K, Hall A (1990) Microinjection of recombinant p21rho induces rapid changes in cell morphology. J Cell Biochem 111:1001–1007

    Google Scholar 

  • Pattengale PK, Stewart TA, Leder A, Sinn E, Muller W, Tepler I, Schmidt E, Leder P (1989) Animal models of human disease. Pathology and molecular biology of spontaneous neoplasms occuring in transgenic mice carrying and expressing activated cellular oncogenes. Am J Pathol 135:39–61

    Google Scholar 

  • Peltomäki P, Aaltonen LA, Sistonen P, Pylkkänen L, Mecklin J-P, Järvinen H, Green JS, Jass JR, Weber JL, Leach FS, Petersen GM, Hamilton SR, De la Chapelle A, Vogelstein B (1993) Genetic mapping of a locus predisposing to human colorectal cancer. Science 260:810–812

    Google Scholar 

  • Pizon V, Lerosey I, Chardin P, Tavitian A (1988a) Nucleotide sequence of a human cDNA encoding a ras-related protein (rap1B). Nucleic Acids Res 16:7719

    Google Scholar 

  • Pizon V, Chardin P, Lerosey I, Olofsson B, Tavitian A (1988b) Human cDNAs rap 1 and rap 2 homologous to the Drosophila gene Dras 3 encode proteins closely related to ras in the “effector” region. Oncogene 3:201–204

    Google Scholar 

  • Polakis PG, Rubinfeld B Evans T, McCormick F (1991) Purification of a plasma membrane-associated GTPase-activating protein specific for rap1/Krev-1 from HL 60 cells. Proc Natl Acad Sci USA 88:239–243

    Google Scholar 

  • Ponder B (1990) Neurofibromatosis gene cloned. Nature 346:703–704

    Google Scholar 

  • Pratt CI, Wu SQ, Bhattacharya M, Kao CH, Gilchrist KW, Reznikoff CA (1992) Chromosome losses in tumorigenic revertants of EJ/ras-expressing somatic cell hybrids. Cancer Genet Cytogenet 59:180–190

    Google Scholar 

  • Quilliam LA, Der CJ, Clark R, O'Rourke EC, Zhang K, McCormick FP, Bokoch GM (1990) Biochemical characterization of Baculovirus-expressed rap1A/Krev-1 and its regulation by GTPase-activating protein. Mol Cell Biol 10:2901–2908

    Google Scholar 

  • Quilliam LA, Mueller H, Bohl BP, Prossnitz V, Sklar LA, Der CJ, Bokoch GM (1991) Rap1A is a substrate for cyclic AMP dependent protein kinase in human neutrophils. J Immunol 147:1628–1635

    Google Scholar 

  • Quinn MT, Parkos CA, Walker L, Orkin SH, Dinauer MC, Jesaitis AJ (1989) Association of a Ras-related protein with cytochrome b of human neutrophils. Nature 342:198–200

    Google Scholar 

  • Quinn MT, Mullen ML, Jesaitis AJ, Linner JG (1992) Subcellular distribution of the Rap1A protein in human neutrophils: colocalization and cotranslocation with cytochrome b559. Blood 79:1563–1573

    Google Scholar 

  • Reddy EP, Reynolds RK, Santos E, Barbacid M (1982) A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene. Nature 300:149–152

    Google Scholar 

  • Ridley AJ, Paterson HF, Noble M, Land H (1988) ras-mediated cell cycle arrest is altered by nuclear oncogenes to induce Schwann cell transformation. EMBO J 7:1635–1645

    Google Scholar 

  • Ridley AJ, Hall A (1992) The small GTP-binding protein rho regulates the assembly of focal adhesions and actin stress fibers in response to growth factors. Cell 70:389–399

    Google Scholar 

  • Roberts TM (1992) A signal chain of events. Nature 360:534–535

    Google Scholar 

  • Rousseau-Merck MF, Pizon V, Tavitian A, Berger R (1990) Chromosome mapping of the human RAS-related RAP1A, RAP1B, and RAP2 genes to chromosomes 1p12–13, 12q14, and 13q34, respectively. Cytogenet Cell Genet 53:2–4

    Google Scholar 

  • Rubinfeld B, Munemitsu S, Clark R, Conroy L, Watt K, Crosier WJ, McCormick F, Polakis P (1991) Molecular cloning of a GTPase activating protein specific for the Krev-1 protein p21rap1. Cell 65:1033–1042

    Google Scholar 

  • Rubinfeld B, Crosier WJ, Albert I, Conroy L, Clark R, McCormick F, Polakis P (1992) Localization of the rap1GAP catalytic domain and sites of phosphorylation by mutational analysis. Mol Cell Biol 12:4634–4642

    Google Scholar 

  • Ruch RJ, Madhukar BV, Trosko JE, Klaunig JE (1993) Reversal of ras-induced inhibition of gap-junctional intercellular communication, transformation, and tumorigenesis by lovastatin. Mol Carcinogen 7:50–59

    Google Scholar 

  • Ruley HE (1983) Adenovirus early region 1A enables viral and cellular transforming genes to transform primary cells in culture. Nature 304:602–606

    Google Scholar 

  • Ryan MP, Higgins PJ (1988) Cytoarchitecture of Kirsten sarcoma virus-transformed rat kidney fibroblasts: Butyrate-induced reorganization within the actin microfilament network. J Cell Physiol 137:25–34

    Google Scholar 

  • Ryan MP, Higgins PJ (1989) Sodium-n-butyrate induces secretion and substrate accumulation of p52 in Kirsten sarcoma virus-transformed rat kidney fibroblasts. Int J Biochem 21:31–37

    Google Scholar 

  • Sager R, Tanaka K, Lau CC, Ebina Y, Anisowicz A (1983) Resistance of human cells to tumorigenesis induced by cloned transforming genes. Proc Natl Acad Sci USA 80:7601–7605

    Google Scholar 

  • Sakoda T, Kaibuchi K, Kishi K, Kishida S, Doi K, Hoshino M, Hattori S, Takai Y (1992) smg/rap-1/Krev-1 p21s inhibit the signal pathway to the c-fos promoter/enhancer from c-Ki-ras p21 but not from c-raf-1 kinase in NIH3T3-cells. Oncogene 7:1705–1711

    Google Scholar 

  • Samid D, Flessate DM, Friedman RM (1987) Interferon-induced revertants of ras-transformed cells: Resistance to transformation by specific oncogenes and retransformation by 5-azacytidine. Mol Cell Biol 7:2196–2200

    Google Scholar 

  • Santos E, Martin-Zanca D, Reddy EP, Pierotti MA, Della Porta G, Barbacid M (1984) Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient. Science 223:661–664

    Google Scholar 

  • Satoh T, Endo M, Nakafuku M, Nakamura S, Kaziro Y (1990) Platelet-derived growth factor stimulates formation of active p21ras. GTP complex in Swiss mouse 3T3. Proc Natl Acad Sci USA 87:5993–5997

    Google Scholar 

  • Satoh T, Nakafuku M, Miyajima A, Kaziro Y (1991) Involvement of ras p21 protein in signal transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4. Proc Natl Acad Sci USA 88:3314–3318

    Google Scholar 

  • Satoh T, Nakafuku M, Kaziro Y (1992) Function of Ras as a molecular switch in signal transduction. J Biol Chem 267:24149–24152

    Google Scholar 

  • Schäfer R, Iyer J, Iten E, Nirkko AC (1988) Partial reversion of the taransformed phenotype in HRAS-trasfered tumorigenic cells by transfer of a human gene. Proc Natl Acad Scie USA 85: 1590–1594

    Google Scholar 

  • Schafer WR, Kim R, Sterne R, Thorner J, Kim S-H, Rine J (1989) Genetic and pharmacological suppression of oncogenic mutations in RAS genes of yeast and humans. Science 245:379–385

    Google Scholar 

  • Schafer WR, Rine J (1992) Protein Prenylation: Genes, Enzymes, Targets, and Functions. Annu Rev Genet 30:209–237

    Google Scholar 

  • Schneider C, King RM, Philipson L (1988) Genes specifically expressed at growth arrest of mammalian cells. Cell 54:787–793

    Google Scholar 

  • Seizinger BR, Rouleau GA, Ozelius LJ, Lane AH, Faryniarz AG, Chao MV, Huson S, Korf BR, Parry DM, Pericak-Vance MA, Collins FS, Hobbs WJ, Falcone BG, Iannazzi JA, Roy JC, StGeorge-Hyslop PH, Tanzi RE, Bothwell MA, Upadyaya M, Harper P, Goldstein AE, Hoover DL, Bader JL, Spence MA, Mulvihill JJ, Aylsworth AS, Vance JM, Rossenwasser GOD, Gaskell PC, Roses AD, Martuza RL, Breakefield XO, Gusella JF (1987) Genetic linkage of von Recklinghausen neurofibromatosis to the nerve growth factor receptor gene. Cell 49:589–594

    Google Scholar 

  • Seliger B, Pfizenmaier K, Schäfer R (1991) Short-time treatment with IFN-gamma induces stable reversion of ras transformed mouse fibroblasts. J Virol 65:6307–6311

    Google Scholar 

  • Seremetis S, Inghirami G, Ferrero D, Newcomb EW, Knowles DM, Dotto G-P, Dalla-Favera R (1989) Transformation and plasmacytoid differentiation of EBV-infected human B lymphoblasts by ras oncogenes. Science 243:660–663

    Google Scholar 

  • Sharma S, Schwarte-Waldhoff I, Oberhuber H, Schäfer R (1993) Functional activity of wild-type and mutant p53 transfected into human tumor cell lines carrying activated ras genes. Cell Growth Diff 4:861–869

    Google Scholar 

  • Sharma SV (1992) Melittin resistance: a counterselection for ras transformation. Oncogene 7:193–201

    Google Scholar 

  • Shen WPV, Aldrich TH, Venta-Perez G, Franza BR, Furth ME (1987) Expression of normal and mutant ras proteins in human acute leukemia. Oncogene 1:157–165

    Google Scholar 

  • Shier WT (1979) Activation of high levels of endogenous phospholipase A2 in cultured cells. Proc Natl Acad Sci USA 76:195–199

    Google Scholar 

  • Shih C, Shilo BZ, Goldfarb MP, Dannenberg A, Weinberg RA (1979) Passage of phenotypes of chemically transformed cells via transfection of DNA and chromatin. Proc Natl Acad Sci USA 76:5714–5718

    Google Scholar 

  • Shindo-Okada N, Makabe O, Nagahara H, Nishimura S (1989) Permanent conversion of mouse and human cells transformed by activated ras or raf genes to apparently normal cells by treatment with the antibiotic azatyrosine. Mol Carcinog 2:159–167

    Google Scholar 

  • Shirasawa S, Furuse M, Yokoyama N, Sasazuki T (1993) Altered growth of human colon cancer cell lines disrupted at activated Ki-ras. Science 260:85–88

    Google Scholar 

  • Simon MA, Bowtell DDL, Dodson GS, Laverty TR, Rubin GM (1991) Ras1 and a putative guanine nucleotide exchange factor perform crucial steps in signaling by the sevenless protein tyrosine kinase. Cell 67:701–716

    Google Scholar 

  • Smith MR, DeGudicibus SJ, Stacey DW (1986) Requirement for c-ras proteins during viral oncogene transformation. Nature 320:540–543

    Google Scholar 

  • Spandidos DA, Wilkie NM (1984) Malignant transformation of early passage rodent cells by a single mutated human oncogene. Nature 310:469–475

    Google Scholar 

  • Spandidos DA, Wilkie NW (1988) The normal human H-ras1 gene can act as an onco-suppressor. Br J Cancer 58,Suppl.IX:67–71

    Google Scholar 

  • Stanbridge EJ (1991) Human tumor suppressor genes. Annu Rev Genet 24:615–657

    Google Scholar 

  • Stephenson JR, Reynolds RK, Aaronson SA (1973) Characterization of morphologic revertants of murine and avian sarcoma virus-transformed cells. J Virol 11:218–222

    Google Scholar 

  • Stern PL (1973) Thy-1 alloantigen on mouse and rat fibroblasts. Nature 246:76–78

    Google Scholar 

  • Stevenson M, Volsky DJ (1986) Activated v-myc and v-ras oncogenes do not transform normal human lymphocytes. Mol Cell Biol 6:3410–3417

    Google Scholar 

  • Stoddart JH, Lane MA, Niles RM (1989) Sodium butyrate suppresses the transforming activity of an activated N-ras oncogene in human colon carcinoma cells. Exp Cell Res 184:16–27

    Google Scholar 

  • Sugimoto Y, Ikawa Y, Nakauchi H (1991) Thy-1 as a negative growth regulator in ras-transformed mouse fibroblasts. Cancer Res 51:99–104

    Google Scholar 

  • Sukumar S, Notario V, Martin-Zanca D, Barbacid M (1983) Induction of mammary carcinomas in rats by nitroso-methylurea involves malignant activation of H-ras-1 locus by single point mutations. Nature 306:658–661

    Google Scholar 

  • Suzuki H, Takahashi K, Kubota Y, Shibahara S (1992) Molecular cloning of a cDNA coding for neurofibromatosis type-1 protein isoform lacking the domain related to ras GTPase-activating protein. Biochem Biophys Res Commun 187:984–990

    Google Scholar 

  • Suzuki N, Choe H-R, Nishida Y, Yamawaki-Kataoka Y, Ohnishi S, Tamaoki T, Kataoka T (1990) Leucine-rich repeats and carboxyl terminus are required for interaction of yeast adenylate cyclase with RAS proteins. Proc Natl Acad Sci USA 87:8711–8715

    Google Scholar 

  • Suzuki Y, Suzuki H, Kayama T, Yoshimoto T, Shibahara S (1991) Brain tumors predominantly express the neurofibromatosis type 1 gene transcripts containing the 63 base insert in the region coding for GTPase activating protein-related domain. Biochem Biophys Res Comm 181:955–961

    Google Scholar 

  • Talbot N, Tagliaferri P, Yanagihara K, Rhim JS, Bassin RH, Benade LE (1988) A ph-dependent differential cytotoxicity of ouabain for human cells transformed by certain oncogenes. Oncogene 3:23–26

    Google Scholar 

  • Tanaka K, Matsumoto K, Toh-e A (1989) IRA1, an inhibitory regulator of the RAS-cyclic AMP pathway in Saccharomyces cerevisiae. Mol Cell Biol 9:757–768

    Google Scholar 

  • Tanaka K, Nakafuku M, Tamanoi F, Kaziro Y, Matsumoto K, Toh-e A (1990a) IRA2, a second gene of Saccharomyces cerevisiae that encodes a protein with a domain homologous to mammalian ras GTPase-activating protein. Mol Cell Biol 10:4303–4313

    Google Scholar 

  • Tanaka K, Nakafuku M, Satoh T, Marshall MS, Gibbs JB, Matsumoto K, Kaziro Y, Toh-e A (1990b) S. cerevisiae genes IRA1 and IRA2 encode proteins that may be functionally equivalent to mammalian ras GTPase activating protein. Cell 60:803–807

    Google Scholar 

  • Tanaka K, Lin BK, Wood DR, Tamanoi F (1991) IRA2, an upstream negative regulator of RAS in yeast, is a RAS GTPase-activating protein. Proc Natl Acad Sci USA 88:468472

    Google Scholar 

  • Teinturier C, Danglot G, Slim R, Pruliere D, Launay JM, Bernheim A (1992) The neurofibromatosis-1 gene transcripts expressed in peripheral nerve and neurofibromas bear the additional exon located in the GAP domain. Biochem Biophys Res Commun 188:851–857

    Google Scholar 

  • The I, Murthy AE, Hannigan GE, Jacoby LB, Menon AG, Gusella JF, Bernards A (1993) Neurofibromatosis type 1 gene mutations in neuroblastoma. Nature Genet 3:62–66

    Google Scholar 

  • Thompson TC, Southgate J, Kitchener G, Land H (1989) Multistage carcinogenesis induced by ras and myc oncogenes in a reconstituted organ. Cell 56:917–930

    Google Scholar 

  • Torti M, Marti KB, Altschuler D, Yamamoto K, Lapetina EG (1992) Erythropoietin induces p21ras activation and p120GAP tyrosine phosphorylation in human erythroleukemia cells. J Biol Chem 267:8293–8298

    Google Scholar 

  • Trackman PC, Pratt AM, Wolanski A, Tang S-S, Offner GD, Troxler RF, Kagan HM (1990) Cloning of rat aorta lysyl oxidase cDNA: Complete codons and predicted amino acid sequence. Biochemistry 29:4863–4870

    Google Scholar 

  • Trahey M, McCormick F (1987) A cytoplasmic protein stimulates normal N-ras p21 GTPase, but does not affect oncogenic mutants. Science 238:542–545

    Google Scholar 

  • Trahey M, Wong G, Halenbeck R, Rubinfeld B, Martin GA, Ladner M, Long CM, Crosier WJ, Watt K, Koths K, McCormick F (1988) Molecular cloning of two types of GAP complementary DNA from human placenta. Science 242:1697–1700

    Google Scholar 

  • Tsai M-H, Yu C-L, Stacey DW (1990) A cytoplasmic protein inhibits the GTPase activity of H-ras in a phospholipid-dependent manner. Science 250:982–985

    Google Scholar 

  • Tse AGD, Barclay AN, Watts A, Williams AF (1985) A glycophospholipid tail at the carboxy terminus of the Thy-1 glycoprotein of neurons and thymocytes. Science 230:1003–1008

    Google Scholar 

  • Tucker RF, Butterfield CE, Folkman J (1981) Interaction of serum and cell spreading affects the growth of neoplastic and nonneoplastic fibroblasts. J Supramol Struct Cell Biochem 15:29–40

    Google Scholar 

  • Viskochil D, Buchberg AM, Xu G, Cawthon RM, Stevens J, Wolff RK, Culver M, Carey JC, Copeland NG, Jenkins NA, White R, O'Connell P (1990) Deletions and a translocation interrupt a cloned gene at the neurofibromatosis type 1 locus. Cell 62:187–192

    Google Scholar 

  • Vogel A, Pollack R (1974) Isolation and characterization of revertant cell lines. VI. Susceptibility of revertants to retransformation by simian virus 40 and murine sarcoma virus. J Virol 14:1404–1410

    Google Scholar 

  • Vogel US, Dixon RAF, Schaber MD, Diehl RE, Marshall MS, Scolnick EM, Sigal IS, Gibbs JB (1988) Cloning of bovine GAP and its interaction with oncogenic ras p21. Nature 335:90–93

    Google Scholar 

  • Vogelstein B, Fearon ER, Hamilton SR, Kern SE, Preisinger AC, Leppert M, Nakamura Y, White R, Smits AMM, Bos JL (1988) Genetic alterations during colorectal-tumor development. N Engl J Med 319:526–532

    Google Scholar 

  • Vogt M, Lesley J, Bogenberger J, Volkman S, Haas M (1986) Coinfection with viruses carrying the v-Ha-ras and v-myc oncogenes lead to growth factor independence by an indirect mechanism. Mol Cell Biol 6:3545–3549

    Google Scholar 

  • Wallace MR, Marchuk DA, Andersen LB, Letcher R, Odeh HM, Saulino AM, Fountain JW, Brereton A, Nicholson J, Mitchell AL, Brownstein BH, Collins FS (1990) Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients. Science 249:181–186

    Google Scholar 

  • Wang S-Y, Bassin RH, Racker E (1988) Effect of high K+ hypertonicity and ouabain on MeAIB uptake and on growth of c-myc and v-ras transfected rat fibroblasts. Oncogene 3:53–57

    Google Scholar 

  • Whitman M, Melton DA (1992) Involvement of p21ras in Xenopus mesoderm induction. Nature 357:252–254

    Google Scholar 

  • Williams AF (1985) Immunoglobulin-related domains for cell surface recognition. Nature 314:579–580

    Google Scholar 

  • Wilson DM, Yang D, Dillberger JE, Dietrich SE, Maher VM, McCormick JJ (1990) Malignant transformation of human fibroblasts by a transfected N-ras oncogene. Cancer Res 50:5587–5593

    Google Scholar 

  • Winter E, Yamamoto F, Almoguera C, Perucho M (1985) A method to detect and characterize point mutations in transcribed genes: amplification and overexpression of the mutant c-Ki-ras allele in human tumors. Proc Natl Acad Sci USA 82:7575–7579

    Google Scholar 

  • Wisdom R, Verma IM (1990) Revertants of v-fos-transformed rat fibroblasts: suppression of transformation is dominant. Mol Cell Biol 10:5626–5633

    Google Scholar 

  • Xu G, Lin B, Tanaka K, Dunn D, Wod D, Gesteland R, White R, Weiss R, Tamanoi F (1990a) The catalytic domain of the neurofibromatosis type 1 gene product stimulates ras GTPase and complements ira mutants of S. cerevisiae. Cell 63:835–841

    Google Scholar 

  • Xu G, O'Connell P, Viskochil D, Cawthon R, Robertson M, Culver M, Dunn D, Stevens J, Gesteland R, White R, Weiss R (1990b) The neurofibromatosis type 1 gene encodes a protein related to GAP. Cell 62:599–608

    Google Scholar 

  • Yagle MK, Parruti G, Yu W, Ponder BAJ, Solomon E (1990) Genetic and physical map of the von Recklinghausen neurofibromatosis (NF1) region on chromosome 17. Proc Natl Acad Sci USA 87:7255–7259

    Google Scholar 

  • Yamada H, Horikawa I, Hashiba H, Oshimura M (1990a) Normal human chromosome 1 carries suppressor activity for various phenotypes of a Kirsten murine sarcoma virustransformed NIH/3T3 cell line. Jpn J Cancer Res 81:1095–1100

    Google Scholar 

  • Yamada H, Omata-Yamada T, Wakabayashi-Ito N, Carter SG, Lengyel P (1990b) Isolation of recessive (mediator-) revertants from NIH 3T3 cells transformed with a c-Ha-ras oncogene. Mol Cell Biol 10:1822–1827

    Google Scholar 

  • Yamamoto T, Kaibuchi K, Mizuno T, Hiroyoshi M, Shirataki H, Takai Y (1990) Purification and characterization from bovine brain cytosol of proteins that regulate the GDP/GTP exchange reaction of smg p21s, ras p21-like GTP-binding proteins. J Biol Chem 265:16626–16634

    Google Scholar 

  • Yamasaki H (1991) Aberrant expression and function of gap junctions during carcinogenesis. Environ Health Perspect 93:191–197

    Google Scholar 

  • Yanagihara K, Ciardiello F, Talbot N, McGready ML, Cooper H, Benade L, Salmon DS, Bassin RH (1990) Isolation of a new class of “flat” revertants from ras-transformed NIH3T3 cells using cis-4-hydroxy-L-proline. Oncogene 5:1179–1186

    Google Scholar 

  • Yatani A, Okabe K, Polakis P, Halenbeck R, McCormick F, Brown AM (1990) Ras p21 and GAP inhibit coupling of muscarinic receptors to atrial K+ channels. Cell 61:769–776

    Google Scholar 

  • Yatani A, Quilliam LA, Brown AM, Bokoch GM (1991) Rap1A antagonizes the ability of ras and ras-GAP to inhibit muscarinic K+ channels. J Biol Chem 266:22222–22226

    Google Scholar 

  • Yoshida Y, Kawata M, Miura Y, Musha T, Sasaki T, Kikuchi A, Takai Y (1992) Microinjection of smg/rap1/Krev-1 p21 into Swiss 3T3-cells induces DNA synthesis and morphological changes. Mol Cell Biol 12:3407–3414

    Google Scholar 

  • Young J, Searle J, Stitz R, Cowen A, Ward M, Chenevix-Trench G (1992) Loss of heterozygosity at the human RAP1A/Krev-1 locus is a rare event in colorectal tumors. Cancer Res 52:285–289

    Google Scholar 

  • Zambetti GP, Olson D, Labow M, Levine AJ (1992) A mutant p53 protein is required for maintenance of the transformed phenotype in cells transformed with p53 plus ras cDNAs. Proc Natl Acad Sci USA 89:3952–3956

    Google Scholar 

  • Zarbl H, Sukumar S, Arthur AV, Martin-Zanca D, Barbacid M (1985) Direct mutagenesis of Ha-ras-1 oncogenes by N-nitroso-N-methylurea during initiation of mammary carcinogenesis in rats. Nature 315:382–385

    Google Scholar 

  • Zarbl H, Latreille J, Jolicoeur P (1987) Revertants of v-fos-transformed fibroblasts have mutations in cellular genes essential for transformation by other oncogenes. Cell 51:357–369

    Google Scholar 

  • Zhang K, Noda M, Vass WC, Papageorge AG, Lowy DR (1990) Identification of small clusters of divergent amino acids that mediate the opposing effects of ras and Krev-1. Science 249:162–165

    Google Scholar 

  • Zucker S, Lysik RM, Malik M, Bauer BA, Caamano J, Kleinszanto AJP (1992) Secretion of gelatinases and tissue inhibitors of metalloproteinases by human lung cancer cell lines and revertant cell lines: not an invariant correlation with metastasis. Int J Cancer 52:366–371

    Google Scholar 

References

  • Brown PH, Alani R, Preis LH, Szabo E, Birrer MJ (1993) Suppression of Oncogene-Induced Transformation by a Deletion Mutant of c-jun. Oncogene 8:877–886

    Google Scholar 

  • Müllauer L, Fujita H, Ishizaki A, Kuzumaki N (1993) Tumor-suppressive function of mutated gelsolin in ras-transformed cells. Oncogene 8:2531–2536

    Google Scholar 

  • Prasad GL, Fuldner RA, Cooper HL (1993) Expression of Transduced Tropomyosin-1 cDNA Suppresses Neoplastic Growth of Cells Transformed by the ras Oncogene. Proc Natl Acad Sci USA 90:7039–7043

    Google Scholar 

  • Yehiely F, Oren M (1992) The gene for the rat heat-shock cognate, hsc70, can suppress oncogene-mediated transformation. Cell Growth Differ 3:803–809

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

Copyright information

© 1994 Springer-Verlag

About this chapter

Cite this chapter

Schäfer, R. (1994). Suppression of ras oncogene-mediated transformation. In: Reviews of Physiology, Biochemistry and Pharmacology, Volume 124. Reviews of Physiology, Biochemistry and Pharmacology, vol 124. Springer, Berlin, Heidelberg. https://doi.org/10.1007/BFb0031031

Download citation

  • DOI: https://doi.org/10.1007/BFb0031031

  • Published:

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-57587-0

  • Online ISBN: 978-3-540-48280-2

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics