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182 related items for PubMed ID: 1992343

  • 1. Raf-1 protein kinase is required for growth of induced NIH/3T3 cells.
    Kolch W, Heidecker G, Lloyd P, Rapp UR.
    Nature; 1991 Jan 31; 349(6308):426-8. PubMed ID: 1992343
    [Abstract] [Full Text] [Related]

  • 2. Differential regulation of the p72-74 RAF-1 kinase in 3T3 fibroblasts expressing ras or src oncogenes.
    Reed JC, Yum S, Cuddy MP, Turner BC, Rapp UR.
    Cell Growth Differ; 1991 May 31; 2(5):235-43. PubMed ID: 1888699
    [Abstract] [Full Text] [Related]

  • 3. Raf revertant cells resist transformation by non-nuclear oncogenes and are deficient in the induction of early response genes by TPA and serum.
    Kolch W, Heidecker G, Troppmair J, Yanagihara K, Bassin RH, Rapp UR.
    Oncogene; 1993 Feb 31; 8(2):361-70. PubMed ID: 8426742
    [Abstract] [Full Text] [Related]

  • 4. Rit, a non-lipid-modified Ras-related protein, transforms NIH3T3 cells without activating the ERK, JNK, p38 MAPK or PI3K/Akt pathways.
    Rusyn EV, Reynolds ER, Shao H, Grana TM, Chan TO, Andres DA, Cox AD.
    Oncogene; 2000 Sep 28; 19(41):4685-94. PubMed ID: 11032018
    [Abstract] [Full Text] [Related]

  • 5. H-ras and raf-1 cooperate in transformation of NIH3T3 fibroblasts.
    Cuadrado A, Bruder JT, Heidaran MA, App H, Rapp UR, Aaronson SA.
    Oncogene; 1993 Sep 28; 8(9):2443-8. PubMed ID: 8361757
    [Abstract] [Full Text] [Related]

  • 6. SCH 51344 inhibits ras transformation by a novel mechanism.
    Kumar CC, Prorock-Rogers C, Kelly J, Dong Z, Lin JJ, Armstrong L, Kung HF, Weber MJ, Afonso A.
    Cancer Res; 1995 Nov 01; 55(21):5106-17. PubMed ID: 7585559
    [Abstract] [Full Text] [Related]

  • 7. Angiotensin II type 1 receptor signals through Raf-1 by a protein kinase C-dependent, Ras-independent mechanism.
    Arai H, Escobedo JA.
    Mol Pharmacol; 1996 Sep 01; 50(3):522-8. PubMed ID: 8794890
    [Abstract] [Full Text] [Related]

  • 8. Ornithine decarboxylase induction in transformation by H-Ras and RhoA.
    Shantz LM, Pegg AE.
    Cancer Res; 1998 Jul 01; 58(13):2748-53. PubMed ID: 9661886
    [Abstract] [Full Text] [Related]

  • 9. PKC epsilon functions as an oncogene by enhancing activation of the Raf kinase.
    Cacace AM, Ueffing M, Philipp A, Han EK, Kolch W, Weinstein IB.
    Oncogene; 1996 Dec 19; 13(12):2517-26. PubMed ID: 9000126
    [Abstract] [Full Text] [Related]

  • 10. Protein kinase C-epsilon associates with the Raf-1 kinase and induces the production of growth factors that stimulate Raf-1 activity.
    Ueffing M, Lovrić J, Philipp A, Mischak H, Kolch W.
    Oncogene; 1997 Dec 11; 15(24):2921-7. PubMed ID: 9416835
    [Abstract] [Full Text] [Related]

  • 11. Transformation by Raf and other oncogenes renders cells differentially sensitive to growth inhibition by a dominant negative c-jun mutant.
    Rapp UR, Troppmair J, Beck T, Birrer MJ.
    Oncogene; 1994 Dec 11; 9(12):3493-8. PubMed ID: 7970709
    [Abstract] [Full Text] [Related]

  • 12. Retroviral gene transfer of dominant negative raf-1 mutants suppresses ha-ras-induced transformation and delays tumor formation.
    Heinicke T, Radziwill G, Nawrath M, Rommel C, Pavlovic J, Moelling K.
    Cancer Gene Ther; 2000 May 11; 7(5):697-706. PubMed ID: 10830717
    [Abstract] [Full Text] [Related]

  • 13. Raf-1 protein is required for growth factor-induced proliferation of primitive hematopoietic progenitors stimulated with synergistic combinations of cytokines.
    Muszynski KW, Ruscetti FW, Gooya JM, Linnekin DM, Keller JR.
    Stem Cells; 1997 May 11; 15(1):63-72. PubMed ID: 9007224
    [Abstract] [Full Text] [Related]

  • 14. A modest reduction in c-myc expression has minimal effects on cell growth and apoptosis but dramatically reduces susceptibility to Ras and Raf transformation.
    Bazarov AV, Adachi S, Li SF, Mateyak MK, Wei S, Sedivy JM.
    Cancer Res; 2001 Feb 01; 61(3):1178-86. PubMed ID: 11221849
    [Abstract] [Full Text] [Related]

  • 15. Raf-1 kinase and ERK2 uncoupled from mitogenic signals in rat fibroblasts.
    Kortenjann M, Shaw PE.
    Oncogene; 1995 Nov 16; 11(10):2105-12. PubMed ID: 7478530
    [Abstract] [Full Text] [Related]

  • 16. High-intensity Raf signals convert mitotic cell cycling into cellular growth.
    Kerkhoff E, Rapp UR.
    Cancer Res; 1998 Apr 15; 58(8):1636-40. PubMed ID: 9563474
    [Abstract] [Full Text] [Related]

  • 17. Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C.
    Kaibuchi K, Fukumoto Y, Oku N, Hori Y, Yamamoto T, Toyoshima K, Takai Y.
    J Biol Chem; 1989 Dec 15; 264(35):20855-8. PubMed ID: 2556385
    [Abstract] [Full Text] [Related]

  • 18. Both v-Ha-Ras and v-Raf stimulate expression of the vascular endothelial growth factor in NIH 3T3 cells.
    Grugel S, Finkenzeller G, Weindel K, Barleon B, Marmé D.
    J Biol Chem; 1995 Oct 27; 270(43):25915-9. PubMed ID: 7592779
    [Abstract] [Full Text] [Related]

  • 19. Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene.
    Ledwith BJ, Manam S, Kraynak AR, Nichols WW, Bradley MO.
    Mol Cell Biol; 1990 Apr 27; 10(4):1545-55. PubMed ID: 1690847
    [Abstract] [Full Text] [Related]

  • 20. Raf-1 protein kinase is an integral component of the oncogenic signal cascade shared by epidermal growth factor and platelet-derived growth factor.
    Kizaka-Kondoh S, Sato K, Tamura K, Nojima H, Okayama H.
    Mol Cell Biol; 1992 Nov 27; 12(11):5078-86. PubMed ID: 1406683
    [Abstract] [Full Text] [Related]

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