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158 related items for PubMed ID: 7693563

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  • 4. Elevated gelsolin and alpha-actin expression in a flat revertant R1 of Ha-ras oncogene-transformed NIH/3T3 cells.
    Müllauer L, Fujita H, Suzuki H, Katabami M, Hitomi Y, Ogiso Y, Kuzumaki N.
    Biochem Biophys Res Commun; 1990 Sep 14; 171(2):852-9. PubMed ID: 2169737
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  • 6. Identification of genes that exhibit increased expression after flat reversion of NIH/3T3 cells transformed by human activated Ha-ras oncogene.
    Müllauer L, Suzuki H, Fujita H, Katabami M, Kuzumaki N.
    Cancer Lett; 1991 Jul 26; 59(1):37-43. PubMed ID: 1878859
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  • 7. [Involvement of cAMP dependent protein kinase in the reversion of a NIH/3T3 cell line transformed by a ras oncogene (EJ-NIH/3T3)].
    Oda A.
    Hokkaido Igaku Zasshi; 1988 Sep 26; 63(5):747-53. PubMed ID: 3071519
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  • 8. Growth-inhibitory functions of a mutated gelsolin (His321) in NIH/3T3 mouse fibroblasts.
    Ishizaki A, Fujita H, Kuzumaki N.
    Exp Cell Res; 1995 Apr 26; 217(2):448-52. PubMed ID: 7698245
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  • 9. [A study on reversion of the human activated c-Ha-ras-transformed cells].
    Ogiso Y.
    Hokkaido Igaku Zasshi; 1988 Sep 26; 63(5):687-97. PubMed ID: 3071518
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  • 10. Functions of [His321]gelsolin isolated from a flat revertant of ras-transformed cells.
    Fujita H, Laham LE, Janmey PA, Kwiatkowski DJ, Stossel TP, Banno Y, Nozawa Y, Müllauer L, Ishizaki A, Kuzumaki N.
    Eur J Biochem; 1995 May 01; 229(3):615-20. PubMed ID: 7758454
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  • 11. Cytoskeletal reorganization in NIH 3T3 fibroblasts expressing the ras oncogene.
    Dartsch PC, Ritter M, Häussinger D, Lang F.
    Eur J Cell Biol; 1994 Apr 01; 63(2):316-25. PubMed ID: 8082656
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  • 12. Sorting of tropomyosin isoforms in synchronised NIH 3T3 fibroblasts: evidence for distinct microfilament populations.
    Percival JM, Thomas G, Cock TA, Gardiner EM, Jeffrey PL, Lin JJ, Weinberger RP, Gunning P.
    Cell Motil Cytoskeleton; 2000 Nov 01; 47(3):189-208. PubMed ID: 11056521
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  • 13. Resistance to apoptosis induced by alkylating agents in v-Ha-ras-transformed cells due to defect in p53 function.
    Kuo ML, Chou YW, Chau YP, Huang TS.
    Mol Carcinog; 1997 Apr 01; 18(4):221-31. PubMed ID: 9142217
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  • 14. Fibroblasts transformed by different ras oncogenes show dissimilar patterns of protease gene expression and regulation.
    Zhang JY, Schultz RM.
    Cancer Res; 1992 Dec 01; 52(23):6682-9. PubMed ID: 1423314
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  • 15. Ultrastructural cytoskeleton alterations and modification of actin expression in the NIH/3T3 cell line after transformation with Ha-ras-activated oncogene.
    Lombardi L, Ballinari D, Bongarzone I, Migliari M, Mondellini P, Traversari C, Modina S.
    Cell Motil Cytoskeleton; 1990 Dec 01; 15(4):220-9. PubMed ID: 1692516
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  • 16. Resistance to oncogenic transformation in revertant R1 of human ras-transformed NIH 3T3 cells.
    Kuzumaki N, Ogiso Y, Oda A, Fujita H, Suzuki H, Sato C, Müllauer L.
    Mol Cell Biol; 1989 May 01; 9(5):2258-63. PubMed ID: 2664473
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  • 17. Increased cell-substrate adhesion accompanies conditional reversion to the normal phenotype in ras-oncogene-transformed NIH-3T3 cells.
    Shumaker DK, Sklar MD, Prochownik EV, Varani J.
    Exp Cell Res; 1994 Oct 01; 214(2):440-6. PubMed ID: 7925639
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  • 18. Induction of p202, a modulator of apoptosis, during oncogenic transformation of NIH 3T3 cells by activated H-Ras (Q61L) contributes to cell survival.
    Xin H, Geng Y, Pramanik R, Choubey D.
    J Cell Biochem; 2003 Jan 01; 88(1):191-204. PubMed ID: 12461788
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  • 19. Decreased retinoylation in NIH 3T3 cells transformed with activated Ha-ras.
    Takahashi N, De Luca LM, Breitman TR.
    Biochem Biophys Res Commun; 1997 Oct 09; 239(1):80-4. PubMed ID: 9345273
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  • 20. Transforming growth factor-beta 1 induces collagen IV gene expression in NIH-3T3 cells.
    Grande J, Melder D, Zinsmeister A, Killen P.
    Lab Invest; 1993 Oct 09; 69(4):387-95. PubMed ID: 8231107
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