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Journal Abstract Search

124 related items for PubMed ID: 3071519

  • 1. [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; 63(5):747-53. PubMed ID: 3071519
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  • 3. [Identification of a specific protein in flat revertant cell lines derived from ras oncogene-transformed cells].
    Fujita H.
    Hokkaido Igaku Zasshi; 1990 Mar; 65(2):210-20. PubMed ID: 2194920
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  • 5. Thy-1 as a negative growth regulator in ras-transformed mouse fibroblasts.
    Sugimoto Y, Ikawa Y, Nakauchi H.
    Cancer Res; 1991 Jan 01; 51(1):99-104. PubMed ID: 1670996
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  • 7. NIH-3T3 cells transformed by the EJ-ras oncogene exhibit reduced platelet-derived growth factor-mediated Ca2+ mobilization.
    Benjamin CW, Connor JA, Tarpley WG, Gorman RR.
    Proc Natl Acad Sci U S A; 1988 Jun 01; 85(12):4345-9. PubMed ID: 3288991
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  • 10. Cyclic AMP-dependent protein kinases from Balb 3T3 cells and other 3T3 derived lines.
    Wehner JM, Malkinson AM, Wiser MF, Sheppard JR.
    J Cell Physiol; 1981 Aug 01; 108(2):175-84. PubMed ID: 6267082
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  • 11. Cyclic AMP can partially restore platelet-derived growth factor-stimulated prostaglandin E2 biosynthesis, and calcium mobilization in EJ-ras-transformed NIH-3T3 cells.
    Olinger PL, Benjamin CW, Gorman RR, Connor JA.
    J Cell Physiol; 1989 May 01; 139(2):335-45. PubMed ID: 2541140
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  • 12. Transformation of NIH/3T3 to anchorage independence by H-ras is accompanied by loss of suppressor activity.
    Tolsma SS, Cohen JD, Ehrlich LS, Bouck NP.
    Exp Cell Res; 1993 Apr 01; 205(2):232-9. PubMed ID: 8482334
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  • 13. 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
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  • 14. 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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  • 15. The effect of n-6 fatty acids on normal and v-Ki ras transformed NIH-3T3 cells.
    Cantrill RC, Ells GW, de Antueno RJ, Elliot M, Raha SK, Horrobin DF.
    Anticancer Res; 1992 Apr 01; 12(6B):2197-201. PubMed ID: 1338278
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  • 16. 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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  • 17. Reduced induction of c-fos but not of c-myc expressions in a nontumorigenic revertant R1 of Ej-ras-transformed NIH/3T3 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA).
    Suzuki H, Fujita H, Ogiso Y, Oda A, Kuzumaki N, Uchino J.
    Exp Cell Res; 1989 Oct 26; 184(2):524-8. PubMed ID: 2509225
    [Abstract] [Full Text] [Related]

  • 18. 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
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  • 19. Cell-free system studies on the phosphorylation of the 17,000-20,000 dalton protein induced by phorbol ester in human leukemic cells and evidence for a similar event in virally transformed murine fibroblasts.
    Feuerstein N, Nishikawa M, Cooper HL.
    Cancer Res; 1985 Jul 01; 45(7):3243-51. PubMed ID: 3159476
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  • 20. 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
    [Abstract] [Full Text] [Related]

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