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Journal Abstract Search

68 related items for PubMed ID: 1532247

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  • 7. Transformation-resistant mos revertant is unable to activate MAP kinase kinase in response to v-mos or v-raf.
    Topol LZ, Marx M, Calothy G, Blair DG.
    Cell Growth Differ; 1995 Jan; 6(1):27-38. PubMed ID: 7718484
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  • 8. Phosphorylation of v-mos Ser 47 by the mitotic form of p34cdc2.
    Bai WL, Singh B, Karshin WL, Shonk RA, Arlinghaus RB.
    Oncogene; 1991 Oct; 6(10):1715-23. PubMed ID: 1833715
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  • 9. The proteins encoded by c-akt and v-akt differ in post-translational modification, subcellular localization and oncogenic potential.
    Ahmed NN, Franke TF, Bellacosa A, Datta K, Gonzalez-Portal ME, Taguchi T, Testa JR, Tsichlis PN.
    Oncogene; 1993 Jul; 8(7):1957-63. PubMed ID: 8510938
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  • 10. Characterization of activated and normal mouse Mos gene in murine 3T3 cells.
    Paules RS, Resnick J, Kasenally AB, Ernst MK, Donovan P, Vande Woude GF.
    Oncogene; 1992 Dec; 7(12):2489-98. PubMed ID: 1461652
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  • 11. v-Rel and c-Rel are differentially affected by mutations at a consensus protein kinase recognition sequence.
    Mosialos G, Gilmore TD.
    Oncogene; 1993 Mar; 8(3):721-30. PubMed ID: 8437855
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  • 12. Mutations in the v-mos gene abolish its ability to induce differentiation but not transformation.
    Kurata N, Akiyama H, Hosoya H, Aoki H, Ishikawa K, Marunouchi T.
    Eur J Cell Biol; 1995 Sep; 68(1):55-61. PubMed ID: 8549590
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  • 14. Ability of the c-mos product to associate with and phosphorylate tubulin.
    Zhou RP, Oskarsson M, Paules RS, Schulz N, Cleveland D, Vande Woude GF.
    Science; 1991 Feb 08; 251(4994):671-5. PubMed ID: 1825142
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  • 19. Mutagenic analysis of functional domains of the mos proto-oncogene and identification of the sites important for MAPK activation and DNA binding.
    Fukasawa K, Zhou R, Matten WT, Armstrong AJ, Daar I, Oskarsson M, Sathyanarayana BK, Maclvor L, Wood TG, Vande Woude GF.
    Oncogene; 1995 Oct 19; 11(8):1447-57. PubMed ID: 7478569
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