Resultados da busca - Richard A. Van Etten

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  1. 1
    Aberrant cytokine signaling in leukemia

    Aberrant cytokine signaling in leukemia por Richard A. Van Etten

    Publicado em 2007
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  2. 2
    Cycling, stressed-out and nervous: cellular functions of c-Abl

    Cycling, stressed-out and nervous: cellular functions of c-Abl por Richard A. Van Etten

    Publicado em 1999
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  3. 3
    Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era

    Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era por Richard A. Van Etten

    Publicado em 2003
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  4. 4
    c-Abl Has High Intrinsic Tyrosine Kinase Activity That Is Stimulated by Mutation of the Src Homology 3 Domain and by Autophosphorylation at Two Distinct Regulatory Tyrosines

    c-Abl Has High Intrinsic Tyrosine Kinase Activity That Is Stimulated by Mutation of the Src Homology 3 Domain and by Autophosphorylation at Two Distinct Regulatory Tyrosines por Bradley Brasher, Richard A. Van Etten

    Publicado em 2000
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  5. 5
    Focus on myeloproliferative diseases and myelodysplastic syndromes

    Focus on myeloproliferative diseases and myelodysplastic syndromes por Richard A. Van Etten, Kevin Shannon

    Publicado em 2004
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  6. 6
    P210 and P190 Induce the Tyrosine Phosphorylation and DNA Binding Activity of Multiple Specific STAT Family Members

    P210 and P190 Induce the Tyrosine Phosphorylation and DNA Binding Activity of Multiple Specific STAT Family Members por Robert Ilaria, Richard A. Van Etten

    Publicado em 1996
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  7. 7
    Right on target: eradicating leukemic stem cells

    Right on target: eradicating leukemic stem cells por Daniela S. Krause, Richard A. Van Etten

    Publicado em 2007
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  8. 8
    Tyrosine Kinases as Targets for Cancer Therapy

    Tyrosine Kinases as Targets for Cancer Therapy por Daniela S. Krause, Richard A. Van Etten

    Publicado em 2005
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  9. 9
    IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1

    IKK-dependent activation of NF-κB contributes to myeloid and lymphoid leukemogenesis by BCR-ABL1 por Mo-Ying Hsieh, Richard A. Van Etten

    Publicado em 2014
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  10. 10
    The <i>PAG</i> gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity

    The <i>PAG</i> gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity por Shih-Te Wen, Richard A. Van Etten

    Publicado em 1997
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  11. 11
    The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase

    The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase por Ryan P. Million, Richard A. Van Etten

    Publicado em 2000
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  12. 12
    Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation

    Dominant Negative Mutants Implicate STAT5 in Myeloid Cell Proliferation and Neutrophil Differentiation por Robert Ilaria, Robert G. Hawley, Richard A. Van Etten

    Publicado em 1999
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  13. 13
    Autoinhibition of Bcr-Abl through Its SH3 Domain

    Autoinhibition of Bcr-Abl through Its SH3 Domain por Kristen M. Smith, Rinat Yacobi, Richard A. Van Etten

    Publicado em 2003
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  14. 14
    Induction of Chronic Myelogenous Leukemia in Mice by the P210 <sup> <i>bcr/abl</i> </sup> Gene of the Philadelphia Chromosome

    Induction of Chronic Myelogenous Leukemia in Mice by the P210 <sup> <i>bcr/abl</i> </sup> Gene of the Philadelphia Chromosome por George Q. Daley, Richard A. Van Etten, David Baltimore

    Publicado em 1990
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  15. 15
    The mouse type IV c-abl gene product is a nuclear protein, and activation of transforming ability is associated with cytoplasmic localization

    The mouse type IV c-abl gene product is a nuclear protein, and activation of transforming ability is associated with cytoplasmic localization por Richard A. Van Etten, Peter K. Jackson, David Baltimore

    Publicado em 1989
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  16. 16
    Blast crisis in a murine model of chronic myelogenous leukemia.

    Blast crisis in a murine model of chronic myelogenous leukemia. por G Q Daley, Richard A. Van Etten, David Baltimore

    Publicado em 1991
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  17. 17
    The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products.

    The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products. por Shih-Te Wen, Peter K. Jackson, Richard A. Van Etten

    Publicado em 1996
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  18. 18
    Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling

    Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling por Shaoguang Li, Anthony D. Couvillon, Bradley Brasher, Richard A. Van Etten

    Publicado em 2001
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  19. 19
    Point mutations in the abl SH2 domain coordinately impair phosphotyrosine binding in vitro and transforming activity in vivo.

    Point mutations in the abl SH2 domain coordinately impair phosphotyrosine binding in vitro and transforming activity in vivo. por Bruce J. Mayer, Peter K. Jackson, Richard A. Van Etten, David Baltimore

    Publicado em 1992
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  20. 20
    The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase

    The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosp... por S. A. Roumiantsev, Isabel E. de Aos, Lyuba Varticovski, Robert Ilaria, Richard A. Van Etten

    Publicado em 2001
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