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C-Jun

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Michael J. Birrer – 1st expert on this subject based on the ideXlab platform

  • Cyclin a is a C-Jun target gene and is necessary for C-Jun-induced anchorage-independent growth in RAT1a cells
    Journal of Biological Chemistry, 2005
    Co-Authors: Motoo Katabami, Howard Donninger, Fumihiro Hommura, Virna D. Leaner, Ichiro Kinoshita, Jeffrey F. B. Chick, Michael J. Birrer

    Abstract:

    Abstract Overexpression of C-Jun enables Rat1a cells to grow in an anchorage-independent manner. We used an inducible C-Jun system under the regulation of doxycycline in Rat1a cells to identify potential C-Jun target genes necessary for C-Jun-induced anchorage-independent growth. Induction of C-Jun results in sustained expression of cyclin A in the nonadherent state with only minimal expression in the absence of C-Jun. The promoter activity of cyclin A2 was 4-fold higher in Rat1a cells in which C-Jun expression was induced compared with the control cells. Chromatin immunoprecipitation demonstrated that C-Jun bound directly to the cyclin A2 promoter. Mutation analysis of the cyclin A2 promoter mapped the C-Jun regulatory site to an ATF site at position –80. C-Jun was able to bind to this site both in vitro and in vivo, and mutation of this site completely abolished promoter activity. Cyclin A1 was also elevated in C-Jun-overexpressing Rat1a cells; however, C-Jun did not regulate this gene directly, since it did not bind directly to the cyclin A1 promoter. Suppression of cyclin A expression via the introduction of a cyclin A antisense sequences significantly reduced the ability of C-Jun-overexpressing Rat1a cells to grow in an anchorage-independent fashion. Taken together, these results suggest that cyclin A is a target of C-Jun and is necessary but not sufficient for C-Jun-induced anchorage-independent growth. In addition, we demonstrated that the cytoplasmic oncogenes Ras and Src transcriptionally activated the cyclin A2 promoter via the ATF site at position –80. Using a dominant negative C-Jun mutant, TAM67, we showed that this transcriptional activation of cyclin A2 requires C-Jun. Thus, our results suggest that C-Jun is a mediator of the aberrant cyclin A2 expression associated with Ras/Src-induced transformation.

  • hmg i y is a c jun activator protein 1 target gene and is necessary for c jun induced anchorage independent growth in rat1a cells
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.

  • HMG-I/Y is a C-Jun/activator protein-1 target gene and is necessary for C-Jun-induced anchorage-independent growth in Rat1a cells.
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.

Fumihiro Hommura – 2nd expert on this subject based on the ideXlab platform

  • Cyclin a is a C-Jun target gene and is necessary for C-Jun-induced anchorage-independent growth in RAT1a cells
    Journal of Biological Chemistry, 2005
    Co-Authors: Motoo Katabami, Howard Donninger, Fumihiro Hommura, Virna D. Leaner, Ichiro Kinoshita, Jeffrey F. B. Chick, Michael J. Birrer

    Abstract:

    Abstract Overexpression of C-Jun enables Rat1a cells to grow in an anchorage-independent manner. We used an inducible C-Jun system under the regulation of doxycycline in Rat1a cells to identify potential C-Jun target genes necessary for C-Jun-induced anchorage-independent growth. Induction of C-Jun results in sustained expression of cyclin A in the nonadherent state with only minimal expression in the absence of C-Jun. The promoter activity of cyclin A2 was 4-fold higher in Rat1a cells in which C-Jun expression was induced compared with the control cells. Chromatin immunoprecipitation demonstrated that C-Jun bound directly to the cyclin A2 promoter. Mutation analysis of the cyclin A2 promoter mapped the C-Jun regulatory site to an ATF site at position –80. C-Jun was able to bind to this site both in vitro and in vivo, and mutation of this site completely abolished promoter activity. Cyclin A1 was also elevated in C-Jun-overexpressing Rat1a cells; however, C-Jun did not regulate this gene directly, since it did not bind directly to the cyclin A1 promoter. Suppression of cyclin A expression via the introduction of a cyclin A antisense sequences significantly reduced the ability of C-Jun-overexpressing Rat1a cells to grow in an anchorage-independent fashion. Taken together, these results suggest that cyclin A is a target of C-Jun and is necessary but not sufficient for C-Jun-induced anchorage-independent growth. In addition, we demonstrated that the cytoplasmic oncogenes Ras and Src transcriptionally activated the cyclin A2 promoter via the ATF site at position –80. Using a dominant negative C-Jun mutant, TAM67, we showed that this transcriptional activation of cyclin A2 requires C-Jun. Thus, our results suggest that C-Jun is a mediator of the aberrant cyclin A2 expression associated with Ras/Src-induced transformation.

  • hmg i y is a c jun activator protein 1 target gene and is necessary for c jun induced anchorage independent growth in rat1a cells
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.

  • HMG-I/Y is a C-Jun/activator protein-1 target gene and is necessary for C-Jun-induced anchorage-independent growth in Rat1a cells.
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.

Motoo Katabami – 3rd expert on this subject based on the ideXlab platform

  • Cyclin a is a C-Jun target gene and is necessary for C-Jun-induced anchorage-independent growth in RAT1a cells
    Journal of Biological Chemistry, 2005
    Co-Authors: Motoo Katabami, Howard Donninger, Fumihiro Hommura, Virna D. Leaner, Ichiro Kinoshita, Jeffrey F. B. Chick, Michael J. Birrer

    Abstract:

    Abstract Overexpression of C-Jun enables Rat1a cells to grow in an anchorage-independent manner. We used an inducible C-Jun system under the regulation of doxycycline in Rat1a cells to identify potential C-Jun target genes necessary for C-Jun-induced anchorage-independent growth. Induction of C-Jun results in sustained expression of cyclin A in the nonadherent state with only minimal expression in the absence of C-Jun. The promoter activity of cyclin A2 was 4-fold higher in Rat1a cells in which C-Jun expression was induced compared with the control cells. Chromatin immunoprecipitation demonstrated that C-Jun bound directly to the cyclin A2 promoter. Mutation analysis of the cyclin A2 promoter mapped the C-Jun regulatory site to an ATF site at position –80. C-Jun was able to bind to this site both in vitro and in vivo, and mutation of this site completely abolished promoter activity. Cyclin A1 was also elevated in C-Jun-overexpressing Rat1a cells; however, C-Jun did not regulate this gene directly, since it did not bind directly to the cyclin A1 promoter. Suppression of cyclin A expression via the introduction of a cyclin A antisense sequences significantly reduced the ability of C-Jun-overexpressing Rat1a cells to grow in an anchorage-independent fashion. Taken together, these results suggest that cyclin A is a target of C-Jun and is necessary but not sufficient for C-Jun-induced anchorage-independent growth. In addition, we demonstrated that the cytoplasmic oncogenes Ras and Src transcriptionally activated the cyclin A2 promoter via the ATF site at position –80. Using a dominant negative C-Jun mutant, TAM67, we showed that this transcriptional activation of cyclin A2 requires C-Jun. Thus, our results suggest that C-Jun is a mediator of the aberrant cyclin A2 expression associated with Ras/Src-induced transformation.

  • hmg i y is a c jun activator protein 1 target gene and is necessary for c jun induced anchorage independent growth in rat1a cells
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.

  • HMG-I/Y is a C-Jun/activator protein-1 target gene and is necessary for C-Jun-induced anchorage-independent growth in Rat1a cells.
    Molecular Cancer Research, 2004
    Co-Authors: Fumihiro Hommura, Motoo Katabami, Howard Donninger, Virna D. Leaner, Takita Felder Sumter, Linda M S Resar, Michael J. Birrer

    Abstract:

    The transcription complex activator protein-1 (AP-1) plays a role in a diverse number of cellular processes including proliferation, differentiation, and apoptosis. To identify AP-1–responsive target genes, we used a doxycycline-inducible C-Jun system in Rat1a cells. The HMG-I/Y chromatin binding protein was found to be up-regulated by C-Jun. Following induction of C-Jun expression, Rat1a cells under nonadherent growth conditions have sustained HMG-I/Y mRNA expression and 2-fold higher protein than uninduced cells. HMG-I/Y promoter reporter assays show that HMG-I/Y promoter activity increases in the presence of C-Jun expression, and gel mobility shift assays demonstrate that induced C-Jun binds to an AP-1 consensus site at position −1,091 in the HMG-I/Y promoter. Suppression of HMG-I/Y expression by its antisense sequence significantly reduces the ability of C-Jun–overexpressing Rat1a cells to grow in an anchorage-independent fashion. HMG-I/Y transforms Rat1a cells (although the colonies are smaller than that observed for the cells overexpressing C-Jun). Taken together, these results suggest that HMG-I/Y is a direct transcriptional target of C-Jun necessary for C-Jun–induced anchorage-independent growth in Rat1a cells.