Joseph F Gera

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi AKT activity determines sensitivity to mammalian target of rapamycin (mTOR) inhibitors by regulating cyclin D1 and c-myc expression
    Joseph F Gera
    Department of Medicine, West Los Angeles Veteran s Administration UCLA Medical Center, University of California School of Medicine, Los Angeles, California 90073, USA
    J Biol Chem 279:2737-46. 2004
  2. ncbi IL-6-induced stimulation of c-myc translation in multiple myeloma cells is mediated by myc internal ribosome entry site function and the RNA-binding protein, hnRNP A1
    Yijiang Shi
    Department of Medicine, Greater Los Angeles VA Healthcare System and University of California at Los Angeles Medical School, Los Angeles, California, USA
    Cancer Res 68:10215-22. 2008

Research Grants

  1. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph F Gera; Fiscal Year: 2010
  2. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph Gera; Fiscal Year: 2007
  3. Regulation of c-myc translation by hnRNP A1: role in multiple myeloma tumor respo
    Joseph Gera; Fiscal Year: 2009
  4. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph Gera; Fiscal Year: 2009
  5. Regulation of c-myc translation by hnRNP A1: role in multiple myeloma tumor respo
    Alan K Lichtenstein; Fiscal Year: 2010

Collaborators

Detail Information

Publications2

  1. ncbi AKT activity determines sensitivity to mammalian target of rapamycin (mTOR) inhibitors by regulating cyclin D1 and c-myc expression
    Joseph F Gera
    Department of Medicine, West Los Angeles Veteran s Administration UCLA Medical Center, University of California School of Medicine, Los Angeles, California 90073, USA
    J Biol Chem 279:2737-46. 2004
    ..These results identify two critical downstream molecular targets whose expression is regulated by AKT activity and whose down-regulation is required for rapamycin/CCI-779 sensitivity...
  2. ncbi IL-6-induced stimulation of c-myc translation in multiple myeloma cells is mediated by myc internal ribosome entry site function and the RNA-binding protein, hnRNP A1
    Yijiang Shi
    Department of Medicine, Greater Los Angeles VA Healthcare System and University of California at Los Angeles Medical School, Los Angeles, California, USA
    Cancer Res 68:10215-22. 2008
    ..These data point to hnRNP A1 as a critical regulator of c-myc translation and a potential therapeutic target in multiple myeloma...

Research Grants8

  1. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph F Gera; Fiscal Year: 2010
    ..The mechanisms of cell intrinsic resistance to these compounds will be investigated, as well as, the pre-clinical evaluation of combination targeted therapies in glioma in vitro and in vivo models. ..
  2. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph Gera; Fiscal Year: 2007
    ..The broad objective of this proposal is understand the molecular events which regulate AKT-dependent hypersensitivity of tumor cells to these agents. ..
  3. Regulation of c-myc translation by hnRNP A1: role in multiple myeloma tumor respo
    Joseph Gera; Fiscal Year: 2009
    ..This is an important pathway of progression of this malignancy in patients. It also elucidates how multiple myeloma tumor cells become resistant to promising new therapeutic agents called mTOR inhibitors. ..
  4. Mechanisms of AKT-dependent sensitivity to rapamycin
    Joseph Gera; Fiscal Year: 2009
    ..The mechanisms of cell intrinsic resistance to these compounds will be investigated, as well as, the pre-clinical evaluation of combination targeted therapies in glioma in vitro and in vivo models. ..
  5. Regulation of c-myc translation by hnRNP A1: role in multiple myeloma tumor respo
    Alan K Lichtenstein; Fiscal Year: 2010
    ..This is an important pathway of progression of this malignancy in patients. It also elucidates how multiple myeloma tumor cells become resistant to promising new therapeutic agents called mTOR inhibitors. ..