DAVID PLAS

Summary

Affiliation: University of Cincinnati
Country: USA

Publications

  1. pmc S6K1 determines the metabolic requirements for BCR-ABL survival
    J F Barger
    Department of Cancer and Cell Biology, University of Cincinnati, Cincinnati, OH 45208 0521, USA
    Oncogene 32:453-61. 2013
  2. ncbi request reprint Akt-dependent transformation: there is more to growth than just surviving
    David R Plas
    Department of Genome Science, The Genome Research Institute, University of Cincinnati, OH 45237, USA
    Oncogene 24:7435-42. 2005
  3. ncbi request reprint AMP-activated protein kinase induces a p53-dependent metabolic checkpoint
    Russell G Jones
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Mol Cell 18:283-93. 2005
  4. ncbi request reprint Cytokine stimulation of aerobic glycolysis in hematopoietic cells exceeds proliferative demand
    Daniel E Bauer
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    FASEB J 18:1303-5. 2004
  5. ncbi request reprint Akt stimulates aerobic glycolysis in cancer cells
    Rebecca L Elstrom
    Department of Cancer Biology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    Cancer Res 64:3892-9. 2004
  6. pmc Akt-directed glucose metabolism can prevent Bax conformation change and promote growth factor-independent survival
    Jeffrey C Rathmell
    Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Mol Cell Biol 23:7315-28. 2003
  7. ncbi request reprint Bcl-x(L) and Akt cooperate to promote leukemogenesis in vivo
    Robyn Karnauskas
    Department of Medicine, University of Chicago, IL 60637, USA
    Oncogene 22:688-98. 2003
  8. ncbi request reprint The CD28 signaling pathway regulates glucose metabolism
    Kenneth A Frauwirth
    Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    Immunity 16:769-77. 2002
  9. ncbi request reprint Homeostatic control of lymphocyte survival: potential origins and implications
    David R Plas
    Abramson Family Cancer Research Institute and Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Nat Immunol 3:515-21. 2002
  10. ncbi request reprint Phosphatidylinositol 3-kinase/Akt signaling is neither required for hypoxic stabilization of HIF-1 alpha nor sufficient for HIF-1-dependent target gene transcription
    Andrew M Arsham
    Committee on Genetics, University of Chicago, Chicago, Illinois 60637, USA
    J Biol Chem 277:15162-70. 2002

Collaborators

  • Yang Xu
  • Craig B Thompson
  • Jeffrey C Rathmell
  • J F Barger
  • Daniel E Bauer
  • Marian H Harris
  • Rebecca L Elstrom
  • Robyn Karnauskas
  • Russell G Jones
  • Monica Buzzai
  • Charles M Rudin
  • Peter S Hammerman
  • Ryan M Cinalli
  • James L Riley
  • Kenneth A Frauwirth
  • Andrew M Arsham
  • A Sullivan
  • H Liu
  • H L Grimes
  • P Tandon
  • C A Gallo
  • James Mu
  • Sara Kubek
  • Morris J Birnbaum
  • Julian J Lum
  • Hongming Zhuang
  • Abass Alavi
  • Casey J Fox
  • Qun Niu
  • Sunit Talapatra
  • Marianne E Greene
  • John D Crispino
  • Richard V Parry
  • M Celeste Simon
  • Carl H June

Detail Information

Publications11

  1. pmc S6K1 determines the metabolic requirements for BCR-ABL survival
    J F Barger
    Department of Cancer and Cell Biology, University of Cincinnati, Cincinnati, OH 45208 0521, USA
    Oncogene 32:453-61. 2013
    ..These data indicate that S6K1 dictates the metabolic requirements mediating BCR-ABL survival and provide a rationale for combining targeted inhibitors of signal transduction, with strategies to interrupt oncogene-induced metabolism...
  2. ncbi request reprint Akt-dependent transformation: there is more to growth than just surviving
    David R Plas
    Department of Genome Science, The Genome Research Institute, University of Cincinnati, OH 45237, USA
    Oncogene 24:7435-42. 2005
    ..Although this conversion promotes cell growth, it also renders cell survival dependent on a continuous supply of extracellular nutrients, which themselves are required regulatory elements in Akt signal transduction...
  3. ncbi request reprint AMP-activated protein kinase induces a p53-dependent metabolic checkpoint
    Russell G Jones
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Mol Cell 18:283-93. 2005
    ..However, persistent activation of AMPK leads to accelerated p53-dependent cellular senescence. Thus, AMPK is a cell-intrinsic regulator of the cell cycle that coordinates cellular proliferation with carbon source availability...
  4. ncbi request reprint Cytokine stimulation of aerobic glycolysis in hematopoietic cells exceeds proliferative demand
    Daniel E Bauer
    Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    FASEB J 18:1303-5. 2004
    ..These data suggest that the high rate of glycolysis observed in response to growth factor stimulation is a primary effect rather than a homeostatic response to increased cell growth...
  5. ncbi request reprint Akt stimulates aerobic glycolysis in cancer cells
    Rebecca L Elstrom
    Department of Cancer Biology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    Cancer Res 64:3892-9. 2004
    ....
  6. pmc Akt-directed glucose metabolism can prevent Bax conformation change and promote growth factor-independent survival
    Jeffrey C Rathmell
    Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    Mol Cell Biol 23:7315-28. 2003
    ..The prevention of Bax activation by posttranscriptional regulation of glucose metabolism may, therefore, be a required aspect of the ability of Akt to maintain long-term cell survival in the absence of growth factors...
  7. ncbi request reprint Bcl-x(L) and Akt cooperate to promote leukemogenesis in vivo
    Robyn Karnauskas
    Department of Medicine, University of Chicago, IL 60637, USA
    Oncogene 22:688-98. 2003
    ..These results implicate activated Akt and growth-factor independence in leukemogenic transformation, and demonstrate the potential for in vivo analysis of genetic determinants of leukemogenesis...
  8. ncbi request reprint The CD28 signaling pathway regulates glucose metabolism
    Kenneth A Frauwirth
    Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    Immunity 16:769-77. 2002
    ..These data suggest that CD28 costimulation functions to increase glycolytic flux, allowing T cells to anticipate energetic and biosynthetic needs associated with a sustained response...
  9. ncbi request reprint Homeostatic control of lymphocyte survival: potential origins and implications
    David R Plas
    Abramson Family Cancer Research Institute and Department of Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Nat Immunol 3:515-21. 2002
    ....
  10. ncbi request reprint Phosphatidylinositol 3-kinase/Akt signaling is neither required for hypoxic stabilization of HIF-1 alpha nor sufficient for HIF-1-dependent target gene transcription
    Andrew M Arsham
    Committee on Genetics, University of Chicago, Chicago, Illinois 60637, USA
    J Biol Chem 277:15162-70. 2002
    ..Therefore, the PI3K/Akt pathway is not necessary for hypoxic induction of HIF-1 subunits or activity, and constitutively active Akt is not itself sufficient to induce HIF-1 activity...
  11. ncbi request reprint Cell metabolism in the regulation of programmed cell death
    David R Plas
    Abramson Family Cancer Research Institute and Department Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Trends Endocrinol Metab 13:75-8. 2002
    ..Here, we review the coordinated effects of growth factor withdrawal on bioenergetics and programmed cell death, and discuss the metabolic consequences of genes that prevent apoptosis, including the BCL2 family of genes and AKT...

Research Grants4

  1. Regulation of Cellular Survival, Size and Metabolism
    DAVID PLAS; Fiscal Year: 2007
    ..Together, these studies will help define the roles of the proto-oncogene Akt and the tumor suppressor genes TSC1 and TSC2 in the deregulation of cell metabolism in cancers associated with these genes. ..
  2. Interrupting Akt-S6K1 metabolic control to enhance apoptotic responses in CML
    DAVID PLAS; Fiscal Year: 2009
    ..Results of these experiments will lead to novel strategies for eliminating the residual cancer cells that can cause relapse in leukemia. ..
  3. Interrupting Akt-S6K1 metabolic control to enhance apoptotic responses in CML
    David R Plas; Fiscal Year: 2010
    ..Results of these experiments will lead to novel strategies for eliminating the residual cancer cells that can cause relapse in leukemia. ..