Affiliation: University of Cincinnati
- S6K1 determines the metabolic requirements for BCR-ABL survivalJ 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...
- Akt-dependent transformation: there is more to growth than just survivingDavid 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...
- AMP-activated protein kinase induces a p53-dependent metabolic checkpointRussell 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...
- Cytokine stimulation of aerobic glycolysis in hematopoietic cells exceeds proliferative demandDaniel 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...
- Akt stimulates aerobic glycolysis in cancer cellsRebecca L Elstrom
Department of Cancer Biology, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
Cancer Res 64:3892-9. 2004....
- Akt-directed glucose metabolism can prevent Bax conformation change and promote growth factor-independent survivalJeffrey 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...
- Bcl-x(L) and Akt cooperate to promote leukemogenesis in vivoRobyn 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...
- The CD28 signaling pathway regulates glucose metabolismKenneth 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...
- Homeostatic control of lymphocyte survival: potential origins and implicationsDavid 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....
- Phosphatidylinositol 3-kinase/Akt signaling is neither required for hypoxic stabilization of HIF-1 alpha nor sufficient for HIF-1-dependent target gene transcriptionAndrew 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...
- Cell metabolism in the regulation of programmed cell deathDavid 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...
- Regulation of Cellular Survival, Size and MetabolismDAVID 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. ..
- Interrupting Akt-S6K1 metabolic control to enhance apoptotic responses in CMLDAVID 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. ..
- Interrupting Akt-S6K1 metabolic control to enhance apoptotic responses in CMLDavid 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. ..