Gary W Reuther

Summary

Affiliation: University of North Carolina
Country: USA

Publications

  1. ncbi request reprint The Ras branch of small GTPases: Ras family members don't fall far from the tree
    G W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, North Carolina 27599 7295, USA
    Curr Opin Cell Biol 12:157-65. 2000
  2. pmc Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia
    G W Reuther
    Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7295, USA
    Mol Cell Biol 20:8655-66. 2000
  3. ncbi request reprint Leukemia-associated Rho guanine nucleotide exchange factor, a Dbl family protein found mutated in leukemia, causes transformation by activation of RhoA
    G W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7295, USA
    J Biol Chem 276:27145-51. 2001
  4. ncbi request reprint RasGRP4 is a novel Ras activator isolated from acute myeloid leukemia
    Gary W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7295, USA
    J Biol Chem 277:30508-14. 2002
  5. ncbi request reprint Tiam1 mediates Ras activation of Rac by a PI(3)K-independent mechanism
    John M Lambert
    Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Nat Cell Biol 4:621-5. 2002
  6. doi request reprint Involvement of fibroblast growth factor receptor 2 isoform switching in mammary oncogenesis
    Jiyoung Y Cha
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7295, USA
    Mol Cancer Res 6:435-45. 2008
  7. ncbi request reprint Activation of Ras proteins by Ras guanine nucleotide releasing protein family members
    Que T Lambert
    H Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida, USA
    Methods Enzymol 407:82-98. 2006
  8. pmc Regulation of MDMX expression by mitogenic signaling
    Daniele M Gilkes
    H Lee Moffitt Cancer Center, MRC3057A, 12902 Magnolia Drive, Tampa, FL 33612, USA
    Mol Cell Biol 28:1999-2010. 2008

Collaborators

Detail Information

Publications8

  1. ncbi request reprint The Ras branch of small GTPases: Ras family members don't fall far from the tree
    G W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, North Carolina 27599 7295, USA
    Curr Opin Cell Biol 12:157-65. 2000
    ..First, the three Ras proteins may not be functionally identical. Second, Ras function involves functional cross-talk with their close relatives...
  2. pmc Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia
    G W Reuther
    Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7295, USA
    Mol Cell Biol 20:8655-66. 2000
    ..Finally, this report is the first to indicate mutations in TrkA may contribute to leukemogenesis...
  3. ncbi request reprint Leukemia-associated Rho guanine nucleotide exchange factor, a Dbl family protein found mutated in leukemia, causes transformation by activation of RhoA
    G W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 7295, USA
    J Biol Chem 276:27145-51. 2001
    ..These data demonstrate that LARG is the first functional Dbl protein mutated in cancer and indicate LARG-mediated activation of RhoA may play a role in the development of human leukemias...
  4. ncbi request reprint RasGRP4 is a novel Ras activator isolated from acute myeloid leukemia
    Gary W Reuther
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7295, USA
    J Biol Chem 277:30508-14. 2002
    ..We conclude that RasGRP4 is a member of the RasGRP family of Ras guanine nucleotide exchange factors that may play a role in myeloid cell signaling growth regulation pathways that are responsive to diacylglycerol levels...
  5. ncbi request reprint Tiam1 mediates Ras activation of Rac by a PI(3)K-independent mechanism
    John M Lambert
    Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
    Nat Cell Biol 4:621-5. 2002
    ..Furthermore, activated Ras and Tiam1 cooperate to cause synergistic formation of Rac-GTP in a PI(3)K-independent manner. Thus, Tiam1 can function as an effector that directly mediates Ras activation of Rac...
  6. doi request reprint Involvement of fibroblast growth factor receptor 2 isoform switching in mammary oncogenesis
    Jiyoung Y Cha
    Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 7295, USA
    Mol Cancer Res 6:435-45. 2008
    ..Our results support cell context distinct mechanisms of FGFR2 IIIb C2 transformation...
  7. ncbi request reprint Activation of Ras proteins by Ras guanine nucleotide releasing protein family members
    Que T Lambert
    H Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida, USA
    Methods Enzymol 407:82-98. 2006
    ..Analyzing the regulation of RasGRP activity should continue to play an important role in understanding the mechanisms by which signal transduction pathways use RasGRP proteins to activate Ras proteins in cells...
  8. pmc Regulation of MDMX expression by mitogenic signaling
    Daniele M Gilkes
    H Lee Moffitt Cancer Center, MRC3057A, 12902 Magnolia Drive, Tampa, FL 33612, USA
    Mol Cell Biol 28:1999-2010. 2008
    ..Therefore, MDMX expression is regulated by mitogenic signaling pathways. This mechanism may protect normal proliferating cells from p53 but also hamper p53 response during tumor development...