Nader Omidvar

Summary

Affiliation: Cardiff University
Country: UK

Publications

  1. pmc PML-RARα co-operates with Sox4 in acute myeloid leukemia development in mice
    Nader Omidvar
    Helen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California San Francisco, USA
    Haematologica 98:424-7. 2013
  2. pmc Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras
    Nader Omidvar
    Department of Haematology, School of Medicine, Cardiff School of Biosciences, Cardiff University, Museum Avenue, Cardiff, United Kingdom
    Mol Cell Biol 26:3966-75. 2006
  3. pmc Expression of glycosylphosphatidylinositol-anchored CD59 on target cells enhances human NK cell-mediated cytotoxicity
    Nader Omidvar
    Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff, United Kingdom
    J Immunol 176:2915-23. 2006
  4. pmc Cutting edge: murine CD59a modulates antiviral CD4+ T cell activity in a complement-independent manner
    M Paula Longhi
    Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Wales, United Kingdom
    J Immunol 175:7098-102. 2005
  5. ncbi request reprint Protein kinase C mediates mutant N-Ras-induced developmental abnormalities in normal human erythroid cells
    Richard L Darley
    Leukaemia Research Fund Differentiation Group, Department of Haematology, University of Wales College of Medicine, Cardiff, United Kingdom
    Blood 100:4185-92. 2002
  6. ncbi request reprint Decay-accelerating factor (CD55) is expressed by neurons in response to chronic but not acute autoimmune central nervous system inflammation associated with complement activation
    Johan van Beek
    Brain Inflammation Immunity Group BIIG, Cardiff University, Cardiff, United Kingdom
    J Immunol 174:2353-65. 2005
  7. ncbi request reprint BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia
    Nader Omidvar
    Institut National de la Sante et de la Recherche Medicale U718 and 728, Universite Paris 7 Denis Diderot, Faculte de Medicine, Institut Universitaire d Hématologie IFR105, Paris, France
    Cancer Res 67:11657-67. 2007
  8. ncbi request reprint Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
    Feyruz V Rassool
    Department of Radiation Oncology, University of Maryland School of Medicine, Baltimore, Maryland 21201 1509, USA
    Cancer Res 67:8762-71. 2007

Detail Information

Publications8

  1. pmc PML-RARα co-operates with Sox4 in acute myeloid leukemia development in mice
    Nader Omidvar
    Helen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California San Francisco, USA
    Haematologica 98:424-7. 2013
    ..The cooperation between these transcription factors is consistent with the paradigm of multiple routes to the disease and reinforces the concept that transcription factor networks are important therapeutic targets in myeloid leukemias...
  2. pmc Ral is both necessary and sufficient for the inhibition of myeloid differentiation mediated by Ras
    Nader Omidvar
    Department of Haematology, School of Medicine, Cardiff School of Biosciences, Cardiff University, Museum Avenue, Cardiff, United Kingdom
    Mol Cell Biol 26:3966-75. 2006
    ..Ral, in turn, appears to influence differentiation through multiple effectors. These data show, for the first time, the importance of Ral in regulating differentiation and self-renewal in hematopoietic cells...
  3. pmc Expression of glycosylphosphatidylinositol-anchored CD59 on target cells enhances human NK cell-mediated cytotoxicity
    Nader Omidvar
    Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff, United Kingdom
    J Immunol 176:2915-23. 2006
    ..The data show that the increased susceptibility of target cells expressing CD59 to NK cytotoxicity requires GPI anchor-mediating signaling events, likely mediated by interactions between GPI-anchored CD59 on targets and NK receptors...
  4. pmc Cutting edge: murine CD59a modulates antiviral CD4+ T cell activity in a complement-independent manner
    M Paula Longhi
    Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Wales, United Kingdom
    J Immunol 175:7098-102. 2005
    ..Collectively, these results demonstrate that CD59a down-modulates CD4+ T cell activity in vitro and in vivo, thereby revealing another link between complement regulators and T cell activation...
  5. ncbi request reprint Protein kinase C mediates mutant N-Ras-induced developmental abnormalities in normal human erythroid cells
    Richard L Darley
    Leukaemia Research Fund Differentiation Group, Department of Haematology, University of Wales College of Medicine, Cardiff, United Kingdom
    Blood 100:4185-92. 2002
    ..This gives rise to phenotypic and functional abnormalities commonly observed in preleukemia, suggesting a direct link between RAS mutations and the pathogenesis of preleukemia...
  6. ncbi request reprint Decay-accelerating factor (CD55) is expressed by neurons in response to chronic but not acute autoimmune central nervous system inflammation associated with complement activation
    Johan van Beek
    Brain Inflammation Immunity Group BIIG, Cardiff University, Cardiff, United Kingdom
    J Immunol 174:2353-65. 2005
    ..We conclude that increased CD55 expression by neurons may represent a key protective signaling mechanism mobilized by brain cells to withstand complement activation and to survive within an inflammatory site...
  7. ncbi request reprint BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia
    Nader Omidvar
    Institut National de la Sante et de la Recherche Medicale U718 and 728, Universite Paris 7 Denis Diderot, Faculte de Medicine, Institut Universitaire d Hématologie IFR105, Paris, France
    Cancer Res 67:11657-67. 2007
    ..The colocalization of BCL-2 and RAS in the bone marrow of MDS/AML patients offers targeting either oncogene as a therapeutic strategy...
  8. ncbi request reprint Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
    Feyruz V Rassool
    Department of Radiation Oncology, University of Maryland School of Medicine, Baltimore, Maryland 21201 1509, USA
    Cancer Res 67:8762-71. 2007
    ..These data suggest treatment strategies that target RAS/RAC pathways and ROS production in human MDS/AML...