Shairaz Baksh

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Identification of novel gene expression targets for the Ras association domain family 1 (RASSF1A) tumor suppressor gene in non-small cell lung cancer and neuroblastoma
    Angelo Agathanggelou
    Section of Medical and Molecular Genetics, Division of Reproductive and Child Health, University of Birmingham, Birmingham B15 2TT, United Kingdom
    Cancer Res 63:5344-51. 2003
  2. ncbi request reprint Identification of the E1A-regulated transcription factor p120 E4F as an interacting partner of the RASSF1A candidate tumor suppressor gene
    Sarah L Fenton
    Section of Medical and Molecular Genetics, Department of Reproductive and Child Health, University of Birmingham, The Medical School, Edgbaston, Birmingham, United Kingdom
    Cancer Res 64:102-7. 2004
  3. ncbi request reprint The tumor suppressor RASSF1A and MAP-1 link death receptor signaling to Bax conformational change and cell death
    Shairaz Baksh
    Cancer Biology Program, Division of Hematology and Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, 1038 NRB, 330 Brookline Avenue, Boston, Massachusetts 02215, USA
    Mol Cell 18:637-50. 2005
  4. pmc Dynamics of RASSF1A/MOAP-1 association with death receptors
    Caitlin J Foley
    Division of Experimental Oncology, Cross Cancer Institute, Edmonton, Alberta, Canada
    Mol Cell Biol 28:4520-35. 2008
  5. pmc Interleukin-3 (IL-3)-induced c-fos activation is modulated by Gab2-calcineurin interaction
    Saiju Pyarajan
    Cancer Institute, NYU School of Medicine, New York University, New York, NY 10016, USA
    J Biol Chem 283:23505-9. 2008

Collaborators

Detail Information

Publications5

  1. pmc Identification of novel gene expression targets for the Ras association domain family 1 (RASSF1A) tumor suppressor gene in non-small cell lung cancer and neuroblastoma
    Angelo Agathanggelou
    Section of Medical and Molecular Genetics, Division of Reproductive and Child Health, University of Birmingham, Birmingham B15 2TT, United Kingdom
    Cancer Res 63:5344-51. 2003
    ..The identified targets are involved in diverse cellular processes; this should help toward understanding mechanisms that contribute to RASSF1A biological activity...
  2. ncbi request reprint Identification of the E1A-regulated transcription factor p120 E4F as an interacting partner of the RASSF1A candidate tumor suppressor gene
    Sarah L Fenton
    Section of Medical and Molecular Genetics, Department of Reproductive and Child Health, University of Birmingham, The Medical School, Edgbaston, Birmingham, United Kingdom
    Cancer Res 64:102-7. 2004
    ..As p120(E4F) has been reported previously to interact with p14ARF, retinoblastoma, and p53, these findings provide an important link between the function of RASSF1A and other major human tumor suppressor genes...
  3. ncbi request reprint The tumor suppressor RASSF1A and MAP-1 link death receptor signaling to Bax conformational change and cell death
    Shairaz Baksh
    Cancer Biology Program, Division of Hematology and Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, 1038 NRB, 330 Brookline Avenue, Boston, Massachusetts 02215, USA
    Mol Cell 18:637-50. 2005
    ..Our findings identify RASSF1A and MAP-1 as important components between death receptors and the apoptotic machinery and reveal a potential link between tumor suppression and death receptor signaling...
  4. pmc Dynamics of RASSF1A/MOAP-1 association with death receptors
    Caitlin J Foley
    Division of Experimental Oncology, Cross Cancer Institute, Edmonton, Alberta, Canada
    Mol Cell Biol 28:4520-35. 2008
    ..The association of RASSF1A and MOAP-1 with death receptors involves an ordered recruitment to receptor complexes to promote cell death and inhibit tumor formation...
  5. pmc Interleukin-3 (IL-3)-induced c-fos activation is modulated by Gab2-calcineurin interaction
    Saiju Pyarajan
    Cancer Institute, NYU School of Medicine, New York University, New York, NY 10016, USA
    J Biol Chem 283:23505-9. 2008
    ..Furthermore Cn dephosphorylates Gab2, resulting in c-fos activation and cell proliferation. We also report that there is a direct interaction between Cn and Gab2 upon IL-3 stimulation, and Akt can regulate this interaction...