Tatyana Ammosova

Summary

Country: Russia

Publications

  1. ncbi Protein phosphatase-1 dephosphorylates the C-terminal domain of RNA polymerase-II
    Kareem Washington
    Center for Sickle Cell Disease, Department of Biochemistry and Molecular Biology, Howard University, 2121 Georgia Avenue, Washington, D C 20059, USA
    J Biol Chem 277:40442-8. 2002
  2. ncbi Phosphorylation of HIV-1 Tat by CDK2 in HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University College of Medicine, Washington, DC 20059, USA
    Retrovirology 3:78. 2006
  3. ncbi Iron chelators ICL670 and 311 inhibit HIV-1 transcription
    Zufan Debebe
    Center for Sickle Cell Disease, Howard University College of Medicine, Washington, DC 20060, USA
    Virology 367:324-33. 2007
  4. ncbi Dephosphorylation of CDK9 by protein phosphatase 2A and protein phosphatase-1 in Tat-activated HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University, 2121 Georgia Ave, N W Washington, DC 20059, USA
    Retrovirology 2:47. 2005
  5. ncbi Nuclear targeting of protein phosphatase-1 by HIV-1 Tat protein
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University, Washington, DC 20059, USA
    J Biol Chem 280:36364-71. 2005
  6. ncbi Nuclear protein phosphatase-1 regulates HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease and Department of Biochemistry and Molecular Biology, Howard University, Washington, D C 20059, USA
    J Biol Chem 278:32189-94. 2003
  7. ncbi Inhibition of PP2A by LIS1 increases HIV-1 gene expression
    Nicolas Epie
    Center for Sickle Cell Disease, Howard University College of Medicine, 520 W Street N W, Washington, DC 20059, USA
    Retrovirology 3:65. 2006
  8. ncbi Regulation of HIV-1 transcription at 3% versus 21% oxygen concentration
    Sharroya Charles
    Center for Sickle Cell Disease, Howard University, Washington, DC 20001, USA
    J Cell Physiol 221:469-79. 2009
  9. ncbi Iron chelators of the di-2-pyridylketone thiosemicarbazone and 2-benzoylpyridine thiosemicarbazone series inhibit HIV-1 transcription: identification of novel cellular targets--iron, cyclin-dependent kinase (CDK) 2, and CDK9
    Zufan Debebe
    Center for Sickle Cell Disease, Department of Medicine, Howard University, Washington DC 20001, USA
    Mol Pharmacol 79:185-96. 2011
  10. ncbi HIV-1 Tat interacts with LIS1 protein
    Nicolas Epie
    Center for Sickle Cell Disease, Howard University, Washington, DC 20059, USA
    Retrovirology 2:6. 2005

Collaborators

Detail Information

Publications12

  1. ncbi Protein phosphatase-1 dephosphorylates the C-terminal domain of RNA polymerase-II
    Kareem Washington
    Center for Sickle Cell Disease, Department of Biochemistry and Molecular Biology, Howard University, 2121 Georgia Avenue, Washington, D C 20059, USA
    J Biol Chem 277:40442-8. 2002
    ..Our data demonstrate that RNAPII CTD is dephosphorylated by PP1 in vitro and by PPP-type phosphatase, distinct from FCP1, in vivo...
  2. ncbi Phosphorylation of HIV-1 Tat by CDK2 in HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University College of Medicine, Washington, DC 20059, USA
    Retrovirology 3:78. 2006
    ..In the present study, we analyzed whether Tat is phosphorylated in cultured cells by CDK2 and whether Tat phosphorylation has a regulatory effect on HIV-1 transcription...
  3. ncbi Iron chelators ICL670 and 311 inhibit HIV-1 transcription
    Zufan Debebe
    Center for Sickle Cell Disease, Howard University College of Medicine, Washington, DC 20060, USA
    Virology 367:324-33. 2007
    ..Further consideration should be given to the development of iron chelators for future anti-retroviral therapeutics...
  4. ncbi Dephosphorylation of CDK9 by protein phosphatase 2A and protein phosphatase-1 in Tat-activated HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University, 2121 Georgia Ave, N W Washington, DC 20059, USA
    Retrovirology 2:47. 2005
    ..In the present study we analyze relative contribution of PP2A and PP1 to dephosphorylation of CDK9 and to HIV-1 transcription in vitro and in vivo...
  5. ncbi Nuclear targeting of protein phosphatase-1 by HIV-1 Tat protein
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University, Washington, DC 20059, USA
    J Biol Chem 280:36364-71. 2005
    ..Our results suggest that Tat might function as a nuclear regulator of PP1 and that interaction of Tat with PP1 is critical for activation of HIV-1 transcription by Tat...
  6. ncbi Nuclear protein phosphatase-1 regulates HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease and Department of Biochemistry and Molecular Biology, Howard University, Washington, D C 20059, USA
    J Biol Chem 278:32189-94. 2003
    ..Our results indicate that PP1 might be a host cell factor that is required for HIV-1 viral transcription. Therefore, nuclear PP1 may represent a novel target for anti-HIV-1 therapeutics...
  7. ncbi Inhibition of PP2A by LIS1 increases HIV-1 gene expression
    Nicolas Epie
    Center for Sickle Cell Disease, Howard University College of Medicine, 520 W Street N W, Washington, DC 20059, USA
    Retrovirology 3:65. 2006
    ..Previously we showed that LIS1 interacts with HIV-1 Tat protein and that this interaction was mediated by WD40 domains of LIS1. In the present study, we analyze the effect of LIS1 on Tat-mediated transcription of HIV-1 LTR...
  8. ncbi Regulation of HIV-1 transcription at 3% versus 21% oxygen concentration
    Sharroya Charles
    Center for Sickle Cell Disease, Howard University, Washington, DC 20001, USA
    J Cell Physiol 221:469-79. 2009
    ....
  9. ncbi Iron chelators of the di-2-pyridylketone thiosemicarbazone and 2-benzoylpyridine thiosemicarbazone series inhibit HIV-1 transcription: identification of novel cellular targets--iron, cyclin-dependent kinase (CDK) 2, and CDK9
    Zufan Debebe
    Center for Sickle Cell Disease, Department of Medicine, Howard University, Washington DC 20001, USA
    Mol Pharmacol 79:185-96. 2011
    ..Our study suggests the potential usefulness of Bp4aT or Bp4eT in antiretroviral regimens, particularly where resistance to standard treatment occurs...
  10. ncbi HIV-1 Tat interacts with LIS1 protein
    Nicolas Epie
    Center for Sickle Cell Disease, Howard University, Washington, DC 20059, USA
    Retrovirology 2:6. 2005
    ..Tat-induced apoptosis of T-cells is attributed, in part, to the distortion of microtubules polymerization. LIS1 is a microtubule-associated protein that facilitates microtubule polymerization...
  11. ncbi RNA interference directed to CDK2 inhibits HIV-1 transcription
    Tatyana Ammosova
    Center for Sickle Cell Disease, Howard University College of Medicine, NW, Washington, DC 20059, USA
    Virology 341:171-8. 2005
    ..1 cells. Our results indicate that CDK2 participates in Tat-mediated HIV-1 transcription and may serve as a potential therapeutic target...
  12. ncbi HIV-1 Tat interaction with RNA polymerase II C-terminal domain (CTD) and a dynamic association with CDK2 induce CTD phosphorylation and transcription from HIV-1 promoter
    Longwen Deng
    Department of Biochemistry and Molecular Biology, George Washington University Medical Center, Washington, D C 20037, USA
    J Biol Chem 277:33922-9. 2002
    ..We suggest that CDK2 is part of a transcription complex that is required for Tat-dependent transcription and that interaction of Tat with CTD and a dynamic association of Tat with CDK2/cyclin E stimulated CTD phosphorylation by CDK2...