Carl Y Sasaki

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Phosphorylation of RelA/p65 on serine 536 defines an I{kappa}B{alpha}-independent NF-{kappa}B pathway
    Carl Y Sasaki
    Laboratory of Immunology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 280:34538-47. 2005
  2. pmc Traf1 induction and protection from tumor necrosis factor by nuclear factor-kappaB p65 is independent of serine 536 phosphorylation
    Carl Y Sasaki
    Laboratory of Immunology, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Cancer Res 67:11218-25. 2007
  3. pmc Resistance to TGF-beta 1 correlates with aberrant expression of TGF-beta receptor II in human B-cell lymphoma cell lines
    Gang Chen
    Lymphocyte Cell Biology Unit, Laboratory of Immunology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Blood 109:5301-7. 2007
  4. pmc Recruitment of RelB to the Csf2 promoter enhances RelA-mediated transcription of granulocyte-macrophage colony-stimulating factor
    Carl Y Sasaki
    Laboratory of Immunology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 286:1093-102. 2011
  5. pmc Antigen-independent IFN-γ production by human naïve CD4 T cells activated by IL-12 plus IL-18
    Rachel B Munk
    Lymphocyte Cell Biology Unit, Laboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 6:e18553. 2011
  6. pmc Transforming growth factor β1 (TGF-β1) suppresses growth of B-cell lymphoma cells by p14(ARF)-dependent regulation of mutant p53
    Gang Chen
    Lymphocyte Cell Biology Unit, Laboratory of Molecular Biology and Immunology, Intramural Research Program, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 287:23184-95. 2012
  7. ncbi request reprint Comparison of the effect of mutant and wild-type p53 on global gene expression
    Thomas J O'Farrell
    Laboratory of Immunology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland 21224, USA
    Cancer Res 64:8199-207. 2004
  8. ncbi request reprint Characterization of H2O2-induced acute apoptosis in cultured neural stem/progenitor cells
    Hsingchi J Lin
    Center for Bio Molecular Science and Engineering, Naval Research Laboratory, Washington, DC 20375, USA
    FEBS Lett 570:102-6. 2004

Collaborators

Detail Information

Publications8

  1. ncbi request reprint Phosphorylation of RelA/p65 on serine 536 defines an I{kappa}B{alpha}-independent NF-{kappa}B pathway
    Carl Y Sasaki
    Laboratory of Immunology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 280:34538-47. 2005
    ....
  2. pmc Traf1 induction and protection from tumor necrosis factor by nuclear factor-kappaB p65 is independent of serine 536 phosphorylation
    Carl Y Sasaki
    Laboratory of Immunology, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Cancer Res 67:11218-25. 2007
    ..These findings suggested that the requirement of serine phosphorylation at residue 536 and the distance between the NF-kappaB response element and the start of transcription may influence which genes will be transcribed...
  3. pmc Resistance to TGF-beta 1 correlates with aberrant expression of TGF-beta receptor II in human B-cell lymphoma cell lines
    Gang Chen
    Lymphocyte Cell Biology Unit, Laboratory of Immunology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Blood 109:5301-7. 2007
    ..These data suggest that promoter methylation plays an important role in T beta RII gene silencing and subsequent development of a TGF-beta1-resistant phenotype by some B-cell lymphoma cells...
  4. pmc Recruitment of RelB to the Csf2 promoter enhances RelA-mediated transcription of granulocyte-macrophage colony-stimulating factor
    Carl Y Sasaki
    Laboratory of Immunology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 286:1093-102. 2011
    ..Moreover, the novel priming process described here underscores the complexity of the interactions between the classical and alternative NF-κB signaling pathways...
  5. pmc Antigen-independent IFN-γ production by human naïve CD4 T cells activated by IL-12 plus IL-18
    Rachel B Munk
    Lymphocyte Cell Biology Unit, Laboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 6:e18553. 2011
    ..Thus, the present study suggests that naïve CD4(+) T cells may participate in innate immunity or amplify adaptive immune responses through cytokine-induced antigen-independent cytokine production...
  6. pmc Transforming growth factor β1 (TGF-β1) suppresses growth of B-cell lymphoma cells by p14(ARF)-dependent regulation of mutant p53
    Gang Chen
    Lymphocyte Cell Biology Unit, Laboratory of Molecular Biology and Immunology, Intramural Research Program, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 287:23184-95. 2012
    ..This work suggests that the high levels of p14(ARF) often found in tumor cells could be a potential therapeutic target...
  7. ncbi request reprint Comparison of the effect of mutant and wild-type p53 on global gene expression
    Thomas J O'Farrell
    Laboratory of Immunology, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Maryland 21224, USA
    Cancer Res 64:8199-207. 2004
    ..However, mutant p53s are likely to be distinct in terms of the extent to which each mechanism contributes to their gain-of-function phenotypes...
  8. ncbi request reprint Characterization of H2O2-induced acute apoptosis in cultured neural stem/progenitor cells
    Hsingchi J Lin
    Center for Bio Molecular Science and Engineering, Naval Research Laboratory, Washington, DC 20375, USA
    FEBS Lett 570:102-6. 2004
    ..We conclude that the transient activation of PI3K-Akt signaling delays the H2O2-induced acute apoptosis in cultured NS/PCs in part through maintaining the basal pGSK3beta level and activating other downstream effectors...