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. pmc Combination therapy with lenalidomide and nanoceria ameliorates CNS autoimmunity
    Erez Eitan
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Exp Neurol 273:151-60. 2015
  8. 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
  9. 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

Publications9

  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. pmc Combination therapy with lenalidomide and nanoceria ameliorates CNS autoimmunity
    Erez Eitan
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Exp Neurol 273:151-60. 2015
    ....
  8. 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...
  9. 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...