NF-kappa B p50 Subunit

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  Subject Areas on Research

  • Alteration of NF-kappa B p50 DNA binding kinetics by S-nitrosylation. 
  • Autophagy enhances NFκB activity in specific tissue macrophages by sequestering A20 to boost antifungal immunity. 
  • Bcl-3 acts as an innate immune modulator by controlling antimicrobial responses in keratinocytes. 
  • Differential effects of nitric oxide-mediated S-nitrosylation on p50 and c-jun DNA binding. 
  • Endotoxin-mediated S-nitrosylation of p50 alters NF-kappa B-dependent gene transcription in ANA-1 murine macrophages. 
  • Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma. 
  • Genome-wide association study of treatment refractory schizophrenia in Han Chinese. 
  • H1 RNA polymerase III promoter-driven expression of an RNA aptamer leads to high-level inhibition of intracellular protein activity. 
  • Inhibition of NF-kappa B by S-nitrosylation. 
  • Inhibition of NF-kappaB activation reduces the tissue effects of transgenic IL-13. 
  • Inhibition of NF-kappaB1 and NF-kappaB2 activation in prostate cancer cells treated with antibody against the carboxyl terminal domain of GRP78: effect of p53 upregulation. 
  • Molecular impact of selective NFKB1 and NFKB2 signaling on DLBCL phenotype. 
  • NF-κB p50 activation associated with immune dysregulation confers poorer survival for diffuse large B-cell lymphoma patients with wild-type p53. 
  • NOS2 regulation of NF-kappaB by S-nitrosylation of p65. 
  • Peripheral blood expression of nuclear factor-kappab-regulated genes is associated with rheumatoid arthritis disease activity and responds differentially to anti-tumor necrosis factor-alpha versus methotrexate. 
  • Proteasome inhibitor attenuates skeletal muscle reperfusion injury by blocking the pathway of nuclear factor-kappaB activation. 
  • The apolipoprotein E-mimetic peptide COG112 inhibits the inflammatory response to Citrobacter rodentium in colonic epithelial cells by preventing NF-kappaB activation. 
  • The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair. 
  • Thioredoxin-mediated denitrosylation regulates cytokine-induced nuclear factor κB (NF-κB) activation.