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One or more keywords matched the following items that are connected to McCall, Charles
Item TypeName
Academic Article Distinct post-receptor alterations generate gene- and signal-selective adaptation and cross-adaptation of TLR4 and TLR2 in human leukocytes.
Academic Article Endotoxin tolerance disrupts chromatin remodeling and NF-kappaB transactivation at the IL-1beta promoter.
Academic Article Alpha2-adrenoceptor stimulation transforms immune responses in neuritis and blocks neuritis-induced pain.
Academic Article Induction of RelB participates in endotoxin tolerance.
Academic Article Toll-like receptor 4-dependent responses to lung injury in a murine model of pulmonary contusion.
Academic Article G9a and HP1 couple histone and DNA methylation to TNFalpha transcription silencing during endotoxin tolerance.
Academic Article RelB sustains IkappaBalpha expression during endotoxin tolerance.
Academic Article Chromatin-specific remodeling by HMGB1 and linker histone H1 silences proinflammatory genes during endotoxin tolerance.
Academic Article The NF-kappaB factor RelB and histone H3 lysine methyltransferase G9a directly interact to generate epigenetic silencing in endotoxin tolerance.
Academic Article Facultative heterochromatin formation at the IL-1 beta promoter in LPS tolerance and sepsis.
Academic Article NAD+-dependent sirtuin 1 and 6 proteins coordinate a switch from glucose to fatty acid oxidation during the acute inflammatory response.
Academic Article Endogenous signals released from necrotic cells augment inflammatory responses to bacterial endotoxin.
Academic Article Epigenetic silencing of tumor necrosis factor alpha during endotoxin tolerance.
Academic Article Dynamic and selective nucleosome repositioning during endotoxin tolerance.
Academic Article MicroRNAs distinguish translational from transcriptional silencing during endotoxin tolerance.
Academic Article NAD+-dependent SIRT1 deacetylase participates in epigenetic reprogramming during endotoxin tolerance.
Academic Article MicroRNA-146a regulates both transcription silencing and translation disruption of TNF-a during TLR4-induced gene reprogramming.
Concept Myeloid Differentiation Factor 88
Concept STAT3 Transcription Factor
Concept Tumor Necrosis Factor-alpha
Concept Transforming Growth Factor beta
Concept Transcription Factor RelB
Concept Transcription Factor RelA
Concept Hypoxia-Inducible Factor 1, alpha Subunit
Academic Article Mitogen-activated protein kinase phosphatase 1 disrupts proinflammatory protein synthesis in endotoxin-adapted monocytes.
Academic Article MicroRNA-146a and RBM4 form a negative feed-forward loop that disrupts cytokine mRNA translation following TLR4 responses in human THP-1 monocytes.
Academic Article RelB: an outlier in leukocyte biology.
Academic Article MicroRNA 21 (miR-21) and miR-181b couple with NFI-A to generate myeloid-derived suppressor cells and promote immunosuppression in late sepsis.
Academic Article Sequential actions of SIRT1-RELB-SIRT3 coordinate nuclear-mitochondrial communication during immunometabolic adaptation to acute inflammation and sepsis.
Academic Article Processing Body Formation Limits Proinflammatory Cytokine Synthesis in Endotoxin-Tolerant Monocytes and Murine Septic Macrophages.
Academic Article GAPDH Binding to TNF-a mRNA Contributes to Posttranscriptional Repression in Monocytes: A Novel Mechanism of Communication between Inflammation and Metabolism.
Academic Article Sirtuin-2 Regulates Sepsis Inflammation in ob/ob Mice.
Academic Article Stat3 and C/EBPß synergize to induce miR-21 and miR-181b expression during sepsis.
Grant Epigenetics of Severe Systemic Inflammation
Grant Function and Metabolic Properties of Toxic Neutrophils
Grant Mitochondrial Biogenesis is Regulated by RelB During Inflammation
Academic Article Mitochondrial Sirtuin 4 Resolves Immune Tolerance in Monocytes by Rebalancing Glycolysis and Glucose Oxidation Homeostasis.
Academic Article Cysteine thiol oxidation on SIRT2 regulates inflammation in obese mice with sepsis.
Academic Article S100A9 maintains myeloid-derived suppressor cells in chronic sepsis by inducing miR-21 and miR-181b.
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