prof. Wim Vanden Berghe
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The interplay between the glucocorticoid receptor and nuclear factor-kappa B or activator protein-1: Molecular mechanisms for gene repression
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DNA binding-independent induction of I kappa B alpha gene transcription by PPAR alpha
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Induction and repression of NF-kappaB-driven inflammatory genes.
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Regulation of the transcriptional activity of the nuclear factor-kappa B p65 subunit.
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Glucocorticoid repression of AP-1 is not mediated by competition for nuclear coactivators.
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Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6.
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In search of the molecular mechanism of gene repression by glucocorticoids
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N-acetyl-L-cysteine inhibits primary human T cell responses at the dendritic cell level: Association with NF-kappa B inhibition.
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Peroxisome proliferator-activated receptor alpha negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-kappa B and AP-1.
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The nuclear factor-kappa B engages CBP/p300 and histone acetyltransferase activity for transcriptional activation of the interleukin-6 gene promoter.