- Dissociated glucocorticoids with anti-inflammatory potential repress interleukin-6 gene expression by a nuclear factor-kappa B-dependent mechanism.
- In search of the molecular mechanism of gene repression by glucocorticoids.
- N-acetyl-L-cysteine inhibits primary human T cell responses at the dendritic cell level: Association with NF-kappa B inhibition.
- The nuclear factor-kappa B engages CBP/p300 and histone acetyltransferase activity for transcriptional activation of the interleukin-6 gene promoter.
- 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.
- The zinc finger protein A20 inhibits TNF-induced NF-kappa B-dependent gene expression by interfering with an RIP- or TRAF2-mediated transactivation signal and directly binds to a novel NF-kappa B-inhibiting protein ABIN.
- In search of the molecular mechanism of gene repression by glucocorticoids
- p38 and extracellular signal-regulated kinase mitogen-activated protein kinase pathways are required for nuclear factor kappa B p65 transactivation mediated by tumor necrosis factor.
- Tumour necrosis factor: intracellular mechanism of action
Glucocorticoid-mediated repression of nuclear factor-κB-dependent transcription involves direct interference with transactivation
1997) PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 94(25). p.13504-13509 Mark(