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Transcriptional activation of the NF‐κB p65 subunit by mitogen‐ and stress‐activated protein kinase‐1 (MSK1)
TLDR
It is shown that the mitogen‐activated protein kinase inhibitors SB203580 and PD98059 or U0126, as well as a potentMitogen‐ and stress‐ activatedprotein kinase‐1 (MSK1) inhibitor H89, counteract tumor necrosis factor (TNF)‐mediated stimulation of p65 transactivation capacity. Expand
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression.
TLDR
The cellular signaling pathways identified as important regulators of inflammation are the signal transduction cascades mediated by the nuclear factor-kappaB and the activator protein-1, which can both be modulated by glucocorticoids. Expand
Peroxisome Proliferator-activated Receptor α Negatively Regulates the Vascular Inflammatory Gene Response by Negative Cross-talk with Transcription Factors NF-κB and AP-1*
TLDR
Fibrates inhibit the vascular inflammatory response via PPARα by interfering with the NF-κB and AP-1 transactivation capacity involving direct protein-protein interaction with p65 and c-Jun. Expand
The p38/RK mitogen‐activated protein kinase pathway regulates interleukin‐6 synthesis response to tumor necrosis factor.
TLDR
It is demonstrated that the stress‐responsive p38 mitogen‐activated protein (MAP) kinase is involved in TNF‐induced cytokine expression and that p38 MAP kinase might be an interesting target to interfere selectively with T NF‐induced gene activation. Expand
p38 and Extracellular Signal-regulated Kinase Mitogen-activated Protein Kinase Pathways Are Required for Nuclear Factor-κB p65 Transactivation Mediated by Tumor Necrosis Factor*
TLDR
It is concluded that, in addition to cytoplasmic activation and DNA binding of NF-κB, the p38 and extracellular signal-regulated kinase MAPK pathways act as necessary cooperative mechanisms to regulate TNF-induced IL-6 gene expression by modulating the transactivation machinery. Expand
A fully dissociated compound of plant origin for inflammatory gene repression.
TLDR
Compound A (CpdA), a plant-derived phenyl aziridine precursor, although not belonging to the steroidal class of GR-binding ligands, does mediate gene-inhibitory effects by activating GR and may be a lead compound of a class of antiinflammatory agents with fully dissociated properties and might hold great potential for therapeutic use. Expand
Minireview: latest perspectives on antiinflammatory actions of glucocorticoids.
TLDR
This minireview aims to highlight some of the latest findings on aspects of the antiinflammatory working mechanisms of GCs. Expand
Crosstalk in inflammation: the interplay of glucocorticoid receptor-based mechanisms and kinases and phosphatases.
TLDR
The integrated interplay between GR signaling and its correlating kinases and phosphatases are illuminated in the context of the clinically important combat of inflammation, giving attention to implications on GC-mediated side effects and therapy resistance. Expand
Interleukin-6, a mental cytokine
TLDR
It is evident that IL-6 has a dichotomic action in the CNS, displaying neurotrophic properties on the one hand, and detrimental actions on the other, in agreement with its central role in neuroinflammation, which evolved as a beneficial process, aimed at maintaining tissue homeostasis, but which can become malignant when exaggerated. Expand
Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6.
TLDR
It is postulated that other components of the enhanceosome complex are sensitive to MAPK cascades and found that MAPK activity is unequivocally linked to the histone acetylation capacity of the enhancesosome to stimulate gene expression in response to TNF. Expand
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