Karolien De Bosscher

ORCID: 0000-0001-5059-9718
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About
Contact & Profiles
Research Areas
  • Estrogen and related hormone effects
  • Cytokine Signaling Pathways and Interactions
  • NF-κB Signaling Pathways
  • Hormonal Regulation and Hypertension
  • Adrenal Hormones and Disorders
  • Immune Response and Inflammation
  • Peroxisome Proliferator-Activated Receptors
  • Immune Cell Function and Interaction
  • Parasitic Infections and Diagnostics
  • Histone Deacetylase Inhibitors Research
  • Immunotherapy and Immune Responses
  • Retinoids in leukemia and cellular processes
  • Heat shock proteins research
  • interferon and immune responses
  • Liver Disease Diagnosis and Treatment
  • Adipose Tissue and Metabolism
  • Asthma and respiratory diseases
  • Stress Responses and Cortisol
  • T-cell and B-cell Immunology
  • Peptidase Inhibition and Analysis
  • Signaling Pathways in Disease
  • Malaria Research and Control
  • Allergic Rhinitis and Sensitization
  • Multiple Myeloma Research and Treatments
  • Nuclear Receptors and Signaling

Cancer Research Institute Ghent
2016-2025

Ghent University
2016-2025

VIB-UGent Center for Medical Biotechnology
2016-2025

Vlaams Instituut voor Biotechnologie
1998-2024

Allegheny Health Network
2022

Weatherford College
2022

VIB-UGent Center for Inflammation Research
2020

Ghent University Hospital
2009-2017

Memorial Sloan Kettering Cancer Center
2013

Chang Gung Memorial Hospital
2012

Interleukin-6 (IL-6) is a pleiotropic cytokine, whose plasma levels are elevated in inflammatory diseases such as atherosclerosis. We have previously reported that peroxisome proliferator-activated receptor alpha (PPARalpha) ligands (fibrates) lower concentrations of IL-6 patients with atherosclerosis and inhibit IL-1-stimulated secretion by human aortic smooth muscle cells (SMC). Here, we show explants isolated from PPARalpha-null mice display an exacerbated response to stimuli,...

10.1074/jbc.274.45.32048 article EN cc-by Journal of Biological Chemistry 1999-11-01

Interleukin-6 (IL-6) is a pleiotropic cytokine, which involved in inflammatory and immune responses, acute phase reactions, hematopoiesis. In the mouse fibrosarcoma cell line L929, nuclear factor (NF)-κB plays crucial role IL-6 gene expression mediated by tumor necrosis (TNF). The levels of activated do not, however, correlate with variations transcription; therefore, other factors and/or regulatory mechanisms presumably modulate mRNA production. Upon analysis various deletion point-mutated...

10.1074/jbc.273.6.3285 article EN cc-by Journal of Biological Chemistry 1998-02-01

Glucocorticoids exert multiple anti-inflammatory activities, one of which is the inhibition transcription dependent on nuclear factor (NF)-κB. It has been suggested that effect dexamethasone (DEX), a glucocorticoid analog, attributed to an increased production inhibitory IκB molecule, in turn would bind and remove activated, DNA-bound NF-κB complexes cell nucleus. Upon investigating DEX-mediated repression interleukin-6 expression induced by tumor necrosis factor, DEX treatment was found act...

10.1073/pnas.94.25.13504 article EN Proceedings of the National Academy of Sciences 1997-12-09

Expression of the pleiotropic cytokine interleukin (IL)-6 can be stimulated by proinflammatory tumor necrosis factor (TNF) and microbial alkaloid staurosporine (STS). In this report, transcriptional mechanisms were thoroughly investigated. Whereas transcription factors binding to activator protein-1-, cAMP-responsive element-, CAAT enhancer-binding protein-responsive sequences are necessary for gene activation STS, nuclear (NF)-kappaB alone is responsible sufficient inducibility TNF, which...

10.1074/jbc.274.45.32091 article EN cc-by Journal of Biological Chemistry 1999-11-01

Glucocorticoids (GCs) are used to combat inflammatory diseases. Their beneficial effect relies mainly on the inhibition of NF-κB- and/or AP-1-driven proinflammatory gene expression. Previously, we have shown that GCs repress tumor necrosis factor-induced IL-6 expression by an NF-κB-dependent nuclear mechanism without changing DNA-binding capacity NF-κB or levels cytoplasmic inhibitor (IκB-α). In present work, investigate GC repression different natural recombinant NF-κB-driven reporter...

10.1073/pnas.97.8.3919 article EN Proceedings of the National Academy of Sciences 2000-04-11

The identification of selective glucocorticoid receptor (GR) modifiers, which separate transactivation and transrepression properties, represents an important research goal for steroid pharmacology. Although the gene-activating properties GR are mainly associated with undesirable side effects, its negative interference activity transcription factors, such as NF-κB, greatly contributes to antiinflammatory immune-suppressive capacities. In present study, we found that Compound A (CpdA), a...

10.1073/pnas.0505554102 article EN Proceedings of the National Academy of Sciences 2005-10-21
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