Katia Vancompernolle
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Tumour necrosis factor induces phosphorylation primarily of the nitric-oxide-responsive form of glyoxalase I
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Tumor necrosis factor modulates glycolysis, the glyoxalase system and induces the formation of specific methylglyoxal-modified proteins in aortic endothelial cells
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Methylglyoxal suppresses TNF-alpha-induced NF-kappa B activation by inhibiting NF-kappa B DNA-binding
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A novel cell death pathway as potential therapeutic target for the treatment of cancer
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Tumor necrosis factor-induced modulation of glyoxalase I activities through phosphorylation by PKA results in cell death and is accompanied by the formation of a specific methyl glyoxal-derived AGE.
(2002) PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 99(2). p.949-954 -
Role of reactive oxygen species in tumor necrosis factor toxicity
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Villin function in the organization of the actin cytoskeleton: correlation of in vivo effects to its biochemical activities in vitro
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Atractyloside-induced release of cathepsin B, a protease with caspase-processing activity.
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- Journal Article
- A1
- open access
A caspase-activated factor (CAF) induces mitochondrial membrane depolarization and cytochrome c release by a nonproteolytic mechanism.
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Identification of two regions in the N-terminal domain of ActA involved in the actin comet tail formation by Listeria monocytogenes.