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Jean-François Dierick

Researcher at Université de Namur

Publications -  18
Citations -  703

Jean-François Dierick is an academic researcher from Université de Namur. The author has contributed to research in topics: Stress-induced premature senescence & Senescence. The author has an hindex of 10, co-authored 17 publications receiving 672 citations. Previous affiliations of Jean-François Dierick include University of Southern Denmark.

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Proteome analysis and identification of symbiosis-related proteins from Medicago truncatula Gaertn. by two-dimensional electrophoresis and mass spectrometry

TL;DR: Internal sequencing with a quadrupole time‐of‐flight mass spectrometer and database searches confirmed the induction of proteins previously described in root symbioses, and revealed the implication of other proteins.
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Stress‐Induced Premature Senescence: Essence of Life, Evolution, Stress, and Aging

TL;DR: The stress syndrome was discovered accidentally by Hans Selye while searching for new hormones in the placenta because he found adrenal enlargements and involution of thymus and lymph nodes, which he thought were specific for a particular hormone.
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Stress-induced premature senescence and replicative senescence are different phenotypes, proteomic evidence

TL;DR: How a proteomic analysis can be useful to approach complex biological problems is illustrated by the concept of stress-induced premature senescence (SIPS), which was induced by two very different stressors: tert-butyhydroperoxide or ethanol.
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Stress-Induced Premature Senescence or Stress-Induced Senescence-Like Phenotype: One In Vivo Reality, Two Possible Definitions?

TL;DR: Irreversible growth arrest after exposure to oxidative stress and generation of DNA damage could be as efficient in avoiding immortalisation as “telomere-dependent” replicative senescence.
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Growth kinetics rather than stress accelerate telomere shortening in cultures of human diploid fibroblasts in oxidative stress-induced premature senescence

TL;DR: The percentage of cells resuming proliferation after stress suggests this telomere shortening is due to the number of cell divisions accomplished to reach confluence during the first PD after stress.