https://www.pierre-francois-roux.com/tags/epigenetics/ Recent content in Epigenetics on Pierre-François Roux Hugo -- gohugo.io en-us © 2021 Pierre-François Roux Fri, 19 Jun 2026 00:00:00 +0000 https://www.pierre-francois-roux.com/teaching/molecular-basis-of-cellular-senescence-and-aging/ Fri, 19 Jun 2026 00:00:00 +0000 https://www.pierre-francois-roux.com/teaching/molecular-basis-of-cellular-senescence-and-aging/ This teaching introduces the molecular basis of cellular senescence and aging, with a focus on how stress-response pathways, chromatin regulation, metabolism and inflammatory programs interact to shape cell fate decisions. Université de Montpellier, Master 2 Biologie-Santé, 2021 Lecture, 4 h The course connects fundamental mechanisms to pathophysiological contexts, including tumor suppression, tissue aging, cancer biology and metabolic homeostasis. It also uses examples from functional genomics and multi-omic studies to show how contemporary molecular biology can move from descriptive profiles to mechanistic hypotheses. https://www.pierre-francois-roux.com/project/p53-e4f1-metabolic-epigenetic-control-of-senescence/ Fri, 19 Jun 2026 00:00:00 +0000 https://www.pierre-francois-roux.com/project/p53-e4f1-metabolic-epigenetic-control-of-senescence/ My current research at the Montpellier Cancer Research Institute focuses on how metabolic rewiring is converted into durable chromatin and transcriptional states during senescence and aging. Cellular senescence relies on checkpoint pathways controlled by pRB and p53, but these regulators do more than arrest the cell cycle: they also control metabolic homeostasis, mitochondrial function, stress adaptation and chromatin regulation. A central entry point of this project is E4F1, a multifunctional component of the p53/pRB network. https://www.pierre-francois-roux.com/project/toward-a-systems-view-of-cellular-senescence/ Fri, 27 Apr 2018 00:00:00 +0000 https://www.pierre-francois-roux.com/project/toward-a-systems-view-of-cellular-senescence/ Cellular senescence is a stress response triggered by telomere dysfunction, oncogene activation, DNA damage, oxidative stress and other insults. It leads to a durable proliferative arrest, but also to profound changes in chromatin organization, transcription, metabolism and secretory activity. This dual nature makes senescence biologically fascinating: it contributes to tumor suppression, wound healing and development, yet persistent senescent cells can also promote chronic inflammation, tissue dysfunction, cancer progression and aging-related pathologies.