LBMCE at Yeast Meeting
The Telomere Biology and Functional Regulation and RNA Surveillance teams participated in the Yeast 2025 conference at Sorbonne University.
Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes
Laboratory of Molecular and Cellular Biology of Eukaryotes
The Telomere Biology and Functional Regulation and RNA Surveillance teams participated in the Yeast 2025 conference at Sorbonne University.
Mitochondria assemble in a dynamic tubular network. Their morphology is governed by mitochondrial fusion and fission, which regulate most mitochondrial functions including oxidative phosphorylation.
Previous studies using ubiquitin traps combined with mass spectrometry revealed that in Bortezomib (BTZ) resistant Mantle Cell Lymphoma (MCL) cells, a selective autophagy mechanism, known as proteaphagy, was a main mechanism eliminating the proteasome and reducing the sensitivity to this treatment.
Telomere shortening ultimately causes replicative senescence.
Northern blot, or RNA blot, is a widely used technique in molecular biology to detect and semi-quantify specific RNAs. The advantage of this method is its ability to simultaneously estimate the sizes and quantities of degraded or processed RNA products.
TELS1 reveals a minor contribution for telomere loops in chromosome end-protection Dr Jérôme Dejardin invité par Maria Teresa Teixeira Lundi 9 Décembre 2024 à 10:30 à l’IBPC – Salle de Conférences 3è étage Chromosome-end protection is crucial for genome stability, Read more
“Molecular and Cellular Responses to the Shortest Telomere in Saccharomyces cerevisiae”
directed by Dr Teresa Teixeira.
The defense will take place on Friday, October 11, 2024, at 2:00 PM, in the Edmond de Rothschild Library at the Institut de Biologie Physico-Chimique (IBPC), located at 13 rue Pierre et Marie Curie, 75005 Paris.
Outer mitochondrial membrane fusion, a vital cellular process, is mediated by mitofusins. However, the underlying molecular mechanism remains elusive.
Telomere maintenance is a universal hallmark of cancers to sustain the unlimited proliferative potential. In ~85% of cancers, telomere shortening is mitigated by reactivated telomerase expression while the other ~15% use a recombination-based mechanism, termed Alternative Lengthening of Telomeres (ALT).
Replicative senescence is triggered when telomeres reach critically short length and activate permanent DNA damage checkpoint-dependent cell cycle arrest.
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