Most degenerative diseases are caused by the toxicity of protein forming aggregates, for example during Parkinson’s or Alzheimer’s diseases. In this article, Oamen et al discovered that the lipid tripentadecanoin has a strong neuroprotective activity. The toxicity of protein aggregates is largely reduced when neurons are pre or post treated by tripentadecanoin. Using baker’s yeast as a model for cellular … Continue reading Tripentadecanoin, a promising molecule to fight neurodegenerative diseases
Cellular senescence is an irreversible proliferation withdrawal that can be initiated after DNA damage-induced cell cycle arrest in G2 phase to prevent genomic instability caused by aberrant mitoses. Its onset requires p53 (TP53) and retinoblastoma protein (RB1) family tumour suppressors, but how a temporary cell cycle arrest is converted into a permanent one remains unknown. We show that a … Continue reading Reciprocal regulation of p21 and Chk1 controls the Cyclin D1-RB pathway to mediate senescence onset after G2 arrest
New publication from the Lagha lab in Nature Communications, by Bellec et al., 2022 Read More: A voir aussi sur les actualités de l’INSB En direct des labos The control of transcriptional memory by stable mitotic bookmarking Maëlle Bellec, Jérémy Dufourt, George Hunt, Hélène Lenden-Hasse, Antonio Trullo, Amal Zine El Aabidine, Marie Lamarque, Marissa M Gaskill, Heloïse Faure-Gautron, Mattias Mannervik, … Continue reading The control of transcriptional memory by stable mitotic bookmarking
Butterworth, Grégoire and colleagues used single molecule fluorescent in situ hybridization to detect hepatitis C virus (HCV) RNA in liver sections of a patient with hepatocellular carcinoma on hepatitis C background. Laser microdissection followed by RNAseq analysis of clusters of infected hepatocytes revealed HCV-related deregulation of genes expression. This work, carried out in the group led by Urszula Hibner, in … Continue reading GOLT1B Activation in Hepatitis C Virus-Infected Hepatocytes Links ER Trafficking and Viral Replication
ABSTRACT Spinal Muscular Atrophy (SMA) is a devastating neurodegenerative disease caused by reduced amounts of the ubiquitously expressed Survival of Motor Neuron (SMN) protein. In agreement with its crucial role in the biogenesis of spliceosomal snRNPs, SMN-deficiency is correlated to numerous splicing alterations in patient cells and various tissues of SMA mouse models. Among the snRNPs whose assembly is impacted … Continue reading Splicing efficiency of minor introns in a mouse model of SMA predominantly depends on their branchpoint sequence and can involve the contribution of major spliceosome components