Publications by authors named "N Loaec"
BCL-x is a master regulator of apoptosis whose pre-mRNA is alternatively spliced into either a long (canonical) anti-apoptotic Bcl-xL isoform, or a short (alternative) pro-apoptotic Bcl-xS isoform. The balance between these two antagonistic isoforms is tightly regulated and overexpression of Bcl-xL has been linked to resistance to chemotherapy in several cancers, whereas overexpression of Bcl-xS is associated to some forms of diabetes and cardiac disorders. The splicing factor RBM25 controls alternative splicing of BCL-x: its overexpression favours the production of Bcl-xS, whereas its downregulation has the opposite effect.
View Article and Find Full Text PDFThe Epstein-Barr virus (EBV) is the first oncogenic virus described in human. EBV infects more than 90% of the human population worldwide, but most EBV infections are asymptomatic. After the primary infection, the virus persists lifelong in the memory B cells of the infected individuals.
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- The Epstein-Barr virus (EBV) uses the EBNA1 protein to maintain its genome while evading the immune system by limiting the translation of its mRNA through a glycine-alanine repeat (GAr).
- The host protein nucleolin (NCL) interacts with G-quadruplexes in the GAr sequence, and its interaction is crucial for suppressing the translation of EBNA1.
- Targeting type I arginine methyltransferases (PRMT1 and PRMT3) can disrupt this interaction, potentially enhancing the immune response against EBV-associated cancers.
CBS encodes a pyridoxal 5'-phosphate-dependent enzyme that catalyses the condensation of homocysteine and serine to form cystathionine. Due to its implication in some cancers and in the cognitive pathophysiology of Down syndrome, the identification of pharmacological inhibitors of this enzyme is urgently required. However, thus far, attempts to identify such molecules have only led to the identification of compounds with low potency and limited selectivity.
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- - Mitochondrial complex V is crucial for ATP production, with most of its subunits encoded by nuclear genes; a specific splice variant (c.87+3A>G) in the ATP5PO gene was found in three individuals suspected of having a mitochondrial disorder.
- - The affected individuals exhibited severe symptoms typical of Leigh syndrome, including developmental issues and cardiomyopathy, and biochemical studies revealed a significant reduction in ATP5PO protein levels and impaired complex V function.
- - Experimental results indicated that the ATP5PO variant leads to a non-functional protein due to the skipping of an essential exon, confirming its pathogenic role and linking it to defects in mitochondrial energy production.