Publications by authors named "M Rogier"
Efficient humoral responses rely on DNA damage, mutagenesis and error-prone DNA repair. Diversification of B cell receptors through somatic hypermutation and class-switch recombination are initiated by cytidine deamination in DNA mediated by activation-induced cytidine deaminase (AID) and by the subsequent excision of the resulting uracils by uracil DNA glycosylase (UNG) and by mismatch repair proteins. Although uracils arising in DNA are accurately repaired, how these pathways are co-opted to generate mutations and double-strand DNA breaks in the context of somatic hypermutation and class-switch recombination is unknown.
View Article and Find Full Text PDFThe autosomal recessive immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome is a genetically heterogeneous disorder. Despite the identification of the underlying gene defects, it is unclear how mutations in any of the four known ICF genes cause a primary immunodeficiency. Here we demonstrate that loss of ZBTB24 in B cells from mice and ICF2 patients affects nonhomologous end-joining (NHEJ) during immunoglobulin class-switch recombination and consequently impairs immunoglobulin production and isotype balance.
View Article and Find Full Text PDFArticle Synopsis
- * Researchers tested urine samples from healthy people and found no major differences between treating them before or after testing.
- * The results suggest that it's not needed to change the urine's acidity before checking calcium levels, which could make testing simpler.
Article Synopsis
- Maintenance of genome integrity relies on cooperation between Fanconi anemia (FA) and homologous recombination (HR) repair pathways, making cells sensitive to DNA damage from acetaldehyde, especially those lacking FANCD2.
- Inactivation of HR factors like BRCA1, BRCA2, or RAD51 increases sensitivity to acetaldehyde, indicating that even with a functioning FA pathway, cells can still be vulnerable to this type of DNA damage.
- The study suggests that inhibiting enzymatic detoxification of acetaldehyde, particularly using disulfiram, could selectively target and eliminate BRCA1/2-deficient cells and tumors, presenting a new potential therapeutic strategy.