Blood: E3 connecting enzyme UBR5 mutation regulates lymphoma B cell maturation

In order to promote B-cell development, activation and survival, coordination of a variety of molecular mechanisms, including transcription, selective splicing, and type switchre, is requiredThe destruction of these pathways can lead to malignant transformationRecently, researchers have found new mutations in patients with set cell lymphoma (MCL) through second-generation sequencing, including the ubiquitin E3-connected enzyme UBR5 mutationabout 18% of MCL patients were found to carry UBR5 mutations, most of which occur in the HECT domain of the protein, which accepts ubiquinone molecules and transfers them to the endto clarify whether UBR5 regulates the maturation of B cells is of great significance for a comprehensive understanding of the malignant transformation of MCLTo illustrate the role of UBR5 in B-cell maturation and activation, the researchers created a mouse model that conditionally destroys the C-end HECT domain of UBR5It was found that the lack of UBR5 HECT domain led to the obstruction of the maturation of b cells in the spleen and the protein associated with mRNA shears was raised through the splicing, this study reveals the new function of UBR5 in B cell maturation, that is, in the process of B cell development, the maturation of B cells by stabilizing the splicing composition, suggesting that UBR5 mutation plays a role in the transformation of set cell lymphoma