Transduction with BBF2H7/CREB3L2 upregulates SEC23A protein in erythroblasts and partially corrects the hypo‐glycosylation phenotype associated with CDAII.

The article offers a study on lentiviral transduction of BBF2H7/7/CREB3L2 into primary human erythroid cells which causes SEC23A upregulation and persistence during terminal erythroid differentiation in both normal and Congenital Dyserythropoietic Anaemia II (CDAII) cells, an autosomal recessive hereditary anaemia caused by mutations in SEC23B gene. Topics include cloning into pXLG3-GFP expression vector and concluded no detrimental effects on erythroblast proliferation or differentiation.