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This project aims to investigate N-linked glycosylation modifications in bone marrow cells (BMCs) of an autosomal dominant osteopetrosis type 2 (ADO2) mouse model carrying the Clcn7 (r284w) mutation. Using LC-MS/MS-based 4D Label-Free N-Glycosylation Proteomics Analysis, we identified significant alterations in the N-glycosylation landscape of ADO2 BMCs compared to wild-type (WT) controls. These findings provide insights into the role of glycosylation in ADO2 pathogenesis, particularly in mononuclear phagocytes.