{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE264nnn/GSE264078/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE264078"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Glycosylation Orchestrates Megakaryocytic Fate of Hematopoietic Stem Cells via Wnt-Muc13 Signaling [scRNA]","description":"The cell-intrinsic and extrinsic programs governing hematopoietic stem and progenitor cells (HSPCs) cell fate determination remain unresolved. Our data reveals that loss of B4GALT1 glycosyltransferase biosynthetic activity restricts HSPC N- and O-glycosylation and reprograms previously unrecognized N-glycan gradients in the bone marrow environment with high expression of complex N-glycans in HSPC-rich regions to accumulate aberrant, cancer-like N-glycan signatures. The loss of B4GALT1 increases the expression of aberrantly glycosylated intracellular oncogenic Mucin13, which is likely to disrupt the destruction complex and mediate Wnt/β-catenin hyperactivation. This enhances metabolic and cell cycle activity, expands the megakaryocyte-primed stem cell pool, and promotes emergence from a steady state, highlighting the essential role of B4GALT1 in modulating the BM glycosylation landscape and its significance in regulating the expansion and differentiation of HSPCs.","dates":{"publication":"2026/06/03"},"accession":"GSE264078","cross_references":{"GSM":["GSM8209858","GSM8209864","GSM8209863","GSM8209862","GSM8209861","GSM8209860","GSM8209859"],"GPL":["24247"],"GSE":["264078"],"taxon":["Mus musculus"]}}