C1GALT1C1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the C1GALT1C1 gene in a near-haploid human cell background. This product provides a powerful loss-of-function model generated through CRISPR/Cas9-mediated gene disruption in HAP1 cells, enabling researchers to investigate the molecular consequences of C1GALT1C1 deficiency in O-glycosylation and related cellular processes. The polyclonal population preserves genetic heterogeneity, making it suitable for pooled screening and robust phenotypic analysis without the limitations of clonal selection.
The host cell line, HAP1, is a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia (CML) cell line. Its near-haploid karyotype minimizes genetic redundancy, allowing uncomplicated interpretation of gene knockout effects, particularly in genetic screens and cancer biology. HAP1 cells retain key signaling and glycosylation machinery relevant to hematopoietic lineages, making them an appropriate platform for studying glycosyltransferase chaperones and their impact on cell surface glycan landscapes.
C1GALT1C1 encodes Cosmc, a dedicated molecular chaperone essential for the proper folding and enzymatic activity of core 1 ??3-galactosyltransferase (C1GALT1). Under normal conditions, Cosmc ensures functional C1GALT1 mediates the synthesis of the core 1 O-glycan structure (Gal??1-3GalNAc-??-Ser/Thr) on mucins such as MUC1 and cell surface receptors like CD43. This process is tightly regulated by the ER stress response and unfolded protein response (UPR). Downstream elongation of core 1 O-glycans is catalyzed by ST6GalNAc1 and ST3Gal1, generating diverse glycan epitopes critical for cell adhesion, signaling, and immune recognition. Disruption of C1GALT1C1 therefore leads to a loss of core 1 O-glycans, accumulation of Tn antigen (GalNAc-??-Ser/Thr), and dysregulation of these pathways.
In the HAP1 context, C1GALT1C1 knockout creates a model that recapitulates key features of Tn syndrome and cancer-associated glycosylation alterations. The near-haploid background amplifies the phenotypic consequences of chaperone loss, facilitating clear detection of shifts in O-glycan profiles. This system is particularly valuable for dissecting the role of C1GALT1C1 in glycoprotein biosynthesis and for screening factors that modulate the ER chaperoning of C1GALT1. The model also supports investigations into how altered glycosylation affects cell proliferation, migration, and immune evasion in a CML-derived lineage.
This polyclonal knockout population is ideally suited for applications in cancer glycobiology, O-glycosylation research, immune cell biology, mucin biology, and biomarker discovery. Representative assays include lectin blotting with PNA or VVA to detect altered glycans, flow cytometry for cell surface Tn antigen expression, Western blotting to assess C1GALT1 levels, RT-qPCR for transcript analysis, glycosylation mass spectrometry for detailed O-glycan profiling, and cell adhesion assays to evaluate functional consequences of glycan loss. Researchers employing this model can elucidate the molecular mechanisms by which C1GALT1C1-dependent glycosylation governs cellular interactions and disease progression. For additional technical information or customized options, please contact Ascent Research.
