The APOBEC3C Knockout HAP1 Polyclonal Cells consist of a population of human near-haploid fibroblast-like cells with CRISPR/Cas9-mediated disruption of the APOBEC3C gene. This polyclonal knockout pool provides a loss-of-function model for studying APOBEC3C function in innate immunity and mutagenesis. The absence of single-cell cloning avoids selection bias and maintains population heterogeneity, making it suitable for bulk assays and pooled screens.
HAP1 is a near-haploid cell line derived from KBM-7 chronic myeloid leukemia cells, widely adopted for genetic screens and functional genomics studies. Its haploid nature permits direct genotype-phenotype correlations and reduces complementation by an additional allele, while rapid proliferation supports high-throughput applications. HAP1 cells are fibroblast-like and are compatible with standard transfection, infection, and molecular biology protocols.
APOBEC3C is a cytidine deaminase that restricts retroviruses and retrotransposons by deaminating cytidine to uridine in viral cDNA, causing G-to-A hypermutations and proviral inactivation. Its expression is induced by interferon-??/?? and -?? signaling through STAT1 and IRF7 downstream of IFNAR. APOBEC3C targets single-stranded DNA and is weakly counteracted by viral Vif proteins. Besides antiviral defense, off-target cellular DNA deamination contributes to cancer-associated mutational signatures.
In the HAP1 background, APOBEC3C knockout eliminates the enzyme’s activity, allowing unambiguous dissection of its role in interferon-stimulated antiviral pathways and endogenous mutagenesis. The polyclonal format enables robust population-level measurements, including Western blotting of APOBEC3C induction upon interferon treatment, RT-qPCR analysis of downstream targets, and HIV-1 infectivity assays to assess restriction. The absence of closely related APOBEC3 family members in HAP1 reduces redundancy, simplifying phenotypic interpretation.
Applications include screening for regulators of APOBEC3C expression using interferon stimulation and immunofluorescence, characterizing HIV-1 host interaction via infectivity assays, and investigating APOBEC-mediated mutation signatures in cancer models through DNA editing assays. The knockout population is also suitable for CRISPR-based modifier screens and validation of genome-wide screen hits, offering a cost-effective alternative to clonal lines. For further information or a quote, please contact Ascent Research.
