The IVNS1ABP Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the human near-haploid HAP1 cell line, featuring targeted disruption of the IVNS1ABP gene. This product provides a heterogeneous pool of edited cells with loss-of-function mutations, enabling functional studies without clonal selection.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia (CML) line, characteristically BCR-ABL positive, near-haploid, p53 functional, and adherent. Their near-haploid karyotype simplifies genetic analysis and knockout generation, while the CML background provides a relevant leukemic model for investigating oncogenic signaling and drug responses.
IVNS1ABP (Influenza Virus NS1A-Binding Protein) is a multifunctional protein that governs pre-mRNA splicing, mRNA nuclear export, and actin cytoskeleton stabilization. It directly binds the influenza A virus NS1 protein, sequestering it to prevent viral suppression of host immune responses. Upstream regulation involves cyclin-dependent kinases and pre-mRNA splicing signals; downstream, IVNS1ABP influences splice site selection, actin filament organization, and NS1 protein localization. Its interaction network includes spliceosome components (U1 snRNP), actin, and mRNA export factors, positioning it at the intersection of RNA processing, cytoskeletal dynamics, and antiviral innate immunity.
In the context of HAP1 CML cells, disrupting IVNS1ABP offers unique advantages. The leukemic background permits dissection of splicing-dependent oncogenic mechanisms and apoptosis regulation, while the near-haploid state facilitates unambiguous genotype-phenotype correlations. This model is particularly suited to studying how IVNS1ABP influences actin-mediated processes in cell adhesion and migration, and its role in modulating drug sensitivity to CDK inhibitors, which are relevant in CML therapy.
Research applications are broad and include investigating influenza A virus?Chost interactions via co-immunoprecipitation of NS1, viral replication assays, and functional splicing analyses using RT-qPCR and RNA-seq. Additional assays such as western blotting, immunofluorescence for nuclear speckles and actin, apoptosis profiling, and drug sensitivity testing (CDK inhibitors) can dissect the molecular consequences of IVNS1ABP loss. For further details or to inquire about this product, please contact Ascent Research.
