The KPNA2 Knockout HEK293T Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from HEK293T human embryonic kidney cells. This heterogeneous pool carries targeted disruption of the KPNA2 gene, generating a loss-of-function model that compromises importin ??2 expression across the population. The polyclonal format ensures diverse mutational events without clonal selection artifacts, providing a robust tool for studying KPNA2-dependent nuclear transport and associated cellular functions.
HEK293T is a female human embryonic kidney epithelial cell line transformed with adenovirus type 5 DNA, conferring constitutive SV40 large T antigen expression. These cells offer high transfection efficiency, rapid proliferation, and outstanding capacity for recombinant protein expression and viral particle production. Their extensive use in genetic perturbation studies ensures reliable CRISPR/Cas9 editing and reproducible experimental outcomes, making them an ideal chassis for KPNA2 knockout generation.
KPNA2 encodes importin ??2, a nuclear import adaptor that recognizes classical NLS motifs on cargo proteins. It forms a complex with importin ?? (KPNB1) and NLS-cargo, docks at the nuclear pore complex via NUP50 and NUP98, and releases cargo upon RanGTP binding. KPNA2 is transcriptionally regulated by E2F1, MYC, and estrogen signaling. It mediates nuclear import of key factors including TP53, RB1, STAT1, and NF-??B (RELA), as well as viral nuclear antigens. Through this mechanism, KPNA2 governs cell cycle progression, DNA repair, circadian rhythms, and viral replication.
In HEK293T cells, endogenous KPNA2 participates in active nuclear transport, and its disruption allows straightforward phenotypic assessment in a human epithelial context. This model is particularly relevant for oncology research, as KPNA2 overexpression is linked to colorectal, breast, lung, gastric, and hepatocellular carcinomas, where it drives proliferation and metastasis via E2F1/MYC-dependent transcription and downstream TP53/RB1 pathway modulation. Studying the loss of importin ??2 in this tractable cell line clarifies its contribution to oncogenic signaling and nuclear import dependencies.
The polyclonal knockout pool supports diverse assays: western blotting validates KPNA2 ablation; immunofluorescence with fluorescent NLS cargo quantifies import defects; CCK-8 and flow cytometry measure proliferation and cell cycle changes; Transwell assays assess migration; and co-immunoprecipitation maps KPNA2?Ccargo interactions. RNA-seq reveals transcriptomic adaptations, while infection models (influenza A, HBV) probe viral nuclear entry. DNA damage response studies can be performed with genotoxic agents. For further information or application support, please contact Ascent Research.
