The EIF3K Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the HEK293T cell line, engineered for targeted disruption of the EIF3K gene. This product provides a heterogeneous loss-of-function model suitable for investigating the role of the eIF3K subunit in translation initiation and cellular signaling. The polyclonal nature ensures representation of diverse editing outcomes across the population, offering a robust tool for functional genomic studies without the limitations of single clonal isolates.
HEK293T cells are adherent epithelial cells derived from human embryonic kidney and stably express the SV40 large T antigen, which facilitates episomal replication of plasmids containing the SV40 origin of replication. This feature enables high-level transient protein expression and efficient retroviral/lentiviral packaging. Widely employed in molecular and cellular biology, HEK293T cells are valued for their robust growth characteristics, ease of transfection, and compatibility with a broad range of functional assays, making them an ideal chassis for generating knockout models via CRISPR/Cas9.
EIF3K encodes a non-essential subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, which facilitates recruitment of the 43S preinitiation complex to mRNA for cap-dependent translation initiation. EIF3K activity is modulated by mTORC1 signaling through downstream effectors S6K and 4E-BP, and its transcription is regulated by MYC. It interacts with eIF3 subunits (A, B, C, G, I), the 40S ribosomal subunit, and eIF4G, linking mTOR pathway signals to the translation machinery. This integration enables selective regulation of mRNAs, including those with TOP motifs or complex 5?? UTRs.
In the HEK293T background, disruption of EIF3K allows dissection of its contributions to translation initiation and growth control. Associations with hepatocellular carcinoma, gastric cancer, and breast cancer make this model valuable for exploring oncogenic translation programs and mTOR dependency. The polyclonal population minimizes clonal artifacts and provides a robust system for genotype-phenotype correlations.
Researchers can employ these cells to examine cap-dependent translation mechanisms using polysome and ribosome profiling, translational efficiency RT-qPCR, and co-immunoprecipitation of eIF3 complex components. Functional assays such as MTT and colony formation evaluate effects of EIF3K loss on cell proliferation and mTOR inhibitor sensitivity. This polyclonal knockout population is suited for screening translation inhibitors, investigating mTOR pathway crosstalk, and validating EIF3K as a cancer target. Contact Ascent Research for more information.
