EIF3K Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line. This product provides a heterogeneous mixture of cells harboring disruptive edits in the EIF3K gene, offering a loss-of-function model without reliance on single-cell clonal isolation. The polyclonal format retains genetic diversity while ensuring robust target-gene disruption, making it suitable for pooled functional genomics screens, inhibitor profiling, and translational studies.
HeLa cells are a widely used immortalized cell line originally derived from a cervical adenocarcinoma of Henrietta Lacks. These epithelial cells are HPV-18 positive and exhibit an aneuploid karyotype. Extensively characterized in cancer biology, cell signaling, and drug discovery, HeLa cells provide a reproducible and accessible platform for investigating molecular mechanisms. Their transformed phenotype and extensive molecular annotation support studies into proliferation, survival, and metastasis.
EIF3K encodes a non-core subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, which coordinates 40S ribosomal subunit recruitment to the 5?? cap of mRNA for start codon scanning. EIF3K integrates upstream signals from mTOR and MAPK pathways, responding to growth factors such as EGF and IGF-1, and to nutrient or energy stress via AMPK. Within the eIF3 holocomplex, EIF3K interacts with core subunits including EIF3A, EIF3B, and EIF3C, and bridges associations with eIF4G and the 40S ribosome. It modulates translation of specific oncogenic mRNAs, notably MYC, CCND1, and BCL2, thereby influencing cell cycle progression and apoptosis. Additionally, EIF3K cooperates with the RNA modifier METTL3 to fine-tune translational output.
In HeLa cells, EIF3K sits at the intersection of mTOR-driven growth signals and cap-dependent translation, making its disruption a valuable tool for dissecting aberrant protein synthesis in cancer. HeLa cells exhibit elevated global translation rates typical of transformed cells, and loss of EIF3K impairs selective translation of proliferation-related transcripts. This model thus enables mechanistic investigation of eIF3K-dependent oncogenic phenotypes, including sustained growth, survival signaling, and metabolic adaptation.
This knockout model supports a broad panel of experimental approaches. Polysome profiling and ribosome profiling can map translation initiation defects and identify EIF3K-dependent translatomes. Puromycin incorporation assays measure de novo protein synthesis, while Western blotting and RT-qPCR verify downstream target expression. Functional studies such as colony formation, cell proliferation, and migration/invasion assays probe tumorigenic potential. The cells also serve as a screening platform for small-molecule translation inhibitors targeting the eIF3 complex or mTOR signaling. For further information, please contact Ascent Research.
