The EIF4E3 Knockout HEK293T Polyclonal Cells are a pool of CRISPR/Cas9-edited HEK293T cells featuring targeted disruption of the endogenous EIF4E3 gene. As a polyclonal knockout population, this product provides a heterogeneous collection of cells with diverse editing outcomes, circumventing the need for single-cell cloning and enabling pooled screening approaches. This loss-of-function model is designed to facilitate investigation of EIF4E3-dependent processes in cap-dependent translation and associated pathways.
The HEK293T host cell line is derived from human embryonic kidney cells and stably expresses the SV40 large T antigen, a feature that underpins its exceptional transfection efficiency and capacity for high-level protein expression. These cells are a cornerstone in molecular and cellular biology, widely employed for lentivirus production, CRISPR screening, and the study of signal transduction. The robust proliferative capacity and well-characterized signaling networks of HEK293T cells make them an ideal chassis for generating knockout models, particularly for cancer-relevant research.
EIF4E3 encodes a cap-binding protein that functions as a translational repressor, competing with the canonical initiation factor eIF4E for the mRNA 5?? cap. By binding to the cap, EIF4E3 prevents assembly of the eIF4F complex, thereby inhibiting 40S ribosomal subunit recruitment and translation initiation of specific mRNA subsets. This repression is mediated through interaction with the nucleocytoplasmic shuttling protein EIF4ENIF1 (4E-T), which facilitates mRNA silencing and decay. The activity of EIF4E3 is subject to regulation by upstream factors such as TP53 and MYC, placing it at the intersection of the mTOR signaling pathway and cellular stress responses. Notably, EIF4E3 post-transcriptionally regulates the expression of key oncogenes, including c-MYC, contributing to its proposed role in tumor suppression.
In the HEK293T context, knockout of EIF4E3 provides a clean system to dissect its repressive functions without interference from endogenous protein. This model is particularly informative for studying cap-dependent translation control, as HEK293T cells maintain intact mTOR signaling. Researchers can use these cells to assess how loss of EIF4E3 impacts the translation of its target mRNAs, alters cell proliferation, and perturbs downstream pathways. Given the implication of EIF4E3 in acute myeloid leukemia and other cancers, this polyclonal knockout model serves as a relevant platform for exploring tumor biology and may reveal synthetic vulnerabilities or resistance mechanisms.
These EIF4E3 knockout cells are suitable for polysome profiling, RNA immunoprecipitation, cap-binding assays, and co-immunoprecipitation to characterize translation control changes and protein interactions. Functional readouts including cell proliferation assays, Western blotting, and dual-luciferase reporters further facilitate investigation of tumor suppressor activity. TIDE analysis can verify editing efficiency in the polyclonal pool. For additional details, contact Ascent Research.
