EIF3M Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the EIF3M gene. This model provides a heterogeneous loss-of-function system derived from HEK293T cells, a widely used human embryonic kidney line. The knockout is generated without clonal selection, enabling studies in a population context that retains the parental line’s favorable growth and transfection characteristics.
HEK293T cells are a transformed human embryonic kidney epithelial line that stably expresses the SV40 large T antigen. This background confers high transfection efficiency and robust protein expression capacity, making it a standard platform for gene overexpression, reporter assays, and recombinant protein production. The line is well-established in biomedical research for mechanistic and translational studies.
EIF3M encodes the M subunit of the eukaryotic translation initiation factor 3 (eIF3) complex, a key assembly that drives cap-dependent translation initiation. EIF3M stabilizes eIF3 binding to the 40S ribosomal subunit, facilitating recruitment of the ternary complex and mRNA to form the 43S preinitiation complex. EIF3M function is regulated by the mTOR pathway, which responds to growth factors and amino acid availability via effectors including 4E-BP1 and S6K. The eIF3 complex interacts with eIF4G, eIF4A, and all other eIF3 subunits (eIF3A-L), and its activity promotes translation of downstream targets such as MYC and cyclins. This places EIF3M at the nexus of growth signaling and translational control.
In HEK293T cells, EIF3M knockout allows precise dissection of eIF3-dependent translational mechanisms. The loss-of-function model is suited for investigating mTOR-mediated regulation, the integrated stress response, and the role of individual eIF3 subunits in ribosome recruitment. The polyclonal format captures population-level effects, providing a physiologically relevant context for studying translation in cancer proliferation and stress adaptation. Researchers can also explore how EIF3M loss impacts eIF3 complex integrity and target mRNA selection.
Applications include polysome profiling to assess ribosome loading, ribosome footprinting for translatome analysis, puromycin incorporation assays to monitor protein synthesis rates, dual luciferase reporter assays for cap-dependent initiation, and RT-qPCR for downstream targets like MYC and cyclins. This model also supports drug-target validation for translation inhibitors and functional genomic screens. For further information or assistance, please contact Ascent Research.
