The EEF1A2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the endogenous EEF1A2 gene in the HEK293T human cell line. This pooled format contains a diverse set of edited alleles, enabling robust loss-of-function studies while minimizing clonal selection biases. It serves as a practical tool for investigating the isoform-specific roles of EEF1A2 in human cells.
The HEK293T host line is a widely utilized human embryonic kidney epithelial cell line that constitutively expresses the SV40 large T antigen, which promotes episomal replication of plasmids carrying the SV40 origin and drives high-level recombinant protein production. These adherent cells exhibit rapid proliferation, high transfection efficiency, and a well-characterized signaling environment, making them a standard choice for functional genomics and protein expression studies.
The EEF1A2 gene encodes a member of the eukaryotic translation elongation factor-1 alpha family, which canonically functions in the GTP-dependent delivery of aminoacyl-tRNA to the ribosomal A site during protein synthesis. In addition, EEF1A2 has non-canonical activities in apoptosis regulation and actin cytoskeleton organization. It functions downstream of PI3K-Akt-mTOR signaling, is transcriptionally regulated by MYC, and activated by growth factors such as IGF-1. EEF1A2 interacts directly with actin filaments and the focal adhesion protein zyxin. Downstream, it modulates global protein synthesis rates and influences the apoptotic regulator Bcl-xL. Disruption of EEF1A2 via CRISPR/Cas9 editing eliminates the gene product, perturbing both translation elongation and its accessory functions.
In HEK293T cells, which endogenously express the highly homologous EEF1A1 isoform, knockout of EEF1A2 permits dissection of isoform-specific contributions to cellular physiology. The polyclonal nature reduces clone-specific artifacts, facilitating unbiased functional genomics screens. This model is particularly relevant for research into neurodevelopmental disorders such as epilepsy and intellectual disability, and for cancer biology, where EEF1A2 dysregulation is linked to enhanced cell survival and proliferation, enabling studies on isoform dependency and therapeutic potential.
Researchers can deploy this knockout model in assays that measure translation rates via puromycin incorporation, assess apoptotic responses via Annexin V staining, visualize actin cytoskeletal changes with immunofluorescence, and profile gene expression by RT-qPCR or Western blotting. It is also well suited for drug sensitivity testing to uncover synthetic lethal interactions or resistance mechanisms associated with EEF1A2 loss. By integrating these approaches, scientists can define the role of EEF1A2 in protein synthesis regulation, apoptosis, and cytoskeletal dynamics. For more detailed product information, please contact Ascent Research.
