EIF4G3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T-lymphocyte line, designed for studying the scaffold protein EIF4G3 in cap-dependent translation initiation. This product features CRISPR/Cas9-mediated disruption of the EIF4G3 gene, producing a heterogeneous pool of cells with targeted loss-of-function alleles, ideal for functional studies without clonal selection artifacts. The polyclonal format provides a representative spectrum of mutations, enabling robust interrogation of EIF4G3-dependent pathways.
Jurkat cells are an immortalized human T-cell line originally derived from a patient with acute T-cell leukemia, widely utilized as a model system for T-cell receptor signaling, apoptosis regulation, and leukemogenesis. Their well-characterized signal transduction networks and rapid suspension growth make them a preferred host for investigating molecular mechanisms underlying immune function and malignant transformation.
EIF4G3 functions as a central scaffold within the eIF4F cap-binding complex, bridging the mRNA 5′ cap structure via eIF4E and the poly(A) tail via PABPC1 to circularize the transcript and enhance ribosome recruitment. Its interactions with eIF4A, an ATP-dependent RNA helicase, and eIF3, which mediates 40S ribosomal subunit binding, are essential for cap-dependent translation initiation. The activity of EIF4G3 is modulated by upstream mTORC1 signaling and the availability of eIF4E, while its scaffolding role directly impacts the synthesis of cyclin D1 and Bcl-xL, linking translation control to cell proliferation and apoptosis. Additional regulatory inputs involve MKNK1-mediated phosphorylation and cooperation with eIF4B.
Disruption of EIF4G3 in Jurkat T lymphocytes is anticipated to suppress cap-dependent translation, reducing protein output of key regulators such as cyclin D1 and Bcl-xL, thereby uncoupling cell cycle progression and anti-apoptotic signaling. This creates a model system to investigate how translational dysregulation contributes to T-cell acute leukemia, including oncogene addiction to protein synthesis and translational reprogramming under stress. The polyclonal knockout population, with its diverse genetic disruptions, provides a robust platform for high-content screens and mechanistic studies.
This polyclonal knockout model is suited for diverse applications including puromycin incorporation and polysome profiling to gauge translation efficiency, western blotting of downstream targets, and MTT or annexin V assays for viability and apoptosis. It can also be employed in drug sensitivity screens targeting eIF4F complex components and flow cytometric cell cycle analysis. For additional information or ordering, please contact Ascent Research.
