The EIF2A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the EIF2A gene. This loss-of-function model enables investigation of EIF2A-dependent translation initiation and stress-response pathways. The polyclonal nature, comprising a heterogeneous pool of edited cells, provides a robust system for functional studies without the biases of single-clone selection.
The Jurkat cell line, an immortalized human T lymphocyte derived from acute T cell leukemia, is a well-established model in immunology and cancer research. Characterized by mutations in PTEN and p53, Jurkat cells are widely used to study T cell biology, apoptosis, and signal transduction, making them an ideal host for exploring mechanisms of leukemia and cellular stress responses.
EIF2A acts as a translation initiation factor that delivers Met-tRNAi to the 40S ribosomal subunit in a GTP-independent manner, particularly under stress conditions such as amino acid deprivation, hypoxia, oxidative stress, or ER stress. When canonical eIF2 activity is inhibited by stress-sensing kinases like PERK and GCN2, EIF2A enables alternative translation initiation of specific mRNAs, often via IRES-dependent mechanisms. It interacts with the 40S subunit, eIF3 complex, and eIF5, and is connected to the integrated stress response, mTOR, and unfolded protein response pathways, ultimately influencing downstream effectors like ATF4 and CHOP.
In the Jurkat context, EIF2A knockout is valuable for dissecting non-canonical translation control in T-cell leukemogenesis. With PTEN and p53 mutations affecting mTOR and apoptosis, loss of EIF2A may reveal stress-adaptive mechanisms supporting leukemic cell survival under nutrient-depleted or hypoxic conditions. This model facilitates the study of how alternative translation initiation contributes to stress-responsive protein expression and highlights potential therapeutic vulnerabilities in T-cell acute lymphoblastic leukemia.
This polyclonal knockout cell pool is suited for applications including Western blotting and RT-qPCR for expression analysis, RNA-seq for transcriptome profiling, polysome and ribosome profiling to study translation events, tunicamycin-induced ER stress and amino acid deprivation assays to probe stress-specific control, IRES reporter assays for functional translation studies, and apoptosis assays (Annexin V staining) to assess cell survival. For further technical details, please contact Ascent Research.
