The EIF5A2 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes in which the EIF5A2 gene has been disrupted, establishing a loss-of-function model essential for investigating the roles of this translation elongation factor. This heterogeneous knockout pool enables robust functional studies without the biases of clonal selection, making it suitable for examining population-level responses.
The parental Jurkat cell line is a well-established human CD4+ T lymphocyte model derived from the peripheral blood of a patient with acute T cell leukemia. Jurkat cells are extensively utilized to dissect T cell receptor signaling, apoptosis, and leukemogenesis, owing to their rapid growth and ease of genetic manipulation. This background provides a physiologically relevant context for studying genes that govern immune cell fate and malignant transformation.
EIF5A2 is a translation elongation factor that specifically promotes the translation of mRNAs with proline-rich motifs, a function critically dependent on its unique hypusination modification. Hypusination is catalyzed sequentially by deoxyhypusine synthase (DHPS) and deoxyhypusine hydroxylase (DOHH), using the polyamine spermidine. EIF5A2 is transcriptionally regulated by c-Myc and is activated downstream of mTOR signaling, which controls polyamine biosynthesis via ornithine decarboxylase. Upon hypusination, eIF5A2 associates with the ribosome and facilitates elongation of nascent peptides, thereby governing the expression of proteins involved in cell cycle progression and apoptosis. Key signaling nodes include mTOR, S6K1, 4E-BP1, and polyamine metabolic enzymes, positioning EIF5A2 at the intersection of nutrient sensing, translational control, and cell fate determination.
In the Jurkat T cell context, knockout of EIF5A2 abrogates its ability to support translation of proline-rich motif-containing transcripts, providing a powerful model to dissect how mTOR-dependent and polyamine-dependent signals converge on the translational machinery to regulate T cell proliferation and survival. This model is particularly valuable for studying the molecular mechanisms underlying T cell leukemia and for validating EIF5A2 as a potential therapeutic target in lymphoid malignancies.
This polyclonal knockout product is suited for diverse research applications, including cancer biology, translational control mechanisms, polyamine metabolism, and drug target validation. Representative experimental approaches include Western blotting and RT-qPCR to confirm gene disruption and analyze downstream targets, MTT and Annexin V assays to evaluate proliferation and apoptosis, flow cytometry for cell cycle profiling, and ribosome profiling to capture translation changes. Additional assays such as migration/invasion assessments and polyamine level measurements further characterize functional consequences of EIF5A2 loss. For further details or technical support, please contact Ascent Research.
