The EIF2D Knockout K-562 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the K-562 chronic myelogenous leukemia suspension line, carrying a targeted disruption of the EIF2D gene. This bulk-selected pool captures heterogeneous editing events, offering a robust loss-of-function model free of clonal artifacts. The cells retain the suspension growth properties and karyotypic features of the parental K-562 line and are supplied as a live culture ready for downstream functional analyses.
The parental K-562 cell line was established from the pleural effusion of a 53-year-old female with chronic myelogenous leukemia in blast crisis and is characterized by the BCR-ABL1 fusion oncogene. As an undifferentiated blast cell line capable of both erythroid and granulocytic differentiation, K-562 serves as a widely used model for hematopoietic differentiation, leukemogenesis, and BCR-ABL signaling. Its suspension growth habit and well-defined response to cytokines and kinase inhibitors facilitate a broad range of mechanistic and screening assays.
EIF2D encodes eukaryotic translation initiation factor 2D, which, in complex with MCTS1 and DENR, binds the 40S ribosomal subunit to promote start codon recognition on internal ribosome entry sites (IRES) within target mRNAs. This cap-independent translation mechanism becomes critical when the canonical eIF2?CeIF4F pathway is inhibited by cellular stress. EIF2D activity is regulated upstream by mTORC1 and by eIF2?? kinases??PERK, GCN2, PKR, and HRI??which sense ER stress, amino acid deprivation, viral infection, and heme deficiency, respectively. Downstream, EIF2D mediates the synthesis of key oncogenic and stress-responsive proteins including c-MYC, XIAP, BCL-2, and VEGF. The factor also interacts with the eIF3 complex and eIF1A, positioning it at the nexus of ribosome recruitment and stress-adaptive translation.
In the K-562 leukemia background, disruption of EIF2D enables investigation of how IRES-dependent translation contributes to malignant cell survival, therapy resistance, and differentiation block. Because BCR-ABL signaling activates mTORC1 and therapeutic stress induces the integrated stress response, this knockout model is particularly suited to dissect the role of EIF2D-driven synthesis of anti-apoptotic and growth-promoting factors under conditions relevant to CML progression and treatment.
Typical research applications include functional dissection of cap-independent translation, stress-response studies in leukemia, and screening for inhibitors of non-canonical translation. The polyclonal knockout cells are compatible with polysome profiling and ribosome footprinting to assess translational control, dual-luciferase reporter assays to validate IRES activity, RT-qPCR for transcript analysis, flow cytometry for cell cycle and apoptosis measurement, and viability assays under mTOR or ISR perturbation. For further technical details or to request a quote, please contact Ascent Research.
