This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EEF1D gene in the K-562 human erythroleukemia cell line. The polyclonal format supplies a heterogeneous pool of edited cells harboring distinct gene-disruption alleles, enabling study of EEF1D’s function in translation elongation while mitigating clonal selection artifacts. By disrupting the delta subunit of the eukaryotic elongation factor 1 (eEF1) complex, this loss-of-function model facilitates investigation of protein synthesis dynamics and associated cellular outcomes.
K-562 cells originate from a 53-year-old female with chronic myelogenous leukemia (CML) in blast crisis and express the BCR-ABL fusion oncogene. This cell line serves as a well-established model for CML and erythroid differentiation, characterized by blast cell properties and inducible erythroid maturation. Its robust proliferation and comprehensive signaling characterization make it ideal for examining oncogene-driven translational control, particularly the crosstalk between BCR-ABL signaling and the EEF1D-dependent translation machinery.
EEF1D encodes the delta subunit of the heterotetrameric eEF1 complex, which mediates GTP-dependent aminoacyl-tRNA delivery to ribosomes during elongation. The complex includes EEF1A, EEF1B, EEF1D, and EEF1G, and interacts with valyl-tRNA synthetase. EEF1D is regulated by mTOR and growth factor pathways, participates in heat shock and MAPK signaling, and influences global protein synthesis, cell proliferation, and apoptotic protein expression. Its disruption impairs elongation factor function, potentially altering synthesis of regulatory proteins and stress sensitivity.
EEF1D knockout in K-562 cells provides a disease-relevant model for studying translation elongation in leukemia. Since K-562 cells rely on BCR-ABL signaling that converges on mTOR to boost protein synthesis, EEF1D loss may compromise this anabolic program, reducing proliferation and modulating stress responses. This model is valuable for elucidating how aberrant translational control contributes to leukemogenesis and for uncovering synthetic lethal interactions between the eEF1 complex and oncogenic kinases.
Researchers can utilize this knockout model for diverse functional genomics studies, including western blotting for EEF1D and downstream targets, RT-qPCR, puromycin incorporation assays, cell viability and apoptosis analyses, and transcriptomic RNA-seq. These methods allow detailed characterization of EEF1D-dependent translation in CML. The polyclonal background also supports drug target validation and screening of eEF1 complex modulators. For further information, please contact Ascent Research.
