The EIF2A Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian endometrioid adenocarcinoma cell line. This product provides a heterogeneous pool of cells with disrupted EIF2A gene expression, generating a loss-of-function model for the alpha subunit of eukaryotic translation initiation factor 2 (eIF2??). The polyclonal format minimizes clonal selection artifacts and is well-suited for population-based functional studies in cancer biology and signal transduction.
MES-OV is a widely used epithelial ovarian cancer cell line established from a patient tumor. As a model of endometrioid carcinoma, it retains pathophysiological features relevant to gynecological oncology research, including aberrant signaling networks and stress responses. This background enables investigation of tumorigenic mechanisms and therapeutic vulnerabilities in a subtype-specific context.
EIF2A encodes eIF2??, a master regulator of translation initiation that delivers initiator tRNA-Met to the ribosome. Under stress, upstream kinases EIF2AK1/HRI, EIF2AK2/PKR, EIF2AK3/PERK, and EIF2AK4/GCN2 phosphorylate eIF2?? at Ser51, inhibiting eIF2B and global protein synthesis while selectively enhancing ATF4 translation. ATF4 subsequently activates targets such as CHOP, GADD34, and ASNS, coordinating the integrated stress response (ISR). Dephosphorylation is mediated by PPP1R15A/GADD34 and PPP1R15B/CReP. eIF2?? interacts with eIF2??, eIF2??, and ribosomal subunits to form the functional initiation complex.
In MES-OV ovarian cancer cells, ablation of EIF2A disrupts ISR-dependent adaptation to microenvironmental stresses like hypoxia and nutrient deprivation, as well as chemotherapeutic challenges. This model permits dissection of eIF2????s role in maintaining protein homeostasis and survival signaling, and it provides a platform to examine how loss of translational control influences malignant phenotypes, drug resistance, and apoptosis decisions.
Typical applications include profiling phospho-eIF2?? and ATF4 expression via Western blotting and luciferase reporters, assessing translational output by puromycin incorporation or polysome profiling, and measuring stress-induced apoptosis with Annexin V assays following tunicamycin or thapsigargin treatment. These cells further enable co-immunoprecipitation of eIF2 complexes and transcriptomic analyses by RNA-seq to map ISR networks. For further inquiries, please contact Ascent Research.
