The EEF1A2 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of EEF1A2 in the Raji B lymphocyte cell line. This polyclonal preparation provides a diverse pool of edited alleles, serving as a robust platform for studying EEF1A2 function in a Burkitt??s lymphoma context without clonal selection.
Raji cells are an EBV-positive lymphoblastoid cell line originally derived from a Burkitt??s lymphoma patient. As B lymphocytes, they are instrumental in antibody production and humoral immunity, and their stable proliferation and MYC-driven oncogenic features make them a widely used model for lymphoma research and viral lymphomagenesis studies.
EEF1A2 is a translation elongation factor that delivers aminoacyl-tRNA to the ribosome. It also participates in actin bundling and apoptosis inhibition, with overexpression linked to oncogenesis. Mechanistically, EEF1A2 promotes cell survival via PI3K/AKT signaling, leading to phosphorylation of AKT and downstream effectors such as mTOR and BAD, while upregulating anti-apoptotic proteins like BCL2. Its activity is regulated by MYC and SP1 transcription factors and involves interactions with HSP90 and MDM2.
In Raji lymphoma cells, EEF1A2 disruption allows interrogation of how translational elongation factor loss influences B-cell malignancy. As EEF1A2 is commonly overexpressed in hematological cancers, its knockout may impair PI3K/AKT-mediated survival signals and enhance sensitivity to apoptosis, providing a model to validate EEF1A2 as a therapeutic target in lymphomas and other cancers such as breast, ovarian, and hepatocellular carcinomas.
This polyclonal knockout cell population supports diverse assays, including Western blotting and RT-qPCR for expression analysis, flow cytometry for apoptosis (e.g., Caspase 3 activation), co-immunoprecipitation for protein interactions (e.g., HSP90), and reporter assays to monitor PI3K/AKT pathway activity. Cell proliferation and drug sensitivity assays can further elucidate functional consequences of EEF1A2 loss. For more information, please contact Ascent Research.
