The METTL13 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated loss-of-function model in the Raji B lymphocyte cell line. This polyclonal knockout population carries a targeted disruption of the METTL13 gene, abrogating its protein-coding function. The product is supplied as a population of cells that have undergone CRISPR/Cas9 genome editing, enabling researchers to study METTL13-dependent effects in a heterogeneous background, typical of cancer cell populations. This format avoids the biases inherent in single-cell clones and provides a robust tool for functional genomic studies.
The Raji cell line, derived from a Burkitt lymphoma patient, is an Epstein-Barr virus (EBV)-immortalized B lymphocyte model that expresses surface IgM. It is extensively utilized in immunology and cancer research due to its well-characterized B-cell receptor (BCR) signaling, lymphomagenic properties, and capacity for immunoglobulin production. Raji cells serve as a relevant system for investigating B-cell malignancies, given their genetic and phenotypic similarities to aggressive lymphomas. Their rapid proliferation and ease of culture make them ideal for high-throughput screening and mechanistic studies.
METTL13 encodes a protein methyltransferase that specifically catalyzes the dimethylation of eukaryotic elongation factor 1A (eEF1A) at lysine 55 (K55me2). This post-translational modification enhances eEF1A function during translation elongation, leading to increased global protein synthesis. Mechanistically, METTL13 is regulated by the mTORC1 signaling pathway and the transcription factor E2F1, placing it at the intersection of growth signaling and translational control. It interacts with eEF1A and the 60S ribosomal subunit, positioning it as a critical modulator of ribosome function. The METTL13-eEF1A axis promotes cell growth and proliferation, contributing to oncogenic processes in various cancer types.
In the context of Raji B lymphocytes, METTL13 plays a pivotal role in sustaining the high translational demand required for rapid proliferation and lymphomagenesis. Abrogation of METTL13 expression disrupts eEF1A K55 dimethylation, potentially impairing translation elongation and reducing protein output. This knockout model enables the dissection of METTL13??s contribution to B-cell receptor signaling outputs and metabolic adaptations in lymphoma cells. It provides a physiologically relevant platform to investigate how dysregulated translation elongation drives B-cell malignancies and to identify METTL13-dependent phenotypic vulnerabilities.
Researchers can employ this knockout cell population in a range of applications, including functional characterization of METTL13 in B-cell translation, mechanistic studies of eEF1A methylation in lymphomagenesis, and screening for synthetic lethal interactions or chemical sensitivities specific to METTL13 loss. Representative assays include Western blot detection of eEF1A K55me2 to confirm target disruption, puromycin incorporation to measure global protein synthesis, proliferation and cell cycle analyses by flow cytometry, and RNA sequencing to assess translation efficiency. This tool is well-suited for translational control studies in cancer and drug discovery programs targeting the translation machinery. For further technical details or ordering information, please contact Ascent Research.
