The MRAS Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout population of Raji B lymphocytes with targeted disruption of the MRAS gene. This format yields a heterogeneous mix of cells carrying various loss-of-function alleles, avoiding clonal bias and offering a reproducible model for interrogating MRAS-mediated signaling in a B-cell context.
Raji is an EBV-positive Burkitt lymphoma-derived B-cell line widely utilized as a model for B-cell malignancies and immune function studies. Originating from a patient with Burkitt lymphoma, these cells maintain characteristic B lymphocyte features, including surface immunoglobulin and functional B-cell receptor (BCR) signaling. The EBV-positive background further supports investigations of virus?Chost interactions relevant to lymphomagenesis.
MRAS is a small GTPase that alternates between an inactive GDP-bound and an active GTP-bound state, transducing signals from cell surface receptors to intracellular effectors. Receptor-mediated activation, through guanine nucleotide exchange factors such as SOS1 and RASGRP, triggers the GTP-bound form to engage RAF1/BRAF, thereby activating the MEK/ERK cascade, the PI3K catalytic subunit to stimulate AKT/mTOR signaling, and RalGDS to control RalA/B-mediated actin regulation. Upstream activators include receptor tyrosine kinases like EGFR and FGFR, G protein-coupled receptors, BCR, and cytokine receptors. MRAS signaling complexes involve RAF1, BRAF, PI3K, SHOC2, and protein phosphatase 1 (PP1C), ultimately affecting transcription factors such as ELK1, c-FOS, c-JUN, and NF-??B to orchestrate proliferation, differentiation, and cytoskeletal dynamics.
In Raji cells, MRAS likely integrates BCR and cytokine signals to sustain proliferative and survival pathways critical for lymphoma progression. Disruption of MRAS in this polyclonal model is expected to impair MAPK/ERK and PI3K/AKT cascades, attenuating cell cycle progression and apoptosis resistance. Given the association of MRAS mutations with Noonan syndrome and RAS pathway dysregulation in B-cell lymphomas, this model provides a powerful system to dissect MRAS contributions to aberrant B-cell behavior, including virus-associated transformation.
This polyclonal knockout cell population is well-suited for functional studies of MRAS-dependent B-cell signaling. Standard applications include Western blotting for MRAS and downstream phospho-proteins, RT-qPCR to confirm gene disruption, flow cytometric analysis of proliferation and apoptosis, cell cycle profiling, and migration/invasion assays. Drug sensitivity tests using MAPK or PI3K pathway inhibitors can identify signaling dependencies, while RNA sequencing enables transcriptome-wide investigation. The polyclonal format also facilitates pooled screening approaches. For further inquiries, please contact Ascent Research.
