The MSRB2 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the methionine sulfoxide reductase B2 (MSRB2) gene in the Raji human B lymphocyte line. This pooled cellular reagent provides a loss-of-function model for dissecting MSRB2-dependent protein repair and antioxidant defense mechanisms within a lymphoid context, enabling robust genotype-phenotype studies without clonal selection artifacts. Researchers can employ this population for stable knockout experiments in suspension culture, with the heterogeneous polyclonal format preserving biological variance and minimizing adaptation biases common to single-cell-derived clones.
The Raji host cell line originates from an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma patient and represents a widely used B lymphocyte model. These cells retain hallmarks of mature B cells, including surface immunoglobulin expression and active antigen presentation pathways, while carrying oncogenic features driven by EBV latency programs. As a suspension-adapted line with rapid proliferation, Raji cells support high-throughput functional genomics, signaling analyses, and drug response profiling in a malignant lymphocyte background relevant to B-cell lymphomas and immune disorders.
MSRB2 encodes a stereospecific methionine-R-sulfoxide reductase that catalyzes thioredoxin-dependent reduction of oxidized methionine residues in proteins, thereby maintaining structural and functional integrity of the proteome. In the NRF2?CKEAP1 oxidative stress response pathway, MSRB2 operates downstream of NRF2 transcriptional activation to repair oxidatively damaged actin, calmodulin, and other critical substrates. The enzyme directly interacts with thioredoxin as a reducing cofactor and forms functional complexes with actin and calmodulin, linking redox sensing to cytoskeletal dynamics and calcium signaling. Disruption of MSRB2 therefore impairs the reduction of methionine sulfoxide back to methionine, leading to accumulation of oxidized proteins and heightened sensitivity to oxidative challenge.
In the Raji B lymphocyte background, MSRB2 knockout significantly attenuates cellular antioxidant capacity, promoting elevated reactive oxygen species (ROS) levels and sensitizing cells to oxidative stress-induced apoptosis. Because methionine oxidation regulates the activity of several signaling proteins, including components of the actin cytoskeleton and calmodulin-dependent pathways, loss of MSRB2 function can dysregulate B-cell receptor-mediated signaling, antigen presentation robustness, and immunoglobulin production under inflammatory conditions. This model thus captures the intersection of oncogenic stress and redox control, making it particularly valuable for studying how lymphoma cells manage oxidative burden and evade programmed cell death.
Typical applications include mechanistic investigations of oxidative stress in lymphoma biology, characterization of protein oxidation repair networks, and screening of antioxidant therapeutic candidates. Researchers commonly pair this knockout pool with parental Raji cells in comparative assays employing western blotting, RT-qPCR, ROS detection probes, cell viability measurements under oxidative insult, annexin V apoptosis staining, flow cytometric immunophenotyping, transcriptomic profiling via RNA-seq, and controlled oxidative stress challenges. For further technical specifications or custom experimental support, please contact Ascent Research.
