The OSMR Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line. Through CRISPR/Cas9-mediated gene disruption targeting the OSMR locus, the cells provide a loss-of-function model for dissecting oncostatin M receptor beta subunit signaling. The polyclonal nature retains heterogeneous editing outcomes, enabling studies of OSMR deficiency in a pool of genetically modified cells without clonal isolation. This product is optimized for use in cellular signaling, immuno-oncology, and cytokine biology research.
The Raji host cell line is a well-characterized lymphoblastoid B cell model originally established from a Burkitt lymphoma patient. These cells are infected with Epstein-Barr virus and exhibit typical B cell features, including robust antibody production and immune-related signaling. Raji cells are widely employed in lymphoma pathogenesis studies, drug screening, and immunological assays, owing to their stable growth and responsiveness to extracellular cytokine stimuli. The lymphoblastoid background provides a physiologically relevant context for examining OSMR-mediated pathways in B lymphocytes.
OSMR encodes the beta subunit of the type II cytokine receptor family, serving as a key co-receptor for oncostatin M (OSM) and interleukin-31 (IL-31). Upon ligand binding, OSMR heterodimerizes with gp130 (IL6ST) or IL31RA, bringing associated Janus kinases (JAK1, JAK2, TYK2) into close proximity. This activates downstream cascades, including JAK-STAT (STAT3, STAT5), MAPK/ERK (ERK1/2), and PI3K-AKT (AKT) pathways, ultimately regulating transcription of target genes such as SOCS3. The receptor complex thus relays extracellular signals to promote cell survival, proliferation, and inflammatory responses.
In the Raji B cell context, OSMR signaling may intersect with pathways critical for lymphomagenesis and immune evasion. Aberrant STAT3 activation is frequently observed in Burkitt lymphoma, and OSM/IL-31 signaling can modulate STAT3 phosphorylation and downstream gene expression. Disrupting OSMR in this model allows precise interrogation of how these cytokine axes influence B cell growth, apoptosis, and interaction with the microenvironment. This knockout tool is therefore valuable for delineating OSMR contributions to lymphoma cell biology and for exploring therapeutic vulnerabilities.
Researchers can apply these polyclonal knockout cells in a range of experimental workflows, including cytokine response profiling after OSM or IL-31 stimulation. Representative assays include Western blot analysis for phosphorylated STAT3 or ERK1/2, flow cytometric detection of surface OSMR expression, RT-qPCR for SOCS3 transcript levels, and cell viability assays under OSM treatment. Co-immunoprecipitation studies can further probe OSMR-gp130 interactions. The model supports drug target validation and STAT3 pathway inhibition studies. For technical inquiries, please contact Ascent Research.
