The NPTN Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population designed to abrogate neuroplastin expression in the Raji B lymphocyte line. This loss-of-function model facilitates the study of neuroplastin-dependent cell adhesion, calcium signaling, and downstream MAPK/ERK pathway modulation in a Burkitt lymphoma background. The polyclonal format provides a pool of cells with NPTN gene disruption, enabling robust population-level analyses without clonal selection biases.
Raji cells are derived from an EBV-positive Burkitt lymphoma patient and represent a widely utilized B lymphocyte model. These lymphoblastoid cells exhibit mature B-cell characteristics, including surface immunoglobulin expression, rapid proliferation, and the capacity to form immunological synapses. Raji cells are commonly employed in cancer biology and immunology to investigate signaling mechanisms underlying B-cell activation, lymphomagenesis, and immune escape.
Neuroplastin (NPTN) encodes a cell adhesion molecule of the immunoglobulin superfamily that engages in homophilic binding and heterophilic interactions with NCAM. A key function of NPTN is its direct association with plasma membrane calcium ATPase (PMCA), which regulates calcium extrusion and intracellular calcium homeostasis. Consequently, NPTN modulates the MAPK/ERK cascade, with downstream effects on ERK1/2 phosphorylation and CaMKII activity, linking to actin cytoskeleton dynamics via integrins. These interactions position NPTN downstream of B cell receptor engagement and upstream of cytoskeletal and signaling effectors, thereby integrating adhesive and calcium signals in immune cells. Upstream regulators include calcium influx through channels, B cell receptor stimulation, inflammatory cytokines, and cell-cell contact, positioning NPTN as a signaling hub in B lymphocytes.
In the Raji context, NPTN knockout is expected to impair cell adhesion, disrupt immunological synapse formation, and alter calcium-dependent B-cell activation. These effects make the model relevant for studying B-cell malignancies, where neuroplastin may contribute to tumor adhesion, migration, and drug resistance. Furthermore, the model may aid in identifying novel therapeutic targets for B-cell lymphomas. Additionally, given NPTN’s role in synaptic plasticity, the model offers insights into neuro-immune interactions and potential links to neurodevelopmental disorders.
Researchers can utilize this polyclonal knockout population in a range of assays, including Western blotting for protein expression, RT-qPCR for transcript analysis, flow cytometry to quantify adhesion markers such as integrins, and calcium flux assays to gauge intracellular Ca2? responses. Co-immunoprecipitation enables investigation of NPTN-PMCA complexes, while cell migration assays and drug sensitivity profiling facilitate functional and pharmacological studies. For further technical details or ordering, please contact Ascent Research.
