The NRP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the neuropilin-1 (NRP1) gene in human Burkitt lymphoma-derived Raji B lymphocytes. This product provides a heterogeneous loss-of-function model, preserving genetic diversity while disrupting NRP1 expression. The polyclonal format enables pooled functional studies and high-throughput screening applications without the need for monoclonal isolation, making it suitable for investigating overall gene function in a population context.
The Raji cell line originates from a Nigerian patient with Burkitt lymphoma and is characterized by Epstein-Barr virus (EBV) positivity and expression of mature B-cell markers such as CD19 and CD20. These immortalized B lymphocytes are a widely established model for EBV latency type III, B-cell receptor signaling, and lymphoma biology. The viral background is particularly relevant for examining immune evasion strategies and oncogenic pathways that depend on both viral and host factors.
NRP1 encodes a transmembrane co-receptor for class 3 semaphorins (e.g., Sema3A) and vascular endothelial growth factor (VEGF) isoforms, including VEGF-A. It forms complexes with plexin receptors, notably Plexin-A1, to mediate semaphorin-induced cytoskeletal collapse, and with VEGFR2 to potentiate VEGF-driven angiogenesis and cell migration. Downstream, NRP1 signals through RhoA activation, AKT phosphorylation, and ERK pathway engagement, influencing cell survival, migration, and immune regulation. NRP1 expression is upregulated by TGF-??, STAT3, and HIF-1??, and it physically interacts with TGF-?? receptors, integrating signaling from multiple pathways critical in cancer and immunity.
In Raji B cells, NRP1 knockout may disrupt semaphorin-mediated repulsion and VEGF-dependent survival signals, potentially impairing lymphoma cell migration and interactions with stromal and endothelial components of the tumor microenvironment. The EBV-positive status combined with NRP1 deficiency offers a unique model to dissect the interplay between viral latency programs and NRP1-mediated immune modulation, including effects on regulatory T-cell function and immune checkpoint molecule expression. This system is well suited for studying how NRP1 loss alters integrin-mediated adhesion, cytokine secretion, and B-cell receptor downstream signaling.
Researchers can utilize this polyclonal knockout population in a variety of assays: western blotting for NRP1 and phosphorylated signaling proteins (e.g., pAKT), RT-qPCR for transcriptional targets, flow cytometry for surface NRP1 and integrin expression, Transwell migration and invasion assays, and co-culture models with endothelial cells to evaluate angiogenic interactions. The model is applicable for drug target validation, particularly for inhibitors of VEGF receptors or semaphorin pathways, and for functional screening in B-cell lymphoma drug sensitivity studies. For additional information or custom applications, please contact Ascent Research.
