The GDPD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human Raji B lymphocyte line, featuring targeted disruption of the GDPD1 gene. This loss-of-function model eliminates glycerophosphodiester phosphodiesterase activity, blocking the conversion of lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA). The polyclonal format maintains a heterogeneous knockout background, suitable for pooled screening and population-level signaling studies without clonal bias. CRISPR/Cas9-mediated gene disruption provides a robust genetic tool for dissecting LPA-dependent processes in lymphoid cells.
Raji cells are EBV-positive Burkitt’s lymphoma-derived B lymphocytes, widely used to study B cell lymphoma biology, EBV latency, and B cell receptor signaling. These immortalized lymphoblastoid cells retain active oncogenic pathways such as NF-??B and STAT3, and are amenable to gene editing. Their established use in cancer research makes them an ideal host for investigating how LPA signaling intersects with lymphomagenesis and viral latency programs.
GDPD1 encodes a glycerophosphodiester phosphodiesterase that hydrolyzes extracellular LPC to produce LPA, a pleiotropic lipid mediator. LPA activates G protein-coupled receptors LPAR1-6, engaging signaling networks including RhoA/ROCK, Ras/Raf/MEK/ERK, and PI3K/AKT cascades. GDPD1 expression is regulated by YAP/TAZ and TEAD transcription factors, linking biomechanical cues to lipid signaling. Downstream, LPA promotes cell migration via Rho GTPases and MMPs, and survival through AKT-mediated pathways.
In the Raji lymphoma context, autocrine LPA generated by GDPD1 may drive tumor cell motility, proliferation, and apoptosis resistance. This knockout polyclonal population allows dissection of endogenous LPA synthesis contributions to malignant phenotypes, independent of exogenous LPA. It also facilitates exploration of crosstalk between LPA signaling and EBV-encoded factors like LMP1 that influence B cell transformation.
Key applications include investigating LPA-driven mechanisms in B cell lymphoma, screening LPAR or GDPD1 inhibitors, and studying immune cell trafficking. Supported assays include Western blotting for p-ERK/p-AKT, RT-qPCR, transwell migration/invasion, flow cytometry, LPA LC-MS quantification, and drug sensitivity testing. For further information, please contact Ascent Research.
