GDE1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the GDE1 gene has been disrupted in the Raji B-lymphoblast cell line. This polyclonal pool retains heterogeneous editing events across the cell population, providing a loss-of-function model suitable for studying the role of GDE1 in glycerophospholipid metabolism and B-cell lymphoma biology. The knockout model avoids clonal selection artifacts and enables population-level assessment of metabolic and signaling phenotypes associated with GDE1 deficiency.
The Raji host cell line is a suspension-adapted, Epstein?CBarr virus (EBV)-positive Burkitt lymphoma-derived lymphoblastoid line. Originally isolated from a human Burkitt lymphoma patient, Raji cells serve as a widely used model for B-cell malignancies and lymphocyte signaling, including oncogenic MYC-driven transformation and immunoglobulin expression. Their EBV status and lymphoblast morphology make them particularly relevant for investigating viral oncogenesis and B-cell receptor (BCR) pathway dependencies.
GDE1 encodes a glycerophosphodiester phosphodiesterase that hydrolyzes glycerophosphocholine to choline and glycerol-3-phosphate. This reaction feeds choline into the Kennedy pathway for de novo phosphatidylcholine synthesis and provides glycerol-3-phosphate for lipid droplet formation and phospholipid remodeling. GDE1 activity is regulated by upstream factors such as MYC, PPAR??, and cellular choline demand, and it directly impacts downstream metabolites including choline, glycerol-3-phosphate, and phosphatidylcholine pools. Interacting partners include choline kinase alpha (CHKA), glycerol-3-phosphate acyltransferase 1 (GPAT1), and lysophosphatidylcholine acyltransferase (LPCAT) enzymes, which together orchestrate membrane phospholipid composition and GPI-anchored protein biosynthesis. Consequently, GDE1 links phospholipid degradation to anabolic lipid pathways critical for membrane homeostasis.
In the context of Raji lymphoma cells, GDE1 knockout provides a powerful tool to dissect how glycerophospholipid catabolism influences B-cell malignant phenotypes. Disruption of GDE1 is expected to perturb membrane phospholipid composition, alter BCR signaling, and potentially impair oncogenic pathways such as AKT/mTOR. This model enables the investigation of metabolic dependencies in lymphomas with high choline demand and MYC-driven proliferation. Furthermore, because EBV-transformed B-cells exhibit altered lipid metabolism, the GDE1-deficient Raji population can be used to explore virus?Chost metabolic interactions.
Key research applications include lipidomics profiling to map changes in glycerophospholipid species, choline uptake assays to quantify metabolic flux, and cell proliferation (MTT) and apoptosis (flow cytometry) assays to assess growth and survival. Phospho-signaling analysis (AKT/mTOR) can reveal downstream pathway alterations, while xenograft tumor growth studies and drug sensitivity screens permit evaluation of GDE1 as a therapeutic target and predictor of response to choline metabolism inhibitors. This polyclonal knockout cell product is suitable for functional genomics, metabolic reprogramming studies, and anti-lymphoma drug discovery. For technical inquiries, please contact Ascent Research.
