The GBE1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the human GBE1 gene in the Raji B lymphocyte cell line. This product is supplied as a heterogeneous pool of edited cells, each carrying CRISPR/Cas9-mediated target-gene disruption without selection for clonal expansion, preserving the polyclonal nature of the knockout pool. The cells provide a robust loss-of-function model for studying glycogen branching enzyme deficiency in a human lymphoid background.
Raji cells are an Epstein-Barr virus (EBV)-immortalized human B lymphocyte line originally derived from a patient with Burkitt lymphoma. These suspension-adapted cells retain key B-cell functionalities, including antibody production and antigen presentation, and have long served as a model system for immunological and oncological research. Their rapid growth in suspension culture makes them amenable to high-throughput screening and metabolic studies.
GBE1 encodes glycogen branching enzyme, a critical enzyme in glycogen biosynthesis that catalyzes the transfer of ??-1,4-linked glucose oligosaccharide segments to form ??-1,6 branch points, thereby determining glycogen??s spherical, soluble structure. The enzyme is transcriptionally regulated by insulin signaling via the transcription factors FOXO1 and PPARGC1A, and it functions in close coordination with glycogen synthase (GYS1), glycogen phosphorylase (PYGL), and glycogenin (GYG1) to synthesize and remodel glycogen particles. Disruption of GBE1 eliminates branching activity, leading to the accumulation of unbranched, poorly soluble polyglucosan that resembles the molecular pathology of glycogen storage disease type IV (Andersen disease) and adult polyglucosan body disease.
In the Raji B-cell context, GBE1 knockout models the metabolic consequences of glycogen branching enzyme deficiency in a lymphoid environment, which is particularly relevant given the role of glycogen as a rapid energy reserve during immune activation and antigen presentation. This knockout cell pool can be used to investigate how impaired glycogen structure alters B-cell proliferation, viability, and effector functions. Moreover, it serves as a platform to explore metabolic vulnerabilities in EBV-positive lymphomas, where dysregulated glycogen metabolism may contribute to oncogenic adaptation.
Researchers can employ this polyclonal knockout population in a range of applications, including functional studies of glycogen metabolism using periodic acid-Schiff (PAS) staining to visualize aberrant polysaccharide accumulation, glucose uptake assays to assess metabolic flux, and RT-qPCR or western blotting to quantify changes in glycogen pathway components such as GYS1, PYGL, and UGP2. The cells are also suited for high-throughput screening of small molecules or biologics aimed at restoring branching activity or alleviating polyglucosan toxicity, as well as for investigating the interplay between glycogen metabolism and B-cell receptor signaling. For further information or to discuss custom projects, please contact Ascent Research.
