The AGL Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line, featuring targeted disruption of the AGL gene. This loss-of-function model eliminates glycogen debranching enzyme activity, providing a robust tool for dissecting glycogen metabolism in a leukemic T cell context.
The Jurkat host cell line originates from the peripheral blood of a 14-year-old male with acute T cell leukemia and represents an immortalized T lymphocyte line extensively employed as an in vitro model for T cell receptor signaling, apoptosis, and leukemia biology. These cells maintain key metabolic pathways, making them suitable for investigating the intersection of energy metabolism and immune function.
AGL encodes the glycogen debranching enzyme, which cleaves ??-1,6-glycosidic bonds in glycogen and limit dextrin, an essential step for complete glycogen degradation. The enzyme functions downstream of hormonal cues from glucagon, epinephrine, and insulin, and interacts directly with glycogen phosphorylase, phosphorylase kinase, and glycogenin to coordinate glycogenolysis. Disruption of AGL leads to accumulation of limit dextrin, impaired glucose release, and altered glycogen breakdown products. This enzymatic step is integrated with the broader glycogen metabolism pathway, which includes glycogen phosphorylase (PYGL/PYGM/PYGB), phosphoglucomutase (PGM1), and glucose-6-phosphatase (G6PC).
In the Jurkat T lymphocyte background, AGL knockout provides a model to explore the significance of glycogen debranching in immune cell metabolism. T cells undergo metabolic reprogramming during activation, and glycogen may serve as a rapid energy source. By eliminating AGL, researchers can assess how impaired glycogen mobilization affects T cell functions such as proliferation, cytokine production, and survival, while also modeling glycogen storage disease type III (Cori disease) in a hematopoietic context.
This product is particularly suited for studies applying assays like PAS staining for glycogen content, glucose release measurements, western blotting for AGL protein, enzymatic activity assays, and RT-qPCR for AGL mRNA expression. Applications range from investigating metabolic reprogramming in T cell leukemia to examining the role of glycogen metabolism in T cell signaling and evaluating therapeutic targets for glycogen storage diseases. For further technical details and ordering information, please contact Ascent Research.
