GPALPP1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the GPALPP1 gene, designed for studying GPI anchor biosynthesis. Generated via CRISPR/Cas9-mediated gene knockout in Jurkat T cells, this heterogeneous pool provides a loss-of-function model that avoids single-cell cloning and captures population-level genetic effects.
The Jurkat cell line, derived from a human T-cell acute lymphoblastic leukemia (T-ALL) patient, is a classic model for T-cell signaling, apoptosis, and leukemia research. Its well-established use in immunology and oncology, along with robust growth and high transfectability, makes it an optimal host for investigating GPALPP1 function in a T lymphocyte context.
GPALPP1 encodes a lipid phosphatase that catalyzes a critical dephosphorylation step in GPI anchor maturation, acting downstream of the PIGA and PIGL enzymes. It interacts with PGAP1 and GPAA1 within the GPI biosynthesis complex and depends on accessory factors including DPM2 and MPDU1. GPALPP1 activity is essential for surface expression of GPI-anchored proteins (GPI-APs) such as CD55 and CD59. Gene disruption impairs GPI anchor processing, reducing GPI-AP presentation and altering cell surface composition.
In Jurkat T cells, GPALPP1 knockout recapitulates features of GPI deficiency syndromes. Reduced surface CD55 and CD59 sensitize cells to complement-mediated lysis and may alter T-cell receptor signaling thresholds. This polyclonal knockout population is a valuable tool for examining how GPI anchor defects intersect with T-ALL pathophysiology and immune cell function, enabling study of population-level compensatory mechanisms.
Researchers can utilize these cells in flow cytometric analysis of surface GPI-AP expression, metabolic labeling to track GPI anchor synthesis, complement lysis assays to assess functional consequences of CD55/CD59 loss, and immunofluorescence microscopy to investigate protein trafficking. Additionally, the cells are suitable for drug screening strategies aimed at restoring GPI-AP surface expression or modulating complement sensitivity. For additional information or to discuss custom projects, please contact Ascent Research.
