The GULP1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte leukemia cell line to disrupt expression of the GULP1 gene. This pool of genetically heterogeneous edited cells provides a robust loss-of-function model for investigating GULP1-dependent pathways in a population-based format, minimizing clonal artifact risks and enabling reproducible functional assays in areas such as phagocytosis, cell migration, and signal transduction.
Jurkat cells, originally derived from the peripheral blood of a 14-year-old male with acute T cell leukemia, are a classic model for T cell receptor signaling, apoptosis, and leukemogenesis. These suspension cells exhibit strong migratory capability and express key components of engulfment signaling, making them an optimal host for studying the role of adaptor proteins like GULP1 in leukemic T cells and immune-related processes.
GULP1 functions as an adaptor that couples activated engulfment receptors??including BAI1, LRP1, TIM-4, integrin ??v??5, and Axl??to the ELMO-Dock180-Rac1 signaling module. Upon receptor engagement by phosphatidylserine-exposing targets, GULP1 recruits the ELMO1-Dock180 complex, which activates Rac1 GTPase. Active Rac1 drives localized actin polymerization and phagocytic cup formation, required for particle internalization and cell migration. Interacting partners such as CrkII, integrin ??5, and APP further modulate GULP1 activity. Loss of GULP1 disrupts this pathway, impairing clearance of apoptotic cells and cellular debris, thereby contributing to chronic inflammation and disease.
In the Jurkat T lymphocyte context, GULP1 knockout cells enable dissection of efferocytosis in a non?professional phagocyte, providing insights into how impaired clearance of dying cells fuels autoimmune disorders, atherosclerosis, and chronic inflammation. Moreover, because GULP1?dependent Rac1 activation drives cell migration, these cells are valuable for studying mechanisms of T cell trafficking and the metastatic dissemination of leukemic cells. The model is thus suited to investigate the dual roles of GULP1 in engulfment and motility within a malignant lymphoid background.
These cells support a variety of experimental workflows, including pHrodo-based phagocytosis assays, transwell migration assays, and Rac1 activation pull-downs. Western blot and co-immunoprecipitation analyses can characterize GULP1 interaction networks, while immunofluorescence microscopy visualizes actin dynamics and phagocytic cup formation. Flow cytometry enables high-throughput quantification of engulfment. The polyclonal population is compatible with drug screening for regulators of engulfment signaling, with rescue experiments using GULP1 overexpression confirming target specificity. For technical inquiries or custom applications, please contact Ascent Research.
