The GPSM1 Knockout Jurkat Polyclonal Cells are a polyclonal knockout cell population generated from the Jurkat human T lymphocyte cell line through CRISPR/Cas9-mediated disruption of the GPSM1 gene. This product comprises a heterogeneous population of cells harboring targeted gene disruptions, providing a robust tool for loss-of-function studies. Supplied as a live cell pool, these polyclonal knockout cells offer a convenient model for investigating GPSM1-mediated signaling pathways without the need for single-cell clonal isolation.
The Jurkat cell line is an immortalized human T lymphocyte line originally derived from the peripheral blood of a patient with acute T-cell leukemia. Jurkat cells are widely employed as a model system for studying T cell receptor (TCR) signaling, apoptosis, and immune cell function. Their well-characterized signaling networks and ease of culture make them a standard platform for genetic manipulation and functional genomics in immunology and oncology research. In the context of GPSM1 knockout, Jurkat cells provide a physiologically relevant background for exploring the role of G-protein regulatory proteins in T cell biology.
GPSM1 (G-protein signaling modulator 1) functions as a receptor-independent activator of heterotrimeric G-protein signaling by acting as a guanine nucleotide dissociation inhibitor (GDI) for G??i/o subunits. By sequestering G??i/o in a GDP-bound state, GPSM1 modulates downstream effectors including adenylyl cyclase, cAMP, and MAPK/ERK pathways. GPSM1 is a key regulator of cell polarity and asymmetric cell division through its interactions with the conserved polarity complex proteins Inscuteable (INSC), LGN (GPSM2), and NuMA. Upstream, GPSM1 expression is subject to regulation by Wnt/??-catenin and Notch signaling, as well as cell cycle-dependent mechanisms. Representative pathway components thus include G??i/o, GPSM1, adenylyl cyclase, cAMP-dependent protein kinase (PKA), MAPK, INSC, LGN, and NuMA.
In Jurkat T cells, GPSM1 knockout disrupts receptor-independent G-protein signaling, potentially impairing the modulation of adenylyl cyclase and MAPK cascades that govern proliferation, survival, and apoptosis. Given the role of G-protein signaling in T cell activation and immune responses, loss of GPSM1 may alter cell polarity and asymmetric division, processes increasingly recognized in hematopoietic cell fate decisions. This polyclonal knockout model therefore enables dissection of GPSM1-dependent pathways in an immortalized T cell environment, providing insights into how GDI-mediated regulation of G??i/o contributes to lymphocyte biology and malignancy.
These polyclonal knockout cells enable various functional assays: Western blotting and RT-qPCR for GPSM1 and partner expression, MTS proliferation and Annexin V apoptosis assays, cAMP measurement for G-protein signaling, and immunofluorescence for LGN/NuMA localization. Migration assays can assess cell motility defects. Applications include T cell signaling, cancer biology, drug target validation, and GPSM1 pathway modulator screening. For further information, contact Ascent Research.
