The GPSM2 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the G protein signaling modulator GPSM2. This product utilizes CRISPR/Cas9-mediated gene disruption to ablate GPSM2 expression in the Jurkat human T lymphocyte cell line, generating a heterogeneous pool of edited cells. The polyclonal format captures the genetic diversity inherent in the knockout population, enabling robust functional analyses without clonal selection artifacts. These cells serve as a versatile research tool for dissecting GPSM2-dependent mechanisms in signal transduction, mitosis, and cell polarity regulation.
The parental Jurkat cell line is an immortalized human T lymphocyte model originally derived from peripheral blood of a 14-year-old male with acute T cell leukemia. Established in 1976, Jurkat cells are extensively employed to investigate T cell receptor signaling, apoptotic pathways, and host?Cpathogen interactions, particularly in HIV infection. Their well-characterized signaling networks and ease of genetic manipulation make them an ideal platform for examining the functional consequences of gene knockout on lymphocyte biology and cancer-related processes.
GPSM2 (LGN) acts as a guanine nucleotide dissociation inhibitor for G??i subunits (GNAI1/2/3, GNAL), binding GDP?bound G??i to inhibit nucleotide exchange. It recruits the adaptor INSC and NUMA to the cell cortex, engaging dynein/dynactin to orient the mitotic spindle. This process is regulated upstream by G??i?coupled receptors, CDK1 phosphorylation, and LATS1/2 kinases, and downstream influences YAP/TAZ transcription cofactors and cell fate determinants, integrating heterotrimeric G protein and Hippo signaling with planar cell polarity.
In Jurkat T lymphocytes, GPSM2 knockout offers a model for studying asymmetric division in immune cells. Polarized divisions during T cell activation may depend on GPSM2?mediated spindle orientation; its loss could affect proliferation, apoptosis, and leukemogenic potential. The model also aids in exploring mechanisms underlying Chudley?McCullough syndrome and DFNB82 hearing loss, where GPSM2 dysfunction is implicated.
Applications include Western blotting and co?immunoprecipitation for GPSM2 and interactors, immunofluorescence for spindle orientation, flow cytometry for cell cycle and apoptosis, RNA?seq for transcriptomic profiling, and live?cell imaging of GFP?LGN dynamics. These polyclonal knockout cells are suited for drug sensitivity screens and functional genomics in immunology and cancer biology. For further information, please contact Ascent Research.
