The GPS2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte cell line, engineered to disrupt the GPS2 gene. This product provides a genetically heterogeneous pool of cells harboring targeted loss-of-function mutations in GPS2, avoiding the limitations of clonal selection and ensuring diverse knockout alleles. The gene disruption effectively abrogates GPS2 protein expression, establishing a flexible model for dissecting the transcriptional regulatory functions of GPS2 in T cell signaling and associated pathways.
The host Jurkat cell line is an immortalized T lymphocyte line originally isolated from the peripheral blood of a 14-year-old male with acute lymphoblastic leukemia, representing an early T cell developmental stage. Jurkat cells are extensively employed in immunology and cancer research to investigate T cell receptor signaling, apoptosis, and gene regulation. The introduction of GPS2 knockout into this well-characterized model enables the study of how GPS2 modulates T cell functions and contributes to leukemic cell behavior.
GPS2 operates as a transcriptional corepressor within a complex containing N-CoR, HDAC3, TBL1, and TBLR1, repressing transcription of genes regulated by nuclear receptors (e.g., PPAR??) and NF-??B. Additionally, GPS2 directly binds and inhibits RAS, thereby blocking downstream ERK in the MAPK cascade. Through these dual mechanisms, GPS2 governs lipid metabolism, inflammation, and cell cycle. Disruption in Jurkat cells is expected to derepress target genes and enhance MAPK/ERK signaling, enabling study of transcriptional and signaling coordination in T lymphocytes.
In Jurkat cells, the GPS2 knockout model is valuable for dissecting the interplay between transcriptional repression and kinase signaling in T cell function and leukemogenesis. Jurkat cells rely on MAPK/ERK and NF-??B pathways for proliferation and survival; thus, loss of GPS2 likely disrupts these cascades, revealing how GPS2 restrains oncogenic and inflammatory signals. The model may elucidate how GPS2-mediated RAS inhibition sets T cell activation thresholds and how its dysfunction contributes to aberrant growth. Given the leukemia origin, this system is particularly relevant for studying tumor-suppressive roles in hematopoietic malignancies.
Researchers can utilize this polyclonal knockout population in a variety of assays, including Western blotting and RT-qPCR to validate GPS2 disruption and measure changes in downstream gene expression, phospho-specific analysis to monitor ERK activation, and co-immunoprecipitation to assess N-CoR-HDAC3 complex integrity. Luciferase reporter assays can quantify transcriptional activities of nuclear receptors and NF-??B, while flow cytometry enables examination of T cell activation markers and apoptosis. These methodologies support investigations in transcriptional regulation, T cell signaling, cancer biology, inflammation, and drug target validation. For further information or customized services, please contact Ascent Research.
