The GPNMB Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line, designed for loss-of-function studies of the GPNMB gene. This product provides a genetically heterogeneous pool of cells with targeted disruption of GPNMB, enabling robust and reproducible investigation of gene function in a physiologically relevant T cell model. The polyclonal format preserves biological variability while ensuring efficient ablation of GPNMB expression, making it suitable for high-throughput screening, pathway analysis, and functional genomics without the bias or resource demands of clonal isolation.
The host Jurkat cell line is an immortalized human T lymphocyte line originally established from a patient with acute T cell leukemia. Jurkat cells are widely employed as a model system for studying T cell receptor (TCR) signaling, activation, and apoptosis due to their ability to recapitulate key aspects of primary T cell responses. Their facile genetic manipulation and robust growth characteristics make them an ideal background for CRISPR-based knockouts, enabling precise dissection of immunoregulatory pathways in a tractable in vitro setting.
GPNMB encodes a type I transmembrane glycoprotein that functions as a co-stimulatory molecule and adhesion receptor. It engages integrins such as ITGB1 and the hyaluronan receptor CD44 to initiate signaling cascades involving focal adhesion kinase (FAK) and SRC family kinases. This leads to downstream phosphorylation of ERK1/2 via the RAS-RAF-MEK pathway and activation of AKT through PI3K signaling, thereby promoting cell survival, proliferation, and migration. GPNMB expression is transcriptionally regulated by MITF, TGF-??, and NF-??B, and can be induced by T cell activation and cytokines including IL-4 and IFN-??. Additionally, GPNMB interacts with syndecan-1 (SDC1) and FXYD5, and its signaling convergence on ERK and AKT modulates matrix metalloproteinases (MMPs) and T cell activation markers such as CD69 and CD25.
In Jurkat T cells, GPNMB knockouts provide critical insights into T cell co-stimulation and immune regulation. Loss of GPNMB is expected to impair integrin-mediated adhesion and TCR-induced activation signals, leading to diminished FAK, ERK1/2, and AKT phosphorylation. Consequently, downstream events such as cytokine production, expression of early activation markers, and migratory capacity may be attenuated. This knockout model thus enables precise delineation of GPNMB??s role in coupling environmental cues to T cell effector functions, and its potential as a checkpoint target in cancer immunotherapy.
Research applications for these polyclonal knockout cells are extensive and include detailed T cell activation studies using flow cytometry to quantify CD69 and CD25 surface expression, ELISA-based cytokine secretion profiling, and western blot analysis of phospho-signaling intermediates. The model is also valuable for cell adhesion and migration assays, co-culture experiments with antigen-presenting cells, drug screening campaigns targeting GPNMB-mediated pathways, and transcriptomic analyses via RNA-seq. By providing a reliable loss-of-function system, these cells accelerate discovery in immune-oncology, inflammation, and signaling biology. For additional information or bulk orders, please contact Ascent Research.
