ABCC1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal T lymphoblastoid cell population carrying a targeted disruption of the ABCC1 gene. This gene-edited product provides a loss-of-function model for the ATP-binding cassette subfamily C member 1 (ABCC1/MRP1), a critical xenobiotic and drug efflux pump. By abolishing ABCC1-mediated transport, these polyclonal knockout cells enable rigorous investigation of multidrug resistance mechanisms in a human T lymphocyte leukemia background.
The Jurkat cell line is an immortalized T lymphocyte line originally derived from the peripheral blood of a 14-year-old male acute T cell leukemia patient. Jurkat cells are widely used as a model system for T cell signaling, apoptosis, and leukemia biology, and they retain constitutive activation of key oncogenic pathways relevant to T-cell acute lymphoblastic leukemia (T-ALL).
ABCC1 encodes MRP1, an ATP-dependent transmembrane transporter that mediates the efflux of structurally diverse endogenous and exogenous substrates, including glutathione-S-conjugates, leukotriene C4, and chemotherapeutic drugs. Its expression is transcriptionally regulated by NRF2 (NFE2L2), p53, NF-??B, the glucocorticoid receptor (NR3C1), and SP1, linking MRP1 activity to oxidative stress responses and survival signaling. MRP1 functions in concert with glutathione (GSH) and glutathione S-transferases (GSTs) to conjugate and eliminate toxic compounds, thereby reducing intracellular drug accumulation. Upstream, NRF2 activation through KEAP1 dissociation promotes MRP1 expression, while p53 and NF-??B modulate transporter levels under stress conditions. Downstream, MRP1-mediated export of leukotriene C4 influences inflammatory mediator clearance, and its efflux of glutathione conjugates contributes to the detoxification of reactive oxygen species.
In Jurkat cells, ABCC1 expression underpins the multidrug resistance phenotype frequently observed in T-ALL, limiting the efficacy of chemotherapeutic agents. CRISPR/Cas9-mediated disruption of ABCC1 in this polyclonal population abrogates the protective efflux mechanism, thereby sensitizing the cells to a range of anticancer drugs. This model allows direct assessment of MRP1 contribution to drug resistance in a well-characterized T lymphoblastoid context, without interference from other multidrug transporters, enabling clean genotype-phenotype correlation.
These ABCC1 knockout Jurkat cells are suited for applications including multidrug resistance studies, chemotherapy screening, functional efflux transporter assays, drug sensitivity profiling, and pharmacological inhibition of ABC transporters. Representative experimental readouts include calcein-AM efflux flow cytometry for transporter activity, intracellular drug accumulation measurements by fluorescence, MTT cell viability assays under drug treatment, ATPase activity assays, and target gene expression analysis via western blotting and RT-qPCR. For further information or custom project inquiries, please contact Ascent Research.
