The IMPA1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte line, engineered to disrupt the IMPA1 gene. This product provides a heterogeneous pool of cells with targeted gene disruption, enabling loss-of-function studies of inositol monophosphatase 1 in a human T cell context. As a polyclonal population, it reflects a range of editing events, offering robust representation of the knockout phenotype across the culture.
The Jurkat cell line is an immortalized human T lymphocyte model originally isolated from the peripheral blood of a patient with acute T cell leukemia. Widely used in immunology and cancer research, Jurkat cells recapitulate key aspects of T cell receptor (TCR) signaling, calcium mobilization, and transcriptional responses, making them a well-established system for dissecting signal transduction cascades and leukemogenic mechanisms.
IMPA1 encodes inositol monophosphatase 1, a magnesium-dependent enzyme that catalyzes the hydrolysis of inositol monophosphates to myo-inositol, a critical step in the recycling of inositol for phosphatidylinositol signaling. Functioning downstream of phospholipase C gamma 1 (PLC??1) and inositol 1,4,5-trisphosphate (IP3) generation, IMPA1 regenerates myo-inositol required for phosphatidylinositol 4,5-bisphosphate (PIP2) resynthesis. This cycle sustains diacylglycerol (DAG)-mediated protein kinase C (PKC) activation and calcium-dependent nuclear factor of activated T cells (NFAT) signaling. IMPA1 is also the molecular target of lithium, a mainstay therapy for bipolar disorder, with inhibition attenuating phosphoinositide turnover and downstream signaling.
In Jurkat T cells, IMPA1 knockout disrupts phosphoinositide recycling, leading to impaired TCR-induced calcium flux and diminished NFAT transcriptional activity. This model replicates lithium??s effect on inositol depletion and offers a genetic tool to dissect the lithium-sensitive signaling node. The polyclonal knockout population thus enables exploration of how IMPA1 deficiency influences T cell activation and provides a human cellular platform for studying mechanisms relevant to mood disorders and lithium pharmacology without pharmacological agents.
Researchers can employ this product in a variety of assay formats, including Western blotting to confirm IMPA1 loss, inositol phosphate accumulation assays, calcium flux measurements, NFAT-reporter luciferase assays, and flow cytometric analysis of phospho-ERK and NFAT nuclear translocation. RNA-sequencing studies can reveal transcriptional changes, while drug sensitivity profiling with lithium or other small molecules facilitates therapeutic discovery. This polyclonal knockout model is particularly suited for high-throughput screening of mood-disorder targets and detailed interrogation of phosphoinositide-dependent immune signaling. For further technical details, please contact Ascent Research.
