The INPP5F Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population providing loss-of-function of INPP5F in a T lymphocyte background. This polyclonal pool avoids clonal biases and enables population-level analysis of INPP5F-dependent phenotypes.
The Jurkat E6-1 cell line, derived from a human acute T cell leukemia patient, is a well-established model for T cell receptor signaling, apoptosis, and cytokine production. Its robust TCR signaling network and genetic tractability make it ideal for dissecting phosphoinositide metabolism and immune signal transduction.
INPP5F is a phosphoinositide 5-phosphatase that hydrolyzes PI(4,5)P2 and PI(3,4,5)P3, key lipid second messengers in membrane trafficking, actin dynamics, and endocytosis. In Jurkat cells, INPP5F functions downstream of TCR stimulation and receptor tyrosine kinases, and interacts with dynamin, amphiphysin, sorting nexin 9, and actin regulators. By depleting phosphoinositide substrates, INPP5F negatively regulates PLC??1-mediated calcium signaling and the PI3K/AKT pathway. Knockout elevates PI(4,5)P2 levels, enhancing TCR-induced PLC??1 phosphorylation, calcium flux, and NFAT-driven transcription, while disturbing actin polymerization and endocytic trafficking.
In the Jurkat T cell context, INPP5F loss underscores the importance of phosphoinositide balance for TCR signaling strength and immune effector functions. Elevated PI(4,5)P2 hyperactivates PLC??1?Ccalcium?CNFAT cascades, influencing cytokine production and cell proliferation. Disruption of INPP5F is relevant to T cell acute lymphoblastic leukemia, glioblastoma, and neurodegenerative conditions, where alterations in phosphoinositide metabolism, membrane trafficking, and actin reorganization contribute to pathogenesis. This model thus facilitates exploration of phosphatase-dependent mechanisms in both leukemic signaling and broader disease contexts.
Researchers can employ the INPP5F Knockout Jurkat Polyclonal Cells for T cell signaling pathway analysis, phosphoinositide metabolism profiling, and immune synapse dynamics studies. Assays include flow cytometry for CD69 or phospho-PLC??1 after TCR ligation, calcium flux measurements using Fluo-4 AM, immunofluorescence imaging of PI(4,5)P2 localization, co-immunoprecipitation of INPP5F interactors, and cell migration analyses. The polyclonal format supports population-based readouts such as western blotting and is well-suited for target validation in leukemia and for screening modulators of phosphoinositide phosphatase function. For further details, contact Ascent Research.
