The INPPL1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human leukemic T-cell line. This product provides a loss-of-function model for the INPPL1 gene, encoding the SHIP2 inositol 5-phosphatase. The polyclonal format circumvents clonal selection, maintaining Jurkat cell heterogeneity while broadly disrupting INPPL1 expression.
The Jurkat cell line is a widely utilized model in T-cell biology, originally established from the peripheral blood of an acute lymphoblastic leukemia patient. These cells are instrumental for investigating T-cell receptor (TCR) signaling, antigen recognition, effector functions, and apoptosis, making them a cornerstone in adaptive immunity and oncological research.
INPPL1 encodes SHIP2, a 5-phosphatase that hydrolyzes PI(3,4,5)P3 to PI(3,4)P2, thereby attenuating PI3K/AKT signaling. SHIP2 is activated downstream of the insulin receptor, growth factor receptors (e.g., EGFR, PDGFR), and integrins, often via Src kinase-mediated phosphorylation. By reducing PIP3 levels, SHIP2 negatively regulates AKT, mTORC1, GSK3, and FOXO transcription factors, and also influences Rac1-dependent actin remodeling. SHIP2 interacts with adaptors including IRS1, Shc, and Grb2, linking receptor activation to signal termination. This positions SHIP2 at the intersection of metabolic, growth, and adhesion pathways, with PIP3 synthesis mediated by PI3K and counterbalanced by PTEN.
In Jurkat T cells, INPPL1 knockout removes a critical brake on PI3K/AKT signaling, leading to enhanced pathway activity that can modulate T-cell activation, proliferation, survival, and metabolic reprogramming. Given SHIP2??s role in insulin signaling and cytoskeletal dynamics, this model facilitates studies on immune-metabolic crosstalk and leukemic cell behavior. The polyclonal nature allows assessment of heterogeneous knockout effects, reflecting physiological variability.
Key applications include dissecting T-cell signaling cascades, characterizing the PI3K/AKT/mTOR axis, exploring immune metabolism in leukemic contexts, and screening pathway-targeting compounds. Compatible assays encompass Western blotting for phospho-AKT and phospho-S6, flow cytometry for activation markers (e.g., CD69, CD25), proliferation and apoptosis analyses, metabolic flux measurements, and migration/invasion studies. These cells are also amenable to co-immunoprecipitation of SHIP2 interactors and phospho-proteomic profiling. For further information, please contact Ascent Research.
