The IREB2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of Jurkat T lymphoblasts, designed to eliminate functional expression of the IREB2 gene. This heterogeneous pool of gene-disrupted cells provides a robust tool for studying the iron-responsive element binding protein 2 (IRP2) and its role in post-transcriptional iron regulation within a human T-cell context.
The parental Jurkat line is a CD4+ T-lymphoblastoid cell line originally derived from a patient with acute T-cell leukemia. It is extensively employed as a model for T-cell signaling, apoptosis, and leukemogenesis. The cells grow in suspension and maintain genetic and biochemical features that facilitate functional genomics and high-throughput screening.
IREB2 (IRP2) functions as an iron-sensing RNA-binding protein that interacts with iron-responsive elements (IREs) in the untranslated regions of mRNAs encoding iron metabolism proteins. Under iron depletion, IRP2 binds to IREs to stabilize transferrin receptor (TFRC) mRNA, promoting iron uptake, while repressing translation of ferritin (FTH1, FTL) and ferroportin (SLC40A1) to reduce iron storage and export. Its stability is directly regulated by intracellular iron levels via the FBXL5 E3 ubiquitin ligase, which targets IRP2 for proteasomal degradation when iron is plentiful. Additional inputs from hypoxia and reactive oxygen species fine-tune IRP2 activity, and downstream targets include DMT1 (SLC11A2) and EPAS1. IRP2 forms complexes with iron?sulfur clusters and can functionally interact with its homolog ACO1 (IRP1), thereby integrating multiple iron-sensing signals.
In leukemic Jurkat T cells, disruption of IREB2 offers a means to interrogate the consequences of aberrant iron regulation on T-cell malignancy. Iron is indispensable for DNA synthesis, mitochondrial function, and cell cycle progression, and leukemic cells often reprogram iron handling to support rapid proliferation. The IREB2 knockout model allows researchers to assess how loss of IRP2 affects proliferation, oxidative stress sensitivity, and apoptotic signaling, thereby revealing potential vulnerabilities in T-cell leukemogenesis linked to iron metabolism.
This polyclonal knockout product is applicable to diverse experimental approaches, including western blot detection of IRP2 and its target proteins, RT?qPCR analysis of TFRC mRNA stability, and flow cytometric measurement of transferrin receptor surface expression. Researchers can carry out intracellular iron quantification and conduct viability assays under iron chelation to screen for iron-modulating compounds. The cells also support RNA immunoprecipitation studies to map IRP2?CRNA interactions. Taken together, they serve as a valuable platform for mechanistic studies of the IRE/IRP system and for drug discovery programs targeting iron homeostasis in cancer and neurodegenerative diseases. For further details, please inquire with Ascent Research.
