The IRF2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat T cells, in which the IRF2 gene has been disrupted using CRISPR/Cas9-mediated gene disruption. This polyclonal pool offers a genetically heterogeneous loss-of-function model for studying IRF2-dependent processes without clonal selection artifacts.
Jurkat cells are an immortalized human T lymphocyte line isolated from a patient with T-cell leukemia. They express CD3 and functional T-cell receptors, making them a widely used model for investigating T-cell receptor signaling, apoptosis, and immune activation. Their leukemic origin also provides a relevant context for studying T-cell malignancies and immune dysregulation.
IRF2 is a transcription factor that modulates interferon-responsive and cell cycle genes. It operates within the JAK-STAT pathway downstream of interferon-alpha/beta (IFNAR1/2) and interferon-gamma receptors, where STAT1 and STAT2 are phosphorylated by JAK1 and TYK2. IRF2 interacts with IRF1, IRF9, and cofactors like CBP/p300 to regulate ISRE-containing promoters. It transcriptionally regulates targets such as CDKN1A (p21), PRDM1 (Blimp-1), MHC class I genes, and numerous ISGs. Upstream regulators include interferon-alpha, interferon-beta, interferon-gamma, and NF-kB. Through these interactions, IRF2 coordinates immune responses, cell cycle progression, and apoptosis.
In Jurkat T cells, IRF2 knockout abrogates both transcriptional repression and activation of interferon-responsive genes, altering ISRE-mediated gene expression. This disruption modulates cell cycle regulators like p21 and apoptotic pathways, potentially affecting T-cell receptor signaling and immune modulation. Given IRF2’s dual role as a repressor and activator, this polyclonal knockout model enables dissection of its context-dependent functions in a T-lymphocyte background, which is critical for understanding interferon biology in leukemia and autoimmune disorders.
This product is suitable for investigating IRF2-mediated transcriptional regulation and interferon signaling in T cells. Typical applications include RT-qPCR profiling of ISGs, Western blotting for IRF2 and downstream targets, RNA-seq transcriptional profiling, and flow cytometric analysis of MHC-I expression. Functional assays such as luciferase reporter assays for ISRE activity, cell proliferation, and apoptosis assays can delineate IRF2’s impact on T-cell fate. Additionally, co-immunoprecipitation and phospho-STAT analysis permit interrogation of IRF2 interactions and JAK-STAT activation status. Cytokine stimulation assays further facilitate study of IRF2’s role in immune dynamics. Researchers seeking technical support or customization of this CRISPR/Cas9-edited polyclonal knockout cell population are invited to contact Ascent Research.
