The IVNS1ABP Knockout Jurkat Polyclonal Cells product comprises a polyclonal population of CRISPR/Cas9-edited Jurkat T lymphocytes with targeted disruption of the IVNS1ABP gene. IVNS1ABP encodes an RNA-binding protein that participates in pre-mRNA splicing regulation and stress granule dynamics, and it is a known interactor of the influenza A virus NS1 protein. By eliminating IVNS1ABP expression, this knockout model enables detailed investigation of its roles in viral immune evasion and host spliceosomal control. The polyclonal format avoids clonal selection constraints, providing a heterogeneous cell pool representative of the diverse responses observed in native cellular environments.
Jurkat cells are an immortalized human T lymphocyte line originally derived from the peripheral blood of a 14-year-old male patient with acute T cell leukemia. These cells serve as a well-established model for studying T cell receptor signaling, leukemia biology, and innate immune responses. Their robust proliferation and susceptibility to viral infection make them particularly suited for examining host?Cpathogen interactions, including those involving influenza A virus. The leukemic origin of Jurkat cells also allows exploration of crosstalk between splicing dysregulation and malignant transformation.
At the molecular level, IVNS1ABP functions as an RNA-binding protein that directly interacts with spliceosomal components, notably SNRPA of the U1 snRNP and SFPQ, to modulate pre-mRNA splicing. It also associates with G3BP1, a core stress granule protein, linking it to RNA metabolism under cellular stress. During influenza A virus infection, IVNS1ABP binds the viral NS1 protein and suppresses the host antiviral response by inhibiting the RIG-I/MDA5 signaling pathway, which includes RIG-I, MDA5, the adaptor MAVS, and the transcription factor IRF3, thereby blocking interferon-?? production. Gene ablation disrupts this NS1-mediated suppression, potentially restoring innate immune signaling and altering the splicing landscape of apoptotic regulators and other targets.
In the Jurkat T cell context, which retains functional RIG-I/MDA5 signaling and is susceptible to influenza A virus, IVNS1ABP knockout provides a relevant system for mechanistic studies of viral immune evasion. The polyclonal knockout population reflects the cellular heterogeneity of a non-clonal model, allowing assessment of gene disruption without the confounding effects of monoclonal selection. Moreover, given the leukemic origin of Jurkat cells, this model can be applied to investigate how splicing regulatory factors like IVNS1ABP contribute to T cell acute lymphoblastic leukemia pathogenesis and how they intersect with antiviral pathways.
These knockout cells are designed for diverse applications, including co-immunoprecipitation to verify IVNS1ABP?CNS1 interaction, RT-qPCR and RNA-seq for splicing analysis, and interferon-?? reporter assays. They are also suited for viral replication studies, drug screening for antivirals or splicing modulators, and flow cytometry for immune markers. For further information, contact Ascent Research.
