The BICC1 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of Jurkat cells, engineered for targeted disruption of the BICC1 gene. This polyclonal format provides a heterogeneous loss-of-function model ideal for studying the functional consequences of BICC1 depletion without clonal selection biases. The product enables robust investigation of BICC1-mediated post-transcriptional regulation within a physiologically relevant T-lymphoblast context.
The parental Jurkat cell line is a widely used immortalized human T lymphocyte model, originally derived from an acute T-cell leukemia patient. These suspension-adapted T lymphoblasts retain key signaling pathways characteristic of T cells, including TCR-mediated activation, apoptosis cascades, and proliferative responses. Jurkat cells are a standard platform for dissecting T-cell signaling dynamics and evaluating therapeutic targets in leukemia and immunology research.
BICC1 encodes an RNA-binding protein that post-transcriptionally orchestrates gene expression by binding to specific mRNA targets, modulating their translation and stability. This regulation is central to the Wnt/planar cell polarity (PCP) pathway, where BICC1 interacts with Dishevelled family members DVL1, DVL2, and DVL3, as well as ANKS6 and INVS, to influence downstream signaling. Additionally, BICC1 interfaces with TGF-beta signaling, collectively controlling cell polarity, proliferation, and differentiation. By fine-tuning PCP component expression, BICC1 serves as a critical node linking extracellular cues to post-transcriptional changes.
In the Jurkat T-cell context, BICC1 knockout offers a powerful system to delineate how RNA-binding protein dysfunction impacts T-lymphocyte biology. Since Jurkat cells exhibit active Wnt and TGF-beta signaling, disruption of BICC1 can reveal its role in modulating T-cell activation, migration, and survival. This model is particularly valuable for probing the contribution of post-transcriptional dysregulation to leukemogenesis and for evaluating BICC1 as a potential therapeutic target in T-cell malignancies.
Researchers can employ this model in diverse workflows, including Western blotting and RT-qPCR for expression analysis, RNA immunoprecipitation and RNA-seq for binding and stability studies, and luciferase reporter assays to assess pathway activity. Functional assays such as flow cytometry for apoptosis and proliferation, transwell migration tests, and co-immunoprecipitation for protein interactions are highly applicable. The BICC1-Jurkat system supports mechanistic studies of post-transcriptional regulation, Wnt/PCP and TGF-beta signaling, and preclinical T-cell leukemia research. For additional product information, please contact Ascent Research.
