The ADARB1 Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte cell line, engineered for loss-of-function analysis of the ADARB1 gene encoding ADAR2. This polyclonal pool offers a heterogeneous knockout model that preserves the diversity of CRISPR/Cas9-mediated gene disruption, avoiding clonal selection bias while enabling robust functional studies of ADAR2-dependent RNA editing in a lymphoid background.
Jurkat cells are immortalized human T lymphocytes originally isolated from the peripheral blood of a patient with acute T cell leukemia. The E6.1 subclone is a widely characterized model for investigating T cell signaling, apoptosis, and HIV infection, exhibiting rapid suspension growth and permissiveness to molecular manipulation. These features make Jurkat an ideal host for generating knockout pools to explore immune cell biology and disease mechanisms.
ADARB1 encodes the adenosine deaminase ADAR2, which catalyzes A-to-I editing of double-stranded RNA (dsRNA) substrates, critically regulating transcript recoding, splicing, and miRNA maturation. ADAR2 is activated by type I interferons and dsRNA, and interacts with ADAR1, NF90/NF45, and RNA helicase A within editing complexes. It modifies key transcripts such as GRIA2 and FLNB, and modulates innate immune sensing by MDA5 and PKR, influencing downstream IRF3 and NF-??B signaling. Knockout of ADARB1 therefore abolishes ADAR2-mediated editing, disrupting dsRNA structural modulation and leading to aberrant interferon responses and altered cellular regulation.
In the Jurkat T cell context, loss of ADAR2 perturbs precise control of dsRNA immunity, potentially resulting in dysregulated T cell activation and apoptosis. This model is especially relevant for dissecting RNA editing roles in T cell leukemia biology and for modeling editing-deficient autoimmune conditions such as Aicardi-Gouti??res syndrome, where unchecked interferon production arises from defective self-RNA editing.
Key applications include RNA-seq for global editing site profiling, RT-qPCR and Western blotting for target validation, and flow cytometry for activation markers (CD69, CD25). Functional assays encompass interferon stimulation, luciferase reporters for dsRNA sensing, and co-immunoprecipitation to map ADAR2 interaction networks. These polyclonal cells also support screening for editing-dependent drug sensitivities. For further information, please contact Ascent Research.
