This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CASZ1 gene in Jurkat cells. The polyclonal format provides a heterogeneous loss-of-function model reflecting a range of gene disruptions within the population, enabling robust analysis of CASZ1-dependent phenotypes without clonal bias. These cells are designed for investigating the tumor-suppressive roles of CASZ1 in T-cell biology.
The Jurkat cell line is a human CD4+ T lymphocyte line derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia. These suspension cells display a mature T-cell phenotype and are extensively used to study T-cell receptor signaling, apoptosis, and HIV infection. Their well-defined signaling pathways and susceptibility to genetic manipulation make Jurkat cells a standard model for leukemia research and drug testing.
CASZ1 is a zinc finger transcription factor that functions as a tumor suppressor by directly binding DNA and regulating genes critical for cell cycle arrest and apoptosis, including CDKN1A (p21) and BAX. CASZ1 is activated by upstream signals from Notch1 intracellular domain, N-Myc, TGF-??, and Wnt, and it cooperates with cofactors such as CSL/RBP-J, MAML1, SMAD2/3, and histone deacetylases to modulate transcription. Through these interactions, CASZ1 integrates Notch, TGF-??/SMAD, and Wnt/??-catenin pathways to control additional targets like MYCN and GATA3, thereby coordinating differentiation and proliferation in T-cells.
In Jurkat T-cells, which harbor a constitutively active Notch1 pathway, CASZ1 knockout abrogates its growth-suppressive functions, potentially leading to unchecked proliferation and reduced apoptosis. Disruption of CASZ1-mediated regulation of CDKN1A and BAX relieves p53-dependent and -independent checkpoints, while aberrant expression of MYCN may further drive oncogenic programs. This polyclonal knockout model is therefore valuable for dissecting the contribution of CASZ1 to T-cell leukemia progression and for examining interplay between Notch1 and TGF-??/SMAD signaling in a T-ALL background.
Key applications include flow cytometry for apoptosis and cell cycle profiling, RT-qPCR and western blotting to quantify target gene expression, ChIP-qPCR to map CASZ1 genomic occupancy, and co-immunoprecipitation to probe interactions with SMAD2/3 or CSL/RBP-J. Proliferation assays and drug dose-response studies facilitate investigation of chemosensitivity and Notch pathway inhibitors. The polyclonal nature makes these cells suitable for pooled CRISPR screens and population-level signaling studies. For additional information, please contact Ascent Research.
