This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line, in which the BCORL1 gene has been disrupted to create a heterogeneous pool of loss-of-function alleles. As a polyclonal population, it retains genomic diversity across cells, enabling robust assessment of BCORL1 function without the potential biases of single-clone isolation. The knockout model provides a versatile experimental system for interrogating BCORL1-dependent transcriptional regulation, signaling pathways, and cellular phenotypes in a T-cell context. This format is particularly suited for pooled screening, dose-response studies, and comparative analyses where population-level effects are paramount.
Jurkat cells are a widely utilized CD4+ T lymphoblastoid cell line originally derived from the peripheral blood of an adolescent male with acute T cell leukemia. These cells serve as a classic model for studying T cell receptor signaling, activation cascades, and apoptosis mechanisms. Their leukemic origin and expression of core T-cell markers make them highly relevant for investigating oncogenic processes and immune cell biology. The immortalized nature of Jurkat cells allows for straightforward genetic manipulation, expansion, and high-throughput assay compatibility, establishing them as a foundational tool in immunological and cancer research.
BCORL1 encodes a transcriptional corepressor that functions by assembling repressor complexes with histone deacetylases HDAC1/2 and C-terminal binding proteins CtBP1/2, facilitating chromatin compaction and silencing of target gene promoters. In the context of T cells, BCORL1 is involved in repressing key regulators of cell cycle and differentiation, including HES1 and MYC, while also modulating CDKN1A. Its activity is integrated into pathways activated by WNT3A and DLL4, which signal through ??-catenin/TCF7/LEF1 and Notch1 intracellular domain, respectively. BCORL1 also interacts with BCL6, RING1, and RNF2, highlighting its role in a broader transcriptional regulatory network that governs hematopoietic development.
In Jurkat T cells, BCORL1 knockout disrupts the normal repressive control over genes that promote proliferation and inhibit apoptosis, mirroring the transcriptional dysregulation observed in T-cell acute lymphoblastic leukemia (T-ALL) and other hematological malignancies. The loss of BCORL1 function can lead to aberrant activation of Notch and Wnt/??-catenin target genes, potentially driving unchecked cell growth. Thus, this polyclonal knockout model recapitulates aspects of leukemogenic transformation and provides a relevant cellular context for exploring tumor suppressor mechanisms, epistatic relationships, and the effects of therapeutic agents targeting these pathways.
This knockout cell population is applicable to a range of experimental workflows, including transcriptional profiling by RNA-seq, chromatin immunoprecipitation (ChIP)-qPCR for histone modification analysis, and protein interaction studies via co-immunoprecipitation to assess BCORL1 complex assembly. Functional assays such as MTT-based proliferation measurements, Annexin V apoptosis detection, and flow cytometry for T-cell activation markers (e.g., CD69) can be employed to quantify phenotypic consequences. Drug screening campaigns for HDAC inhibitors, Notch antagonists, or Wnt modulators are facilitated by the population??s uniform genetic background. For further technical details and ordering information, please contact Ascent Research.
