The BHLHE40 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the BHLHE40 gene in the Jurkat human T lymphocyte cell line. This product provides a loss-of-function model for investigating BHLHE40-dependent transcriptional regulation. The polyclonal format offers a heterogeneous pool of edited cells, enabling population-level studies without clonal selection bias. This knockout tool is suitable for functional genomics, signaling pathway analysis, and phenotypic screening in T cell biology and leukemia research.
Jurkat cells are an immortalized human CD4+ T lymphocyte line originally derived from an acute lymphoblastic leukemia (ALL) patient. They serve as a widely recognized model for T cell receptor signaling, activation, and apoptosis, as well as for studying leukemogenesis and immune response mechanisms. The Jurkat background is particularly valuable for dissecting signaling cascades relevant to T cell-mediated immunity and cancer biology.
BHLHE40 (basic helix-loop-helix family member e40) is a transcriptional repressor that modulates gene expression by binding to E-box elements and recruiting histone deacetylases such as HDAC1 and HDAC2. It is a core component of the circadian clock, forming regulatory loops with CLOCK and BMAL1 (ARNTL), and directly represses targets like PER1. In hypoxic conditions, BHLHE40 is induced by HIF1A and regulates downstream effectors including TP53, CDKN1A, and BCL2L11, thereby influencing cell cycle arrest and apoptosis. Additionally, it integrates signals from TGF-beta (via SMAD2/3) and inflammatory pathways (STAT3, NFKB1) to control immune cell differentiation and cytokine expression, including IL2.
In Jurkat T cells, BHLHE40 knockout disrupts the normal transcriptional programs governing circadian rhythmicity, hypoxia adaptation, and T cell activation. This model enables researchers to dissect how BHLHE40-mediated repression affects proliferation and apoptosis in a leukemic background. The interaction of BHLHE40 with core clock proteins and HIF1A provides a unique platform to explore the intersection of circadian biology and cancer cell metabolism. Moreover, the knockout can unveil BHLHE40??s role in modulating T cell receptor-driven responses and cytokine production, offering insights into autoimmune disorders and leukemia progression.
The BHLHE40 Knockout Jurkat Polyclonal Cells are ideal for a wide range of experimental approaches, including quantitative real-time PCR (RT-qPCR), western blotting, RNA sequencing (RNA-seq), and chromatin immunoprecipitation (ChIP-qPCR) to assess transcriptional and epigenetic changes. Functional studies may involve flow cytometry analysis of activation markers, proliferation assays (e.g., CFSE labeling), apoptosis assays (e.g., annexin V staining), and luciferase-based reporter assays for E-box activity. This polyclonal knockout population supports drug sensitivity screening and investigation of circadian or hypoxia-modulated pathways in T cell leukemia. For further information, please contact Ascent Research.
