This product consists of a polyclonal population of Jurkat T-cell leukemia cells engineered with CRISPR/Cas9 to disrupt the CCNY gene, encoding cyclin Y. The polyclonal knockout format preserves genetic heterogeneity, minimizing clonal bias and providing a reliable loss-of-function model. These cells lack functional cyclin Y protein, enabling dissection of its roles in Wnt signaling and cell cycle control in a human T-lymphocyte background.
Jurkat cells, derived from a male adolescent with acute lymphoblastic leukemia, are a classic model for studying T-cell signaling, apoptosis, and leukemogenesis. They retain key aspects of T-cell biology and offer high transfectability, making them ideal for targeted gene ablation. In the context of CCNY disruption, this model allows investigation of cyclin Y function in a malignant T-cell environment with intact Wnt pathway machinery.
Cyclin Y is a membrane-associated cyclin that activates CDK14 and CDK16. Upon Wnt stimulation, the CCNY?CCDK14 complex phosphorylates the co-receptor LRP6, stabilizing ??-catenin, which translocates to the nucleus to co-activate TCF/LEF transcription factors. This stimulates expression of proliferation and survival genes such as MYC and CCND1. CCNY also interfaces with core Wnt components DVL and Axin, and its activity is influenced by mitogenic inputs. Thus, CCNY links Wnt ligand reception at the plasma membrane to cell cycle machinery and transcriptional responses.
In T-cell acute lymphoblastic leukemia, Wnt/??-catenin signaling is frequently dysregulated, promoting disease progression. The CCNY knockout Jurkat cells enable researchers to interrogate how cyclin Y contributes to leukemic growth, survival, and drug response. The model facilitates the study of Wnt pathway dependency, identification of downstream effectors, and evaluation of therapeutic strategies targeting Wnt. Additionally, it permits analysis of potential crosstalk between cyclin Y-associated kinases and other oncogenic drivers in T-cell malignancies.
Applications include Western blot detection of ??-catenin, TOPFlash/FOPFlash reporter assays, RT-qPCR for Wnt targets, flow cytometric cell cycle analysis, and co-immunoprecipitation of CCNY?CCDK14/LRP6 complexes. The polyclonal population is suitable for Wnt inhibitor screening and functional genomics studies. For further technical details or custom inquiries, please contact Ascent Research.
