The CCNYL1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-mediated gene-edited population of Jurkat cells in which the CCNYL1 gene has been disrupted to create a loss-of-function model. This polyclonal knockout cell product enables investigation of cyclin Y-like 1 function without clonal selection, providing a heterogeneous population that reflects the genetic diversity of the editing outcome.
The Jurkat cell line is an immortalized human T lymphocyte line derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Widely used as a model system, Jurkat cells are instrumental for dissecting T-cell signaling, activation, and apoptosis, offering a robust cellular context for studying molecular mechanisms underlying leukemia and immune cell biology.
CCNYL1 encodes a cyclin Y-like protein that acts as a regulatory subunit for cyclin-dependent kinases, primarily CDK2 and CDK1, to govern cell cycle progression. This protein interacts with and activates these CDKs, leading to phosphorylation of retinoblastoma protein (RB1) and subsequent release of E2F transcription factors, which drive expression of genes required for G1/S transition and S-phase entry. The pathway is modulated by upstream regulators such as E2F and MYC transcription factors and is counterbalanced by CDK inhibitors p21 and p27, with additional interactions involving cyclin E and cyclin A to ensure precise cell cycle control.
In the Jurkat T-cell leukemia background, disruption of CCNYL1 provides a valuable model for studying the intersection of cell cycle regulation and leukemogenesis. Because aberrant cyclin-dependent kinase signaling is a hallmark of many cancers, this knockout cell population allows researchers to examine how loss of CCNYL1 affects T-lymphocyte proliferation, survival, and response to anti-mitogenic signals, thereby contributing to the identification of therapeutic targets in lymphoid malignancies.
This knockout product is suited for a broad spectrum of functional studies, including flow cytometry-based cell cycle analysis using propidium iodide staining, western blotting for cyclin and CDK expression, RT-qPCR profiling of cell cycle genes, and apoptosis assays with Annexin V. Proliferation assays such as MTT and BrdU incorporation, as well as transcriptomic analysis via RNA-seq, can be employed to characterize CCNYL1-dependent networks. The cells are particularly useful for screening small-molecule inhibitors of cell cycle kinases and investigating novel cyclin biology in T-cell leukemia. For further technical information, please contact Ascent Research.
