CCNY Knockout HAP1 Polyclonal Cells constitute a human cell population generated through CRISPR/Cas9-mediated disruption of the CCNY gene, resulting in a functional loss of cyclin Y expression. As a polyclonal knockout pool, this product provides a versatile system for investigating CCNY-dependent signaling and cell cycle regulation, allowing researchers to study gene function in a mixed population that reflects the heterogeneous nature of genetic perturbation studies. The cells are produced using the well-characterized HAP1 cell line and are intended for advanced applications in cancer biology, signal transduction, and drug discovery.
The host cell line, HAP1, is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. HAP1 cells display fibroblast-like morphology and adhere robustly to culture surfaces, making them suitable for a wide range of standard cell-based assays. Their near-haploid karyotype, lacking a second set of chromosomes except for a disomic region, simplifies genetic analyses and reduces the likelihood of functional compensation by alternate alleles, thereby facilitating clean loss-of-function studies and genetic interaction screens.
Cyclin Y, encoded by CCNY, is a key cell cycle regulator that activates CDK14 kinase upon binding. The cyclin Y/CDK14 complex phosphorylates the LRP6 co-receptor in response to WNT ligand stimulation, allowing recruitment of AXIN and DVL, which leads to GSK3?? inhibition and subsequent ??-catenin stabilization. Stabilized ??-catenin translocates to the nucleus and partners with TCF/LEF transcription factors to drive expression of targets such as CCND1 and MYC. In parallel, cyclin Y contributes to G2/M phase transition, linking cell cycle progression with Wnt/??-catenin signaling. Representative pathway components include WNT3A, LRP6, DVL, AXIN, GSK3??, ??-catenin, and CDK14.
The HAP1 background offers a distinct advantage when studying CCNY function because the near-haploid state minimizes interference from residual functional alleles, enabling more penetrant phenotypes. This model is particularly valuable for probing Wnt pathway deregulation, a hallmark of myeloid leukemias and other malignancies. Researchers can leverage these knockout cells to investigate CCNY??s role in cancer cell proliferation, apoptosis, and therapeutic response, as well as to validate CCNY as a potential target in acute myeloid leukemia, breast cancer, or colorectal cancer.
These CCNY knockout cells are well suited for a broad range of experimental workflows. Investigators can monitor Wnt/??-catenin pathway activity using TCF/LEF luciferase reporter assays, quantify ??-catenin stabilization by western blotting, and measure target gene expression (CCND1, MYC) by RT-qPCR. Cell cycle distribution can be assessed via flow cytometry after propidium iodide staining, and proliferation rates can be evaluated by growth curve or MTT assays. Furthermore, the cells enable drug sensitivity screens and genetic modifier studies to uncover novel regulators of the CCNY signaling axis. For additional product details or technical support, please contact Ascent Research.
