The CCNYL1 Knockout HAP1 Polyclonal Cells product comprises a population of HAP1 cells modified by CRISPR/Cas9-mediated disruption of the CCNYL1 gene, generating a heterogeneous polyclonal loss-of-function model. This product is supplied as a pool of edited cells, suitable for functional studies where population-level responses to CCNYL1 ablation are of interest, rather than clonal isolates.
The HAP1 host cell line is a near-haploid human cell line derived from the KBM-7 chronic myelogenous leukemia line. It exhibits adherent, fibroblast-like morphology and carries a predominantly haploid karyotype, with only a small diploid fraction. The haploid nature of HAP1 cells makes them a powerful platform for genetic perturbation screens, as single-allele targeting can unmask recessive phenotypes, enabling efficient functional genomics and drug target discovery.
CCNYL1 encodes a cyclin Y-like protein that functions as a regulatory subunit of cyclin-dependent kinases, primarily CDK14 (PFTK1) and possibly CDK16, to modulate Wnt/??-catenin signaling. The CCNYL1?CCDK14 complex phosphorylates the Wnt co-receptor LRP6 at key residues, thereby enhancing signalosome assembly and downstream pathway activation. In response to Wnt ligands such as Wnt3a, this kinase activity promotes ??-catenin stabilization by inhibiting the Axin destruction complex (composed of APC, GSK3??, and CK1). Stabilized ??-catenin translocates to the nucleus, where it partners with TCF/LEF transcription factors to drive expression of Wnt target genes, including MYC, CCND1, and AXIN2, which are implicated in cell cycle progression and proliferation.
In the HAP1 cell background, disruption of CCNYL1 is expected to impair canonical Wnt signaling by reducing LRP6 phosphorylation and subsequent ??-catenin accumulation, providing a clean experimental system for dissecting CCNYL1??s contribution to signal transduction. Because HAP1 cells are near-haploid, knockout phenotypes are generally more penetrant than in diploid models, enabling sensitive detection of functional changes in Wnt-responsive transcription and cell cycle regulation. This knockout pool is particularly well-suited for studying the mechanistic role of CCNYL1 in cancer biology, given HAP1??s origin from a CML-derived line, as well as for modeling signaling defects linked to Wnt-related disorders.
Researchers can employ these CCNYL1 knockout polyclonal cells in a variety of assays to probe Wnt pathway activity and cell cycle dynamics. The population is amenable to TOPFlash/FOPFlash luciferase reporter assays for measuring ??-catenin/TCF-driven transcription, western blotting to assess LRP6 phosphorylation and ??-catenin levels, and RT-qPCR to quantify expression of Wnt target genes such as AXIN2 and CCND1. Co-immunoprecipitation experiments can be used to examine the CCNYL1?CCDK14 interaction, while flow cytometry and cell proliferation assays enable functional evaluation of cell cycle progression. Additionally, the polyclonal nature supports pooled high-throughput genetic screens and RNA-seq studies to explore transcriptome-wide effects of CCNYL1 loss. For further details or custom configurations, please contact Ascent Research.
