The CCDC112 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to abolish target gene expression in the human HAP1 cell line. This product provides a heterogeneous pool of edited cells with targeted disruption of the CCDC112 locus, enabling loss-of-function studies without clonal selection bias. The polyclonal format captures the diversity of CRISPR-mediated gene disruption events, offering a robust and reproducible model for investigating CCDC112 function.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line, exhibiting adherent fibroblast-like morphology. Its haploid karyotype facilitates straightforward genetic manipulation and phenotype-to-genotype correlation, as only one allele must be targeted for functional knockout. The CML origin provides a relevant cellular context for cancer-related studies, while the adherent growth supports a variety of imaging and biochemical assays.
CCDC112 encodes a putative coiled-coil domain-containing protein, suggesting a role in mediating protein-protein interactions. Although its precise molecular function remains uncharacterized, CCDC112 has been associated with cilium assembly and cell cycle regulation pathways. Potential interaction partners may include intraflagellar transport (IFT) proteins and primary cilium structural components, positioning CCDC112 within ciliary biology networks. The absence of well-defined upstream regulators, downstream targets, or established binding partners underscores the need for functional models to elucidate its signaling role.
The combination of CCDC112 knockout with the near-haploid HAP1 background creates a powerful system for dissecting gene function in ciliary and cell cycle processes. Polyclonal populations minimize the risk of clonal artifacts, ensuring that observed phenotypes reflect loss of CCDC112 rather than off-target effects or secondary mutations. This model is particularly valuable for studying primary cilium dynamics, as HAP1 cells can be induced to form cilia, and for exploring potential tumor-suppressive or oncogenic roles in leukemia and other cancers.
Researchers can employ this polyclonal knockout model in a range of experimental workflows, including Western blotting and RT-qPCR for validation of CCDC112 depletion, cell proliferation and cell cycle assays to assess growth regulatory functions, and immunofluorescence microscopy to visualize primary cilia using markers such as acetylated tubulin or ARL13B. Genotyping PCR can confirm gene disruption at the population level. These cells are suitable for investigating ciliary assembly mechanisms, cell cycle control, and cancer biology. For additional information or technical support, please contact Ascent Research.
