The CCDC167 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell pool targeting the CCDC167 gene in the HAP1 cell line. This genetically heterogeneous population harbors loss-of-function mutations, enabling functional studies of CCDC167 in a near-haploid human context. The polyclonal format maintains genetic diversity while ensuring target protein depletion, suitable for experiments that benefit from population-level knockout effects without clonal isolation.
The HAP1 cell line is an adherent, fibroblast-like line derived from a male chronic myeloid leukemia (CML) patient, carrying the BCR-ABL fusion oncogene. Its near-haploid karyotype reduces genetic redundancy, simplifying the interpretation of knockout phenotypes, making it an ideal model system for CRISPR-based gene disruption studies. HAP1 cells provide a clean genetic background for dissecting gene functions in cancer-relevant pathways, with the near-haploid state ensuring high knockout efficiency and unambiguous phenotypic interpretation.
CCDC167 encodes a coiled-coil domain protein that localizes to centrosomes and regulates centrosome duplication and cell cycle progression. Its expression is driven by cell cycle transcription factors E2F and FOXM1. Functionally, CCDC167 interacts with centrosomal components PLK4 and CEP192, and operates downstream of CDK1/Cyclin B. The protein also associates with microtubule-associated proteins, influencing microtubule organization. Disruption of CCDC167 leads to defects in centrosome number control and cell division fidelity.
Combining CCDC167 knockout with the BCR-ABL oncogenic driver in the HAP1 CML model permits investigation of centrosome-associated defects in a leukemic context. Researchers can explore synthetic lethal interactions and cooperative mechanisms between centrosome integrity and tyrosine kinase signaling. This model is particularly relevant for studying CCDC167 dysregulation observed in hepatocellular carcinoma and colorectal cancer, aiding the identification of therapeutic targets that exploit centrosome vulnerabilities.
This knockout cell pool supports Western blotting for CCDC167 depletion, immunofluorescence to assess centrosome number and localization, cell proliferation assays (MTS, BrdU), and flow cytometric cell cycle analysis. RNA sequencing can reveal transcriptome-wide effects of CCDC167 loss. These applications facilitate functional studies of centrosome biology, high-throughput anti-cancer drug screening, and mechanistic dissection of coiled-coil proteins in cell division. For further information, contact Ascent Research.
