The CCDC97 Knockout HAP1 Polyclonal Cells are a human knockout cell product generated through CRISPR/Cas9-mediated disruption of the CCDC97 gene in the HAP1 haploid cell background. This product is supplied as a polyclonal cell population, representing a mixture of edited cells each carrying distinct gene-disrupting events at the target locus. As a pooled knockout model, it avoids the limitations of single clonal isolates and enables the study of CCDC97 loss-of-function in a genetically heterogeneous yet controlled human cell context. The polyclonal format is particularly suited for applications where clonal variation may confound phenotypic interpretation.
The host cell line, HAP1, is a near-haploid human cell line derived from the chronic myeloid leukemia cell line KBM-7. It displays adherent growth characteristics and retains a stable haploid karyotype, making it an invaluable tool for genetic perturbation studies. The haploid nature simplifies the generation of complete loss-of-function models because only one allele needs to be disrupted, eliminating the complexity of biallelic targeting. HAP1 cells are widely employed in functional genomics, drug target validation, and high-throughput screening due to their ease of genetic manipulation and the unambiguous genotype-phenotype relationships they provide.
CCDC97 encodes a protein containing coiled-coil domains, structural motifs known to mediate protein-protein interactions and serve as scaffolds for the assembly of multi-protein complexes. Despite these predicted features, the molecular function of CCDC97 remains poorly characterized. No validated upstream regulators, downstream effectors, or interacting partners have been reported, and the protein has not been assigned to any defined signaling pathway or cellular process. This lack of functional annotation designates CCDC97 as an uncharacterized gene whose biological significance awaits discovery. The present knockout model therefore offers a clean experimental system to interrogate its roles through loss-of-function analysis.
Introduction of the CCDC97 knockout into the HAP1 haploid background creates a potent model for investigating the cellular consequences of CCDC97 deficiency. The absence of a second gene copy ensures that any phenotypic changes following CRISPR/Cas9 editing can be attributed directly to CCDC97 loss. Combined with the well-characterized HAP1 framework, researchers can compare knockout and wild-type cells under standardized culture conditions, mining for alterations in proliferation, morphology, apoptosis, or signaling. The polyclonal makeup further strengthens statistical robustness and minimizes biases arising from random clonal events that may arise during single-cell expansion.
These CCDC97 knockout polyclonal cells support a diverse range of experimental workflows. Confirmation of knockout efficiency can be achieved through western blotting for CCDC97 protein levels or RT-qPCR for mRNA transcript analysis. Immunofluorescence microscopy allows visualization of potential subcellular relocalization of candidate interactors in the absence of CCDC97. Co-immunoprecipitation coupled with mass spectrometry provides a direct avenue to identify protein binding partners that depend on CCDC97 expression. Flow cytometry enables quantitative phenotypic screening, such as cell cycle or viability assays. These applications collectively enable the systematic functional characterization of CCDC97 in a human haploid context. For additional details or technical support, please contact Ascent Research.
