The CCDC126 Knockout HAP1 Polyclonal Cells comprise a population of CRISPR/Cas9-edited HAP1 cells in which the CCDC126 gene has been disrupted to generate a loss-of-function model. This polyclonal knockout pool, derived from the HAP1 chronic myeloid leukemia cell line, enables gene function studies without the confounding effects of clonal selection. The heterogeneous mixture of edited alleles provides a robust tool for investigating the biological roles of CCDC126 in a near-haploid background.
HAP1 cells are a near-haploid, Philadelphia chromosome-positive human cell line expressing the BCR-ABL1 fusion oncoprotein, a hallmark of chronic myeloid leukemia. Originating from the KBM-7 cell line, HAP1 cells possess a reduced genome complexity with a single copy of most chromosomes, which facilitates loss-of-function genetic screens and minimizes compensation by redundant alleles. This unique genetic background makes HAP1 particularly well-suited for CRISPR-based functional genomics, providing a clean system to assess gene knockout phenotypes in the context of leukemic signaling.
The CCDC126 gene encodes a protein containing coiled-coil domains, motifs typically involved in mediating protein-protein interactions, yet its precise molecular function remains uncharacterized. Current knowledge suggests CCDC126 may participate in uncharacterized signaling or scaffolding complexes, potentially influencing cellular processes through interactions yet to be identified. The absence of known upstream regulators, downstream effectors, or pathway associations underscores the need for systematic functional analysis. Disruption of CCDC126 in HAP1 cells is expected to interfere with any protein complexes or signaling events that require intact coiled-coil-mediated interactions, providing a hypothesis-generating tool for pathway discovery.
Utilizing the HAP1 cell line to ablate CCDC126 capitalizes on the model??s haploid nature, which eliminates heterozygosity and simplifies phenotypic interpretation, particularly for genes with unknown functions. The BCR-ABL-driven leukemic background further allows investigation of CCDC126??s potential involvement in oncogenic signaling networks. Although no direct link to CML pathogenesis has been established, the knockout model offers a defined system to explore synthetic lethality, drug-gene interactions, and novel regulatory nodes within the BCR-ABL signaling axis.
This knockout cell pool is suitable for a broad range of assays, including CRISPR-based functional screens, protein interactome mapping via co-immunoprecipitation, and phenotypic analyses using flow cytometry, immunofluorescence, and cell proliferation measurements. Researchers can employ western blotting and RT-qPCR to confirm target disruption and assess compensatory transcriptional changes. Additionally, the polyclonal population is amenable to drug sensitivity profiling, enabling evaluation of how loss of CCDC126 modulates responses to tyrosine kinase inhibitors or other therapeutic agents. For further technical details or to inquire about custom modifications, please contact Ascent Research.
