The CCDC85C Knockout K-562 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CCDC85C gene. This product features a heterogeneous pool of K-562 cells that have undergone CRISPR/Cas9-mediated disruption of the CCDC85C locus, providing a versatile model to investigate the biological functions of this poorly characterized coiled-coil domain-containing protein. Unlike clonal knockout lines, the polyclonal format captures a spectrum of genetic alterations, enabling population-level analyses that can reflect the complexity of loss-of-function phenotypes in a leukemia context.
The host K-562 cell line is a widely used human chronic myelogenous leukemia (CML) model established from a patient in blast crisis. K-562 cells carry the Philadelphia chromosome and express the BCR-ABL1 fusion oncoprotein, which drives constitutive tyrosine kinase activity and aberrant signaling. This cell line is a canonical system for studying hematopoietic differentiation, as it retains the capacity to differentiate along erythroid, granulocytic, and monocytic lineages in response to chemical inducers. K-562 cells are also pivotal in drug development for BCR-ABL1-targeted therapies, such as imatinib, and are extensively employed in functional genomics to elucidate oncogenic mechanisms.
The CCDC85C gene encodes a protein with predicted coiled-coil domains, structural motifs that typically mediate protein-protein interactions, suggesting a role in macromolecular complex assembly or scaffolding. However, the specific molecular functions, interaction partners, and associated signaling pathways of CCDC85C remain largely undefined. Disruption of CCDC85C in this CRISPR-edited population may perturb unknown protein interaction networks, potentially affecting downstream cellular processes such as signal transduction, cytoskeletal organization, or transcriptional regulation. The mechanistic consequences of CCDC85C loss are expected to provide insights into the protein??s contributions to leukemia cell biology, though careful phenotypic characterization is required to dissect these effects.
Within the K-562 leukemic background, CCDC85C knockout offers a unique opportunity to explore the interplay between an uncharacterized coiled-coil protein and the BCR-ABL1-driven oncogenic network. This model is particularly valuable for identifying novel modulators of BCR-ABL1-associated phenotypes, including proliferation, apoptosis, and drug sensitivity. The polyclonal nature of the knockout population allows for the assessment of phenotypic variability and the selection of subclones with distinct attributes, enhancing the discovery of gene function in a heterogeneous tumor cell environment. Researchers can utilize this system to probe whether CCDC85C influences key oncogenic processes or modulates response to tyrosine kinase inhibitors.
This knockout product is suited for a range of experimental applications, including functional characterization of CCDC85C through transcriptomic profiling (RNA-seq), protein interaction screening via co-immunoprecipitation or proximity labeling, and quantitative assays such as western blotting and RT-qPCR to confirm knockout effects. Flow cytometry-based assessments of cell surface markers and viability, as well as drug sensitivity assays with agents like imatinib, enable the investigation of CCDC85C??s impact on leukemia-specific phenotypes. The cells can also be employed in differentiation studies using chemical inducers, providing a comprehensive platform for deciphering CCDC85C biology. For additional details or technical support, please contact Ascent Research.
