The CCDC91 Knockout K-562 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CCDC91 gene in the K-562 human lymphoblast host cell line. This polyclonal format provides a heterogeneous population of edited cells, enabling loss-of-function studies without clonal selection artifacts. The CRISPR/Cas9 system introduces targeted gene disruption, rendering the resulting cell pool suitable for investigating the functional consequences of CCDC91 ablation in a leukemia-relevant background.
The K-562 host cell line is a widely used model derived from the pleural effusion of a patient with chronic myelogenous leukemia (CML) in blast crisis. This cell line carries the hallmark Philadelphia chromosome, which encodes the BCR-ABL1 fusion tyrosine kinase driving oncogenic signaling. K-562 cells are pluripotent hematopoietic precursors capable of differentiating along erythroid, granulocytic, and monocytic lineages, thus serving as a versatile platform for studying hematopoietic differentiation, leukemia biology, and drug response.
CCDC91 encodes a coiled-coil domain-containing protein, with such structural motifs typically mediating protein?Cprotein interactions that contribute to the assembly of macromolecular complexes. Although the precise regulatory network of CCDC91 remains undefined, its expression is presumably controlled by basal transcriptional machinery. The protein is predicted to interact with other coiled-coil domain proteins and cytoskeletal components, potentially participating in cellular organization or signaling pathways. However, specific downstream targets and interacting partners have not been experimentally validated, leaving its functional integration into broader signaling networks an open area of investigation.
In the context of K-562 leukemia cells, CCDC91 knockout may perturb protein interaction networks that are critical for maintenance of the transformed phenotype or differentiation capacity. Given that chromosome 1p36 alterations??a region harboring CCDC91??have been associated with various cancers, this model allows researchers to explore the gene’s role in leukemogenesis and to assess whether its disruption alters cell proliferation, cell cycle progression, or apoptosis. The polyclonal knockout population is particularly valuable for unbiased screens that minimize clone-specific effects.
Typical applications include using western blotting to confirm loss of CCDC91 protein expression, co-immunoprecipitation to identify binding partners, and proliferation assays to evaluate growth phenotypes under normal or drug-treated conditions. Flow cytometry-based cell cycle analysis can further delineate functional consequences. This knockout cell population is also suited for synthetic lethal screening to uncover therapeutic vulnerabilities in CML cells. For further details or assistance with experimental design, please contact Ascent Research.
