The CCDC71L Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for the targeted disruption of the CCDC71L gene through CRISPR/Cas9-mediated gene disruption. This product provides a pooled population of HeLa cells carrying heterogeneous CCDC71L knockout alleles, enabling robust loss-of-function studies without the clonal selection biases associated with monoclonal knockouts. By leveraging CRISPR/Cas9 technology, the product offers a genetically heterogeneous knockout model that reflects population-level gene targeting, useful for studying gene function in a cellular context with high biological diversity.
HeLa cells, the host line for this knockout, are derived from a human cervical adenocarcinoma and are immortalized epithelial cells that maintain a stable karyotype and vigorous proliferation in vitro. These cells are positive for human papillomavirus 18 (HPV18), which contributes to their transformed phenotype and makes them a classic model for cancer biology. HeLa cells have been extensively used to investigate mechanisms of tumorigenesis, cell cycle regulation, and cellular responses to oncogenic stress. Their epithelial origin and consistent growth characteristics provide a reproducible platform for genetic perturbation and phenotypic analysis.
CCDC71L encodes a coiled-coil domain-containing protein with a putative role in mediating protein?Cprotein interactions. Based on current knowledge, CCDC71L is predicted to link intracellular signaling cascades to cytoskeletal reorganization. The protein likely interacts with actin filaments, microtubules, and motor proteins, positioning it as a potential scaffold that coordinates cytoskeletal dynamics. Although the full regulatory network remains poorly characterized, CCDC71L may be regulated by cell cycle-dependent kinases and is thought to function downstream of signals affecting cell morphology and migration. Its interacting partners include other coiled-coil domain proteins and key cytoskeletal components, implying involvement in pathways governing cytoskeletal regulation and cell cycle control.
In the HeLa cell context, disruption of CCDC71L is expected to perturb cellular architecture and migration, as the protein??s coiled-coil domains facilitate interactions essential for maintaining cytoskeletal integrity and dynamic remodeling. HeLa cells depend on precise spatial and temporal control of actin and tubulin networks for processes such as division, adhesion, and motility. Therefore, CCDC71L knockout may compromise these activities, offering a model to study how cytoskeletal dysregulation contributes to cancer cell phenotypes. This polyclonal population is particularly suitable for probing the functional roles of CCDC71L in tumorigenesis and identifying phenotypes that arise from gene disruption in a heterogeneous cell pool.
This CCDC71L knockout model is applicable across a range of biomedical research areas, including cancer cell biology, cytoskeletal dynamics, protein interaction studies, and high-throughput phenotypic screening. Researchers can employ this product in Western blotting to confirm protein loss, immunofluorescence to visualize changes in actin or tubulin organization, migration and invasion assays to assess motility, and cell proliferation assays to measure growth effects. The heterogeneous nature of the polyclonal population enables robust detection of dominant phenotypes while mitigating clonal artifacts. For further technical information and custom inquiries, please contact Ascent Research.
