The CCSER1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line. This product features targeted disruption of the CCSER1 gene via CRISPR/Cas9-mediated gene editing, providing a loss-of-function model for investigating the role of the CCSER1 protein in centrosome biology and ciliogenesis. The polyclonal nature of the knockout population ensures a heterogeneous mix of edited alleles, reflecting the complexity of gene disruption in a cellular context.
HeLa cells are an immortalized human epithelial cell line originally derived from a cervical adenocarcinoma. They have been a cornerstone of biomedical research for decades, offering robust growth characteristics and extensive characterization. Their epithelial origin and transformed nature make them particularly relevant for studies in cancer biology, cell cycle regulation, and signal transduction. The well-documented genetic and proteomic landscape of HeLa cells facilitates the integration of CCSER1 knockout data with existing knowledge.
The CCSER1 gene encodes a coiled-coil protein that localizes to centrosomes and is essential for proper centriole duplication and primary cilium formation. Mechanistically, CCSER1 interacts with centrosomal components such as CEP135 and SAS-6, and it functions within a network that includes key regulators like PLK4 and STIL. It is hypothesized to act as a scaffold or regulator that ensures the fidelity of centriole duplication, and its activity may be influenced by cell cycle-dependent expression and transcriptional regulation. Disruption of CCSER1 leads to centrosome amplification and impaired ciliogenesis, underscoring its critical role in maintaining centrosome homeostasis.
In the HeLa cell context, knockout of CCSER1 results in aberrant centrosome numbers and defective primary cilium assembly, phenotypes that are directly linked to genomic instability and tumorigenesis. The tumor suppressor potential of CCSER1, suggested by its association with cancer and microcephaly, makes this model valuable for dissecting the molecular mechanisms by which centrosome dysfunction contributes to oncogenesis. HeLa cells provide a controllable system to explore how loss of CCSER1 affects cell cycle progression, mitotic fidelity, and the balance between proliferation and differentiation.
This polyclonal knockout cell product is ideally suited for a range of research applications, including the study of centrosome duplication, primary cilium biogenesis, and the molecular pathology of cancer. Researchers can employ immunofluorescence microscopy to visualize centrosome markers, RT-qPCR to assess CCSER1 transcript levels, and Western blotting to analyze CCSER1 and its interacting partners such as CEP135 and SAS-6. Functional assays, including cilium formation and centrosome duplication assays, can be combined with flow cytometric cell cycle analysis to delineate the downstream consequences of CCSER1 loss. For further inquiries and technical support, please contact Ascent Research.
