The JPT1 Knockout HeLa Polyclonal Cells offer a CRISPR/Cas9-mediated gene disruption model targeting JPT1 in a polyclonal HeLa cell population. This heterogeneous knockout pool avoids clonal selection bias, enabling robust phenotypic assessment of JPT1 loss-of-function across multiple editing events. The polyclonal format is ideal for large-scale genetic screening and functional studies where population-level responses are informative.
HeLa cells, derived from HPV18-positive cervical adenocarcinoma, are a widely used human cell line with well-characterized mitotic and cell cycle properties. Their rapid proliferation and genetic tractability facilitate CRISPR-based gene editing, making them an excellent host for JPT1 knockout. The HeLa background supports investigation of mitotic regulation in a transformed epithelial context relevant to cancer biology.
JPT1 encodes a microtubule-associated protein critical for mitotic spindle assembly and chromosome segregation. It interacts with gamma-tubulin and TPX2 to promote bipolar spindle formation, and its activity is regulated by mitotic kinases such as CDK1/Cyclin B and PLK1. JPT1 also collaborates with Aurora kinase A to coordinate microtubule dynamics. Disruption of JPT1 impairs the G2/M checkpoint, leading to aberrant spindle morphology, chromosome misalignment, and genomic instability.
In HeLa cells, JPT1 knockout directly perturbs mitosis, providing a model to study spindle-related pathways and their deregulation in cancer. JPT1 dysfunction has been implicated in glioblastoma and hepatocellular carcinoma, underscoring its relevance in tumor biology. The HPV18-positive host further allows exploration of viral oncoprotein interactions with the mitotic machinery.
This polyclonal knockout population is suitable for immunofluorescence analysis of spindle morphology, flow cytometry-based cell cycle profiling, western blot detection of mitotic markers, and proliferation assays. It supports drug target validation for mitotic inhibitors and synthetic lethality screens. For further information, contact Ascent Research.
