The DIP2A Knockout HeLa Polyclonal Cells is a CRISPR/Cas9-edited polyclonal knockout population derived from HeLa cells, offering a heterogeneous loss-of-function model for DIP2A. This polyclonal format avoids single-cell cloning artifacts and retains population diversity, making it suitable for pooled functional assays and screens. CRISPR/Cas9-mediated gene disruption generates a mix of DIP2A-deficient cells, enabling robust investigation of DIP2A-dependent pathways without clonal uniformity requirements.
The parental HeLa cell line is an immortalized human cervical adenocarcinoma epithelial model, originally derived from Henrietta Lacks, with HPV-18 integration and a hypertriploid karyotype. HeLa cells are a widely used system in cancer biology and functional genomics due to their robust proliferation and experimental tractability. Their transformed epithelial phenotype provides a relevant context for studying genes involved in oncogenesis, epigenetic regulation, and cell motility.
DIP2A acts as an adaptor protein downstream of SLIT-ROBO signaling, interacting with ROBO1 to regulate cytoskeletal dynamics via RAC1 during axon guidance and neuronal development. Additionally, DIP2A recruits the DMAP1?CDNMT1 complex to mediate DNA methylation-dependent gene silencing, linking extracellular signals to epigenetic reprogramming. DIP2A is regulated by miR-137 and its dysfunction is implicated in autism spectrum disorder and intellectual disability. These dual roles position DIP2A at the crossroads of signal transduction and epigenetic control.
In HeLa cells, which express SLIT-ROBO pathway components and maintain active DNA methylation machinery, DIP2A knockout enables dissection of its functions in a cancer-relevant background. This model facilitates the study of DIP2A??s contributions to epigenetic regulation, cell migration, and proliferation, aspects relevant to both neurodevelopmental disorders and cancer biology. The polyclonal nature of the knockout population ensures representative functional heterogeneity, mirroring biological complexity.
This product supports diverse assays, including western blotting and RT-qPCR for knockout validation, RNA-seq for transcriptome analysis, and bisulfite sequencing to evaluate DNA methylation changes. Co-immunoprecipitation can confirm DIP2A interactions with ROBO1, DMAP1, and DNMT1, while functional studies utilizing cell migration, invasion, proliferation, and apoptosis assays elucidate phenotypic consequences of DIP2A loss. Researchers may apply these cells to investigate DIP2A??s role in SLIT-ROBO signaling in cancer, model neurodevelopmental gene regulation, or validate DIP2A as a therapeutic target. For additional details, please contact Ascent Research.
