The BICD2 Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, engineered to disrupt the BICD2 gene locus. This product provides a heterogeneous pool of cells carrying loss-of-function mutations, enabling robust functional studies of BICD2-dependent processes without clonal selection. The polyclonal format preserves population-level genetic diversity while ensuring reliable gene disruption, making it suitable for experiments demanding physiological relevance.
HeLa cells, the chosen host line, originate from a human cervical adenocarcinoma and are positive for human papillomavirus type 18 (HPV18). These immortalized epithelial cells are a widely used model in cell biology, offering robust growth, ease of transfection, and well-characterized subcellular architecture. Their susceptibility to CRISPR/Cas9 gene editing makes them a versatile platform for generating knockout models to dissect molecular mechanisms underlying intracellular transport and organelle organization.
BICD2 encodes a dynein adaptor protein linking cargo to the dynein-dynactin motor complex for minus-end-directed microtubule transport. It directly interacts with dynein light chains DYNLL1 and DYNLRB1, and is regulated by RAB6 GTPase and the LIS1/NDEL1 complex (PAFAH1B1 and NDEL1). This positions BICD2 as central to dynein-mediated trafficking, necessary for Golgi positioning, vesicle transport, and microtubule organization. BICD2 loss disrupts dynein (DYNC1H1) and dynactin recruitment, impairing cargo translocation and organelle homeostasis.
In HeLa cells, BICD2 deficiency compromises dynein-dependent transport, offering a tractable system to dissect adaptor-mediated motor complex assembly. This model is relevant for studying diseases such as spinal muscular atrophy, lower extremity-predominant (SMA-LED) and hereditary spastic paraplegia, linked to BICD2 mutations. Perturbing microtubule-based trafficking allows researchers to mimic disease-relevant phenotypes, including aberrant Golgi morphology and altered cargo distribution, providing mechanistic insights into motor neuron pathologies.
Applications span live-cell imaging to track dynein-mediated transport, immunofluorescence for Golgi integrity, and co-immunoprecipitation to probe BICD2 interactions with dynein components. Western blotting confirms protein ablation, while functional assays quantify defects in organelle positioning. This polyclonal pool is ideal for high-content screening, disease modeling, or BICD2-rescue experiments. For further details, please contact Ascent Research.
