Dual C2 domain-containing protein A (DOC2A) Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the DOC2A gene, enabling loss-of-function studies of DOC2A-mediated exocytosis regulation. The polyclonal format maintains genetic diversity while eliminating functional DOC2A protein expression across the cell population, facilitating robust functional comparisons in experimental models of calcium-dependent secretion.
The host HeLa cell line is an immortalized human epithelial cell line originally derived from cervical adenocarcinoma and is positive for human papillomavirus type 18 (HPV18). These cells are widely employed as a robust and well-characterized model for epithelial cell biology, viral oncogenesis, and cancer research. Their high transfection efficiency and stable growth properties make them an ideal platform for generating CRISPR-edited knockout populations to study genes involved in cellular secretion and membrane trafficking.
DOC2A encodes a calcium-sensing protein that plays a critical role in calcium-triggered exocytosis by promoting SNARE complex assembly and synaptic vesicle priming. Upstream, DOC2A function is activated by calcium influx and diacylglycerol (DAG) signaling in response to synaptic activity. It interacts with key exocytosis regulators including Munc13-1 and Munc18-1, and directly associates with core SNARE proteins syntaxin-1, SNAP-25, and VAMP2. In concert with the calcium sensor synaptotagmin, DOC2A facilitates the transition of primed vesicles to fusion-competent states, integrating calcium signals into the regulation of SNARE-mediated membrane fusion.
In HeLa cells, the DOC2A knockout model enables dissection of calcium-regulated exocytosis pathways within an epithelial cancer context. HeLa cells possess a functional SNARE secretion machinery and exhibit both constitutive and calcium-evoked exocytotic events, making them suitable for studying DOC2A’s role in vesicle fusion regulation. Disruption of DOC2A in these cells may impair calcium-dependent secretory responses, providing insights into how aberrant expression of exocytosis regulators contributes to altered secretion in cancer cells and potentially in neurosecretion-related pathologies. This model thus bridges a gap between basic exocytosis mechanisms and disease-relevant secretory dysfunctions.
Typical research applications include investigating calcium-triggered exocytosis, neurotransmitter release machinery, and SNARE complex regulation using this knockout population. The DOC2A knockout HeLa cells serve as a powerful tool for studying how calcium sensor proteins modulate secretory vesicle dynamics in cancer cells, with potential implications for understanding aberrant exocytosis in neurodegenerative disorders and intellectual disability. Standard downstream assays include calcium imaging to monitor calcium transients, co-immunoprecipitation and western blotting to assess SNARE complex interactions, RT-qPCR for gene expression analysis, and vesicle release assays or electrophysiological recordings to measure exocytotic activity. For detailed product information, validation data, or custom gene-editing services, please contact Ascent Research.
