The ACBD3 Knockout HeLa Cell Line is a CRISPR/Cas9-edited knockout cell line derived from HeLa cervical adenocarcinoma cells, engineered to disrupt the ACBD3 gene. This product provides a stable loss-of-function model for investigating ACBD3-dependent cellular processes without the constraints of transient knockdown approaches. The cell line is offered as a bulk population and is suitable for applications requiring constitutive gene disruption in a widely used human cancer model.
The parental HeLa cell line is an immortalized epithelial cell line originating from a human cervical adenocarcinoma. HeLa cells are HPV18-positive, leading to E6-mediated inactivation of wild-type p53, and they display an aneuploid karyotype. These genetic properties, combined with their robust growth and well-characterized signaling networks, have established HeLa as a principal model in cancer biology, virology, and cell signaling research. The ACBD3 knockout thus builds upon a host system with extensive experimental precedent.
At the molecular level, ACBD3 encodes a Golgi-associated scaffold protein essential for maintaining Golgi architecture and facilitating intracellular trafficking. ACBD3 directly interacts with PI4KB and recruits this kinase to Golgi membranes to produce phosphatidylinositol 4-phosphate (PI4P), a phosphoinositide required for vesicle biogenesis and cargo sorting. Additionally, ACBD3 forms complexes with GOLGB1/giantin and NUMB, connecting it to Notch signaling: NUMB-mediated endosomal trafficking of the Notch intracellular domain is influenced by ACBD3, thereby modulating expression of downstream targets such as HES1. This circuitry is perturbed by enterovirus infection, as the viral 3A protein hijacks ACBD3 to redirect PI4KB activity toward replication organelle formation.
In HeLa cells, disruption of ACBD3 is expected to compromise Golgi integrity and impair secretory and endocytic pathways that are active in these transformed cells. Given ACBD3??s involvement in gastric cancer pathobiology and its exploitation by enteroviruses, the knockout model enables dissection of how this scaffold coordinates membrane trafficking and signaling in a cancer cell background. The HPV-driven inactivation of p53 and aneuploid genome of HeLa cells provide a permissive context for probing interplay between Golgi stress responses, oncogenic signaling, and viral subversion.
This knockout cell line serves as a versatile platform for experimental investigations. Researchers can apply immunofluorescence microscopy using antibodies against Golgi markers such as GM130 to assess morphological changes, western blotting to quantify ACBD3 protein loss, and RT-qPCR to measure Notch target gene expression (e.g., HES1). Flow cytometry permits analysis of surface protein trafficking, while enterovirus replication assays reveal the dependency of viral life cycles on ACBD3. Additionally, cell proliferation and viability studies address the role of ACBD3 in cancer cell growth. For further details or custom inquiries, please contact Ascent Research.
