The ACAP2 Knockout HeLa Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population of HeLa cervical adenocarcinoma epithelial cells with targeted disruption of the ACAP2 gene, resulting in loss of ACAP2 protein expression. This polyclonal knockout model is designed for loss-of-function studies of ACAP2 in endocytic recycling and cell migration.
HeLa is an immortalized cell line derived from a cervical adenocarcinoma of Henrietta Lacks, widely used in biomedical research. These cells exhibit robust growth and retain epithelial characteristics, making them a standard host for gene-editing studies. Their transformed phenotype and cervical origin make them particularly suited for investigating processes such as cell adhesion, migration, and invasion, functions regulated by ACAP2.
ACAP2 encodes a GTPase-activating protein (GAP) for the small GTPase ARF6, catalyzing GTP hydrolysis to inactivate ARF6. ACAP2 thereby regulates ARF6-dependent endocytic recycling of integrins and other cargo, modulating cell migration and actin cytoskeleton organization. It acts downstream of growth factor receptors and phosphoinositides, and interacts with ARF6, clathrin adaptors, and endosomal coat proteins. The ACAP2-ARF6 module is balanced by the exchange factor EFA6; ACAP2 inactivation of ARF6 is critical for proper integrin trafficking and downstream signaling via Rac1 and actin polymerization.
In HeLa cervical adenocarcinoma cells, the ACAP2-ARF6 pathway controls integrin surface dynamics and actin remodeling, processes frequently dysregulated in cancer metastasis. ACAP2 knockout in this model enables dissection of its role in endosomal trafficking and cell invasion. The polyclonal population reflects tumor cell heterogeneity and allows examination of collective versus single-cell migration behaviors, providing insight into cervical cancer progression.
This knockout model is well-suited for cell migration and invasion assays such as wound healing and Transwell assays. It supports integrin trafficking studies via immunofluorescence and recycling assays, ARF6 activity measurements using GTP-loading assays, and downstream signaling analysis by Western blotting for targets including integrin ??1, Rac1, and actin. These applications facilitate investigation of endocytic recycling and its role in cancer metastasis. For additional details, please contact Ascent Research.
