The MICAL3 Knockout AGS Polyclonal Cells are a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the MICAL3 gene in the AGS human gastric adenocarcinoma cell line. This polyclonal product comprises a heterogeneous mixture of cells with varied loss-of-function alleles, offering a robust and artifact-free model for studying MICAL3-dependent functions without the clonal limitations of single-cell-derived lines.
The AGS parental line, derived from a human gastric adenocarcinoma, is a well-established epithelial model for gastric cancer research. It recapitulates key features of gastric carcinogenesis and is routinely employed to investigate molecular pathways governing cell proliferation, migration, and invasion, making it an ideal host for interrogating actin and trafficking regulators.
MICAL3 is a flavoprotein monooxygenase that selectively oxidizes actin methionine residues, promoting filament disassembly and remodeling of the actin cytoskeleton. Its localization and activity are controlled by direct binding to Rab GTPases (Rab8A, Rab10, Rab15), which recruit MICAL3 to vesicle membranes and cortical actin structures. Upstream signals via semaphorin 3A and plexin A1/A2 receptors activate Rac1 GTPase, which in turn modulates MICAL3-mediated F-actin depolymerization. This molecular network positions MICAL3 as a key node connecting extracellular cues to actin dynamics and vesicle trafficking.
In AGS cells, MICAL3 contributes to the coordination of membrane trafficking and cytoskeletal reorganization required for cell migration and invasion??hallmarks of metastatic gastric adenocarcinoma. Disruption of MICAL3 via knockout is predicted to perturb actin polymerization, vesicle transport, and cellular motility, thereby enabling researchers to directly assess its role in tumor cell behavior and identify downstream targets affected by its loss.
The MICAL3 Knockout AGS Polyclonal Cells support diverse experimental approaches, including immunofluorescence microscopy of actin and vesicle markers, Transwell migration/invasion assays, actin polymerization measurements, and co-immunoprecipitation of MICAL3 with Rab-family proteins. Additional applications encompass Rab GTPase activity assays and direct MICAL3 oxidation assays to confirm loss of monooxygenase function. These cells are a valuable tool for functional genomics, drug target validation, and mechanistic studies in gastric cancer and actin-related pathologies. For detailed inquiries, please contact Ascent Research.
