The MYO19 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the MYO19 gene in a human gastric adenocarcinoma background. This product consists of a heterogeneous pool of AGS cells that have undergone CRISPR/Cas9-mediated disruption of the MYO19 locus, resulting in ablation of functional MYO19 protein expression. As a polyclonal population, the cells represent a range of editing outcomes, making them suitable for experiments that benefit from population-level phenotypic assessment without single-cell clone selection. The knockout model enables investigation of MYO19-dependent mitochondrial dynamics, cell migration, and metabolic regulation within an epithelial tumor context.
The parental AGS cell line is derived from malignant gastric tissue and displays epithelial morphology characteristic of gastric adenocarcinoma. AGS cells are widely utilized as an in vitro model for studying the molecular mechanisms of gastric cancer progression, including proliferation, invasion, and metastasis. Their relevance to gastric adenocarcinoma makes them particularly valuable for dissecting pathways that drive tumor cell motility and mitochondrial adaptation. The epithelial origin of AGS cells provides a physiologically relevant platform for exploring how cytoskeletal and mitochondrial networks intersect in cancer biology.
MYO19 encodes an actin-based myosin motor protein that localizes to the outer mitochondrial membrane and plays a central role in mitochondrial positioning and fission. MYO19 functions by tethering mitochondria to the actin cytoskeleton, facilitating their transport toward the cell periphery and recruiting the fission factor DRP1 to promote mitochondrial division. The activity of MYO19 is transcriptionally regulated by PGC-1??, NRF1, and ATF5, and is integrated with the mitochondrial unfolded protein response and PI3K/AKT signaling. Downstream, MYO19 interacts with the mitochondrial adaptors TRAK1, MIRO1 (RHOT1), and MIRO2 (RHOT2) to coordinate motor-cargo linkage, and cooperates with DRP1 at sites of mitochondrial constriction. Together, these molecular players form a axis that couples actin dynamics to mitochondrial quality control and energy distribution.
In AGS gastric cancer cells, MYO19 knockout disrupts the normal subcellular distribution of mitochondria, leading to perinuclear clustering, decreased DRP1-mediated fission, and impaired cell migration. Because gastric adenocarcinoma cells exhibit elevated metabolic plasticity and migratory capacity, loss of MYO19 provides a powerful tool to dissect how mitochondrial dynamics contribute to tumor cell invasiveness and metabolic reprogramming. This knockout model thus enables systematic analysis of the interplay between the actin cytoskeleton and mitochondrial homeostasis in a disease-relevant epithelial context.
Typical research applications include mechanistic studies of mitochondrial transport and fission, comparative migration and invasion assays (transwell and wound healing), metabolic flux analyses using Seahorse technology, and drug screening targeting mitochondrial function. Researchers can employ complementary techniques such as Western blotting, RT-qPCR, immunofluorescence with MitoTracker staining, ATP measurement, and co-immunoprecipitation of MYO19 complexes. Mitochondrial isolation and functional assays further support detailed biochemical characterization. For further technical information or customization options, please contact Ascent Research.
