The INF2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HT29 cells harboring targeted disruption of the INF2 gene. This heterogeneous pool of knockout cells is derived from the HT29 colorectal adenocarcinoma line and is supplied as a mixed population, enabling robust loss-of-function studies without the limitations of single-clone artifacts. The INF2 gene encodes a formin protein, and its disruption via CRISPR/Cas9 creates a versatile model for investigating INF2-dependent cellular processes.
The HT29 parental cell line is an established human colorectal adenocarcinoma model originating from a 44-year-old Caucasian female. These epithelial cells are characterized by their mucin-secreting phenotype and are widely used in colorectal cancer research to study intestinal barrier function, tumorigenesis, and drug response. Their adherent growth and well-defined signaling pathways make them an ideal host for genetic perturbation.
INF2 is a diaphanous-related formin that uniquely accelerates both actin polymerization and depolymerization, thereby regulating cytoskeletal dynamics and mitochondrial morphology. Activated by RhoA and Cdc42, INF2 promotes actin filament assembly at endoplasmic reticulum?Cmitochondria contact sites, facilitating the recruitment of DRP1 and subsequent mitochondrial fission. INF2 additionally modulates focal adhesion turnover and communicates with the Hippo pathway through YAP/TAZ signaling, linking cytoskeletal tension to transcriptional responses. Key interacting partners include DRP1, actin, profilin, myosin II, and calmodulin.
In the context of colorectal adenocarcinoma, INF2 knockout provides a valuable tool for dissecting the interplay between actin remodeling, mitochondrial fragmentation, and cancer cell behavior. HT29 cells rely on dynamic cytoskeletal reorganization for migration and invasion, and INF2??s role in these processes makes the knockout model particularly relevant for studying metastasis and focal adhesion dynamics. Moreover, INF2 mutations are linked to podocytopathies such as focal segmental glomerulosclerosis, underscoring its significance in cell biology across different tissues.
This polyclonal knockout product supports a wide array of experimental approaches. Researchers can employ mitochondrial morphology analysis and co-immunoprecipitation of DRP1 to assess mitochondrial fission defects; actin cytoskeleton staining and migration assays to evaluate motility; and phospho-YAP analysis or flow cytometry to probe downstream signaling. Applications extend to high-content screening for mitochondrial health and drug discovery targeting formin-dependent pathways. For detailed protocols or further inquiries, please contact Ascent Research.
