The INO80C Knockout HT29 Polyclonal Cells product consists of a CRISPR/Cas9-edited heterogeneous pool of HT29 human colorectal adenocarcinoma cells carrying targeted disruption of the INO80C gene. This polyclonal knockout population, generated without single-cell cloning, preserves genetic diversity and avoids clonal artifacts, thereby offering a robust model for population-level functional studies of INO80C loss.
The HT29 cell line, originally isolated from a 44-year-old female patient, is a widely employed model of colorectal adenocarcinoma. These colon epithelial cells are characterized by aberrant Wnt pathway activation and robust proliferative potential, and they serve as a relevant system for investigating DNA damage repair pathways, chromatin dynamics, and oncogenic signaling in a malignant epithelial context.
INO80C encodes an essential subunit of the ATP-dependent INO80 chromatin remodeling complex, which catalyzes nucleosome sliding and regulates histone variant H2A.Z exchange. The complex includes core components INO80, RVBL1, RVBL2, ACTL6A, ARP5, and ARP8. INO80 is recruited to DNA double-strand breaks upon activation by the upstream kinases ATM and ATR, where it promotes the assembly of repair foci containing ??H2AX, 53BP1, and RAD51. Additionally, the complex modulates transcription of cell cycle regulators. Disruption of INO80C impairs nucleosome dynamics and the DNA damage response, leading to defective genome maintenance.
In the HT29 colorectal adenocarcinoma background, INO80C knockout provides a valuable tool for dissecting the role of chromatin remodeling in cancer biology. The INO80 complex is critical for genome integrity; its dysfunction may increase genomic instability and alter sensitivity to DNA-damaging chemotherapeutics. This model enables investigation of how INO80C loss influences repair pathway choice, cell cycle checkpoints, and epigenetic modifications, potentially revealing therapeutic vulnerabilities in colorectal tumors.
These polyclonal knockout cells are suitable for diverse assays, including Western blotting and RT-qPCR to assess INO80C expression and downstream targets, ChIP-qPCR to evaluate histone modifications and H2A.Z occupancy, and immunofluorescence detection of ??H2AX foci after genotoxic stress. Functional studies can utilize flow cytometry for cell cycle profiling, clonogenic survival assays following DNA damage, and RNA-seq for transcriptome-wide analysis. Researchers can apply this model to study chromatin remodeling, DNA damage response, and colorectal cancer biology. For further information or technical support, please contact Ascent Research.
