The INO80C Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, engineered for the loss-of-function analysis of the human INO80C gene. This product provides a heterogeneous population of cells with disrupted INO80C alleles, suitable for studying the gene??s role in chromatin remodeling, DNA damage repair, and transcriptional regulation. The polyclonal format enables robust assessment of INO80C-dependent phenotypes without clonal selection biases, making it ideal for pooled functional genomic screens and population-level assays.
HeLa cells are an immortalized epithelial cell line originating from human cervical adenocarcinoma. They are extensively characterized and widely used in cancer biology, DNA repair, and chromatin dynamics research due to their stable karyotype, rapid growth, and well-defined signaling pathways. Their genetic tractability and relevance to human disease make them a preferred platform for CRISPR-based knockout studies targeting genome stability factors.
INO80C is a core subunit of the INO80 chromatin remodeling complex, an ATP-dependent molecular machine that mobilizes nucleosomes to regulate DNA accessibility. The complex is activated by upstream DNA damage signals via ATM and ATR kinases, which phosphorylate components to promote recruitment to double-strand breaks. INO80C interacts with ACTR5, ACTR8, and the transcription factor YY1 to facilitate nucleosome sliding at damaged chromatin and gene regulatory regions. This remodeling enables the recruitment of downstream effectors such as the histone variant H2AX (phosphorylated as ??H2AX), the repair proteins BRCA1 and RAD51, and transcription factors that execute DNA repair and cell cycle checkpoint programs. INO80C thus coordinates chromatin architecture with genome stability and gene expression networks, working alongside other remodelers like the SWI/SNF complex.
In HeLa cells, CRISPR/Cas9-mediated disruption of INO80C impairs the INO80 complex??s ability to remodel chromatin in response to genotoxic stress, leading to defective DNA repair, aberrant gene transcription, and increased genomic instability. This knockout model phenocopies aspects of chromosomal instability syndromes and provides a tractable system to investigate how compromised chromatin remodeling contributes to oncogenesis, metastasis, and resistance to DNA-damaging therapies. It also allows dissection of INO80C??s separate roles in repair versus transcription, offering insights into its dual functions.
These polyclonal knockout cells are suited for a wide range of assays. Validation of INO80C loss can be performed by western blotting. DNA damage accumulation can be monitored by ??H2AX immunofluorescence or comet assay. Chromatin remodeling defects can be assessed by ChIP-seq to map nucleosome positioning and histone modifications. Transcriptional changes are detectable via RNA-seq, and cellular recovery after irradiation or drug treatment can be measured by clonogenic survival assays. These applications collectively elucidate INO80C??s contributions to genome maintenance and gene control. For further information, please contact Ascent Research.
