The INO80D Knockout NCI-H1975 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the INO80D gene has been disrupted in the NCI-H1975 human lung adenocarcinoma cell line. This product offers a heterogeneous pool of cells with targeted gene disruption, enabling loss-of-function studies without clonal selection. The polyclonal format preserves population-level diversity while effectively interrogating INO80D-dependent cellular processes.
The NCI-H1975 host cell line was established from a non-smoking female patient with non-small cell lung adenocarcinoma and serves as a well-characterized model for human lung adenocarcinoma. It is widely employed in cancer biology research and drug screening due to its retention of key oncogenic mutations and signaling pathways relevant to lung adenocarcinoma. The cell line??s adherent growth and established protocols for genetic manipulation make it suitable for advanced genomic modification.
INO80D is a subunit of the INO80 chromatin remodeling complex, which catalyzes nucleosome sliding and eviction. The INO80 complex is recruited to DNA double-strand breaks (DSBs) through interactions with ??-H2AX and is activated by the ATM and ATR kinases. INO80D contributes to complex integrity and interacts with core INO80 components such as INO80, ACTR5, and ACTR8, as well as DNA repair proteins including RAD51 and BRCA1. Functionally, the complex facilitates homologous recombination repair by promoting nucleosome displacement at damage sites, enabling assembly of repair foci and accurate restoration of genomic integrity. INO80D also participates in transcriptional regulation through nucleosome positioning at target genes, impacting RNA polymerase II activity. Disruption of INO80D compromises complex stability, leading to impaired DSB repair, altered chromatin architecture, and dysregulated gene expression, which can affect cellular proliferation and genome stability.
In the context of NCI-H1975 lung adenocarcinoma cells, loss of INO80D function provides a powerful system to investigate the interplay between chromatin remodeling and DNA damage responses in a cancer-relevant background. NCI-H1975 cells harbor intrinsic genomic alterations that sensitize them to defects in DNA repair pathways, making INO80D knockout a valuable tool for probing mechanisms of genome instability and resistance to genotoxic therapies. The polyclonal population mimics heterogeneous tumor cell responses and is particularly suited for studying how INO80D modulates cancer cell fitness under DNA-damaging conditions.
This knockout cell model supports diverse applications, including homologous recombination reporter assays, immunofluorescence for ??-H2AX foci, ChIP-qPCR for chromatin occupancy, RNA-seq for transcriptome profiling, comet assays for DNA damage quantification, and cell viability assays for drug sensitivity screening. Research uses include chromatin remodeling in cancer, DNA damage response mechanisms, and oncology drug screening. For additional details, please contact Ascent Research.
