The KDM7A Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout cell population engineered for loss-of-function studies of the KDM7A gene. This polyclonal pool consists of HEK293T cells carrying heterogeneous targeted disruptions of the KDM7A locus, generated without single-cell cloning. The product provides a physiologically relevant model for examining KDM7A-dependent pathways while preserving the host line??s high transfectivity and robust growth. By avoiding clonal selection, the polyclonal format reduces the risk of incidental genetic drift and offers a more representative population for gene function analysis.
HEK293T cells, derived from the HEK293 human embryonic kidney line, constitutively express the SV40 large T antigen, which enhances episomal replication of plasmids with the SV40 origin. This feature confers exceptionally high transfection efficiency, making the line ideal for recombinant protein expression, lentivirus production, and transcriptional reporter assays. These characteristics provide an optimal background for studying chromatin-modifying factors like KDM7A.
KDM7A encodes a histone demethylase that targets dimethylated lysine 9 and lysine 27 on histone H3 (H3K9me2 and H3K27me2) for demethylation, thereby relieving transcriptional repression. As a transcriptional coactivator, KDM7A directly interacts with the androgen receptor (AR) and is recruited to AR-responsive promoters, promoting expression of genes such as KLK2 and KLK3 that drive proliferation in prostate cancer. Its activity is modulated by upstream regulatory signals and cooperation with chromatin-remodeling complexes and the related demethylase PHF8. This positions KDM7A at a key intersection between epigenetic modification and hormone-driven gene regulation.
The HEK293T background offers a highly tractable system for exploring KDM7A??s role in histone demethylation and AR-mediated transcription. Although not derived from prostate tissue, HEK293T cells express core epigenetic machinery and can be readily engineered to reconstitute AR signaling pathways. Gene editing of KDM7A in this context enables researchers to dissect epigenetic regulatory mechanisms without confounding factors present in cancer cell lines. The model is particularly suited for studying how KDM7A loss alters global H3K9me2/H3K27me2 levels and downstream gene programs relevant to cancer and neurodevelopmental disorders.
Researchers can utilize this polyclonal knockout pool in a variety of experimental workflows. Western blotting for histone methylation marks and KDM7A protein confirms target disruption, while RT-qPCR quantifies changes in AR target gene expression such as KLK2 and KLK3. Chromatin immunoprecipitation (ChIP-qPCR) enables locus-specific assessment of H3K9me2 and H3K27me2 occupancy. Androgen receptor reporter assays and cell proliferation studies further probe functional consequences of KDM7A loss. Together, these approaches support drug target validation, epigenetics research, and high-throughput screens. For additional technical details or inquiries, please contact Ascent Research.
