The HDAC10 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the HDAC10 gene in human HEK293T cells. This product provides a pooled population of cells harboring heterogeneous gene disruptions, enabling loss-of-function studies of the class IIb histone deacetylase HDAC10. As a polyclonal knockout model, it avoids clonal artifacts and facilitates the assessment of HDAC10-dependent phenotypes in a genetically diverse cellular background.
HEK293T cells are a widely used human embryonic kidney epithelial cell line transformed with sheared adenovirus 5 DNA and constitutively expressing the SV40 large T antigen. This enables high-level episomal replication of plasmids containing the SV40 origin, leading to robust recombinant protein expression and efficient production of lentiviral and retroviral vectors. Their reliable growth, ease of transfection, and broad utility in protein expression, viral packaging, and biochemical assays make HEK293T an optimal host for studying HDAC10 function.
HDAC10 is a class IIb histone deacetylase that catalyzes the removal of acetyl groups from lysine residues on histones H3 and H4, as well as on non-histone proteins such as HSP70. Through chromatin condensation, HDAC10 acts as a transcriptional repressor and is regulated by p53 and miR-130a. It interacts with HDAC3 and the SMRT/N-CoR corepressor complex to modulate gene expression. Notably, HDAC10 deacetylates HSP70 to promote autophagic flux, linking its activity to key autophagy components LC3 and p62/SQSTM1, and positioning it at the intersection of chromatin remodeling, DNA repair, and cellular homeostasis.
In the HEK293T context, disruption of HDAC10 impairs histone deacetylation and HSP70-mediated autophagy, providing a versatile platform for dissecting epigenetic regulation and stress responses. This knockout model is particularly relevant for investigating how HDAC10 influences cancer-relevant pathways, given HEK293T cells’ utility in signaling and drug-response studies. Loss of HDAC10 may alter sensitivity to HDAC inhibitors, enabling mechanistic insights into autophagy-related disorders and DNA damage signaling.
Research applications include autophagy mechanism studies using fluorescence-based flux assays, cancer cell biology investigations related to hepatocellular carcinoma and breast cancer, DNA damage response profiling, and HDAC inhibitor screening via drug sensitivity assays. Representative techniques such as Western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation (probing interactions with HDAC3, HSP70, and SMRT/N-CoR), and HDAC activity assays are well-suited to this polyclonal knockout model. For additional technical details or consultation, please contact Ascent Research.
