H1-10 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from HEK293T cells, targeting the H1-10 (H1FX) gene. This gene encodes a replication-independent linker histone variant essential for higher-order chromatin structure and transcriptional regulation. The polyclonal pool contains heterogeneous cells with CRISPR/Cas9-mediated disruptions in H1-10, providing a loss-of-function model that maintains genetic diversity for functional studies.
HEK293T cells are a human embryonic kidney epithelial line immortalized by adenovirus 5 E1A/E1B expression and stable SV40 large T antigen. These properties enable high transfection efficiency and episomal replication of SV40 ori plasmids, making the line ideal for viral packaging, protein expression, and gene editing. Their epithelial morphology and CRISPR/Cas9 permissiveness support consistent knockout population generation.
Linker histone H1-10 (H1FX) binds nucleosomes and linker DNA, facilitating chromatin compaction and global transcriptional repression. Its expression is controlled by E2F transcription factors and p53. H1-10 interacts with core histones and chromatin remodeling complexes, limiting transcription factor access. In p53 signaling, H1-10 modulates p53-dependent transcriptional programs influencing apoptosis or senescence. Knockout removes this regulation, leading to decondensed chromatin and altered expression of cell cycle regulators like p21, RB1, E2F1, and cyclin D1.
In HEK293T, H1-10 knockout creates a model to dissect chromatin?Csignal transduction interplay. The embryonic kidney epithelial origin plus SV40-mediated transformation allows probing linker histone function in a pro-tumorigenic background. H1-10 loss-induced chromatin decompaction may alter sensitivity to genotoxic stress and downstream transcriptional responses. This polyclonal population captures heterogeneity in chromatin states, aiding identification of H1-10-dependent programs intersecting with SV40 large T-driven p53 and RB1 inactivation.
Research applications span ATAC-seq and RNA-seq for chromatin accessibility and transcriptome profiling. Co-immunoprecipitation with western blotting or mass spectrometry identifies altered protein interactions. Flow cytometry and senescence-associated ??-galactosidase assays evaluate cell cycle and senescence changes, while immunofluorescence visualizes chromatin reorganization. This model supports drug discovery targeting epigenetic modifiers or p53 pathway reactivation. For detailed information, contact Ascent Research.
