The KRT9 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout pool for the KRT9 gene in HAP1 cells. This heterogeneous population carries diverse gene disruptions, eliminating keratin 9 protein expression without requiring single-cell cloning. Since KRT9 is not endogenously expressed in HAP1 cells, this knockout line serves as an ideal host for ectopic expression studies or as a rigorous negative control in genetic screens.
HAP1 is a near-haploid human myeloid leukemia cell line derived from KBM-7, originally from a male chronic myeloid leukemia patient in blast crisis. Its haploid genome simplifies CRISPR-based gene knockout, making it a preferred platform for genetic screening. HAP1 cells are well-characterized and stably maintained, enabling high-throughput functional genomics applications in a leukemic background.
Keratin 9 (KRT9) is a type I cytokeratin essential for intermediate filament assembly in palmoplantar epidermis. It heterodimerizes with KRT1 and links to desmosomes via desmoplakin (DSP), junction plakoglobin (JUP), and plakophilin-1 (PKP1). Transcription is regulated by TP63, NOTCH1, AP-1, calcium, and VDR. Mutations cause epidermolytic palmoplantar keratoderma, a skin fragility disorder.
Because HAP1 cells lack endogenous KRT9, this knockout provides a clean background for reintroduction studies to probe filament formation and desmosome linkage. Co-immunoprecipitation with DSP or JUP and assembly assays are feasible after ectopic expression. The line is an ideal negative control for haploid screens and enables dissection of upstream KRT9 regulators.
This polyclonal knockout population supports immunocytochemistry, Western blotting, RT-qPCR, co-immunoprecipitation, and adhesion assays. Genotyping PCR and TIDE confirm editing. Applications include keratin biology, desmosome research, skin disease modeling, and genetic interactions. For further details, contact Ascent Research.
