The C15orf40 Knockout HAP1 Polyclonal Cells product consists of a polyclonal population of HAP1 cells that have undergone CRISPR/Cas9-mediated disruption of the C15orf40 gene. This polyclonal knockout model is designed for loss-of-function studies of the uncharacterized C15orf40 locus in a near-haploid human cell background, providing a powerful tool for functional genomics and phenotypic screening applications.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line, widely adopted for CRISPR-based genetic screens due to its haploid karyotype which simplifies knockout generation and phenotype interpretation. These cells grow in suspension and exhibit features of the leukemic lineage, making them suitable for hematopoietic cancer research and high-throughput screening assays.
C15orf40 is predicted to encode a protein of unknown function, with no characterized molecular interactions, upstream regulators, or downstream targets. There are currently no established links to specific signaling pathways or disease associations. Consequently, this knockout tool enables de novo investigation of the gene’s potential roles in cellular processes such as proliferation, survival, or differentiation.
The disruption of C15orf40 in the HAP1 background leverages the cell line’s well-defined genetic landscape and near-haploid state to reduce confounding variables, allowing researchers to directly interrogate the gene’s contribution to leukemic cell biology. This model may reveal either essential or modulatory functions of C15orf40 that could be relevant to cancer cell fitness or normal cellular homeostasis.
Typical applications include functional characterization of C15orf40 through phenotypic profiling assays such as cell viability, apoptosis, and proliferation measurements. The polyclonal population is compatible with transcriptomic analyses (e.g., RNA-seq) and, where validated antibodies are available, western blotting to confirm protein loss-of-function. The model also supports genetic interaction screens and comparative studies with wild-type HAP1 cells. For further information or custom requests, please contact Ascent Research.
