The CD209 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of the HAP1 human cell line in which the CD209 gene has been disrupted to create a loss-of-function model. CD209 encodes DC-SIGN, a C-type lectin receptor that recognizes carbohydrate structures on pathogens and modulates immune responses. The polyclonal format captures a diverse set of gene disruptions, reducing clonal bias and enhancing the reproducibility of downstream functional assays.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. These adherent, fibroblast-like cells contain a single copy of most chromosomes, simplifying knockout studies by avoiding heterozygous alleles. Their genetic uniformity and ease of culture make HAP1 a robust platform for high-throughput functional genomics, particularly for genes involved in innate immunity and signal transduction.
DC-SIGN functions as a pattern recognition receptor that binds mannose-rich glycans and fucose-containing structures on viruses, bacteria, and fungi. Ligand engagement triggers intracellular signaling through adaptors such as LSP1 and kinase RAF1, leading to ERK1/2 phosphorylation and activation of the IKK complex, which drives NF-??B transcriptional responses. These pathways regulate cytokine production and T-cell activation. CD209 expression is induced by IL-4, GM-CSF, TNF-??, and IL-13, and controlled by transcription factor PU.1. Additionally, DC-SIGN mediates cell adhesion via interactions with ICAM-3 and ICAM-2, and serves as an attachment factor for HIV-1 gp120.
In HAP1 cells, disruption of CD209 eliminates DC-SIGN surface expression and downstream signaling, offering a clean genetic background for dissecting its role in pathogen recognition, adhesion, and innate immune activation. The near-haploid nature ensures that phenotypes directly result from the targeted knockout, enabling unambiguous interpretation of experimental data. This model is particularly suited for screening compounds that block DC-SIGN?Cpathogen interactions or for structure-function analyses using ectopic receptor mutants.
Typical research applications include investigation of host-pathogen interactions with viral, bacterial, and fungal species; screening of antiviral agents blocking DC-SIGN-mediated entry; analysis of dendritic cell adhesion and migration; and mechanistic studies of innate immune signaling. Supporting assays include flow cytometry for knockout validation, western blotting and RT-qPCR for pathway readouts, adhesion and pathogen binding assays, NF-??B reporter systems, and co-immunoprecipitation to map protein interactions. For technical inquiries, please contact Ascent Research.
