The DMBT1 Knockout HAP1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human near-haploid cell line, designed to disrupt the DMBT1 gene. This pooled knockout model eliminates the heterogeneity of single-cell clones and offers a robust representation of loss-of-function effects across a polyclonal population. The gene disruption is achieved via CRISPR/Cas9-mediated targeting, resulting in a genetically mixed population with DMBT1 inactivation. This product is particularly suited for functional genomics studies requiring a consistent and reproducible knockout background without the isolation of monoclonal lines.
The HAP1 host cell line is a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia cell line. Its haploid karyotype simplifies genetic manipulations and facilitates precise knockout experiments by minimizing the need for biallelic editing. HAP1 cells are widely employed in genetic screening and pathway dissection due to their stable growth characteristics and amenability to a range of molecular and cellular assays. Their use as a model system enables straightforward interpretation of gene function, especially in the context of cellular processes such as differentiation, immune response, and tumor biology.
DMBT1 encodes a large secreted glycoprotein characterized by multiple scavenger receptor cysteine-rich (SRCR) domains that function as pattern recognition receptors at mucosal surfaces. The protein is transcriptionally regulated by pro-inflammatory stimuli including TNF-alpha, IL-1beta, and bacterial lipopolysaccharide (LPS), as well as androgens. Upon secretion, DMBT1 interacts with host factors such as surfactant proteins A and D, complement C1q, MUC5B, and IgA, and directly binds bacteria, thereby mediating pathogen agglutination and mucus stabilization. Downstream, DMBT1 modulates innate immune signaling pathways, including the TLR4/NF-kB axis and IL-8 production, influencing epithelial barrier integrity and immune cell recruitment. These interactions position DMBT1 at the intersection of mucosal defense and tumor suppression mechanisms.
In HAP1 polyclonal knockout cells, loss of DMBT1 expression provides a powerful model to dissect its roles in epithelial homeostasis and host-pathogen interactions. The haploid background ensures that even single-allele disruptions result in a clear loss-of-function phenotype across the polyclonal pool, streamlining experimental design. This model is valuable for investigating how DMBT1 influences innate immune responses to bacterial challenges and its involvement in suppressing malignant transformation, as evidenced by its downregulation in various cancers. The polyclonal format preserves biological variability while still delivering consistent knockout effects, which is advantageous for studies requiring broad representation of genetic perturbation.
Researchers can employ these DMBT1 knockout HAP1 polyclonal cells in a variety of experimental setups, including bacterial binding assays to study pathogen adhesion, NF-kB luciferase reporter assays to assess signaling pathway activity, and colony formation assays to evaluate tumor suppressive functions. The cells are also suitable for Western blotting, RT-qPCR, ELISA, and immunofluorescence applications to validate DMBT1 deletion and downstream effector changes. This product supports functional genomics in innate immunity, cancer biology, and drug target validation. For additional technical details or ordering information, please contact Ascent Research.
