The CD55 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD55 gene has been disrupted, generating a loss-of-function model for investigating complement regulation and immune evasion. This polyclonal pool ensures a heterogeneous mix of edited alleles, enabling robust and reproducible functional studies without the need for clonal isolation. The knockout population is derived from the HAP1 cell line, a well-characterized near-haploid human chronic myeloid leukemia model, and is designed for researchers seeking to interrogate CD55-dependent mechanisms in a simplified genetic background.
HAP1 cells originate from the KBM-7 chronic myeloid leukemia line and possess a near-haploid karyotype, making them uniquely suited for genetic manipulation and CRISPR-based screens. The haploid genome reduces gene redundancy and simplifies the interpretation of knockout phenotypes, particularly in pathways where biallelic disruption is critical. HAP1 cells maintain key signaling properties of myeloid leukemia, allowing investigation of CD55 function within a malignant context. Their robust growth characteristics and compatibility with high-throughput assays further enhance their utility in drug discovery and functional genomics.
CD55, also known as decay-accelerating factor (DAF), is a glycosylphosphatidylinositol (GPI)-anchored protein that accelerates decay of C3 and C5 convertases, protecting cells from autologous complement-mediated lysis. Its expression is activated by TNF-alpha, IL-1beta, and LPS through NF-kB-dependent transcriptional regulation. CD55 directly interacts with C3b, C4b, complement convertases, and the adhesion-class G protein-coupled receptor CD97. By dissociating these convertases, CD55 limits C3b deposition on the cell surface and prevents assembly of the membrane attack complex (MAC). The regulatory network also includes Factor I and Factor H, which cooperate with CD55 to inactivate C3b and maintain host cell protection.
In HAP1 cells, CD55 knockout abolishes this protective mechanism, leading to increased C3b deposition and enhanced susceptibility to complement-dependent cytotoxicity (CDC). This phenotype models paroxysmal nocturnal hemoglobinuria (PNH), where loss of GPI-anchored proteins including CD55 results in complement-mediated hemolysis. Additionally, CD55 contributes to immune evasion in leukemia, and its deletion provides a system to study tumor cell clearance by innate immunity. The near-haploid background facilitates clean genetic dissection and identification of synthetic lethal interactions or resistance mechanisms.
This polyclonal knockout population is suitable for flow-cytometric quantification of C3b deposition, complement-dependent cytotoxicity assays, western blotting, immunofluorescence, and RT-qPCR. The cells are compatible with arrayed and pooled CRISPR screens for genetic interaction mapping and drug target validation. Applications include complement biology, hematological disease modeling, inflammatory and autoimmune condition research. For additional details, product specifications, or technical support, please contact Ascent Research.
