The C1QBP Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the C1QBP gene in the human near-haploid HAP1 cell line. This polyclonal product offers a functional knockout pool, avoiding the clonal artifacts associated with single-cell?Cderived lines while providing a robust system for loss-of-function studies. The C1QBP gene, encoding the gC1qR/p32 protein, is disrupted to enable investigation of its pleiotropic roles in complement activation, mitochondrial homeostasis, apoptosis, cell cycle control, and viral pathogenesis.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia line, originating from a male patient, and retain a near-haploid karyotype. This haploid nature simplifies genetic knockout studies by eliminating the complexity of diploid gene dosage, making HAP1 a powerful platform for functional genomics, drug target validation, and pathway dissection. The hematopoietic origin of HAP1 renders this model especially relevant for studying malignancies and immune-related signaling networks.
C1QBP encodes a multifunctional scaffolding protein that binds complement component C1q, kininogen, and hyaluronan, thereby linking innate immunity to mitochondrial physiology. As an upstream regulator of apoptosis, gC1qR/p32 interacts with BCL2, BAX, and cytochrome c to govern mitochondrial outer membrane permeabilization and caspase-3 activation in response to stimuli such as TNF-??, IL-1??, and genotoxic stress. It also promotes cell proliferation through modulation of CDK1 and cyclin D1, and activates NF-??B signaling via NFKB1 and RELA downstream of TLR4/MYD88. Concurrently, C1QBP engages MAPK1/ERK2 and AKT1 within the MAPK and PI3K/AKT pathways, influencing survival and growth. In viral infection, C1QBP serves as a co-receptor for HIV-1 gp41 and HCV core protein, facilitating entry and pathogenesis.
In the haploid HAP1 background, disruption of C1QBP permits unambiguous dissection of its contributions to leukemogenesis and complement-dependent inflammation. Since a single functional allele is present, the polyclonal knockout population exhibits a uniform loss-of-function phenotype, enabling clear readouts in assays for proliferation, apoptosis, and viral susceptibility. This model is particularly suitable for comparative studies with wild-type HAP1 cells to delineate C1QBP-dependent downstream effectors.
Key applications include mechanistic studies of complement-mediated inflammation via C1q binding assays, mitochondrial apoptosis profiling using flow cytometry for mitochondrial membrane potential and Annexin V/PI staining, and investigation of viral entry mechanisms through infectivity assays with HIV-1 or HCV. The polyclonal format further supports genetic interaction screens, high?content imaging, and drug-response profiling in a near-haploid system. For further technical inquiries or to request a quotation, please contact Ascent Research.
