The ATAD3B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HAP1 human near-haploid cells. This pool of cells carries targeted disruption of ATAD3B, enabling loss-of-function studies without single-cell cloning. The polyclonal format preserves genetic heterogeneity while ensuring robust knockout representation, suitable for high-throughput screening and reproducible functional assays.
HAP1 is a fibroblast-like, near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. Its haploid karyotype facilitates complete gene disruption in one allele, simplifying knockout phenotype interpretation. Widely used in functional genomics, HAP1 cells provide a versatile platform for mitochondrial research due to stable adherent growth and tractability for biochemical and imaging assays.
ATAD3B is an inner mitochondrial membrane AAA+ ATPase coordinating mitochondrial nucleoid organization, mtDNA replication, and cholesterol trafficking. It interacts with the nucleoid and cholesterol transfer complex, linking mtDNA maintenance to steroidogenesis and mitochondrial dynamics. Transcriptional regulation involves PPARGC1A, NRF1, ESRRA, and TFAM, while ATAD3B influences STAR, POLG, TFAM, and CYP11A1. Binding partners include ATAD3A, MFN2, STAR, VDAC1, and MT-CO2, positioning ATAD3B at the interface of mitochondrial homeostasis, membrane architecture, and bioenergetic signaling.
Loss of ATAD3B disrupts mitochondrial ultrastructure, reduces mtDNA copy number, impairs cholesterol metabolism, and compromises oxidative phosphorylation. In near-haploid HAP1 cells, the knockout provides a clean model to dissect these phenotypes without a second allele. The polyclonal population reduces clonal variation and enables genome-wide modifier screens, making it ideal for exploring mitochondrial biology and genetic interactions linked to mitochondrial disorders and cancer.
This product is suited for Western blotting of ATAD3B and mitochondrial markers, RT-qPCR-based mtDNA copy number quantification, immunofluorescence with MitoTracker or Tomm20 for morphology, flow cytometry for membrane potential (TMRE/JC-1), and cholesterol efflux assays. It also supports co-immunoprecipitation of ATAD3B interactors and haploid genetic screens. Researchers in mitochondrial biology, mtDNA instability, drug discovery, and cancer metabolism will find this model valuable. For further information, contact Ascent Research.
