The ANXA7 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the ANXA7 gene in the HAP1 human near-haploid cell line. This polyclonal knockout model provides a heterogeneous collection of edited cells, representing a spectrum of gene disruptions that collectively abolish ANXA7 function. The product is designed for loss-of-function studies without the need for clonal isolation, avoiding potential clone-specific artifacts. By disrupting ANXA7 in a haploid background, this system simplifies genetic analysis and supports robust phenotypic screening.
HAP1 cells are a near-haploid human cell line derived from the chronic myeloid leukemia line KBM-7, widely used for genetic screens and knockout studies due to their haploid karyotype. The haploid genome reduces redundancy and allows single-allele gene disruption to produce a null phenotype, making HAP1 an efficient platform for CRISPR/Cas9-mediated functional genomics. HAP1 cells maintain key signaling pathways and are amenable to high-throughput applications, making them a relevant model for investigating cancer-related gene functions and drug responses.
ANXA7 is a calcium-dependent phospholipid-binding protein that facilitates membrane fusion during exocytosis. It is phosphorylated by EGFR, PKC, and Src kinase, and interacts with Galectin-3 and SNARE proteins (syntaxin-4, SNAP-23, VAMP) to promote vesicle-plasma membrane fusion. ANXA7 integrates calcium signals with the exocytic machinery and has been implicated in caspase-3 activation during apoptosis. Loss of ANXA7 disrupts these processes, affecting regulated secretion and apoptotic sensitivity, and is linked to cancers, neurofibromatosis type 1, and platelet disorders.
In the HAP1 polyclonal knockout population, ANXA7 deficiency allows exploration of its role in exocytosis regulation and apoptosis in a leukemic background. This model is valuable for dissecting ANXA7??s contextual tumor suppressor functions in cancers such as glioblastoma, prostate, and breast cancer. The polyclonal format mimics the genetic heterogeneity of tumor populations, enabling assessment of population-level phenotypes in proliferation, survival, and drug response without clonal selection bias.
Key applications include studying tumor suppressor mechanisms, screening for genetic interactors, and investigating EGFR signaling dynamics. Researchers can employ western blotting for knockout verification, apoptosis assays (caspase activation), co-immunoprecipitation with SNARE components, calcium imaging, and drug sensitivity profiling. The polyclonal knockout cells are particularly suited for high-throughput genetic screens and rescue experiments. For technical inquiries or to order this product, please contact Ascent Research.
