The ANAPC7 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the ANAPC7 gene in the HAP1 human near-haploid cell line. This heterogeneous cell pool contains diverse loss-of-function mutations at the target locus, offering a robust system for studying ANAPC7 biology without clonal artifacts.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia line and exhibit a near-haploid karyotype, simplifying genetic analysis and phenotypic readouts. As a myeloid hematopoietic model, they maintain relevant signaling pathways while enabling efficient knockout generation and functional studies.
ANAPC7 encodes a subunit of the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase that controls mitotic progression. APC/C is activated by the coactivators CDC20 and CDH1, which target substrates such as cyclin B1 and securin for proteasomal degradation. Upstream regulators include CDK1 and PLK1, and the complex interacts with the mitotic checkpoint components MAD2, BUBR1, and BUB3. The APC/C also ubiquitinates downstream effectors like SKP2, linking mitotic exit to cell cycle regulation.
In the HAP1 background, ANAPC7 knockout reinforces the study of mitosis in a genetically simplified system, amplifying phenotypes such as mitotic arrest and chromosomal instability characteristic of cancer. This model is particularly suited for investigating how APC/C dysfunction drives malignancy in hematopoietic contexts and for testing mitotic-targeting therapeutics.
These polyclonal cells support a range of applications, including flow cytometry-based cell cycle profiling, live-cell mitotic imaging, and ubiquitination assays. Researchers can quantify cyclin B1 and securin levels via western blotting, assess proliferation, and evaluate drug responses to mitotic inhibitors. Combined with functional genomics approaches, the model facilitates substrate discovery and checkpoint analysis. For inquiries, please contact Ascent Research.
