ANPEP Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ANPEP gene in the HAP1 human near-haploid hematopoietic cell line. This product provides a functional loss-of-model for dissecting aminopeptidase N (CD13) biology without the complexity of a diploid genome. The polyclonal pool is generated through CRISPR/Cas9-mediated gene disruption, enabling efficient interrogation of ANPEP-dependent cellular processes. It is a powerful tool for genetic screens and mechanistic studies in cancer biology, virology, and signal transduction.
The HAP1 host cell line is derived from the chronic myeloid leukemia line KBM-7, exhibiting a stable near-haploid karyotype and fibroblast-like morphology. Its haploid nature minimizes compensation from second alleles, making it exceptionally suitable for gene knockout experiments and genome-wide screens. HAP1 cells retain hematopoietic lineage characteristics and are widely adopted for functional genomics, drug target discovery, and pathway analysis. This genetic background is particularly valuable for studying oncogenic mechanisms and host?Cpathogen interactions relevant to myeloid malignancies.
ANPEP encodes the type II membrane protein CD13, a zinc-dependent metalloprotease that removes neutral amino acids from the N-terminus of peptides. It plays critical roles in peptide metabolism, cell adhesion, and serves as a receptor for coronaviruses. ANPEP is transcriptionally regulated by cytokines such as interleukin-4, phorbol esters, retinoic acid, and the transcription factor C/EBP??. Downstream, its enzymatic activity generates bioactive peptides including angiotensin III and enkephalins, modulates focal adhesion kinase signaling, and shapes extracellular matrix interactions. CD13 interacts with integrins, other aminopeptidases, and viral spike proteins, positioning it at the nexus of remodeling, signaling, and infection.
In the HAP1 near-haploid leukemia background, ANPEP deletion permits rigorous dissection of CD13 functions in cell proliferation, adhesion, invasion, and hematopoietic signaling. The knockout eliminates enzymatic trimming and viral receptor activity, unmasking direct consequences on peptide-receptor crosstalk and the renin-angiotensin system. Because HAP1 cells are amenable to high-throughput screening, this model enables systematic genetic modifier and drug sensitivity studies in a leukemia-relevant context. It also provides a clean system to analyze CD13-dependent entry of coronaviruses such as SARS-CoV-2, bypassing confounding factors present in diploid or primary cells.
Typical applications include functional characterization of aminopeptidase N in acute myeloid leukemia, investigation of CD13 as a viral receptor for COVID-19 research, screening of novel aminopeptidase inhibitors, and elucidation of peptide-mediated signaling cascades. The polyclonal knockout population is compatible with assays such as aminopeptidase activity measurements, flow cytometry for CD13 surface expression, western blotting and RT-qPCR for confirmation of gene disruption, cell adhesion and viral entry assays, proliferation and apoptosis analyses, and drug sensitivity profiling. It also serves as a robust platform for haploid genetic screens to identify synthetic lethal partners or regulators of CD13. For additional details or to inquire about this product, please contact Ascent Research.
