The APLP2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 near-haploid chronic myeloid leukemia cell line, designed for functional disruption of the APLP2 gene. This polyclonal pool, generated by CRISPR/Cas9-mediated gene targeting, provides a loss-of-function model suitable for investigating APLP2-dependent cellular mechanisms without the isolation of single-cell clones. The product enables researchers to study the consequences of APLP2 depletion across a heterogeneous cell population, maintaining the inherent genetic background of HAP1 cells.
The HAP1 host cell line originates from the KBM-7 chronic myeloid leukemia line and is characterized by a near-haploid karyotype (one copy of most chromosomes), male origin, and expression of the BCR-ABL1 fusion oncogene. This unique genomic architecture eliminates the confounding effects of heterozygous mutations, making HAP1 a powerful platform for CRISPR/Cas9-based knockout screens and functional genomics studies. The near-haploid state ensures that targeting the single APLP2 allele results in efficient gene disruption, facilitating robust phenotypic readouts in subsequent assays.
APLP2 (Amyloid Beta Precursor Like Protein 2) is a type I transmembrane protein homologous to APP. It undergoes sequential proteolytic processing by ADAM10 (??-secretase), BACE1 (??-secretase), and the ??-secretase complex, releasing an intracellular domain (AICD) that translocates to the nucleus. There, AICD forms a complex with Fe65 and Tip60 to regulate genes such as GSK-3?? and Rac1. Upstream regulators include retinoic acid, protein kinase C, and calcium influx. APLP2 also mediates cell adhesion and migration via interactions with integrin ??5, LRP1, and adaptor proteins JIP1 and Mint1, and modulates metal ion homeostasis through copper and zinc binding.
In the HAP1 near-haploid background, APLP2 disruption enables unambiguous functional analysis. The polyclonal pool allows assessment of heterogeneous knockout effects. This model is ideal for dissecting integrin-mediated signaling and secretase-dependent transcriptional regulation, free from wild-type interference. HAP1 is also suited for high-throughput screens, and this pool can validate hits related to Alzheimer??s, cancer metastasis, and neurodevelopment.
The APLP2 Knockout HAP1 Polyclonal Cells are suited for functional studies of the APP family in Alzheimer’s disease, analysis of secretase substrate specificity, and investigation of cell adhesion and metal homeostasis. Key assays include Western blotting, RT-qPCR, Sanger sequencing, immunofluorescence, cell adhesion and migration assays, co-immunoprecipitation with APP or integrin ??5, and ??-secretase cleavage assays. Transcriptomic analysis via RNA-seq and qPCR for targets such as GSK-3?? and Rac1 can further characterize the signaling network. For validation data and culture conditions, please contact Ascent Research.
