AAMP Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human AAMP gene in the HAP1 cell line. This pooled loss-of-function model, generated by CRISPR/Cas9-mediated gene disruption, provides a genetically diverse background for studying AAMP-dependent phenotypes without clonal selection artifacts.
HAP1 is a near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells, displaying fibroblastoid adherent morphology and disomy for chromosome 8. Its haploid genome simplifies knockout generation, requiring disruption of a single allele, making it ideal for functional genomics and genetic screening. Widely used in cancer biology and signal transduction research, HAP1 enables efficient CRISPR/Cas9-mediated gene disruption for oncogenic pathway analysis.
AAMP encodes an angio-associated migratory cell protein with immunoglobulin-like and heparin-binding domains. It promotes cell migration and angiogenesis by interacting with heparan sulfate proteoglycans, integrins, and extracellular matrix proteins. Acting downstream of VEGFA, FGF2, hypoxia, and HIF1A, AAMP facilitates focal adhesion turnover and cytoskeletal reorganization. Mechanistically, it activates SRC and FAK, leading to RHOA and RAC1-mediated signal transduction, culminating in MAPK1/3 (ERK1/2) and AKT1 phosphorylation. Knockout of AAMP impairs these signaling cascades, reducing endothelial tube formation and migratory capacity.
In the HAP1 background, this knockout model enables dissection of AAMP’s role in migration and angiogenic pathways. HAP1 cells express VEGFA and its receptor KDR, supporting analysis of AAMP-mediated signaling. Disruption of AAMP is expected to attenuate integrin-dependent adhesion and downstream RHOA/RAC1-MAPK/AKT activation, providing a robust system to study mechanisms relevant to cancer metastasis and cardiovascular diseases. The polyclonal format minimizes clonal bias, ensuring representative loss-of-function phenotypes.
Applications include angiogenesis research, cancer metastasis studies, cell migration assays, and drug target validation. Representative assays: Western blotting for phospho-ERK1/2 and phospho-AKT, RT-qPCR for target gene expression, immunofluorescence for focal adhesion analysis, tube formation assays, and migration/invasion assays. Flow cytometry can assess integrin surface expression. For technical inquiries, contact Ascent Research.
