The EGFL7 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population disrupting the human EGFL7 gene in the HAP1 cell line. This heterogeneous cell pool contains diverse loss-of-function alleles generated by targeted gene disruption, providing a versatile tool for studying EGFL7 function in a near-haploid background.
HAP1 cells are a near-haploid human chronic myeloid leukemia line derived from KBM-7. The haploid karyotype simplifies genetic manipulation, facilitating homozygous knockout generation and straightforward genotype-phenotype analysis. Widely used for CRISPR screens and gene disruption studies, this background reduces genetic complexity, making it ideal for functional genomics applications.
EGFL7 is a secreted angiogenic factor that antagonizes Notch signaling to regulate vascular morphogenesis. Its expression is driven by ETS transcription factors (e.g., ERG) and induced by VEGF and HIF1A. EGFL7 interacts with Notch receptors (Notch1, Notch4) and the ligand DLL4, as well as integrin ??v??3 and extracellular matrix components fibronectin and collagen. Through these interactions, EGFL7 suppresses Notch downstream targets RBPJ, HES1, and HEY1, thereby promoting endothelial migration and sprouting. Additionally, EGFL7 engages integrin?CFAK?CSrc pathways to modulate cell adhesion and cytoskeletal dynamics.
Disruption of EGFL7 in the haploid HAP1 background establishes a potent loss-of-function model. The near-haploid state enables functional homozygous knockout within the polyclonal population, eliminating residual EGFL7 activity. This system is well-suited for dissecting EGFL7??s role in Notch modulation, integrin signaling, and angiogenesis. The polyclonal format permits bulk assays and pooled screening approaches, facilitating drug target validation in cancers with aberrant angiogenesis, such as glioblastoma and hepatocellular carcinoma.
This product supports diverse applications including angiogenesis tube formation and endothelial migration assays to examine vascular effects. Notch signaling can be probed using reporter assays or target gene expression analysis. Standard techniques such as Western blot, RT-qPCR, and Sanger sequencing confirm EGFL7 disruption. Co-immunoprecipitation studies can explore altered protein interactions. The haploid platform is ideal for functional genomics and genetic interaction screens. For additional information, contact Ascent Research.
