The EDN1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the EDN1 gene has been disrupted, providing a loss-of-function model for endothelin-1. This polyclonal pool is suitable for functional assays without clonal selection.
The HAP1 cell line is a near-haploid human line derived from the chronic myeloid leukemia KBM-7 cells, exhibiting fibroblast morphology. Its near-haploid genome facilitates genetic knockout studies by eliminating the complexity of a second allele, making it ideal for functional genomics and screening applications.
EDN1 encodes endothelin-1, a potent vasoconstrictor peptide that binds G protein-coupled receptors EDNRA and EDNRB. Ligand engagement activates G??q/11, stimulating PLC?? to generate IP3 and DAG, which mobilize Ca2+ and activate PKC. Downstream, the MAPK cascades (ERK1/2, JNK, p38) and PI3K/Akt pathways are triggered, promoting cell proliferation and inflammation. Endothelin-1 expression is regulated by TGF-??, IL-1??, TNF-??, angiotensin II, HIF-1??, and shear stress, and it transcriptionally induces c-Fos, c-Jun, VEGF, and CTGF. The pro-peptide is processed by endothelin-converting enzyme-1 (ECE1).
In HAP1 cells, EDN1 knockout eliminates autocrine endothelin-1 signaling, enabling dissection of its roles in vasoconstriction, proliferation, and inflammation. This model is valuable for studying hypertension, pulmonary arterial hypertension, atherosclerosis, heart failure, and cancer, where endothelin-1 drives vascular remodeling and tumor?Cstroma interactions.
This polyclonal knockout pool can be applied in RT-qPCR, western blotting, and ELISA to confirm EDN1 loss. Functional assays for calcium flux, MAPK phosphorylation, cell proliferation, migration, and AP-1 reporter activity are used to investigate downstream signaling. It is suited for drug target validation and mechanistic studies in vascular biology and oncology. For further information, please contact Ascent Research.
