NPR1 Knockout Cell Line (Hela)

The choice depends on whether you are studying NPR1 (NPR-A, GC-A)'s role as the principal ANP/BNP receptor or its functions in cardiovascular and renal physiology. The Knockout line is the standard tool for asking whether NPR-A is required for ANP/BNP-induced cGMP generation in heterologous expression contexts — NPR-A is a transmembrane guanylyl cyclase responsible for cardiac, renal, and vascular natriuretic peptide effects including natriuresis, vasodilation, and anti-hypertrophic responses. Overexpression is useful for studying NPR-A in heterologous expression contexts or for testing disease-associated mutations. For natriuretic peptide research, the EDITGENE NPR1 Knockout in HeLa enables biochemical and structure-function studies of NPR-A. This product complements the parallel Npra Knockout in HL-1 (also available); HeLa is preferred for biochemistry, HL-1 for cardiomyocyte-relevant studies. NPR1 polymorphisms have been associated with hypertension and heart failure risk. Rescue with wild-type or guanylyl cyclase-dead NPR-A is the standard specificity control. The knockout is valuable for sacubitril/valsartan (Entresto) mechanism studies and ANP/BNP analog drug development.

Primary applications: • ANP/BNP-induced cGMP signaling: cGMP measurement following ANP or BNP stimulation to quantify NPR-A-dependent guanylyl cyclase activity. • Polymorphism studies: rescue with NPR1 polymorphic variants associated with hypertension and heart failure risk for pharmacogenomic studies. • Structure-function studies: rescue with wild-type or guanylyl cyclase-dead NPR-A in clean heterologous background. • Sacubitril/valsartan mechanism: studies of Entresto's cardioprotective effects mediated through enhanced ANP/BNP signaling at NPR-A. EDITGENE recommends this HeLa-based model for NPR-A biochemistry; the parallel Npra Knockout in HL-1 (also available) is preferred for cardiomyocyte-relevant studies.

Yes. NPR-A rescue experiments in HeLa are well-suited for biochemistry: • Construct design: use a codon-modified NPR1 sequence with a small intracellular C-terminal tag (FLAG, HA). NPR-A has the canonical particulate guanylyl cyclase architecture — preserve all elements. • Guanylyl cyclase-dead rescue: catalytic domain mutations abolish cGMP generation and serve as the standard specificity control. • Polymorphism rescue: cardiovascular disease-associated NPR1 polymorphisms enable pharmacogenomic studies. • Functional readout: rescue should restore ANP/BNP-induced cGMP generation. HeLa transduces efficiently with lentivirus and supports stable rescue line generation.