NPR2 Knockout Cell Line (Hela)

The choice depends on whether you are studying NPR2 (NPR-B, GC-B)'s role as the CNP receptor regulating skeletal growth or modeling acromesomelic dysplasia type Maroteaux (AMDM). The Knockout line is the standard tool for asking whether NPR-B is required for CNP-induced cGMP generation — NPR-B is a transmembrane guanylyl cyclase activated by C-type natriuretic peptide (CNP) binding, with established roles in endochondral ossification and skeletal growth. Overexpression is useful for studying NPR-B signaling or for testing disease-associated mutations. For natriuretic peptide research, the EDITGENE NPR2 Knockout in HeLa enables biochemical study of CNP-NPR-B signaling. NPR2 loss-of-function mutations cause AMDM (autosomal recessive dwarfism with vertebral and limb deformities); gain-of-function cause overgrowth syndrome. Rescue with wild-type or disease-associated mutant NPR-B enables genotype-function studies. The knockout is valuable for studying vosoritide (CNP analog approved for achondroplasia) and emerging CNP-NPR-B-targeted therapeutics. This product complements parallel NPR1, NPR3 Knockouts in HeLa for comprehensive NPR family dissection.

Primary applications: • CNP-induced cGMP signaling: cGMP measurement following CNP stimulation to quantify NPR-B-dependent guanylyl cyclase activity. • Acromesomelic dysplasia modeling: rescue with patient-derived NPR2 mutations for genotype-function studies of AMDM and overgrowth syndromes. • Vosoritide pharmacology: critical genetic control for vosoritide (FDA-approved CNP analog for achondroplasia) and emerging NPR-B-targeted therapeutics. • Endochondral ossification mechanism: studies of CNP-NPR-B signaling in skeletal growth biology. EDITGENE recommends this model for researchers investigating CNP signaling, skeletal dysplasia mechanisms, and NPR-B-targeted achondroplasia therapeutics.

Yes. NPR-B rescue experiments require attention to guanylyl cyclase architecture: • Construct design: use a codon-modified NPR2 sequence with a small intracellular C-terminal tag (FLAG, HA). NPR-B has extracellular CNP-binding domain, single transmembrane span, KHD, dimerization domain, and C-terminal guanylyl cyclase domain — preserve all elements. • Guanylyl cyclase-dead rescue: catalytic domain mutations abolish cGMP generation. • AMDM mutation rescue: patient-derived NPR2 mutations enable disease genotype-function studies. • Functional readout: rescue should restore CNP-induced cGMP generation measured by cGMP ELISA or biosensor imaging. HeLa transduces efficiently with lentivirus and supports stable rescue line generation.