Fig 1: Neprilysin (NEP)-deficient mice have increased fasting and amino acid-stimulated glucagon and urea concentrations. Plasma concentrations of A, glucagon and B, corresponding incremental areas under the curve (iAUCs); C, blood glucose concentrations, plasma concentrations of D, insulin; E, body weight; plasma concentrations of F, amino acids; and G, corresponding iAUCs, plasma concentrations of H, urea; and I, corresponding iAUCs; and plasma concentrations of J, ∆ urea in male NEP–/– mice (black circles) and NEP+/+ mice (open circles)-challenged amino acids (equivalent to 1% of body weight) at time 0 minutes (n = 5-6). Data are presented as mean ± SEM and are analyzed by A, C, D, F, H, and J, repeated-measures 2-way analysis of variance, and B, E, G and I, unpaired t tests. –/– indicates NEP–/– mice and +/+ indicates NEP+/+ mice.
Fig 2: Neprilysin (NEP) degrades glucagon into metabolites (Gcg1-21, Gcg1-19, Gcg1-18, Gcg5-18, and Gcg1-13) that do not activate the glucagon receptor (GCGR). Matrix-assisted laser desorption/ionization time of flight identified m/zs in the m/z spectra 1500 to 4500 after recombinant A, human, and B, mouse NEP (10 ng) mixed with glucagon (1 µg) after 15, 30, and 60 minutes’ incubation, and after 60 minutes’ incubation with glucagon, NEP, and the NEP inhibitor sacubitrilat (0.5 nmol, 10% dimethyl sulfoxide) (active form of the prodrug, sacubitril). C, GCGR activation (dose-response curve) for native glucagon (Gcg1-29)-induced 3′,5′-cyclic adenosine 5′-monophosphate (cAMP) accumulation in COS-7 cells transiently transfected with human GCGR. D, Dose-response curves for cAMP accumulation with glucagon-degradation products in COS-7 cells transiently transfected with human GCGR (3 technical replicates).
Supplier Page from R&D Systems, a Bio-Techne Brand for Neprilysin/CD10 Protein
Available conjugates: Sizes Available: 10 ug