Brain Natriuretic Peptide-45, mouse (TFA)

Mouse BNP-45 (CAS No. 1816939-52-2) is the major active form of mouse B-type natriuretic peptide. It is generated from a 121-amino acid precursor by specific cleavage with the furin enzyme. The C-terminal 45 amino acids constitute the active peptide, which contains an essential 17-membered intramolecular ring structure with highly conserved key residues. Endogenous Mouse BNP-45 is mainly expressed in mouse atria, ventricles, and AT-1 cardiomyocytes; its mRNA has not been detected in other tissues, and there is an additional transcription initiation site in ventricular tissue. Its biological functions include promoting renal natriuresis, diuresis, and vasodilation, which are achieved by binding to A/B-type receptors and activating the intracellular cGMP signaling pathway. The C-type receptor is responsible for clearing BNP-45 from the bloodstream, thereby maintaining its homeostasis. Its expression is regulated by cis-acting elements in the 5' flanking region, while AT-rich sequences in the 3' untranslated region modulate mRNA stability. Mouse BNP-45 is an important molecular tool for studying cardiovascular regulation and related diseases in mice, and it helps to elucidate the functional conservation and species specificity of the BNP family.

References：

[1] Steinhelper ME. Structure, expression, and genomic mapping of the mouse natriuretic peptide type-B gene. Circ Res. 1993 May;72(5):984-92. doi: 10.1161/01.res.72.5.984. PMID: 8097440.

Ser-Gln-Gly-Ser-Thr-Leu-Arg-Val-Gln-Gln-Arg-Pro-Gln-Asn-Ser-Lys-Val-Thr-His-Ile-Ser-Ser-Cys-Phe-Gly-His-Lys-Ile-Asp-Arg-Ile-Gly-Ser-Val-Ser-Arg-Leu-Gly-Cys-Asn-Ala-Leu-Lys-Leu-Leu (Disulfide bridge:Cys23-Cys39)