Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a key mediator of vascular homeostasis. eNOS enzymatic activity appears to be determined by the availability of its cofactor tetrahydrobiopterin (BH4). BH4 bioavailability is limited by oxidative degradation in dysfunctional endothelium, and by alterations in the rate of its biosynthesis, governed by the rate-limiting enzyme GTP cyclohydrolase 1 (GTPCH). In this project novel targeted transgenic mouse lines were generat
以下为对购买帮助不大的评价