ACBC has the binding profile of an antagonist at the glycine site of the NMDA receptor. ACBC and HA-966, a known glycine antagonist, blocked NMDA responses in a non-competitive manner and blocked the potentiation of NMDA responses by glycine in a competitive manner[2]. Promoters with medium to strong expression were included into the pSET152-system, leading to an overexpression of the acbC gene. AcbC catalyzes the first step of acarbose biosynthesis and connects primary to secondary metabolism. By overexpression, the acarbose formation was not enhanced, but slightly reduced in case of strongest overexpression[3]. ACBC has the potential as a tool for physicians to identify individual patient preferences as a practical basis for concordant prescribing for OA (osteoarthritis) in clinical practice[4]. AcbC also plays important roles not only in controlling the activity level after the last-reward collection but also in motivational learning for setting the activity level of reward-seeking behavior. Rats receiving training after AcbC lesioning showed a reduction in motivation for reward seeking[5].
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