受体
腺苷受体
腺苷
腺苷A2B受体
腺苷酸环化酶
基因剔除小鼠
生物
腺苷A3受体
转基因小鼠
细胞生物学
G蛋白偶联受体
嘌呤能信号
腺苷A1受体
腺苷A2A受体
转基因
内科学
内分泌学
生物化学
医学
兴奋剂
基因
作者
Ron Yaar,Matthew R. Jones,Jiang‐Fan Chen,Katya Ravid
摘要
Abstract Adenosine receptors represent a family of G‐protein coupled receptors that are ubiquitously expressed in a wide variety of tissues. This family contains four receptor subtypes: A1 and A3, which mediate inhibition of adenylyl cyclase; and A2a and A2b, which mediate stimulation of this enzyme. Currently, all receptor subtypes have been genetically deleted in mouse models except for the A2b adenosine receptor, and some have been overexpressed in selective tissues of transgenic mice. Studies involving these transgenic mice indicated that receptor levels are rate limiting, as effects were amplified upon increases in receptor level. The knockout models pointed to clusters of activities related to the physiologies of the cardiovascular and the nervous systems, which are either reduced or enhanced upon specific receptor deletion. Interestingly, the trend of effects on these systems is similar in the A1 and A3 adenosine receptor knockout mice and opposite to the effects observed in the A2a adenosine receptor knockout model. This review summarizes in vitro studies on pathways affected by each adenosine receptor, and primarily focuses on the above in vivo models generated to investigate the physiologic role of adenosine receptors. Furthermore, it illustrates the need for multiple adenosine receptor subtype deficiency studies in mice and the deletion of the A2b subtype. © 2005 Wiley‐Liss, Inc.
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