Adenosine A2A receptor

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Revision as of 17:19, 18 October 2017

spinqualitylabelsall models Human A2AR (mutant) complex with adenosine 2ydo Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image Contents 1 Function 2 Disease 3 Relevance 4 Structural highlights Function Adenosine A2A receptor (A2AR) is one of the G protein-coupled receptors. The protein uses adenosine as the preferred endogenous agonist and is involved in increasing intracellular cAMP levels.[1] Disease A2AR antagonists are being tested in the treatment of Alzheimer's Disease. Relevance A2AR is responsible for regulating myocardial blood flow. It is involved in cerebral and renal blood flow, immune function, pain regulation and sleep. For details see G protein-coupled receptor. A2AR is blocked by caffeine producing the arousal effect.[2] For details see Caffeine. Structural highlights Like other G proteins, . .

3D Structures of adenosine A2A receptor

Updated on 18-October-2017

3eml – hA2AR/lysozyme + antagonist – human
5k2a, 5k2b, 5k2c, 5k2d – hA2AR/cytochrome b562
5iu4, 5iu7, 5iu8, 5iua, 5iub – hA2AR/cytochrome b562 (mutant) + inhibitor
4ug2, 4uhr – hA2AR (mutant) + inhibitor
5g53 – hA2AR + G protein
3qak – hA2AR/lysozyme + agonist
2ydo – hA2AR (mutant) + adenosine
2ydv – hA2AR (mutant) + agonist
3pwh, 3rey, 3rfm, 3uza, 3uzc – hA2AR (mutant) + antagonist
3rfm – hA2AR (mutant) + caffeine
3vg9, 3vga – hA2AR (mutant) + antibody
4eiy – hA2AR/cytochrome b562 + antagonist
5uig – hA2AR/cytochrome b562 (mutant) + antagonist

References

1. ↑ Lebon G, Warne T, Edwards PC, Bennett K, Langmead CJ, Leslie AG, Tate CG. Agonist-bound adenosine A(2A) receptor structures reveal common features of GPCR activation. Nature. 2011 May 18. PMID:21593763 doi:10.1038/nature10136
2. ↑ Lazarus M, Shen HY, Cherasse Y, Qu WM, Huang ZL, Bass CE, Winsky-Sommerer R, Semba K, Fredholm BB, Boison D, Hayaishi O, Urade Y, Chen JF. Arousal effect of caffeine depends on adenosine A2A receptors in the shell of the nucleus accumbens. J Neurosci. 2011 Jul 6;31(27):10067-75. doi: 10.1523/JNEUROSCI.6730-10.2011. PMID:21734299 doi:http://dx.doi.org/10.1523/JNEUROSCI.6730-10.2011