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Crystal structure of a constitutive active mutant of adenosine A2A receptor.
Cui, Min; Zhou, Qingtong; Xu, Yueming; Weng, Yuan; Yao, Deqiang; Zhao, Suwen; Song, Gaojie.
Afiliación
  • Cui M; Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, People's Republic of China.
  • Zhou Q; Department of Pharmacology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, People's Republic of China.
  • Xu Y; Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, People's Republic of China.
  • Weng Y; Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, People's Republic of China.
  • Yao D; State Key Laboratory of Oncogenes and Related Genes, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, People's Republic of China.
  • Zhao S; iHuman Institute, ShanghaiTech University, Shanghai 201210, People's Republic of China.
  • Song G; School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, People's Republic of China.
IUCrJ ; 9(Pt 3): 333-341, 2022 May 01.
Article en En | MEDLINE | ID: mdl-35546802
The adenosine A2A receptor (A2AAR) is a prototypical member of the class A subfamily of G-protein-coupled receptors (GPCRs) that is widely distributed in various tissues and organs of the human body, and participates in many important signal-regulation processes. We have previously summarized a common activation pathway of class A GPCRs in which a series of conserved residues/motifs undergo conformational change during extracellular agonist binding and finally induce the coupling of intracellular G protein. Through this mechanism we have successfully predicted several novel constitutive active or inactive mutations for A2AAR. To reveal the molecular mechanism of mutation-induced constitutive activity, we determined the structure of a typical mutant I92N complexed with the agonist UK-432097. The mutated I92N forms a hydrophilic interaction network with nearby residues including Trp6.48 of the CWxP motif, which is absent in wild-type A2AAR. Although the mutant structure is similar overall to the previously determined intermediate-state A2AAR structure (PDB ID 3qak) [Xu, Wu, Katritch, Han, Jacobson, Gao, Cherezov & Stevens (2011). Science, 332, 322-327 ▸], molecular dynamics simulations suggest that the I92N mutant stabilizes the metastable intermediate state through the hydrophilic interaction network and favors the conformational transition of the receptor towards the active state. This research provides a structural template towards the special pharmacological outcome triggered by conformational mutation and sheds light on future structural or pharmaco-logical studies among class A GPCRs.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: IUCrJ Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: IUCrJ Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido