Nature Search

Allosteric mechanisms underlie GPCR signaling to SH3-domain proteins through arrestin

NMR and in vitro reconstitution indicate that GPCRs signal through SH3-containing proteins downstream of β-arrestin 1 proline regions and that arrestin allosterically activates downstream kinases by disrupting their autoinhibitory conformation.

Fan Yang
Peng Xiao
Jiangyun Wang
Research17 Aug 2018
Nature Chemical Biology

Volume: 14, P: 876-886
DeSiphering receptor core-induced and ligand-dependent conformational changes in arrestin via genetic encoded trimethylsilyl ¹H-NMR probe

Characterization of dynamic conformational changes in membrane protein complexes by NMR spectroscopy remains challenging. Here authors report the site-specific incorporation of 4-trimethylsilyl phenylalanine (TMSiPhe) into proteins, which enabled the characterization of multiple conformational states of a phospho-β2 adrenergic receptor/β-arrestin-1 complex in response to different receptor ligands.

Qi Liu
Qing-tao He
Jin-peng Sun
ResearchOpen Access25 Sept 2020
Nature Communications

Volume: 11, P: 1-17
Phospho-selective mechanisms of arrestin conformations and functions revealed by unnatural amino acid incorporation and ¹⁹F-NMR

G-protein-coupled receptors (GPCRs) signal via G proteins or arrestin-mediated pathways; the plasticity of arrestin proteins is thought to underlie their function. Here, the authors use NMR to examine how β-arrestin-1 recognizes different GPCR phospho-barcodes, and how this triggers structural rearrangements to fulfill selective functions.

Fan Yang
Xiao Yu
Jin-Peng Sun
ResearchOpen Access08 Sept 2015
Nature Communications

Volume: 6, P: 1-15
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling

Angiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca²⁺channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.

Chun-Hua Liu
Zheng Gong
Jin-Peng Sun
ResearchOpen Access09 Feb 2017
Nature Communications

Volume: 8, P: 1-17

Quick links

Search

Filter By:

Allosteric mechanisms underlie GPCR signaling to SH3-domain proteins through arrestin

DeSiphering receptor core-induced and ligand-dependent conformational changes in arrestin via genetic encoded trimethylsilyl 1H-NMR probe

Phospho-selective mechanisms of arrestin conformations and functions revealed by unnatural amino acid incorporation and 19F-NMR

Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling

Search

Quick links

DeSiphering receptor core-induced and ligand-dependent conformational changes in arrestin via genetic encoded trimethylsilyl ¹H-NMR probe

Phospho-selective mechanisms of arrestin conformations and functions revealed by unnatural amino acid incorporation and ¹⁹F-NMR