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Articles by Andy Chevigne
Chemokine and opioid peptide scavenging through constitutive and ligand-induced release of ACKR3-bearing extracellular vesicles
Abstract Atypical chemokine receptors (ACKRs) are non-signaling GPCRs that regulate ligand availability, with ACKR3 functioning as a dual scavenger of chemokines and opioid peptides. Here, we demonstrate that following ligand stimulation, besides the canonical internalization, ACKR3 is released on extracellular vesicles (EVs). ACKR3 was also found on EVs released under basal conditions, although to a lesser extent.
Encoding and decoding selectivity and promiscuity in the human chemokine-GPCR interaction network
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Keywords chemokine GPCR unstructured protein short linear motif selectivity determinants chemotaxis polymorphism protein-protein interaction data science machine learning Introduction In humans, cell migration is coordinated by interactions between secreted chemokine ligands and their chemokine receptors of the G-protein-coupled receptors (GPCRs) superfamily that are expressed on the surface of the migrating cell (Figure 1A).
By Andrew B. Kleist, Martyna Szpakowska, Lindsay Talbot Verified, Greg Slodkowicz, Duccio Malinverni, Monica Thomas, Kyler S. Crawford, Daniel J. McGrail, Acacia F. Dishman, Michael J. Wedemeyer, Madison N. Sluter, S. Stephen Yi, Nidhi Sahni, Francis C. Peterson, Andy Chevigne, Brian F Volkman, M. Madan Babu
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Cell Press
Verified
Molecular basis of promiscuous chemokine binding and structural mimicry at the C-X-C chemokine receptor, CXCR2
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Keywords signal transduction GPCRs chemokine receptors biased signaling ligand promiscuity dimerization structural mimicry cryo-EM drug discovery β-arrestin Get full text access Log in, subscribe or purchase for full access. References 1. Hughes, C.E. ∙ Nibbs, R.J.B. A guide to chemokines and their receptors FEBS Journal. 2018; 285:2944-2971 2. Viola, A. ∙ Luster, A.D. Chemokines and their receptors: drug targets in immunity and inflammation Annu. Rev. Pharmacol. Toxicol. 2008; 48:171-197 3.
By Shirsha Saha, Fumiya Sano, Saloni Sharma, Manisankar Ganguly, Sudha Mishra, Annu Dalal, Hiroaki Akasaka, Takaaki Kobayashi, Nashrah Zaidi, Divyanshu tiwari, Nabarun Roy, Manish Yadav, Nilanjana Banerjee, Sayantan Saha, Samanwita Mohapatra, Yuzuru Itoh, Andy Chevigne, Ramanuj Banerjee, Wataru Shihoya, Osamu Nureki, Arun Shukla
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Cell Press
Verified
Molecular basis of promiscuous chemokine binding and structural mimicry at the C-X-C chemokine receptor, CXCR2
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Keywords signal transduction GPCRs chemokine receptors biased signaling ligand promiscuity dimerization structural mimicry cryo-EM drug discovery β-arrestin Introduction Chemokines are small proteins secreted by immune cells that play critical roles in a myriad of physiological processes, including cellular migration and inflammatory responses, by activating chemokine receptors.1,2 Chemokine receptors belong to the superfamily of G-protein-coupled receptors (GPCRs) with primary coupling to...
By Shirsha Saha, Fumiya Sano, Saloni Sharma, Manisankar Ganguly, Sudha Mishra, Annu Dalal, Hiroaki Akasaka, Takaaki Kobayashi, Nashrah Zaidi, Divyanshu tiwari, Nabarun Roy, Manish Yadav, Nilanjana Banerjee, Sayantan Saha, Yuzuru Itoh, Andy Chevigne, Ramanuj Banerjee, Wataru Shihoya, Osamu Nureki, Arun Shukla, Samanwita Mohapatra
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Cell Press
Verified
International Union of Basic and Clinical Pharmacology. CXVIII. Update on the Nomenclature for Atypical Chemokine Receptors including ACKR5
Abstract Chemokines signal through classical G protein-coupled receptors (GPCRs) to induce cell migration during development, immune homeostasis and multiple diseases. Over the last decade a subfamily of atypical chemokine receptors (ACKRs) was delineated from GPCRs based on their inability to trigger conventional G protein signaling or mediate cell migration in response to chemokines.
GRK specificity and Gβγ dependency determines the potential of a GPCR for arrestin-biased agonism - Communications Biology
Abstract G protein-coupled receptors (GPCRs) are mainly regulated by GPCR kinase (GRK) phosphorylation and subsequent β-arrestin recruitment. The ubiquitously expressed GRKs are classified into cytosolic GRK2/3 and membrane-tethered GRK5/6 subfamilies. GRK2/3 interact with activated G protein βγ-subunits to translocate to the membrane. Yet, this need was not linked as a factor for bias, influencing the effectiveness of β-arrestin-biased agonist creation.
Systematic Assessment of Human CCR7 Signalling Using NanoBRET Biosensors Points towards the Importance of the Cellular Context
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Reply to: How carvedilol does not activate β2-adrenoceptors - Nature Communications
replying to R.J. Lefkowitz et al. Nature Communications https://doi.org/10.1038/s41467-023-42848-5 (2023) We thank Dr. Robert Lefkowitz and co-authors for their comments on our article “How carvedilol activates β2-adrenoceptors”1. In their critique2, they state that our study concludes that intrinsic sympathomimetic activity (ISA) is the mechanism responsible for the beneficial actions of carvedilol and that this is incorrect.
G protein-receptor kinases 5/6 are the key regulators of G protein-coupled receptor 35-arrestin interactions
Abstract Human G protein-coupled receptor 35 is regulated by agonist-mediated phosphorylation of a set of five phospho-acceptor amino acids within its C-terminal tail. Alteration of both Ser300 and Ser303 to alanine in the GPR35a isoform greatly reduces the ability of receptor agonists to promote interactions with arrestin adapter proteins.
How Carvedilol activates β2-adrenoceptors - Nature Communications
Abstract Carvedilol is among the most effective β-blockers for improving survival after myocardial infarction. Yet the mechanisms by which carvedilol achieves this superior clinical profile are still unclear. Beyond blockade of β1-adrenoceptors, arrestin-biased signalling via β2-adrenoceptors is a molecular mechanism proposed to explain the survival benefits. Here, we offer an alternative mechanism to rationalize carvedilol’s cellular signalling.
Computationally designed GPCR quaternary structures bias signaling pathway activation - Nature Communications
Abstract Communication across membranes controls critical cellular processes and is achieved by receptors translating extracellular signals into selective cytoplasmic responses. While receptor tertiary structures can be readily characterized, receptor associations into quaternary structures are challenging to study and their implications in signal transduction remain poorly understood.
Emerging roles of the protease allergen Der p 1 in house dust mite-induced airway inflammation
The first fully documented report on isolation of the house dust mite (HDM) allergen Der p 1 was published by Chapman and Platts-Mills in 1980,1x1Chapman, M.D. and Platts-Mills, T.A. Purification and characterization of the major allergen from Dermatophagoides pteronyssinus-antigen P1. J Immunol.
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