G Protein-Coupled Receptors: Molecular Mechanisms Involved in Receptor Activation and Selectivity: Second Edition
A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Genetics and Genomics".
Deadline for manuscript submissions: 30 April 2025 | Viewed by 988
Special Issue Editors
Interests: G protein-coupled receptor; signal transduction; chemokines; protein-protein interactions; yeast genetic analysis; alternative splicing; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals
Interests: G protein-coupled receptor; chemokines; prokineticins; pain; neuroinflammation; in vivo and in vitro pharmacological analysis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
G protein-coupled receptors (GPCRs) are seven-transmembrane receptors that, upon activation, predominately transduce their signals through the alpha subunits of heterotrimeric G proteins. GPCRs are present in all cell types and regulate a plethora of physiological functions, whose alterations lead to a pathogenic readout.
Many GPCRs show basal activity that can be modulated by ligands with different efficacy. Full agonists are able to induce the maximal signaling response, while some ligands, known as biased ligands, selectively activate certain receptor-associated pathways at the expense of others. The interaction of GPCRs with extracellular ligands induces an extremely variable response due to the distinct distribution of active conformations of these receptors. Ligand binding and downstream signaling have also been shown to be influenced by the dimeric nature of the receptors.
This Special Issue aims to present novel data focused on biochemical, pharmacological, and structural evidence regarding the molecular mechanisms of GPCR activation, whose understanding is crucial to designing new highly specific drugs with reduced side effects.
Dr. Rossella Miele
Dr. Roberta Lattanzi
Guest Editors
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Keywords
- G protein-coupled receptors
- chemokines
- dimerization
- beta arrestin
- biased agonist
- pain
- inflammation
- neuroinflammation
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