ReviewFrontiers in medicine2019
Discovery of Pathologic GPCR Aggregation.
Review in Frontiers in medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Improved Method for Predicting GPCR-GPCR Interaction Pairs.Proteins · 2026Article
- The interplay of serotonin 5-HT1A and 5-HT7 receptors in chronic stress.Journal of cell science · 2024Article
- Chemokine receptor hetero-oligomers regulate monocyte chemotaxis.Life science alliance · 2024Article
- RNA therapeutics in targeting G protein-coupled receptors: Recent advances and challenges.Molecular therapy. Nucleic acids · 2024Review
- Article
- αInternational journal of molecular sciences · 2023Review
- The World of GPCR dimers - Mapping dopamine receptor DComputational and structural biotechnology journal · 2023Article
- CXCR4-CCR7 Heterodimerization Is a Driver of Breast Cancer Progression.Life (Basel, Switzerland) · 2021Article
- Review
- Class A G protein-coupled receptors assemble into functional higher-order hetero-oligomers.FEBS letters · 2021Article
- Neural network strategies for plasma membrane selection in fluorescence microscopy images.Biophysical journal · 2021Article
- Plasticity of seven-transmembrane-helix receptor heteromers in human vascular smooth muscle cells.PloS one · 2021Article
- Structural Complexity and Plasticity of Signaling Regulation at the Melanocortin-4 Receptor.International journal of molecular sciences · 2020Review
- Characterization of heteromeric complexes between chemokine (C-X-C motif) receptor 4 and αBiochemical and biophysical research communications · 2020Article
- GPCRs, G Proteins, and Their Impact on β-cell Function.Comprehensive Physiology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The family of G-protein-coupled receptors (GPCRs) is one of the most important drug targets. Mechanisms underlying GPCR activation and signaling are therefore of great pharmacologic interest. It was long thought that GPCRs exist and function as monomers. This feature was considered to distinguish GPCRs from other membrane receptors such as receptor tyrosine kinases or cytokine receptors, which signal from dimeric receptor complexes. But during the last two decades it was increasingly recognized that GPCRs can undergo aggregation to form dimers and higher order oligomers, resulting in homomeric and/or heteromeric protein complexes with different stoichiometries. Moreover, this protein complex formation could modify GPCR signaling and function. We contributed to this paradigm shift in GPCR pharmacology by the discovery of the first pathologic GPCR aggregation, which is the protein complex formation between the angiotensin II AT1 receptor and the bradykinin B2 receptor. Increased AT1-B2 heteromerization accounts for the angiotensin II hypersensitivity of pregnant women with preeclampsia hypertension. Since the discovery of AT1-B2, other pathologic GPCR aggregates were found, which contribute to atherosclerosis, neurodegeneration and Alzheimer's disease. As a result of our findings, pathologic GPCR aggregation appears as an independent and disease-specific process, which is increasingly considered as a novel target for pharmacologic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.