ArticleThe Journal of biological chemistry2011
Cross-talk between carboxypeptidase M and the kinin B1 receptor mediates a new mode of G protein-coupled receptor signaling.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Bradykinin B2 Receptor Signaling Increases Glucose Uptake and Oxidation: Evidence and Open Questions.Frontiers in pharmacology · 2020Pooled it
- Bradykinin's carbamylation as a mechanistic link to impaired wound healing in patients with kidney dysfunction.BMC biology · 2025Article
- A comprehensive review on current understanding of bradykinin in COVID-19 and inflammatory diseases.Molecular biology reports · 2022Review
- Angiotensin-Converting Enzyme Inhibitor Protects Against Cisplatin Nephrotoxicity by Modulating Kinin B1 Receptor Expression and Aminopeptidase P Activity in Mice.Frontiers in molecular biosciences · 2020Article
- Kinins in Glioblastoma Microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2019Article
- Interactions between carboxypeptidase M and kinin B1 receptor in endothelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- The kinin BInflammopharmacology · 2019Article
- HAE Pathophysiology and Underlying Mechanisms.Clinical reviews in allergy & immunology · 2016Review
- Optical probes based on G protein-coupled receptors - added work or added value?British journal of pharmacology · 2016Review
- Downregulation of kinin B1 receptor function by B2 receptor heterodimerization and signaling.Cellular signalling · 2015Article
- Carboxypeptidase M is a positive allosteric modulator of the kinin B1 receptor.The Journal of biological chemistry · 2013Article
- ACE inhibition enhances bradykinin relaxations through nitric oxide and B1 receptor activation in bovine coronary arteries.Biological chemistry · 2013Article
- Carboxypeptidase M augments kinin B1 receptor signaling by conformational crosstalk and enhances endothelial nitric oxide output.Biological chemistry · 2013Review
- Endothelial nitric-oxide synthase activation generates an inducible nitric-oxide synthase-like output of nitric oxide in inflamed endothelium.The Journal of biological chemistry · 2013Article
- Characterization of dual agonists for kinin B1 and B2 receptors and their biased activation of B2 receptors.Cellular signalling · 2012Article
- Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms.Progress in neurobiologyReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
G protein-coupled receptor (GPCR) signaling is affected by formation of GPCR homo- or heterodimers, but GPCR regulation by other cell surface proteins is not well understood. We reported that the kinin B1 receptor (B1R) heterodimerizes with membrane carboxypeptidase M (CPM), facilitating receptor signaling via CPM-mediated conversion of bradykinin or kallidin to des-Arg kinin B1R agonists. Here, we found that a catalytically inactive CPM mutant that still binds substrate (CPM-E264Q) also facilitates efficient B1R signaling by B2 receptor agonists bradykinin or kallidin. This response required co-expression of B1R and CPM-E264Q in the same cell, was disrupted by antibody that dissociates CPM from B1R, and was not found with a CPM-E264Q-B1R fusion protein. An additional mutation that reduced the affinity of CPM for C-terminal Arg and increased the affinity for C-terminal Lys inhibited the B1R response to bradykinin (with C-terminal Arg) but generated a response to Lys(9)-bradykinin. CPM-E264Q-mediated activation of B1Rs by bradykinin resulted in increased intramolecular fluorescence resonance energy transfer (FRET) in a B1R FRET construct, similar to that generated directly by a B1R agonist. In cytokine-treated human lung microvascular endothelial cells, disruption of B1R-CPM heterodimers inhibited B1R-dependent NO production stimulated by bradykinin and blocked the increased endothelial permeability caused by treatment with bradykinin and pyrogallol (a superoxide generator). Thus, CPM and B1Rs on cell membranes form a critical complex that potentiates B1R signaling. Kinin peptide binding to CPM causes a conformational change in the B1R leading to intracellular signaling and reveals a new mode of GPCR activation by a cell surface peptidase.
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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.