Subcellular hot spots of GPCR signaling promote vascular inflammation
© 2020 Published by Elsevier Ltd..
G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes, and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFκB activation mediated by β-arrestins and CARMA-BCL10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-β-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:16 |
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| Enthalten in: |
Current opinion in endocrine and metabolic research - 16(2021) vom: 10. Feb., Seite 37-42 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Birch, Cierra A [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Revised 17.03.2021 published: Print-Electronic Citation Status PubMed-not-MEDLINE |
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| doi: |
10.1016/j.coemr.2020.07.011 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM314114963 |
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| 520 | |a G-coupled protein receptors (GPCRs) comprise the largest class of druggable targets. Signaling by GPCRs is initiated from subcellular hot spots including the plasma membrane, signalosomes, and endosomes to contribute to vascular inflammation. GPCR-G protein signaling at the plasma membrane causes endothelial barrier disruption and also cross-talks with growth factor receptors to promote proinflammatory signaling. A second surge of GPCR signaling is initiated by cytoplasmic NFκB activation mediated by β-arrestins and CARMA-BCL10-MALT1 signalosomes. Once internalized, ubiquitinated GPCRs initiate signaling from endosomes via assembly of the transforming growth factor-β-activated kinase binding protein-1 (TAB1)-TAB2-p38 MAPK complex to promote vascular inflammation. Understanding the complexities of GPCR signaling is critical for development of new strategies to treat vascular inflammation such as that associated with COVID-19 | ||
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| 650 | 4 | |a Endosomes | |
| 650 | 4 | |a Endothelial | |
| 650 | 4 | |a G protein-coupled receptor, GPCR | |
| 650 | 4 | |a JAK-STAT | |
| 650 | 4 | |a Janus kinase, JAK | |
| 650 | 4 | |a MALT1 | |
| 650 | 4 | |a NFκB | |
| 650 | 4 | |a adherens junctions, AJ | |
| 650 | 4 | |a angiotensin II type 1 receptor, AT1 | |
| 650 | 4 | |a angiotensin converting enzyme-2, ACE2 | |
| 650 | 4 | |a caspase recruitment domain-containing protein, CARMA | |
| 650 | 4 | |a coronavirus disease of 2019, COVID-19 | |
| 650 | 4 | |a fibroblast-growth-factor, FGF | |
| 650 | 4 | |a inhibitor of NFκB kinase, IKK | |
| 650 | 4 | |a mitogen-activated protein kinase, MAPK | |
| 650 | 4 | |a mucosa-associated lymphoid tissue lymphoma translocation protein 1, (MALT1) | |
| 650 | 4 | |a neural precursor cell expressed developmentally downregulated protein 4, NEDD4 | |
| 650 | 4 | |a nuclear factor kappa-light-chain-enhancer of activated B cells, NFκB | |
| 650 | 4 | |a p38 MAPK | |
| 650 | 4 | |a platelet activating factor, PAF | |
| 650 | 4 | |a protease-activated receptor-1, PAR1 | |
| 650 | 4 | |a severe acute respiratory syndrome coronavirus 2, SARS-CoV-2 | |
| 650 | 4 | |a signal transducer and activator of transcription, STAT | |
| 650 | 4 | |a transforming growth factor-α-activated kinase binding protein-1, TAB1 | |
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| 700 | 1 | |a Trejo, JoAnn |e verfasserin |4 aut | |
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