Publications by authors named "M J Canals"

Knowledge about seafloor depth, or bathymetry, is crucial for various marine activities, including scientific research, offshore industry, safety of navigation, and ocean exploration. Mapping the central Arctic Ocean is challenging due to the presence of perennial sea ice, which limits data collection to icebreakers, submarines, and drifting ice stations. The International Bathymetric Chart of the Arctic Ocean (IBCAO) was initiated in 1997 with the goal of updating the Arctic Ocean bathymetric portrayal.

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The formyl-peptide receptor 2 (FPR2) is a G-protein-coupled receptor that responds to pathogen-derived peptides and regulates both proinflammatory and proresolution cellular processes. While ligand selectivity and G-protein signaling of FPR2 have been well characterized, molecular mechanisms controlling subsequent events such as endocytosis and recycling to the plasma membrane are less understood. Here, we show the key role of the G-protein-coupled receptor kinase 5 (GRK5) in facilitating FPR2 endocytosis and postendocytic trafficking.

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  • - The study explores how mu-opioid receptors (MORs) interact with neuroinflammation and glial cells, revealing a complex, bidirectional relationship rather than a straightforward immunosuppression effect.
  • - Researchers found that activated microglia and certain proinflammatory cytokines boost neuronal MOR expression and enhance activation in response to the opioid DAMGO.
  • - The results suggest a feedback loop where microglial activation and cytokine release influence neuronal MOR dynamics, indicating a need for further investigation into the implications for opioid use in pain management.
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  • The chemokine CCL18 attracts T cells and is elevated in inflammatory diseases, but its receptor is not yet confirmed.
  • Experiments showed that CCR8-expressing mouse cells responded to the ligand CCL1, but not to CCL18, which suggests CCR8 isn’t the receptor for CCL18.
  • Additionally, CCL18 was found to inhibit migration through another receptor, CCR3, reinforcing the idea that CCR8 does not effectively bind CCL18 without additional factors.
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