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  1. Article ; Online: CCR3-dependent eosinophil recruitment is regulated by sialyltransferase ST3Gal-IV.

    Immler, Roland / Nussbaumer, Katrin / Doerner, Axel / El Bounkari, Omar / Huber, Silke / Abisch, Janine / Napoli, Matteo / Schmidt, Sarah / Margraf, Andreas / Pruenster, Monika / Rohwedder, Ina / Lange-Sperandio, Baerbel / Mall, Marcus A / de Jong, Renske / Ohnmacht, Caspar / Bernhagen, Juergen / Voehringer, David / Marth, Jamey D / Frommhold, David /
    Sperandio, Markus

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Volume 121, Issue 19, Page(s) e2319057121

    Abstract: Eosinophil recruitment is a pathological hallmark of many allergic and helminthic diseases. Here, we investigated chemokine receptor CCR3-induced eosinophil recruitment in ... ...

    Abstract Eosinophil recruitment is a pathological hallmark of many allergic and helminthic diseases. Here, we investigated chemokine receptor CCR3-induced eosinophil recruitment in sialyltransferase
    MeSH term(s) Animals ; Receptors, CCR3/metabolism ; Receptors, CCR3/genetics ; Sialyltransferases/metabolism ; Sialyltransferases/genetics ; Eosinophils/metabolism ; Eosinophils/immunology ; Mice ; beta-Galactoside alpha-2,3-Sialyltransferase ; Mice, Knockout ; Chemokine CCL11/metabolism ; Mice, Inbred C57BL ; Ovalbumin/immunology ; Bronchoalveolar Lavage Fluid
    Chemical Substances Receptors, CCR3 ; Sialyltransferases (EC 2.4.99.-) ; beta-Galactoside alpha-2,3-Sialyltransferase (EC 2.4.99.4) ; Ccr3 protein, mouse ; Chemokine CCL11 ; Ccl11 protein, mouse ; Ovalbumin (9006-59-1)
    Language English
    Publishing date 2024-04-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2319057121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: E-selectin-mediated rapid NLRP3 inflammasome activation regulates S100A8/S100A9 release from neutrophils via transient gasdermin D pore formation.

    Pruenster, Monika / Immler, Roland / Roth, Jonas / Kuchler, Tim / Bromberger, Thomas / Napoli, Matteo / Nussbaumer, Katrin / Rohwedder, Ina / Wackerbarth, Lou Martha / Piantoni, Chiara / Hennis, Konstantin / Fink, Diana / Kallabis, Sebastian / Schroll, Tobias / Masgrau-Alsina, Sergi / Budke, Agnes / Liu, Wang / Vestweber, Dietmar / Wahl-Schott, Christian /
    Roth, Johannes / Meissner, Felix / Moser, Markus / Vogl, Thomas / Hornung, Veit / Broz, Petr / Sperandio, Markus

    Nature immunology

    2023  Volume 24, Issue 12, Page(s) 2021–2031

    Abstract: S100A8/S100A9 is a proinflammatory mediator released by myeloid cells during many acute and chronic inflammatory disorders. However, the precise mechanism of its release from the cytosolic compartment of neutrophils is unclear. Here, we show that E- ... ...

    Abstract S100A8/S100A9 is a proinflammatory mediator released by myeloid cells during many acute and chronic inflammatory disorders. However, the precise mechanism of its release from the cytosolic compartment of neutrophils is unclear. Here, we show that E-selectin-induced rapid S100A8/S100A9 release during inflammation occurs in an NLRP3 inflammasome-dependent fashion. Mechanistically, E-selectin engagement triggers Bruton's tyrosine kinase-dependent tyrosine phosphorylation of NLRP3. Concomitant potassium efflux via the voltage-gated potassium channel K
    MeSH term(s) Humans ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Gasdermins ; Neutrophils/metabolism ; E-Selectin/metabolism ; Calgranulin A/metabolism ; Calgranulin B/metabolism ; Inflammation/metabolism
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Gasdermins ; E-Selectin ; Calgranulin A ; Calgranulin B
    Language English
    Publishing date 2023-10-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01656-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 42: Show issues

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  3. Article ; Online: NOS inhibition reverses TLR2-induced chondrocyte dysfunction and attenuates age-related osteoarthritis.

    Shen, Ping / Serve, Sebastian / Wu, Peihua / Liu, Xiaohui / Dai, Yujie / Durán-Hernández, Nayar / Nguyen, Dan Thi Mai / Fuchs, Michael / Maleitzke, Tazio / Reisener, Marie-Jacqueline / Dzamukova, Maria / Nussbaumer, Katrin / Brunner, Tobias M / Li, Yonghai / Holecska, Vivien / Heinz, Gitta A / Heinrich, Frederik / Durek, Pawel / Katsoula, Georgia /
    Gwinner, Clemens / Jung, Tobias / Zeggini, Eleftheria / Winkler, Tobias / Mashreghi, Mir-Farzin / Pumberger, Matthias / Perka, Carsten / Löhning, Max

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 29, Page(s) e2207993120

    Abstract: Osteoarthritis (OA) is a joint disease featuring cartilage breakdown and chronic pain. Although age and joint trauma are prominently associated with OA occurrence, the trigger and signaling pathways propagating their pathogenic aspects are ill defined. ... ...

    Abstract Osteoarthritis (OA) is a joint disease featuring cartilage breakdown and chronic pain. Although age and joint trauma are prominently associated with OA occurrence, the trigger and signaling pathways propagating their pathogenic aspects are ill defined. Following long-term catabolic activity and traumatic cartilage breakdown, debris accumulates and can trigger Toll-like receptors (TLRs). Here we show that TLR2 stimulation suppressed the expression of matrix proteins and induced an inflammatory phenotype in human chondrocytes. Further, TLR2 stimulation impaired chondrocyte mitochondrial function, resulting in severely reduced adenosine triphosphate (ATP) production. RNA-sequencing analysis revealed that TLR2 stimulation upregulated nitric oxide synthase 2 (
    MeSH term(s) Humans ; Mice ; Animals ; Chondrocytes/metabolism ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism ; Osteoarthritis/metabolism ; Toll-Like Receptors/metabolism ; Cartilage, Articular/metabolism ; Cells, Cultured
    Chemical Substances Toll-Like Receptor 2 ; Toll-Like Receptors ; TLR2 protein, human
    Language English
    Publishing date 2023-07-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2207993120
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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