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  1. AU="van der Stoel, Miesje M"
  2. AU="Hifumi, Toru"
  3. AU="Jie Chen"
  4. AU="Ballarin, Barbara"
  5. AU="Thiel, Nadine"
  6. AU="Gerti Pishtari"
  7. AU="Alexander Hammers, ProfPhD"
  8. AU="Dessimoz, Christophe"
  9. AU="Planchuelo-Gómez, Álvaro"
  10. AU="McKay, Lindsay G A"
  11. AU="Laude, Marie-Charlotte"
  12. AU="Hale, Lillian V A"
  13. AU="Hassan Hartman"
  14. AU="Song, Mengwei"
  15. AU="Yimin Geng"
  16. AU="Wang, Chang-Sheng"
  17. AU="Doyle, Andrew D"
  18. AU="Redpath, Sophie H A"
  19. AU="Hopman, Maria Te"
  20. AU="Pomputius, William"
  21. AU="Agrawal, Sonali"
  22. AU="Martinez, Luis R"
  23. AU="Passoni, Lorena"
  24. AU="Slimani, Wafa"
  25. AU="Jin, J"
  26. AU="Xia, Hongmin"
  27. AU="Akdemir, İrem"
  28. AU=Ciccone Giovannino

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  1. Artikel ; Online: Vinculin strengthens the endothelial barrier during vascular development.

    van der Stoel, Miesje M / Kotini, Maria P / Schoon, Rianne M / Affolter, Markus / Belting, Heinz-Georg / Huveneers, Stephan

    Vascular biology (Bristol, England)

    2023  Band 5, Heft 1

    Abstract: Remodelling of cell-cell junctions is crucial for proper tissue development and barrier function. The cadherin-based adherens junctions anchor via β-catenin and α-catenin to the actomyosin cytoskeleton, together forming a junctional mechanotransduction ... ...

    Abstract Remodelling of cell-cell junctions is crucial for proper tissue development and barrier function. The cadherin-based adherens junctions anchor via β-catenin and α-catenin to the actomyosin cytoskeleton, together forming a junctional mechanotransduction complex. Tension-induced conformational changes in the mechanosensitive α-catenin protein induce junctional vinculin recruitment. In endothelial cells, vinculin protects the remodelling of VE-cadherin junctions. In this study, we have addressed the role of vinculin in endothelial barrier function in the developing vasculature. In vitro experiments, using endothelial cells in which α-catenin was replaced by a vinculin-binding-deficient mutant, showed that junctional recruitment of vinculin promotes endothelial barrier function. To assess the role of vinculin within blood vessels in vivo, we next investigated barrier function in the vasculature of vcl knockout zebrafish. In the absence of vinculin, sprouting angiogenesis and vessel perfusion still occurred. Intriguingly, the absence of vinculin made the blood vessels more permeable for 10 kDa dextran molecules but not for larger tracers. Taken together, our findings demonstrate that vinculin strengthens the endothelial barrier and prevents vascular leakage in developing vessels.
    Sprache Englisch
    Erscheinungsdatum 2023-01-27
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 2516-5658
    ISSN (online) 2516-5658
    DOI 10.1530/VB-22-0012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: DLC1 promotes mechanotransductive feedback for YAP via RhoGAP-mediated focal adhesion turnover.

    Hooglugt, Aukie / van der Stoel, Miesje M / Shapeti, Apeksha / Neep, Beau F / de Haan, Annett / van Oosterwyck, Hans / Boon, Reinier A / Huveneers, Stephan

    Journal of cell science

    2024  Band 137, Heft 8

    Abstract: Angiogenesis is a tightly controlled dynamic process demanding a delicate equilibrium between pro-angiogenic signals and factors that promote vascular stability. The spatiotemporal activation of the transcriptional co-factors YAP (herein referring to ... ...

    Abstract Angiogenesis is a tightly controlled dynamic process demanding a delicate equilibrium between pro-angiogenic signals and factors that promote vascular stability. The spatiotemporal activation of the transcriptional co-factors YAP (herein referring to YAP1) and TAZ (also known WWTR1), collectively denoted YAP/TAZ, is crucial to allow for efficient collective endothelial migration in angiogenesis. The focal adhesion protein deleted-in-liver-cancer-1 (DLC1) was recently described as a transcriptional downstream target of YAP/TAZ in endothelial cells. In this study, we uncover a negative feedback loop between DLC1 expression and YAP activity during collective migration and sprouting angiogenesis. In particular, our study demonstrates that signaling via the RhoGAP domain of DLC1 reduces nuclear localization of YAP and its transcriptional activity. Moreover, the RhoGAP activity of DLC1 is essential for YAP-mediated cellular processes, including the regulation of focal adhesion turnover, traction forces, and sprouting angiogenesis. We show that DLC1 restricts intracellular cytoskeletal tension by inhibiting Rho signaling at the basal adhesion plane, consequently reducing nuclear YAP localization. Collectively, these findings underscore the significance of DLC1 expression levels and its function in mitigating intracellular tension as a pivotal mechanotransductive feedback mechanism that finely tunes YAP activity throughout the process of sprouting angiogenesis.
    Mesh-Begriff(e) Animals ; Humans ; Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/genetics ; Cell Cycle Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Movement ; Feedback, Physiological ; Focal Adhesions/metabolism ; Focal Adhesions/genetics ; GTPase-Activating Proteins/metabolism ; GTPase-Activating Proteins/genetics ; Human Umbilical Vein Endothelial Cells/metabolism ; Mechanotransduction, Cellular/genetics ; Neovascularization, Physiologic ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/genetics ; YAP-Signaling Proteins/metabolism
    Chemische Substanzen Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; DLC1 protein, human ; GTPase-Activating Proteins ; rho GTPase-activating protein ; Tumor Suppressor Proteins ; YAP-Signaling Proteins ; YAP1 protein, human
    Sprache Englisch
    Erscheinungsdatum 2024-04-30
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.261687
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: Endothelial YAP/TAZ Signaling in Angiogenesis and Tumor Vasculature.

    Hooglugt, Aukie / van der Stoel, Miesje M / Boon, Reinier A / Huveneers, Stephan

    Frontiers in oncology

    2021  Band 10, Seite(n) 612802

    Abstract: Solid tumors are dependent on vascularization for their growth. The hypoxic, stiff, and pro-angiogenic tumor microenvironment induces angiogenesis, giving rise to an immature, proliferative, and permeable vasculature. The tumor vessels promote tumor ... ...

    Abstract Solid tumors are dependent on vascularization for their growth. The hypoxic, stiff, and pro-angiogenic tumor microenvironment induces angiogenesis, giving rise to an immature, proliferative, and permeable vasculature. The tumor vessels promote tumor metastasis and complicate delivery of anti-cancer therapies. In many types of tumors, YAP/TAZ activation is correlated with increased levels of angiogenesis. In addition, endothelial YAP/TAZ activation is important for the formation of new blood and lymphatic vessels during development. Oncogenic activation of YAP/TAZ in tumor cell growth and invasion has been studied in great detail, however the role of YAP/TAZ within the tumor endothelium remains insufficiently understood, which complicates therapeutic strategies aimed at targeting YAP/TAZ in cancer. Here, we overview the upstream signals from the tumor microenvironment that control endothelial YAP/TAZ activation and explore the role of their downstream targets in driving tumor angiogenesis. We further discuss the potential for anti-cancer treatments and vascular normalization strategies to improve tumor therapies.
    Sprache Englisch
    Erscheinungsdatum 2021-02-04
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2020.612802
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Early adipogenesis is repressed through the newly identified FHL2-NFAT5 signaling complex.

    Clemente-Olivo, Maria P / Hernández-Quiles, Miguel / Sparrius, Rinske / van der Stoel, Miesje M / Janssen, Vera / Habibe, Jayron J / van den Burg, Janny / Jongejan, Aldo / Alcaraz-Sobrevals, Paula / van Es, Robert / Vos, Harmjan / Kalkhoven, Eric / de Vries, Carlie J M

    Cellular signalling

    2023  Band 104, Seite(n) 110587

    Abstract: The LIM-domain-only protein FHL2 is a modulator of signal transduction and has been shown to direct the differentiation of mesenchymal stem cells towards osteoblast and myocyte phenotypes. We hypothesized that FHL2 may simultaneously interfere with the ... ...

    Abstract The LIM-domain-only protein FHL2 is a modulator of signal transduction and has been shown to direct the differentiation of mesenchymal stem cells towards osteoblast and myocyte phenotypes. We hypothesized that FHL2 may simultaneously interfere with the induction of the adipocyte lineage. Therefore, we investigated the role of FHL2 in adipocyte differentiation. For these studies pre-adipocytes isolated from mouse adipose tissue and the 3T3-L1 (pre)adipocyte cell line were applied. We performed FHL2 gain of function and knockdown experiments followed by extensive RNAseq analyses and phenotypic characterization of the cells by oil-red O (ORO) lipid staining. Through affinity-purification mass spectrometry (AP-MS) novel FHL2 interacting proteins were identified. Here we report that FHL2 is expressed in pre-adipocytes and for accurate adipocyte differentiation, this protein needs to be downregulated during the early stages of adipogenesis. More specifically, constitutive overexpression of FHL2 drastically inhibits adipocyte differentiation in 3T3-L1 cells, which was demonstrated by suppressed activation of the adipogenic gene expression program as shown by RNAseq analyses, and diminished lipid accumulation. Analysis of the protein-protein interactions mediating this repressive activity of FHL2 on adipogenesis revealed the interaction of FHL2 with the Nuclear factor of activated T-cells 5 (NFAT5). NFAT5 is an established inhibitor of adipocyte differentiation and its knockdown rescued the inhibitory effect of FHL2 overexpression on 3T3-L1 differentiation, indicating that these proteins act cooperatively. We present a new regulatory function of FHL2 in early adipocyte differentiation and revealed that FHL2-mediated inhibition of pre-adipocyte differentiation is dependent on its interaction with NFAT5. FHL2 expression increases with aging, which may affect mesenchymal stem cell differentiation, more specifically inhibit adipocyte differentiation.
    Mesh-Begriff(e) Mice ; Animals ; Adipogenesis/genetics ; Cell Differentiation ; Adipocytes/metabolism ; Signal Transduction ; Lipids ; 3T3-L1 Cells ; Transcription Factors/metabolism ; Muscle Proteins/metabolism ; LIM-Homeodomain Proteins/genetics ; LIM-Homeodomain Proteins/metabolism ; LIM-Homeodomain Proteins/pharmacology
    Chemische Substanzen Lipids ; Nfat5 protein, mouse ; Transcription Factors ; Fhl2 protein, mouse ; Muscle Proteins ; LIM-Homeodomain Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-01-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2023.110587
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 2579: Hefte anzeigen Standort:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Artikel ; Online: Vinculin controls endothelial cell junction dynamics during vascular lumen formation.

    Kotini, Maria P / van der Stoel, Miesje M / Yin, Jianmin / Han, Mitchell K / Kirchmaier, Bettina / de Rooij, Johan / Affolter, Markus / Huveneers, Stephan / Belting, Heinz-Georg

    Cell reports

    2022  Band 39, Heft 2, Seite(n) 110658

    Abstract: Blood vessel morphogenesis is driven by coordinated endothelial cell behaviors. Active remodeling of cell-cell junctions promotes cellular plasticity while preserving vascular integrity. Here, we analyze the dynamics of endothelial adherens junctions ... ...

    Abstract Blood vessel morphogenesis is driven by coordinated endothelial cell behaviors. Active remodeling of cell-cell junctions promotes cellular plasticity while preserving vascular integrity. Here, we analyze the dynamics of endothelial adherens junctions during lumen formation in angiogenic sprouts in vivo. Live imaging in zebrafish reveals that lumen expansion is accompanied by the formation of transient finger-shaped junctions. Junctional fingers are positively regulated by blood pressure, whereas flow inhibition prevents their formation. Using fluorescent reporters, we show that junctional fingers contain the mechanotransduction protein vinculin. Furthermore, genetic deletion of vinculin prevents finger formation, a junctional defect that could be rescued by transient endothelial expression of vinculin. Our findings suggest a mechanism whereby lumen expansion leads to an increase in junctional tension, triggering recruitment of vinculin and formation of junctional fingers. We propose that endothelial cells employ force-dependent junctional remodeling to counteract external forces in order to maintain vascular integrity during sprouting angiogenesis.
    Mesh-Begriff(e) Adherens Junctions/metabolism ; Animals ; Cadherins/metabolism ; Endothelial Cells/metabolism ; Intercellular Junctions/metabolism ; Mechanotransduction, Cellular ; Neovascularization, Physiologic ; Vinculin/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins/metabolism
    Chemische Substanzen Cadherins ; Zebrafish Proteins ; Vinculin (125361-02-6)
    Sprache Englisch
    Erscheinungsdatum 2022-04-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110658
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis.

    Malinova, Tsveta S / Angulo-Urarte, Ana / Nüchel, Julian / Tauber, Marina / van der Stoel, Miesje M / Janssen, Vera / de Haan, Annett / Groenen, Anouk G / Tebbens, Merel / Graupera, Mariona / Plomann, Markus / Huveneers, Stephan

    Nature communications

    2021  Band 12, Heft 1, Seite(n) 2610

    Abstract: Angiogenic sprouting relies on collective migration and coordinated rearrangements of endothelial leader and follower cells. VE-cadherin-based adherens junctions have emerged as key cell-cell contacts that transmit forces between cells and trigger ... ...

    Abstract Angiogenic sprouting relies on collective migration and coordinated rearrangements of endothelial leader and follower cells. VE-cadherin-based adherens junctions have emerged as key cell-cell contacts that transmit forces between cells and trigger signals during collective cell migration in angiogenesis. However, the underlying molecular mechanisms that govern these processes and their functional importance for vascular development still remain unknown. We previously showed that the F-BAR protein PACSIN2 is recruited to tensile asymmetric adherens junctions between leader and follower cells. Here we report that PACSIN2 mediates the formation of endothelial sprouts during angiogenesis by coordinating collective migration. We show that PACSIN2 recruits the trafficking regulators EHD4 and MICAL-L1 to the rear end of asymmetric adherens junctions to form a recycling endosome-like tubular structure. The junctional PACSIN2/EHD4/MICAL-L1 complex controls local VE-cadherin trafficking and thereby coordinates polarized endothelial migration and angiogenesis. Our findings reveal a molecular event at force-dependent asymmetric adherens junctions that occurs during the tug-of-war between endothelial leader and follower cells, and allows for junction-based guidance during collective migration in angiogenesis.
    Sprache Englisch
    Erscheinungsdatum 2021-05-10
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-22873-y
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  7. Artikel ; Online: Disentangling mechanisms involved in collagen pyridinoline cross-linking: The immunophilin FKBP65 is critical for dimerization of lysyl hydroxylase 2.

    Gjaltema, Rutger A F / van der Stoel, Miesje M / Boersema, Miriam / Bank, Ruud A

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

    2016  Band 113, Heft 26, Seite(n) 7142–7147

    Abstract: Collagens are subjected to extensive posttranslational modifications, such as lysine hydroxylation. Bruck syndrome (BS) is a connective tissue disorder characterized at the molecular level by a loss of telopeptide lysine hydroxylation, resulting in ... ...

    Abstract Collagens are subjected to extensive posttranslational modifications, such as lysine hydroxylation. Bruck syndrome (BS) is a connective tissue disorder characterized at the molecular level by a loss of telopeptide lysine hydroxylation, resulting in reduced collagen pyridinoline cross-linking. BS results from mutations in the genes coding for lysyl hydroxylase (LH) 2 or peptidyl-prolyl cis-trans isomerase (PPIase) FKBP65. Given that the immunophilin FKBP65 does not exhibit LH activity, it is likely that LH2 activity is somehow dependent on FKPB65. In this report, we provide insights regarding the interplay between LH2 and FKBP65. We found that FKBP65 forms complexes with LH2 splice variants LH2A and LH2B but not with LH1 and LH3. Ablating the catalytic activity of FKBP65 or LH2 did not affect complex formation. Both depletion of FKBP65 and inhibition of FKBP65 PPIase activity reduced the dimeric (active) form of LH2 but did not affect the binding of monomeric (inactive) LH2 to procollagen Iα1. Furthermore, we show that LH2A and LH2B cannot form heterodimers with each other but are able to form heterodimers with LH1 and LH3. Collectively, our results indicate that FKBP65 is linked to pyridinoline cross-linking by specifically mediating the dimerization of LH2. Moreover, FKBP65 does not interact with LH1 and LH3, explaining why in BS triple-helical hydroxylysines are not affected. Our results provide a mechanistic link between FKBP65 and the loss of pyridinolines and may hold the key to future treatments for diseases related to collagen cross-linking anomalies, such as fibrosis and cancer.
    Mesh-Begriff(e) Amino Acids/chemistry ; Amino Acids/metabolism ; Arthrogryposis/enzymology ; Arthrogryposis/genetics ; Arthrogryposis/metabolism ; Collagen/chemistry ; Collagen/genetics ; Collagen/metabolism ; Collagen Type I/chemistry ; Collagen Type I/genetics ; Collagen Type I/metabolism ; Cross-Linking Reagents/chemistry ; Dimerization ; Humans ; Osteogenesis Imperfecta/enzymology ; Osteogenesis Imperfecta/genetics ; Osteogenesis Imperfecta/metabolism ; Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase/genetics ; Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase/metabolism ; Protein Binding ; Protein Processing, Post-Translational ; Tacrolimus Binding Proteins/genetics ; Tacrolimus Binding Proteins/metabolism
    Chemische Substanzen Amino Acids ; Collagen Type I ; Cross-Linking Reagents ; collagen type I, alpha 1 chain ; pyridinoline (63800-01-1) ; Collagen (9007-34-5) ; PLOD2 protein, human (EC 1.14.11.4) ; Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase (EC 1.14.11.4) ; Tacrolimus Binding Proteins (EC 5.2.1.-) ; FKBP10 protein, human (EC 5.2.1.8)
    Sprache Englisch
    Erscheinungsdatum 2016--28
    Erscheinungsland United States
    Dokumenttyp 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.1600074113
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  8. Artikel ; Online: Microembolus clearance through angiophagy is an auxiliary mechanism preserving tissue perfusion in the rat brain.

    van der Wijk, Anne-Eva / Georgakopoulou, Theodosia / Majolée, Jisca / van Bezu, Jan S M / van der Stoel, Miesje M / van Het Hof, Bert J / de Vries, Helga E / Huveneers, Stephan / Hordijk, Peter L / Bakker, Erik N T P / van Bavel, Ed

    Acta neuropathologica communications

    2020  Band 8, Heft 1, Seite(n) 195

    Abstract: Considering its intolerance to ischemia, it is of critical importance for the brain to efficiently process microvascular occlusions and maintain tissue perfusion. In addition to collateral microvascular flow and enzymatic degradation of emboli, the ... ...

    Abstract Considering its intolerance to ischemia, it is of critical importance for the brain to efficiently process microvascular occlusions and maintain tissue perfusion. In addition to collateral microvascular flow and enzymatic degradation of emboli, the endothelium has the potential to engulf microparticles and thereby recanalize the vessel, through a process called angiophagy. Here, we set out to study the dynamics of angiophagy in relation to cytoskeletal remodeling in vitro and reperfusion in vivo. We show that polystyrene microspheres and fibrin clots are actively taken up by (brain) endothelial cells in vitro, and chart the dynamics of the actin cytoskeleton during this process using live cell imaging. Whereas microspheres were taken up through the formation of a cup structure by the apical endothelial membrane, fibrin clots were completely engulfed by the cells, marked by dense F-actin accumulation surrounding the clot. Both microspheres and fibrin clots were retained in the endothelial cells. Notably, fibrin clots were not degraded intracellularly. Using an in vivo microembolization rat model, in which microparticles are injected into the common carotid artery, we found that microspheres are transported by the endothelium from the microvasculature into the brain parenchyma. Microembolization with microspheres caused temporal opening of the blood-brain barrier and vascular nonperfusion, followed by microsphere extravasation and restoration of vessel perfusion over time. Taken together, angiophagy is accompanied by active cytoskeletal remodeling of the endothelium, and is an effective mechanism to restore perfusion of the occluded microvasculature in vivo.
    Mesh-Begriff(e) Animals ; Brain ; Cerebrovascular Circulation ; Endothelial Cells/pathology ; Endothelial Cells/physiology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiology ; Female ; Human Umbilical Vein Endothelial Cells/pathology ; Human Umbilical Vein Endothelial Cells/physiology ; Humans ; Intracranial Embolism/pathology ; Male ; Microspheres ; Microvessels/pathology ; Microvessels/physiology ; Phagocytosis/physiology ; Rats ; Thrombosis
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2020-11-17
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-020-01071-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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