M
Monika Julia Wolf
Researcher at University of Zurich
Publications - 47
Citations - 2688
Monika Julia Wolf is an academic researcher from University of Zurich. The author has contributed to research in topics: Hemodynamics & Tumor necrosis factor alpha. The author has an hindex of 20, co-authored 44 publications receiving 2233 citations. Previous affiliations of Monika Julia Wolf include École Polytechnique Fédérale de Lausanne.
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Journal ArticleDOI
Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes
Monika Julia Wolf,Arlind Adili,Kira Piotrowitz,Zeinab Abdullah,Yannick Boege,Kerstin Stemmer,Marc Ringelhan,Nicole Simonavicius,Michèle Egger,Dirk Wohlleber,Anna Lorentzen,Claudia Einer,Sabine Schulz,Thomas Clavel,Ulrike Protzer,Christoph Thiele,Hans Zischka,Holger Moch,Matthias H. Tschöp,Alexei V. Tumanov,Dirk Haller,Kristian Unger,Michael Karin,Manfred Kopf,Percy A. Knolle,Achim Weber,Mathias Heikenwalder +26 more
TL;DR: A mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet is developed, demonstrating that distinct molecular mechanisms determine NASH and H CC development.
Journal ArticleDOI
A Lymphotoxin-Driven Pathway to Hepatocellular Carcinoma
Johannes Haybaeck,Nicolas Zeller,Monika Julia Wolf,Achim Weber,Ulrich Wagner,Michael O. Kurrer,Juliane Bremer,Giandomenica Iezzi,Rolf Graf,Pierre-Alain Clavien,Robert Thimme,Hubert E. Blum,Sergei A. Nedospasov,Kurt Zatloukal,Muhammad Ramzan,Sandra Ciesek,Thomas Pietschmann,Patrice N. Marche,Michael Karin,Manfred Kopf,Jeffrey L. Browning,Adriano Aguzzi,Mathias Heikenwalder +22 more
TL;DR: S sustained LT signaling represents a pathway involved in hepatitis-induced HCC, and in vivo LTbetaR stimulation implicates hepatocytes as the major LT-responsive liver cells, and LT betaR inhibition in LTalphabeta-transgenic mice with hepatitis suppresses HCC formation.
Journal ArticleDOI
Endothelial CCR2 Signaling Induced by Colon Carcinoma Cells Enables Extravasation via the JAK2-Stat5 and p38MAPK Pathway
Monika Julia Wolf,Alexandra Hoos,Judith Bauer,Steffen Boettcher,Markus Knust,Achim Weber,Nicole Simonavicius,Christoph Schneider,Matthias Lang,Michael Stürzl,Roland S. Croner,Andreas Konrad,Markus G. Manz,Holger Moch,Adriano Aguzzi,Geert van Loo,Manolis Pasparakis,Marco Prinz,Lubor Borsig,Mathias Heikenwalder,Mathias Heikenwalder +20 more
TL;DR: CCL2 upregulation in metastatic UICC stage IV colon carcinomas is described and it is demonstrated that tumor cell-derived CCL2 activates the CCR2(+) endothelium to increase vascular permeability in vivo.
Journal ArticleDOI
RIP3, a kinase promoting necroptotic cell death, mediates adverse remodelling after myocardial infarction
Mark Luedde,Matthias Lutz,Natalie Carter,Justyna Sosna,Christoph Jacoby,Mihael Vucur,Jérémie Gautheron,Christoph Roderburg,Nadine Borg,Florian Reisinger,Hans-Joerg Hippe,Andreas Linkermann,Monika Julia Wolf,Stefan Rose-John,Renate Lüllmann-Rauch,Dieter Adam,Ulrich Flögel,Mathias Heikenwalder,Tom Luedde,Norbert Frey +19 more
TL;DR: It is shown that RIP3-dependent necroptosis modulates post-ischaemic adverse remodelling in a mouse model of MI, and this novel signalling pathway may be an attractive target for future therapies that aim to limit the adverse consequences of myocardial ischaemia.
Journal ArticleDOI
TAK1 suppresses a NEMO-dependent but NF-kappaB-independent pathway to liver cancer.
Kira Bettermann,Mihael Vucur,Johannes Haybaeck,Christiane Koppe,Jörn Janssen,Felix Heymann,Achim Weber,Ralf Weiskirchen,Christian Liedtke,Nikolaus Gassler,Michael Müller,Rita Vos,Monika Julia Wolf,Yannick Boege,Gitta Maria Seleznik,Nicolas Zeller,Daniel Erny,Thomas J. Fuchs,Stefan Zoller,Stefano Cairo,Marie-Annick Buendia,Marco Prinz,Shizuo Akira,Frank Tacke,Mathias Heikenwalder,Christian Trautwein,Tom Luedde +26 more
TL;DR: Conditional ablation of TAK1 in liver parenchymal cells causes hepatocyte dysplasia and early-onset hepatocarcinogenesis, coinciding with biliary ductopenia and cholestasis and serves as a gatekeeper for a protumorigenic, NF-kappaB-independent function of NEMO in parenChymal liver cells.