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Axel Ullrich
Researcher at Max Planck Society
Publications - 436
Citations - 63142
Axel Ullrich is an academic researcher from Max Planck Society. The author has contributed to research in topics: Receptor tyrosine kinase & Tyrosine kinase. The author has an hindex of 124, co-authored 436 publications receiving 61445 citations. Previous affiliations of Axel Ullrich include Institute of Molecular and Cell Biology & Agency for Science, Technology and Research.
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Journal ArticleDOI
The E3 ligase Cbl-b and TAM receptors regulate cancer metastasis via natural killer cells
Magdalena Paolino,Axel Choidas,Stephanie Wallner,Blanka Pranjic,Iris Uribesalgo,Stefanie Loeser,Amanda M. Jamieson,Wallace Y. Langdon,Fumiyo Ikeda,Juan Pablo Fededa,Shane J. F. Cronin,Roberto Nitsch,Carsten Schultz-Fademrecht,Jan Eickhoff,Sascha Menninger,Anke Unger,Robert Torka,Thomas Gruber,Reinhard Hinterleitner,Gottfried Baier,Dominik Wolf,Axel Ullrich,Bert Klebl,Josef M. Penninger +23 more
TL;DR: This novel TAM/Cbl-b inhibitory pathway shows that it might be possible to develop a ‘pill’ that awakens the innate immune system to kill cancer metastases, and the anticoagulant warfarin exerts anti-metastatic activity in mice via Cbl- b/TAM receptors in NK cells.
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The EGF receptor as central transducer of heterologous signalling systems
TL;DR: The current state of knowledge regarding the role of epidermal growth factor (EGF) in such a network is described and the recent advances made in the elucidation of the mechanism underlying EGF receptor transactivation are discussed.
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TACE cleavage of proamphiregulin regulates GPCR‐induced proliferation and motility of cancer cells
TL;DR: Evidence is presented that blockade of the TACE by the tissue inhibitor of metalloprotease‐3, a dominant‐negative TACE mutant or RNA interference suppresses GPCR‐stimulated AR release, EGFR activation and downstream events, suggesting TACE can function as an effector of G PCR‐mediated signalling and represents a key element of the cellular receptor cross‐talk network.
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Interplay between mycobacteria and host signalling pathways.
TL;DR: This review highlights the strategies employed by mycobacteria to subvert host-cell signalling and identifies key molecules involved in these processes that might serve as potential targets for new antimycobacterial therapies.
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ERK6, a mitogen-activated protein kinase involved in C2C12 myoblast differentiation
TL;DR: These findings suggest ERK6 to be a tissue-specific, differentiation signal-transducing factor that is connected to phosphotyrosine-mediated signaling pathways distinct from those activating other members of the MAP kinase family such as LRK1 and ERK2.