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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
Formation of Signal Transfer Complexes between Stem Cell and Platelet-Derived Growth Factor Receptors and SH2 Domain Proteins in Vitro
TL;DR: In vitro association experiments indicate that PLC gamma and PI3'-K bind the beta PDGF-R simultaneously, while these two SH2 proteins compete for association to p145c-kit binding sites, with p85/PI3-K exhibiting higher affinity.
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90K (Mac‐2 BP) gene expression in breast cancer and evidence for the production of 90K by peripheral‐blood mononuclear cells
Ornella Fusco,Patrizia Querzoli,Italo Nenci,Clara Natoli,Cord Brakebush,Axel Ullrich,Stefano Iacobelli +6 more
TL;DR: Investigating 90K‐gene expression in peripheral‐blood mononuclear cells (PBMC) revealed higher levels of 90K message in PBMC of breast‐cancer patients than in healthy individuals, which suggests that PBMC activated in response to tumor growth and progression may be an important source of serum 90K in breast cancer.
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Inhibition of Ret oncogene activity by the protein tyrosine phosphatase SHP1.
Anita M. Hennige,Reiner Lammers,Wolfgang Höppner,Dorit Arlt,Volker Strack,Reinhard Teichmann,Fausto Machicao,Axel Ullrich,Hans-Ulrich Häring,Monika Kellerer +9 more
TL;DR: The data suggest that SHP1 caused a moderate reduction of Ret autophosphorylation, which led to a strong suppression of the Ret oncogene activity.
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Structural gene for beta-nerve growth factor not defective in familial dysautonomia
Xandra O. Breakefield,Gregory Orloff,Carmela M. Castiglione,Lisa M. Coussens,Felicia B. Axelrod,Axel Ullrich +5 more
TL;DR: This analysis excludes the beta-NGF gene region as the cause of this neurologic disease but does not eliminate other genes involved in beta- NGF action, such as those coding for processing enzymes, receptors, or other subunits of the NGF complex.
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Differential effects of W mutations on p145c-kit tyrosine kinase activity and substrate interaction.
TL;DR: The results suggest that the location of W mutations may be an important determinant of the specificity of substrate association and phosphorylation, and may explain, at least in part, the cell type-specific defects associated with certain W alleles.