D
Dieter E. Jenne
Researcher at Max Planck Society
Publications - 137
Citations - 13380
Dieter E. Jenne is an academic researcher from Max Planck Society. The author has contributed to research in topics: Proteinase 3 & Proteases. The author has an hindex of 50, co-authored 131 publications receiving 11998 citations. Previous affiliations of Dieter E. Jenne include Chugai Pharmaceutical Co..
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Journal ArticleDOI
Lifeact: a versatile marker to visualize F-actin
Julia Riedl,Alvaro H. Crevenna,Kai Kessenbrock,Jerry Haochen Yu,Dorothee Neukirchen,Michal Bista,Frank Bradke,Dieter E. Jenne,Tad A. Holak,Zena Werb,Michael Sixt,Roland Wedlich-Söldner +11 more
TL;DR: Lifeact, a 17-amino-acid peptide, is described, which stained filamentous actin (F-actin) structures in eukaryotic cells and tissues and in its chemically modified peptide form allowed visualization of actin dynamics in nontransfectable cells.
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Netting neutrophils in autoimmune small-vessel vasculitis.
Kai Kessenbrock,Markus Krumbholz,Ulf Schönermarck,Walter Back,Wolfgang Gross,Zena Werb,Hermann-Josef Gröne,Volker Brinkmann,Dieter E. Jenne +8 more
TL;DR: It is shown that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 and myeloperoxidase (MPO).
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Peutz-Jeghers syndrome is caused by mutations in a novel serine threonine kinase.
Dieter E. Jenne,Heike Reimann,J.-I. Nezu,W. Friedel,Steffan Loff,R. Jeschke,Oliver Müller,Walter Back,Michael Zimmer +8 more
TL;DR: It is concluded that germline mutations in STK11, probably in conjunction with acquired genetic defects of the second allele in somatic cells, cause the manifestations of PJ syndrome.
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Neutrophil Elastase, Proteinase 3, and Cathepsin G as Therapeutic Targets in Human Diseases
TL;DR: The physicochemical functions of hematopoietic serine proteases are described, toward a goal of better delineating their role in human diseases and identifying new therapeutic strategies based on the modulation of their bioavailability and activity.
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Induction of MHC class I genes in neurons
TL;DR: Transcription of MHC class I genes was very rare in neurons with spontaneous action potentials, and expression of beta 2-microglobulin under tighter control than in class I heavy chain molecules occurred only in electrically silent neurons treated with interferon gamma.