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Josef Mautner

Researcher at Technische Universität München

Publications -  58
Citations -  6103

Josef Mautner is an academic researcher from Technische Universität München. The author has contributed to research in topics: Antigen & Epstein–Barr virus. The author has an hindex of 26, co-authored 55 publications receiving 5594 citations. Previous affiliations of Josef Mautner include Helmholtz Zentrum München.

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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Pancreatic cancers require autophagy for tumor growth

TL;DR: Inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on Autophagy.
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Blood diffusion and Th1-suppressive effects of galectin-9-containing exosomes released by Epstein-Barr virus-infected nasopharyngeal carcinoma cells.

TL;DR: Results indicate that blocking galectin-9/Tim-3 interaction in vivo might alleviate the Th1-suppressive effect of NPC exosomes and sustain antitumoral T-cell responses and thereby improve clinical efficacy of immunotherapeutic approaches against NPC.
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Effective and long-term control of EBV PTLD after transfer of peptide-selected T cells

TL;DR: A rapid and sustained reconstitution of a protective EBV-specific T-cell memory occurred after the infusion of small numbers of directly isolated EBV -specific T cells in patients with PTLD.
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Infectious Epstein-Barr Virus Lacking Major Glycoprotein BLLF1 (gp350/220) Demonstrates the Existence of Additional Viral Ligands

TL;DR: The results suggest the hypothesis that additional cellular molecules, apart from CD21, allow virus entry into these cells, indicating that viral molecules other than BLLF1 can mediate the binding of EBV to its target cells.