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Thomas Brunner

Researcher at University of Konstanz

Publications -  511
Citations -  26076

Thomas Brunner is an academic researcher from University of Konstanz. The author has contributed to research in topics: Apoptosis & Medicine. The author has an hindex of 75, co-authored 448 publications receiving 23438 citations. Previous affiliations of Thomas Brunner include University Medical Center Freiburg & University of Oxford.

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Activation-induced cell death in murine T cell hybridomas. Differential regulation of Fas (CD95) versus Fas ligand expression by cyclosporin A and FK506

Thomas Brunner, +4 more
- 01 Jul 1996 - 
TL;DR: It is concluded that CsA and FK506 block activation-induced apoptosis in T cell hybridomas predominantly by interfering with activation signals leading to FasL expression and that the regulation of the expression of Fas and FasL on activated T cells is differentially controlled.
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The nuclear receptor LRH-1 critically regulates extra-adrenal glucocorticoid synthesis in the intestine

Matthias Mueller, +7 more
- 04 Sep 2006 - 
TL;DR: It is shown here that LRH-1 promotes the expression of the steroidogenic enzymes and the synthesis of corticosterone in murine intestinal epithelial cells in vitro and is proposed as an important regulator of intestinal tissue integrity and immune homeostasis.
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Fas (CD95/Apo-1) ligand regulation in T cell homeostasis, cell-mediated cytotoxicity and immune pathology

Thomas Brunner, +5 more
- 01 Jun 2003 - 
TL;DR: In this review, various aspects of FasL regulation in cell-mediated cytotoxicity, immune homeostasis and the immunopathology of diseases are discussed.
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Human pancreatic tumor cells are sensitized to ionizing radiation by knockdown of caveolin-1.

Nils Cordes, +8 more
- 18 Oct 2007 - 
TL;DR: The data presented show, for the first time, that disruption of interactions of Cav-1 with β1-integrin or FAK affects radiation survival and proliferation of pancreatic carcinoma cells and suggest that Cav- 1 is critical to these processes.
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Stromal SPARC expression and patient survival after chemoradiation for non-resectable pancreatic adenocarcinoma.

Tine S. Mantoni, +8 more
- 01 Nov 2008 - 
TL;DR: The hypothesis of a detrimental effect of PSC on patient survival in LAPC after chemoradiation is supported by the inverse correlation of SPARC in distal stromal cells with patients survival and in vitro data indicate that paracrine SPARC from PSC increases the invasion of pancreatic cancer cells.