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Michael Hahne

Researcher at Centre national de la recherche scientifique

Publications -  118
Citations -  14052

Michael Hahne is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: Apoptosis & Tumor necrosis factor alpha. The author has an hindex of 44, co-authored 116 publications receiving 13445 citations. Previous affiliations of Michael Hahne include University of Amsterdam & University of Lausanne.

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Inhibition of death receptor signals by cellular FLIP

Martin Irmler, +12 more
- 10 Jul 1997 - 
TL;DR: The characterization of an inhibitor of apoptosis is reported, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues and may be implicated in tissue homeostasis as an important regulator of apoptotic regulation.
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Melanoma Cell Expression of Fas(Apo-1/CD95) Ligand: Implications for Tumor Immune Escape

Michael Hahne, +11 more
- 22 Nov 1996 - 
TL;DR: In vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation and tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL.
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Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways

Bente Lowin, +3 more
- 25 Aug 1994 - 
TL;DR: Two complementary, specific cytotoxic mechanisms are functional in CTLs, one based on the secretion of lytic proteins and one which depends on cell-surface ligand–receptor interaction, which is triggered upon T-cell receptor occupancy and directed to the cognate target cell.
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Conversion of Membrane-bound Fas(CD95) Ligand to Its Soluble Form Is Associated with Downregulation of Its Proapoptotic Activity and Loss of Liver Toxicity

Pascal Schneider, +6 more
- 20 Apr 1998 - 
TL;DR: The results indicate that the mere trimerization of the Fas and TRAIL receptors may not be sufficient to trigger death signals, and the observation that sFasL is less cytotoxic than membrane-bound FasL may explain why in certain types of cancer, systemic tissue damage is not detected, even though the levels of circulating sFAsL are high.
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APRIL, a New Ligand of the Tumor Necrosis Factor Family, Stimulates Tumor Cell Growth

Michael Hahne, +12 more
- 21 Sep 1998 - 
TL;DR: A novel member of the TNF family designated APRIL (for a proliferation-inducing ligand) is described and it is suggested that APRIL may be implicated in the regulation of tumor cell growth.