Michael Thiele

TL;DR: MIF can directly promote cell survival through activation of the PI3K/Akt pathway and this effect is critical for tumor cell survival.

TL;DR: A novel MIF-driven signalling pathway and an intricate regulatory system involving extra- and possibly intracellular MIF, and which likely critically participates in controlling cell proliferation and survival is unravelled.

TL;DR: Inhibition of MIF resulted in a shift in the cellular composition of neointimal plaques toward a stabilized phenotype with reduced macrophage/foam cell content and increased SMC content, which might be attributable to a reduction of monocyte recruitment mediated by endothelial MIF.

TL;DR: The findings show that Mif has potent antiapoptotic activities and suggest that MIF is a modulator of pro-oxidative stress-induced apoptosis, as well as investigating the effects of MIF on apoptosis.

TL;DR: The biochemical and biological evidence for a role of the TPOR activity for various MIF functions is summarized and discussed, and the marked functional homologies with Trx proteins, the MIF redox/MHC II link, and recent attempts to discern the intra- versus extracellular roles are dealt with.