Transforming growth factor-beta (TGF-beta) plays an important role during the 
period of developmental cell death in the nervous system. Using the 
oligodendroglial precursor cell line OLI-neu, we have previously established an 
in vitro system to analyze TGF-beta-mediated cell death on the molecular level. 
We could show that the Krüppel-like Zn-finger transcription factor TIEG1 was 
up-regulated after TGF-beta stimulation of OLI-neu cells and mimicked TGF-beta 
effects in these cells; i.e., overexpression of TIEG1 in OLI-neu cells induced 
apoptosis as shown by apoptosis ELISA, DNA fragmentation, and caspases-3 
activation. The apoptotic pathway seemed to be initiated by repressing the 
expression of the antiapoptotic protein Bcl-XL. In contrast, the reporter 
activity of a SMAD consensus promoter was induced, whereas the promoter activity 
of the inhibitory SMAD7 was reduced, suggesting that SMAD-dependent TGF-beta 
responses, such as TGF-beta-induced apoptosis, are enhanced in the presence of 
TIEG1.