Figure 2 | Cell Death & Disease

Figure 2

From: TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease

Figure 2

TIAF1 self-binding leads to apoptosis. (a) TGF-β-sensitive mink lung Mv1Lu epithelial cells, overexpressing ECFP/EYFP, ECFP-TIAF1/EYFP-TIAF1 or EYFP-TIAF1(E22/23A), were exposed to TGF-β1 (5 ng/ml). Time-lapse microscopy was carried out (total 8 h; one picture taken per 5 min). TGF-β1 rapidly induced apoptosis of TIAF1/TIAF1-expressing cells, but not ECFP/EYFP-expressing cells, in 1 h. No apoptosis was observed in cells overexpressing a dominant-negative TIAF1(E22/23A) or in non-transfected cells. (b) Human neuroblastoma SK-N-SH cells overexpressing TIAF1/TIAF1 were sensitive to UV light-induced apoptosis, but ECFP/EYFP-overexpressing cells were resistant. (c) Human TβRII-deficient colon HCT116 cells, overexpressing TIAF1/TIAF1, were treated with TGF-β1 (5 ng/ml) and imaged by time-lapse FRET microscopy. TGF-β1 significantly increased the self-binding of TIAF1/TIAF1 (left panel). When the binding reached a maximal strength (measured as FRETc),14 the cell underwent apoptosis (left panel). When cells were co-transfected with TIAF1 and Smad4, apoptosis was blocked (right panel). The expression of Smad4 was optimized to a low level, so as to prevent apoptosis by the overexpressed Smad4 (see Figure 3)

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