Fig. 6: Elimination of the CD95 amino terminal region enhances pro-survival signaling pathways in a CD95L-independent manner.
From: MMP7 cleavage of amino-terminal CD95 death receptor switches signaling toward non-apoptotic pathways
A Serum starved CEM-IRC cells reconstituted with full-length CD95, CD95-Δ58 or empty vector were lyzed and the indicated immunoblots were performed. Activation status of the PI3K and MAPK kinase pathways was evaluated by phosphorylation of Akt at Ser473 and ERK at T202/Y204, respectively. Data are representative of three independent experiments. B Growth curves for full-length CD95, CD95-Δ58 or empty vector transfected CEM-IRC clones. Cells (104) were plated onto 6-well tissue culture dishes and incubated in RPMI containing 8% or 0% FCS. Cells were counted at 0, 1, 2, and 3 days. C Indicated cells were incubated with non-cytotoxic concentrations of the PI3K (wortmannin) and ERK (UO126) inhibitors. Data are representative of three independent experiments. D Western blot analysis of total cell lysates from CEM-IRC cells reconstituted with full-length CD95 (CD95), CD95-Δ58 or empty vector (numbering indicates clones). Human CD95L-expressing 1A12 cells serve as positive control. Tubulin is used as a loading control. Note: 1A12 is a mouse T-cell line and the anti-tubulin antibody was specific for human tubulin, therefore mouse tubulin was not recognized in 1A12 cells.
