Figure 3.

Effects of alterations in N-glycosylation on Chi3l1 signaling and tunicamycin-induced apoptosis. Peritoneal macrophages isolated from wild-type (WT) (+/+) and IL-13Rα2–null mutant mice (−/−) were stimulated with recombinant (r) Chi3l1 (rChi3l1) with and without tunicamycin treatment (2 μg/ml). (A) After overnight incubation, WT cells were harvested and total cell lysates were subjected to IB assays with phospho-specific antibodies against Erk (pErk), Akt (pAkt), together with antibodies detecting total forms of Erk and Akt. (B) Nuclear fractions of the cell lysates were used to detect the levels of β-catenin and c-Fos expression. (C and D) Cells isolated from WT and IL-13Rα2^−/− mice were subjected to IB assays with antibodies used in A and B. (E) Western blot evaluations of inhibitor of caspase-activated DNase (ICAD) in cells from WT and IL-13Rα2–null mice after treatment of tunicamycin and rChi3l1. Each panel is representative of a minimum of three evaluations. Erk = extracellular regulated kinase.