Figure 4.
Figure 4. CXCR3 agonists stimulate activation of Akt in T lymphocytes. (A-C) T cells were stimulated for different periods of time with 10, 30, and 100 nM CXCL11 (Ai-iii), CXCL10 (Bi-iii), CXCL9 (Bi-iii), or CXCL12 (C), and phosphorylation of Akt was determined by Western blot analysis using specific anti–phosho-Akt (P-Akt) antibodies. Phosphorylation was quantified by chemiluminescence and corrected for total Akt (T-Akt) expression on stripped blots. (D-E) Involvement of Gi- (D) and PI3K–signaling pathway (E) in CXCL11-induced Akt phosphorylation. T cells were grown in serum-free medium in the presence of PTX (100 ng/mL, 48 h; D) or wortmannin (wort) (100 nM, 30 minutes; E) and exposed to CXCL11 (1 minute, 30 nM) before lysis and Western blot analysis. A representative experiment of at least 2 independent experiments is shown.

CXCR3 agonists stimulate activation of Akt in T lymphocytes. (A-C) T cells were stimulated for different periods of time with 10, 30, and 100 nM CXCL11 (Ai-iii), CXCL10 (Bi-iii), CXCL9 (Bi-iii), or CXCL12 (C), and phosphorylation of Akt was determined by Western blot analysis using specific anti–phosho-Akt (P-Akt) antibodies. Phosphorylation was quantified by chemiluminescence and corrected for total Akt (T-Akt) expression on stripped blots. (D-E) Involvement of Gi- (D) and PI3K–signaling pathway (E) in CXCL11-induced Akt phosphorylation. T cells were grown in serum-free medium in the presence of PTX (100 ng/mL, 48 h; D) or wortmannin (wort) (100 nM, 30 minutes; E) and exposed to CXCL11 (1 minute, 30 nM) before lysis and Western blot analysis. A representative experiment of at least 2 independent experiments is shown.

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