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. Author manuscript; available in PMC: 2009 Sep 1.
Published in final edited form as: J Immunol. 2008 Sep 1;181(5):3575–3585. doi: 10.4049/jimmunol.181.5.3575

FIGURE 8. Effect of inhibitors on PMA-induced TGF-β production.

FIGURE 8

A, 3T3TβRII cells were pre-treated with rapamycin (Rapa, 100 nM) overnight, SB 203580 (SB, 10 µM), PD 98059 (PD, 30 µM), JNK inhibitor II (JNKII, 30 µM) or wortmannin (Wort, 100 nM) for 1 h and then stimulated with PMA (100 nM) for 18 h. Total TGF-β in the conditioned medium was analyzed by ELISA. *, significantly different from PMA alone. B, 3T3TβRII cells were pre-treated with rapamycin (Rapa, 100 nM) overnight, SB 203580 (SB, 10 µM), PD 98059 (PD, 50 µM), JNK inhibitor II (JNKII, 50 µM) or wortmannin (Wort, 100 nM) for 1 h and then stimulated with PMA (100 nM) for 4 h. TGF-β mRNA levels were analyzed using Relative Quantitative RT-PCR. C, 3T3TβRII cells were pre-treated with rapamycin (Rapa, 100 nM) overnight, SB 203580 (SB, 10 µM), PD 98059 (PD, 50 µM), JNK inhibitor II (JNKII, 50 µM) or wortmannin (Wort, 100 nM) for 1 h and then stimulated with PMA (100 nM) for 30 min. Total cell lysates were immunoblotted for phospho-eIF4E.