Figure 4
Figure 4. Aberrant activation of stress-response pathways in FA-C cells. (A) NF-κB transcriptional activity in lymphoblasts. NF-κB transcriptional activity was evaluated as increased luciferase activity in cell extracts isolated 48 hours after transfection with the reporter pNF-κB-Luc and phRL-TK. Luciferase activity in AHH1 cells was fixed to 1 in each experiment. Data presented are the mean (± SD) of at least 3 independent experiments done in triplicate. (B) Immunoblot showing the level of phosphorylation of key players of the MAPK pathways. Proteins were isolated from exponentially growing lymphoblasts. (C) TNF-α level in FA-C cells as function of MAPK activity. HSC536 and HSC536Neo cells were treated with SB203580 (p38 inhibitor, 10 μM), PD98059 (ERK inhibitor, 30 μM), and SP600125 (JNK inhibitor, 25 μM). Supernatants were collected 24 hours after subculturing and cytokine release was determined by ELISA. Data presented are the mean (± SD) of at least 3 independent experiments. *P < .01.

Aberrant activation of stress-response pathways in FA-C cells. (A) NF-κB transcriptional activity in lymphoblasts. NF-κB transcriptional activity was evaluated as increased luciferase activity in cell extracts isolated 48 hours after transfection with the reporter pNF-κB-Luc and phRL-TK. Luciferase activity in AHH1 cells was fixed to 1 in each experiment. Data presented are the mean (± SD) of at least 3 independent experiments done in triplicate. (B) Immunoblot showing the level of phosphorylation of key players of the MAPK pathways. Proteins were isolated from exponentially growing lymphoblasts. (C) TNF-α level in FA-C cells as function of MAPK activity. HSC536 and HSC536Neo cells were treated with SB203580 (p38 inhibitor, 10 μM), PD98059 (ERK inhibitor, 30 μM), and SP600125 (JNK inhibitor, 25 μM). Supernatants were collected 24 hours after subculturing and cytokine release was determined by ELISA. Data presented are the mean (± SD) of at least 3 independent experiments. *P < .01.

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