Fig. 5: Loss of CYLD leads to decreased efficacy of IKK inhibitors in inducing apoptosis and necroptosis in MT4 cells. | Cell Death & Disease

Fig. 5: Loss of CYLD leads to decreased efficacy of IKK inhibitors in inducing apoptosis and necroptosis in MT4 cells.

From: Reversal of CYLD phosphorylation as a novel therapeutic approach for adult T-cell leukemia/lymphoma (ATLL)

Fig. 5

a MT4 cells were transduced with lentiviruses encoding a non-targeting or CYLD-targeting shRNA. After selection for stable knockdown of CYLD, the two lines were treated with a combination of 10 µM MRT67307 and TPCA for 24 h. Cell viability was assayed by CellTiter-Glo. The ATP level for each cell line treated with DMSO was set at 100%. The bars represent the mean ± S.D. from three independent experiments. **p < 0.01. b Control or CYLD-deficient cells were treated for 24 h with a combination of the kinase inhibitors in the absence or presence of zVAD-FMK (10 µM). Lysates were sequentially blotted for Procaspase-8, cleaved Caspase-8, cleaved Caspase-3, cleaved PARP-1, phospho-RIPK3, RIPK3, CYLD, and β-actin. A separate membrane with identical samples was also blotted for phospho-MLKL, MLKL, and GAPDH. Cleaved Caspase-3 and PARP-1 are biochemical signatures for apoptosis. Phospho-RIPK3 and phospho-MLKL are biochemical signatures for necroptosis.

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