Fig. 4: Inhibiting CYLD phosphorylation activates RIPK1-dependent apoptosis and necroptosis. | Cell Death & Disease

Fig. 4: Inhibiting CYLD phosphorylation activates RIPK1-dependent apoptosis and necroptosis.

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

Fig. 4

a MT4 cells were treated for 24 h with a combination of MRT67307 (10 µM), TPCA (10 µM), zVAD-FMK (10 µM), and necrostatin-1 (30 µM) as indicated. Cellular viability was analyzed using CellTiter-Glo. The viability of cells treated with DMSO was set at 100%. The bars represent the mean ± S.D. from three independent experiments. *p < 0.05; **p < 0.01. b MT4 cells were treated as in (a). Lysates were sequentially blotted for Procaspase-8, cleaved Caspase-3, cleaved PARP-1, and β-actin. A separate membrane with identical samples was also blotted for phospho-RIPK3, RIPK3, and GAPDH. Cleaved Caspase-3 and PARP-1 are biochemical signatures for apoptosis. Phospho-RIPK3 is a biochemical signature for necroptosis.

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