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. 2024 May 13;10:227. doi: 10.1038/s41420-024-01984-7

Fig. 6. Oligomerization of NT-GSDMD, NT-GSDME, and p-MLKL triggers PANoptosis after co-treatment of IFN-γ + TNF-α.

Fig. 6

Immunoblot analysis of pro-(P53), activated (P30), oligomerized GSDMD, and pro-(P53), activated (P34), oligomerized GSDME (a); tMLKL, phosphorylated MLKL (pMLKL) and oligomerized pMLKL (b) induced by PBS or IFN-γ and TNF-α in DLD1 or HCT116; the active NT-GSDMD, NT-GSDME, p-MLKL could form oligomers, 100kD, 130KD, 180KD, and bigger oligomers. The active NT-GSDMD, NT-GSDME mainly in the cytosolic fraction and membrane fraction, little in the nuclear fraction; the active p-MLKL is mainly in the nuclear fraction, little in the cytosolic fraction and membrane fraction. ATP, GAPDH, and Lamin B1 were used as membrane, cytosolic, and nuclear internal control respectively. Data are representative of at least three independent experiments.