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. 2016 Mar 11;310(10):G844–G854. doi: 10.1152/ajpgi.00407.2015

Fig. 2.

Fig. 2.

TNF-mediated increases in LDs are independent of EGF receptor (EGFR) and IKK but depend on phosphatidylinositol 3-kinase (PI3K). A: HT-29 cells were treated with TNF (6 h) in the presence of pharmacological inhibitors for EGFR (AG1517), IKK-β (PS1145), or PI3K (wortmannin) and stained for LDs (BODIPY 493/503) (representative images from 3 independent experiments, scale bar = 5 μm). B: protein from TNF-stimulated HT-29 cells (6 h) in the presence of AG1517, PS1145, or wortmannin was immunoblotted for the LD coat protein PLIN2. Densitometric analysis of n = 3, *P < 0.05, compared with Con, #P < 0.05, compared with TNF alone, ANOVA. C: TNF-treated NCM460 cells (6 h) with and without wortmannin were stained by BODIPY 493/503 (representative images from 3 independent experiments, scale bar = 5 μm).