Fig. 3: Usp8 acts downstream of Traf2, and upstream of Tak1.
From: Usp8 promotes tumor cell migration through activating the JNK pathway
a Simplified schematic illustrating the cascade of JNK pathway. Egr, Eiger; Tnfr, Tumor necrosis factor receptors; Traf2, TNF-receptor-associated factor 2; Tak1, TGF-β-associated kinase 1; Hep, Hemipterous; Mkk4, MAP kinase kinase 4; Bsk, Basket; puc, puckered; mmp1, matrix metalloproteinase 1. b A wing disc with usp8 ectopic expression by ptc-gal4 was stained to show GFP (green) and puc-lacZ (white). c Knockdown of bsk inhibited Usp8-induced puc-lacZ upregulation. d Knockdown of hep attenuated puc-lacZ expression caused by usp8 ectopic expression. e Knockdown of tak1 inhibited puc-lacZ expression caused by usp8 ectopic expression. f Knockdown of traf2 failed to decrease puc-lacZ expression caused by usp8 ectopic expression. g The adult wing of ptc-gal4 was used as a control. h Overexpression of usp8 resulted in the loss of ACV phenotype. i-n The loss of ACV caused by usp8 overexpression is rescued by depletion of usp8 (i), or bsk (j), or hep (k), or mkk4 (l), or tak1 (m), but not traf2 (n). o Statistical analyses of the presence of ACV in g–n were presented as mean ± SD. Numbers of wings for statistical analyses were shown in columns. Above all, the t-test was used for statistical analyses, ns (not significant), p > 0.05; ***p < 0.001; ****p < 0.0001. Scale bars: 50 μm for all disc images, 200 μm for all adult wing images.
