TABLE 1.

The antiviral effect of TCDC is independent of known bile acid signal cascades^a

Inhibitor	Target	Relative MCMV-dependent luciferase activity (mean ± SD) with:
		Inhibitor alone	Inhibitor + TCDC
None	None	1.0 ± 0.0	0.5 ± 0.1
SU6656	Yes kinase	1.5 ± 0.3	0.6 ± 0.1
PP2	Src kinase	0.9 ± 0.4	0.4 ± 0.1
Protein kinase inhibitor	Protein kinase A	1.2 ± 0.3	0.4 ± 0.2
PD98059	Erk kinase	1.0 ± 0.2	0.5 ± 0.2
SB203580	p38MAPK	0.9 ± 0.2	0.6 ± 0.2
Rapamycin	mTOR	0.8 ± 0.3	0.5 ± 0.1
Sp600125	JNK1/2	0.8 ± 0.2	0.3 ± 0.1
Bafilomycin A1	Autophagy	1.1 ± 0.3	0.6 ± 0.1
LY294002	PI3 kinase	0.4 ± 0.1	0.1 ± 0.0

^aHepatocytes were incubated for 30 min with inhibitors of the indicated signal cascades (Yes kinase, SU6656 [10μM]; Src kinase, PP2 [10 μM]; protein kinase A, protein kinase inhibitor [2.3 nM]; Erk kinase, PD98059 [10 μM]; p38^MAPK, SB203580 [10 μM]; mTOR, rapamycin [10 nM]; JNK1/2, Sp600125 [10 μM]; autophagy, bafilomycin A1 [250 nM]; PI3 kinase, LY294002 [50 μM]) before being treated for 3 h with 25 μM TCDC prior to infection with Δm157-MCMV-luciferase. After 24 h, cells were lysed and luciferase activity was quantified.