“…The activity of mouse XenoRs, including pregnane X receptor (PXR), CAR, liver X receptor α (LXR α), farnesoid X receptor (FXR), vitamin D receptor (VDR), PPARα, PPARβ, PPARγ, estrogen receptor α (ERα), ERβ, and glucocorticoid receptor (GR) in response to TCS (10 μM) was monitored. CV-1 cells were maintained in DMEM (Life Technologies) supplemented with 10% FBS, seeded in 96-well plates, and transfected with an expression vector containing a specific nuclear receptor (i.e., PXR, CAR, LXRα, VDR, FXR, PPARα, PPARδ, PPARγ, or GR) and RXR, along with a luciferase reporter containing the appropriate DNA response element, as described previously (9). The assay was first validated with known nuclear receptor ligands as positive controls, including pregnenolone 16α-carbonitrile (10 μm; Sigma) for PXR, 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene (250 nM; Sigma) for CAR, β-estradiol (10 nM; Sigma) for ER, T0901317 (1 μM; CAYMAN Chemical) for LXRα, calcipotriol (10 μM; Sigma) for VDR, GW4064 (1 μM; Sigma) for FXR, WY14643 (30 μM; Sigma) for PPARα, GW501516 (100 nM) for PPARδ, rosiglitazone (1 μM; Cayman Chemical) for PPARγ, and dexamethasone (100 nM; Sigma) for GR.…”