| First Author | Nishiumi S | Year | 2007 |
| Journal | Arch Biochem Biophys | Volume | 466 |
| Issue | 2 | Pages | 267-73 |
| PubMed ID | 17880909 | Mgi Jnum | J:126932 |
| Mgi Id | MGI:3762319 | Doi | 10.1016/j.abb.2007.08.007 |
| Citation | Nishiumi S, et al. (2007) Curcumin suppresses the transformation of an aryl hydrocarbon receptor through its phosphorylation. Arch Biochem Biophys 466(2):267-73 |
| abstractText | Halogenated and polycyclic aromatic hydrocarbons induce diverse biochemical responses through the transformation of a cytosolic aryl hydrocarbon receptor (AhR). In mouse hepatoma Hepa-1c1c7 cells, curcumin, a yellow pigment of Curcuma longa, did not inhibit the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced translocation of the AhR into the nucleus, but rather accelerated it. In the nucleus, curcumin inhibited the TCDD-induced heterodimerization of the AhR with an AhR nuclear translocator (Arnt), an essential partner for the transformation, and also dose-dependently inhibited the TCDD-evoked phosphorylation of both the AhR and Arnt. Moreover, curcumin significantly inhibited the TCDD-induced activation of protein kinase C (PKC), which is involved in the transformation, decreased the TCDD-induced DNA-binding activity of the AhR/Arnt heterodimer, and downregulated CYP1A1 expression. In a cell-free system, curcumin inhibited the binding of 3-methylcholanthrene, an AhR agonist, to the receptor. These results indicate that curcumin is able to bind to the AhR as a ligand, but suppresses its transformation by inhibiting the phosphorylation of AhR and Arnt, probably by PKC. |
