Fig 1: Per2 inhibit Id3 expression via regulating PTEN/AKT/Smad5 signaling pathway. The protein levels of PTEN, AKT, p-AKT(T308), p-AKT(S473), Smad5, p-Smad5, GAPDH were analyzed by Western blot in U87 and U251 cells.
Fig 2: Immunohistochemistry of the liver clock components Per2 and CRY1 in liver sections of control and diclofenac-treated animals after daily dosing for 28 days. A complex relationship exists between the circadian clock and inflammation. Panel AI–III: Liver sections of three individual control animals: Disseminated throughout the liver lobule are Per2-positive macrophages. Panel BI–III: Diclofenac low-dose treatment caused a marked increase in activated Per2-positive macrophages. Some hepatocytes and sinusoidal endothelium also stained positive. Panel CI–III: High-dose diclofenac treatment. Hepatocytes of an inflamed liver lobule abundantly express Per2 (CIII). Panel DI–III: Liver sections of three individual control animals. In one control (DI) bile duct epithelium appeared slightly positive; none of the controls expressed the protein (DI–III). Panel EI–III: Diclofenac low-dose treatment. Shown in panel EI is the liver section of a low-dose-treated animal with marked CRY1-positive macrophage infiltrates within an inflamed hepatic lobule. Conversely, EIII illustrates marked portal histiocytic infiltrates of monocytes and macrophages; however, none express CRY1, while panel F1 documents CRY-positive histiocytic infiltrates forming a granuloma adjacent to the central vein of an inflamed liver lobule. Panel FI–III: High-dose diclofenac treatment. We observed a clear dose-related increase in CRY1 expression.
Supplier Page from Abcam for Anti-PER2 antibody