Bis(5-chloro­salicylato-κO)bis­(1,10-phenanthroline-κ2 N,N′)cadmium(II)

In the title complex, [Cd(C7H4ClO3)2(C12H8N2)2], the Cd atom is coordinated by two 5-chloro­salicylate ligands and two 1,10-phenanthroline ligands, displaying a distorted octa­hedral coordination geometry. The crystal structure is stabilized by O—H⋯O and C—H⋯O hydrogen bonds and π–π inter­actions between the 1,10-phenanthroline ligands and 5-chloro­salicylate ligands, with a centroid–centroid distance between neighbouring aromatic rings of 3.730 (1) Å

(E)-2-Meth­oxy-6-(thia­zol-2-ylimino­meth­yl)phenol

The title compound, C11H10N2O2S, displays an E configuration about the C=N bond. The mean planes of the thia­zole and benzene rings make a dihedral angle of 9.32 (18)°. Intra­molecular O—H⋯N hydrogen bonds are found in the crystal structure

Mediator MED23 Links Insulin Signaling to the Adipogenesis Transcription Cascade

SummaryAdipocyte differentiation is orchestrated by multiple signaling pathways and a temporally regulated transcriptional cascade. However, the mechanisms by which insulin signaling is linked to this cascade remain unclear. Here we show that the Med23 subunit of the Mediator Complex and its interacting transcription factor Elk1 are critical regulators of adipogenesis. Med23−/− embryonic fibroblast cells were refractory to hormone-induced adipogenesis. Knockdown of either Med23 or Elk1, or overexpression of dominant-negative Elk1, inhibited adipogenesis. In the absence of either Elk1 or Med23, Krox20, an immediate early gene stimulated by insulin during adipogenesis, was uninducible. Moreover, the adipogenic defect in Med23-deficient cells was rescued by ectopic expression of Krox20 or one of its downstream factors, C/EBPβ or PPARγ. Mechanistically, the insulin-stimulated, Med23-deficient preinitiation complex failed to initiate robust transcription of Krox20. Collectively, our results suggest that Med23 serves as a critical link transducing insulin signaling to the transcriptional cascade during adipocyte differentiation