Triflumizole

In the title compound {systematic name: 4-chloro-N-[1-(1H-imidazol-1-yl)-2-propoxyethyl­idene]-2-(trifluoro­meth­yl)aniline}, C15H15ClF3N3O, the dihedral angle between the aniline and imidazole ring planes is 81.80 (4)°. In the crystal structure, weak inter­molecular C—H⋯X (X = N, O or F) hydrogen bonds and C—H⋯π inter­actions help to consolidate the packing

Role of G{alpha}12 and G{alpha}13 as Novel Switches for the Activity of Nrf2, a Key Antioxidative Transcription Factor

G{alpha}12 and G{alpha}13 function as molecular regulators responding to extracellular stimuli. NF-E2-related factor 2 (Nrf2) is involved in a protective adaptive response to oxidative stress. This study investigated the regulation of Nrf2 by G{alpha}12 and G{alpha}13. A deficiency of G{alpha}12, but not of G{alpha}13, enhanced Nrf2 activity and target gene transactivation in embryo fibroblasts. In mice, G{alpha}12 knockout activated Nrf2 and thereby facilitated heme catabolism to bilirubin and its glucuronosyl conjugations. An oligonucleotide microarray demonstrated the transactivation of Nrf2 target genes by G{alpha}12 gene knockout. G{alpha}12 deficiency reduced Jun N-terminal protein kinase (JNK)-dependent Nrf2 ubiquitination required for proteasomal degradation, and so did G{alpha}13 deficiency. The absence of G{alpha}12, but not of G{alpha}13, increased protein kinase C {delta} (PKC {delta}) activation and the PKC {delta}-mediated serine phosphorylation of Nrf2. G{alpha}13 gene knockout or knockdown abrogated the Nrf2 phosphorylation induced by G{alpha}12 deficiency, suggesting that relief from G{alpha}12 repression leads to the G{alpha}13-mediated activation of Nrf2. Constitutive activation of G{alpha}13 promoted Nrf2 activity and target gene induction via Rho-mediated PKC {delta} activation, corroborating positive regulation by G{alpha}13. In summary, G{alpha}12 and G{alpha}13 transmit a JNK-dependent signal for Nrf2 ubiquitination, whereas G{alpha}13 regulates Rho-PKC {delta}-mediated Nrf2 phosphorylation, which is negatively balanced by G{alpha}12

Diclomezine: 6-(3,5-dichloro-4-methyl­phen­yl)pyridazin-3(2H)-one

In the title compound, C11H8Cl2N2O, the benzene and pyridazine rings are tilted by 8.6 (1)° relative to each other. In the crystal, pairs of inter­molecular N—H⋯O hydrogen bonds form centrosymmetric dimers. π–π contacts with centroid–centroid distances of 3.698 (2) and 3.751 (1) Å and halogen–halogen inter­actions [3.379 (1) Å] also stabilize the structure

N-(Pyridin-2-ylmeth­yl)pyridin-2-amine

The title compound, C11H11N3, crystallizes with two mol­ecules (A and B) in the asymmetric unit. The geometries of both mol­ecules are very similar, with the exception of the torsion angles of the inter-ring chains; the values for C—N—C—C are 67.4 (5) and −69.3 (5)° for mol­ecules A and B, respectively. The dihedral angles between the pyridyl ring planes are 84.0 (2) and 83.2 (2)° for mol­ecules A and B, respectively. In the crystal, weak inter­molecular N—H⋯N hydrogen bonds and C—H⋯π inter­actions contribute to the stabilization of the packing

Bis[μ-N-(pyridin-2-ylmeth­yl)pyridin-2-amine-κ2 N:N′]disilver(I) bis(trifluoro­methane­sulfonate)

In the binuclear title compound, [Ag2(C11H11N3)2](CF3O3S)2, the complex cation is centrosymmetric, with the unique Ag+ cation coordinated by two pyridine N atoms from two symmetry-related N-(pyridin-2-ylmeth­yl)pyridin-2-amine ligands in a geometry slightly distorted from linear [N—Ag—N 161.02 (7)°]. This set-up leads to the formation of a 14-membered cyclic dimer. The two pyridine rings coordinated to the Ag+ cation are tilted by 80.19 (7)° with respect to each other. Inter­molecular N—H⋯O hydrogen-bonding inter­actions between the cyclic dimer and the anion exist. A two-dimensional network parallel to the ac plane is constructed by three weak Ag⋯(O,N) inter­actions as well as an F⋯F contact of 2.890 (4) Å