In view of this hypothesis, it will be challenging to study molecular clocks in organisms that have both a photolyase with a dual function and cryptochromes, as is the case of marsupials, such as Potorous and Monodelphis. The genome of Monodelphis domesticus has been sequenced and reveals the presence of cryptochrome genes, as well as photolyase. It will be of interest to determine how the clock of non-placental mammals will respond to the loss of photolyase. On the basis of our data, one would predict a change in tau, suggesting that the circadian clock of placental mammals has adapted to the loss of photolyase by adjusting period. Studying the marsupial circadian system at the cellular and molecular level will answer these AbMole Nortriptyline questions and shed light on the functional evolution of the CPF. The present study has identified the Potorous tridactylus CPD photolyase as an attractive candidate for further structure-function studies, aiming at understanding the functional diversity between cryptochromes and photolyases. Progressive liver fibrosis due to chronic viral hepatitis, autoimmune, metabolic or hereditary disorders is a leading cause of morbidity and mortality in the Western world. Regardless of the underlying etiology, liver fibrosis is characterized by an excessive deposition and reorganization of extracellular matrix with a dramatic increase in noncollagenous and collagenous ECM proteins. The fibrillar collagen type I, is encoded by two different genes, col1A1 and col1A2, and accounts for 36% of the total collagens in ECM of healthy liver. During liver fibrogenesis, collagen type I is the predominant isoform deposited into the perisinusoidal space. However, collagen type IV, that constitutes less than 10% of total collagen in the normal liver, is most dramatically upregulated in fibrosis. In the fibrotic liver, hepatic stellate cells undergo myofibroblastic transdifferentiation. These myofibroblastic HSC are regarded as the main source of ECM production although portal myofibroblasts, infiltrating fibroblasts and fibrocytes may also participate in the synthesis and restructuring of the connective tissue. HSC get activated in response to chronic liver injury by proinflammatory and profibrogenic mediators such as transforming growth AbMole Ganciclovir factor-b and plateletderived growth factor b. TGF-b is recognized as the main profibrogenic mediator, triggering the myofibroblastic transition of HSC. Furthermore, it promotes the synthesis of ECM proteins, and inhibits expression and activity of matrix degrading enzymes in HSC. TGF-b stimulated matrix production and deposition has been shown in a wide range of models of experimental fibrosis and in patients with chronic hepatitis and cirrhosis. Interestingly, there is good evidence for hepatic growth factor opposing TGF-b signalling by reducing TGF-b mRNA levels. HGF is a multifunctional cytokine that elicits mitogenic, motogenic, and morphogenic properties by activation of the tyrosine kinase receptor Met, a product of the proto-oncogene c-met.