Human MAFA peptide

In the frame of the UPStrat-MAFA "Urban Disaster Prevention Strategies Using MAcroseismic Fields and FAult Sources" project, seismic hazard has been assessed in Portugal in terms of macroseismic intensity. Assessment has been performed by using a probabilistic approach based on the statistical analysis of local seismic histories (i.e., the record of seismic effects at each locality) performed by a new version of the SASHA code (D'Amico and Albarello in Res Lett 79(5):663-671, 2008) on purpose modified to account for this specific area of study. Local seismic histories are reconstructed by considering documented effects or indirect estimates deduced from epicentral information or numerical simulations. All these pieces of evidence are combined taking into account relevant uncertainty and statistical completeness of information locally available. Distribution of expected maximum intensity (i.e., the maximum intensity characterized by a fixed exceedance probability for a exposure time of 50 years) has been obtained and compared with the one deduced from alternative approaches.

The large-Maf transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) has been found to be crucial for insulin transcription and synthesis and for pancreatic beta-cell function and maturation. However, insights about the effects of small Maf factors on beta-cells are limited. Our goal was to elucidate the function of small-Maf factors on beta-cells using an animal model of endogenous small-Maf dysfunction. Transgenic (Tg) mice with beta-cell-specific expression of dominant-negative MafK (DN-MafK) experiments, which can suppress the function of all endogenous small-Mafs, were fed a high-fat diet, and their in vivo phenotypes were evaluated. Phenotypic analysis, glucose tolerance tests, morphologic examination of beta-cells, and islet experiments were performed. DN-MafK-expressed MIN6 cells were also used for in vitro analysis. The results showed that DN-MafK expression inhibited endogenous small-Maf binding to insulin promoter while increasing MafA binding. DN-MafK Tg mice under high-fat diet conditions showed improved glucose metabolism compared with control mice via incremental insulin secretion, without causing changes in insulin sensitivity or MafA expression. Moreover, up-regulation of insulin and glucokinase gene expression was observed both in vivo and in vitro under DN-MafK expression. We concluded that endogenous small-Maf factors negatively regulates beta-cell function by competing for MafA binding, and thus, the inhibition of small-Maf activity can improve beta-cell function.