Catálogo de publicaciones - revistas

<jats:title>Moving Bricks with MraY</jats:title> <jats:p> Peptidoglycan, the building brick of bacterial cell walls, is synthesized in the cytoplasm and must be transported across the cell membrane. To achieve this, it is attached to a carrier lipid by the integral membrane protein MraY. MraY is targeted by natural antibacterials and is a promising antibiotic target. <jats:bold> Chung <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6149" page="1012" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1236501">1012</jats:related-article> ) report the crystal structure of MraY at 3.3 Ã… resolution. The structure, together with mutational mapping, outlines the location of the active site and provides interesting hints for how the enzyme binds the substrate and catalyzes attachment to the carrier lipid. </jats:p>

<jats:title>Depression and the Habenula</jats:title> <jats:p> The lateral habenula (LHb) appears to have a role in depression. However, the underlying mechanisms are poorly understood, and by using multiple rodent models of depression, <jats:bold> Li <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6149" page="1016" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1240729">1016</jats:related-article> ) identified a signaling pathway and associated neuronal adaptations in which the enzyme βCaMKII was selectively up-regulated in the LHb. Manipulations that enhanced βCaMKII levels increased depression-related phenotypes, and RNA interference of CaMKIIb blunted depression. Enhanced βCaMKII levels in the habenula promoted excitatory synaptic transmission on these neurons and increased action potential firing mediated by an up-regulation of a specific subtype of glutamate receptors. </jats:p>

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<jats:p>Noncoding RNAs make up the majority of transcribed RNA and have a wide range of functions in cellular and developmental processes. Consequently, they are also implicated in the development and pathophysiology of many diseases and represent potential targets for therapeutic intervention. microRNAs are one class of noncoding RNA that has been intensely studied. Effective inhibition (or silencing) of microRNAs in vivo has enabled scientists to make groundbreaking discoveries about the contribution of these short regulating RNAs to some of the major human diseases, such as cancer, heart disease, and diabetes. Long noncoding RNAs are less well studied, but have recently emerged as another novel class of therapeutic targets in a variety of diseases. Both long and short noncoding RNAs represent new avenues of investigation for drug discovery with several advantages over traditional protein-based targets; however, they come with their own unique set of challenges.</jats:p>

<jats:title>Transforming Fat to Thin</jats:title> <jats:p> How much does the microbiota influence the host's phenotype? <jats:bold> Ridaura <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6150/1241214.full">1241214</jats:ext-link> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6150" page="1069" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1243787"> <jats:bold>Walker and Parkhill</jats:bold> </jats:related-article> ) obtained uncultured fecal microbiota from twin pairs discordant for body mass and transplanted them into adult germ-free mice. It was discovered that adiposity is transmissible from human to mouse and that it was associated with changes in serum levels of branched-chain amino acids. Moreover, obese-phenotype mice were invaded by members of the Bacteroidales from the lean mice, but, happily, the lean animals resisted invasion by the obese microbiota. </jats:p>