Catálogo de publicaciones - revistas

<jats:p>Improved breeding of a plant that produces a major antimalarial compound is now possible based on knowledge of its genetic map.</jats:p>

<jats:p> The reaction of ions such as NO <jats:sup>+</jats:sup> with networks of only a few water molecules has implications for understanding chemistry in the ionosphere. </jats:p>

<jats:p>A major figure in international economics laid the foundation for modern economics and transformed the atmosphere of economic study.</jats:p>

<jats:p>Virus infection in mammals elicits a variety of defense responses that are initiated by signals from virus-sensing receptors expressed by the host. These receptors include the ubiquitously expressed RIG-I–like receptor (RLR) family of RNA helicases. RLRs are cytoplasmic proteins that act in cell-intrinsic antiviral defense by recognizing RNAs indicative of virus presence. Here, we highlight recent progress in understanding how RLRs discriminate between the RNA content of healthy versus virus-infected cells, functioning as accurate sensors of virus invasion.</jats:p>

<jats:p>NLR (nucleotide-binding domain, leucine-rich repeat–containing) proteins have rapidly emerged as central regulators of immunity and inflammation with demonstrated relevance to human diseases. Much attention has focused on the ability of several NLRs to activate the inflammasome complex and drive proteolytic processing of inflammatory cytokines; however, NLRs also regulate important inflammasome-independent functions in the immune system. We discuss several of these functions, including the regulation of canonical and noncanonical NF-κB activation, mitogen-activated protein kinase activation, cytokine and chemokine production, antimicrobial reactive oxygen species production, type I interferon production, and ribonuclease L activity. We also explore the mechanistic basis of these functions and describe current challenges in the field.</jats:p>

<jats:p>Twenty years after the proposal that pattern recognition receptors detect invasion by microbial pathogens, the field of immunology has witnessed several discoveries that have elucidated receptors and signaling pathways of microbial recognition systems and how they control the generation of T and B lymphocyte–mediated immune responses. However, there are still many fundamental questions that remain poorly understood, even though sometimes the answers are assumed to be known. Here, we discuss some of these questions, including the mechanisms by which pathogen-specific innate immune recognition activates antigen-specific adaptive immune responses and the roles of different types of innate immune recognition in host defense from infection and injury.</jats:p>

<jats:p>Interleukin-1β (IL-1β), reactive oxygen species (ROS), and thioredoxin-interacting protein (TXNIP) are all implicated in the pathogenesis of type 2 diabetes mellitus (T2DM). Here we review mechanisms directing IL-1β production and its pathogenic role in islet dysfunction during chronic hyperglycemia. In doing so, we integrate previously disparate disease-driving mechanisms for IL-1β, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. The NLRP3 inflammasome also drives IL-1β maturation and secretion in another disease of metabolic dysregulation, gout. Thus, we propose that the NLRP3 inflammasome contributes to the pathogenesis of T2DM and gout by functioning as a sensor for metabolic stress.</jats:p>

<jats:p>During translation of mitochondrial genes, shifting the ribosome reading frame avoids unconventional arginine codons.</jats:p>

<jats:title>Adaptive Girdle Loss in Sticklebacks</jats:title> <jats:p> How do molecular changes give rise to phenotypic adaptation exemplified by the repeated reduction in the pelvic girdle observed in separate populations of sticklebacks? Now <jats:bold> Chan <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="302" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182213">302</jats:related-article> , published online 10 December) have identified the specific DNA changes that control this major skeletal adaptation. The key locus controlling pelvic phenotypes mapped to a noncoding regulatory region upstream of the <jats:italic>Pituitary homeobox transcription factor 1</jats:italic> gene, which drives a tissue-specific pelvic enhancer. Multiple populations showed independent deletions in this region and enhancer function was inactivated. Reintroduction of the enhancer restored pelvic development in a pelvic-reduced stickleback. </jats:p>