Catálogo de publicaciones - revistas

<jats:title>Dissecting Serotonin Receptors</jats:title> <jats:p> Serotonin receptors are the targets for many widely used drugs prescribed to treat ailments from depression to obesity and migraine headaches (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6132" page="562" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1238521">Palczewski and Kiser</jats:related-article> </jats:bold> ). <jats:bold> C. Wang <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="6132" page="610" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1232807">610</jats:related-article> , published online 21 March) and <jats:bold> Wacker <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="6132" page="615" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1232808">615</jats:related-article> , published online 21 March) describe crystal structures of two members of the serotonin family of receptors bound to antimigraine medications or to a precursor of the hallucinogenic drug LSD. Subtle differences in the way particular ligands bind to the receptors cause substantial differences in the signals generated by the receptor and the consequent biological responses. The structures reveal how the same ligand can activate one or both of the two main serotonin receptor signaling mechanisms, depending on which particular receptor it binds. </jats:p>

<jats:title>Dissecting Serotonin Receptors</jats:title> <jats:p> Serotonin receptors are the targets for many widely used drugs prescribed to treat ailments from depression to obesity and migraine headaches (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6132" page="562" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1238521">Palczewski and Kiser</jats:related-article> </jats:bold> ). <jats:bold> C. Wang <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="6132" page="610" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1232807">610</jats:related-article> , published online 21 March) and <jats:bold> Wacker <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="6132" page="615" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1232808">615</jats:related-article> , published online 21 March) describe crystal structures of two members of the serotonin family of receptors bound to antimigraine medications or to a precursor of the hallucinogenic drug LSD. Subtle differences in the way particular ligands bind to the receptors cause substantial differences in the signals generated by the receptor and the consequent biological responses. The structures reveal how the same ligand can activate one or both of the two main serotonin receptor signaling mechanisms, depending on which particular receptor it binds. </jats:p>

<jats:title>Making Antisense of Flowering</jats:title> <jats:p> The recent discovery of biological roles for long noncoding RNAs raises important questions as to how they are themselves regulated. <jats:bold> Sun <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="6132" page="619" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1234848">619</jats:related-article> ) adopted a genetic approach to identify regulators of <jats:italic>COOLAIR</jats:italic> —a set of antisense transcripts from the locus encoding the major <jats:italic>Arabidopsis</jats:italic> floral repressor, <jats:italic>FLC</jats:italic> . Analysis of a mutant misregulating <jats:italic>COOLAIR</jats:italic> revealed a homeodomain protein that repressed <jats:italic>COOLAIR</jats:italic> expression via an R-loop covering the <jats:italic>COOLAIR</jats:italic> promoter. Thus, R-loop stabilization is an integral part of <jats:italic>COOLAIR</jats:italic> regulation, <jats:italic>FLC</jats:italic> expression, and flowering time. </jats:p>

<jats:title>IDHology</jats:title> <jats:p> Among the most exciting drug targets to emerge from cancer genome sequencing projects are two related metabolic enzymes, isocitrate dehydrogenases 1 and 2 (IDH1, IDH2). Mutations in the <jats:italic>IDH1</jats:italic> and <jats:italic>IDH2</jats:italic> genes are common in certain types of human cancer. Whether inhibition of mutant IDH activity might offer therapeutic benefits is unclear (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6132" page="558" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1238523">Kim and DeBerardinis</jats:related-article> </jats:bold> ). <jats:bold> F. Wang <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="6132" page="622" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1234769">622</jats:related-article> , published online 4 April) isolated a small molecule that selectively inhibits mutant IDH2, describe the structural details of its binding to the mutant enzyme, and show that this compound suppresses the growth of patient-derived leukemia cells harboring the <jats:italic>IDH2</jats:italic> mutation. <jats:bold> Rohle <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="6132" page="626" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1236062">626</jats:related-article> , published online 4 April) show that a small molecule inhibitor of IDH1 selectively slows the growth of patient-derived brain tumor cells with the <jats:italic>IDH1</jats:italic> mutation. </jats:p>

<jats:title>IDHology</jats:title> <jats:p> Among the most exciting drug targets to emerge from cancer genome sequencing projects are two related metabolic enzymes, isocitrate dehydrogenases 1 and 2 (IDH1, IDH2). Mutations in the <jats:italic>IDH1</jats:italic> and <jats:italic>IDH2</jats:italic> genes are common in certain types of human cancer. Whether inhibition of mutant IDH activity might offer therapeutic benefits is unclear (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6132" page="558" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1238523">Kim and DeBerardinis</jats:related-article> </jats:bold> ). <jats:bold> F. Wang <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="6132" page="622" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1234769">622</jats:related-article> , published online 4 April) isolated a small molecule that selectively inhibits mutant IDH2, describe the structural details of its binding to the mutant enzyme, and show that this compound suppresses the growth of patient-derived leukemia cells harboring the <jats:italic>IDH2</jats:italic> mutation. <jats:bold> Rohle <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="6132" page="626" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1236062">626</jats:related-article> , published online 4 April) show that a small molecule inhibitor of IDH1 selectively slows the growth of patient-derived brain tumor cells with the <jats:italic>IDH1</jats:italic> mutation. </jats:p>

<jats:title>Dynamic Protection</jats:title> <jats:p> During an immune response, CD8 <jats:sup>+</jats:sup> T cells are recruited to provide protection. Most cells differentiate into short-lived effectors that help to clear the pathogen, whereas others form long-lived memory cells to protect against reinfection. <jats:bold> Gerlach <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="6132" page="635" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1235487">635</jats:related-article> , published online 14 March) and <jats:bold> Buchholz <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="6132" page="630" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1235454">630</jats:related-article> , published online 14 March) used in vivo fate mapping of mouse T cells with a defined specificity during a bacterial infection to show that the dynamics of the single-cell response are not uniform. The response of a particular T cell population is the average of a small number of clones that expand greatly (“large clones”) and many clones that only proliferate at low amounts (“small clones”). The memory pool arises largely from small clones whereas effectors are primarily made up of large clones. </jats:p>

<jats:title>Dynamic Protection</jats:title> <jats:p> During an immune response, CD8 <jats:sup>+</jats:sup> T cells are recruited to provide protection. Most cells differentiate into short-lived effectors that help to clear the pathogen, whereas others form long-lived memory cells to protect against reinfection. <jats:bold> Gerlach <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="6132" page="635" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1235487">635</jats:related-article> , published online 14 March) and <jats:bold> Buchholz <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="6132" page="630" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1235454">630</jats:related-article> , published online 14 March) used in vivo fate mapping of mouse T cells with a defined specificity during a bacterial infection to show that the dynamics of the single-cell response are not uniform. The response of a particular T cell population is the average of a small number of clones that expand greatly (“large clones”) and many clones that only proliferate at low amounts (“small clones”). The memory pool arises largely from small clones whereas effectors are primarily made up of large clones. </jats:p>

<jats:title>Reading Dreams</jats:title> <jats:p> How specific visual dream contents are represented by brain activity is unclear. Machine-learning–based analyses can decode the stimulus- and task-induced brain activity patterns that represent specific visual contents. <jats:bold> Horikawa <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="6132" page="639" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1234330">639</jats:related-article> , published online 4 April) examined patterns of brain activity during dreaming and compared these to waking responses to visual stimuli. The findings suggest that the visual content of dreams is represented by the same neural substrate as observed during awake perception. </jats:p>

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