Catálogo de publicaciones - revistas

<jats:title>New Horizons' views of Pluto</jats:title> <jats:p> The flyby of Pluto and its moon Charon by the New Horizons spacecraft generated news coverage around the world. Now Stern <jats:italic>et al.</jats:italic> report the first scientific results from the high-speed encounter. The surface of Pluto is surprisingly diverse, with large regions of differing brightness and composition. There is ample evidence for ongoing rich geological processes that act to sculpt its surface. Charon's surface is similarly complex, with numerous relief structures and varied coloration. Pluto's atmosphere is extensive but less dense than expected, whereas Charon has no detectable atmosphere. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aad1815">10.1126/science.aad1815</jats:related-article> </jats:p>

<jats:title>A tripartite gene silencing complex</jats:title> <jats:p>The formation of specialized cell types during development involves the silencing of genes not required in those cell types. An important player in this silencing process is the polycomb repressive complex 2 (PRC2), which methylates histone H3 on lysine residue 27 (H3K27me). Jiao and Liu determined the x-ray crystal structure of a functional PRC2 complex from a thermophilic yeast species (see the Perspective by Schapira). The intimate association of the three subunits confers stability to PRC2. The structure also reveals how the reaction product, H3K27me, stimulates PRC2 allosterically and how a cancer-associated histone mutation blocks the PRC2 active site.</jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aac4383">10.1126/science.aac4383</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6258" page="278" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aad5203">278</jats:related-article> </jats:p>

<jats:title>Keeping a leash on cancer-killing cells</jats:title> <jats:p> Redirecting the immune system to attack tumor cells is proving to be an effective therapy against cancer. However, when patients are exposed to T cells engineered to recognize and attack cancer cells, there is a risk of runaway or excessive activity or of off-target effects, both of which can themselves be deadly. Wu <jats:italic>et al.</jats:italic> designed T cells expressing chimeric antigen receptors that recognize and attack cancer cells with an additional control system. This mechanism would allow a doctor administering the therapy to turn the engineered T cell “on” or “off” by administering a small molecule that is required along with cancer cell antigen to stimulate the T cells and activate their tumor cell–killing properties. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aab4077">10.1126/science.aab4077</jats:related-article> </jats:p>