Catálogo de publicaciones - revistas

<jats:title>Viruses pack antiviral mediators</jats:title> <jats:p> Viruses often hijack host proteins for their own use, turning host cells into virion-spewing machines. However, Bridgeman <jats:italic>et al.</jats:italic> and Gentili <jats:italic>et al.</jats:italic> now report a sneaky way that the host can fight back (see the Perspective by Schoggins). Host cells that expressed the enzyme cGAS, an innate immune receptor that senses cytoplasmic DNA, packaged the cGAS-generated second messenger cGAMP into virions. Virions could then transfer cGAMP to neighboring cells, triggering an antiviral gene program in these newly infected cells. Such transfer of an antiviral mediator may help to speed up the immune response to put the brakes on viral spread. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue pp. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1228" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aab3632">1228</jats:related-article> and <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1232" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aab3628">1232</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1166" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aad0942">1166</jats:related-article> </jats:p>

<jats:title>Viruses pack antiviral mediators</jats:title> <jats:p> Viruses often hijack host proteins for their own use, turning host cells into virion-spewing machines. However, Bridgeman <jats:italic>et al.</jats:italic> and Gentili <jats:italic>et al.</jats:italic> now report a sneaky way that the host can fight back (see the Perspective by Schoggins). Host cells that expressed the enzyme cGAS, an innate immune receptor that senses cytoplasmic DNA, packaged the cGAS-generated second messenger cGAMP into virions. Virions could then transfer cGAMP to neighboring cells, triggering an antiviral gene program in these newly infected cells. Such transfer of an antiviral mediator may help to speed up the immune response to put the brakes on viral spread. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue pp. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1228" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aab3632">1228</jats:related-article> and <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1232" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aab3628">1232</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6253" page="1166" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aad0942">1166</jats:related-article> </jats:p>

<jats:title>A misstep in the chromosomes' dance</jats:title> <jats:p> The chromosomes of most cancer cells are unstable, suffering breaks and rearrangements. These aberrations perturb normal gene-regulatory programs and contribute to cancer progression. Tanno <jats:italic>et al.</jats:italic> studied several human cell lines that show chromosome instability. Homologous chromosomes did not pair very well with each other during cell division. These chromosomes had lost a specific chromatin covalent modification, methylation of histone H3 lysine 9, and/or the protein “glue” cohesin at the chromosomes' centromeres. Either of these losses interfered with the binding of the shugoshin 1 protein, which is required for proper chromosome pairing and segregation. </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" issue="6253" page="1237" related-article-type="in-this-issue" vol="349" xlink:href="10.1126/science.aaa2655">1237</jats:related-article> </jats:p>

<jats:p> Between alternative transcription start sites, alternative splicing, and posttranslational modifications, a given gene may produce dozens of protein variants, each with a different biological activity. Teasing apart those structure-function relationships requires mapping specific variants to their associated biological functions, and the tool of the trade for doing so is mass spectrometry. But not just any mass spec will do. Researchers need a holistic view of protein structure, data that is lost with the popular “bottom-up” proteomics strategy. Powered by today’s ultrahigh-resolution, high massaccuracy mass specs, protein biochemists are increasingly turning bottom-up upside-down. Their new alternative: topdown proteomics. <jats:list list-type="bullet"> <jats:list-item> <jats:p> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/site/products/lst_20150911.xhtml">Read the Feature (Full-Text HTML)</jats:ext-link> </jats:p> </jats:list-item> <jats:list-item> <jats:p> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/site/products/lst_20150911.pdf">Read the Feature (PDF)</jats:ext-link> </jats:p> </jats:list-item> <jats:list-item> <jats:p> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/site/products/lst_20150911_np.pdf">Read New Products (PDF)</jats:ext-link> </jats:p> </jats:list-item> </jats:list> </jats:p>

<jats:p>A weekly roundup of information on newly offered instrumentation, apparatus, and laboratory materials of potential interest to researchers.</jats:p>

<jats:p> While technological breakthroughs of the last decade have greatly advanced our understanding of the cancer genome, they have also revealed the immense complexity and heterogeneity of tumors. The key to further advancing our understanding and treatment of cancer is to distinguish between genes and pathways that drive tumorigenesis (driver events) and neutral, passenger events. A growing body of evidence has shown that not all DNA-level alterations have biological implications, making it necessary to examine multiple ꞌomics levels including the transcriptome and proteome, to identify critical driver events. In this webinar, our expert panel will discuss how using a multi-omics–based approach to cancer research can advance our understanding of cancer biology as well as lead to the discovery of novel biomarkers. <jats:list list-type="bullet"> <jats:list-item> <jats:p> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://webinar.sciencemag.org/webinar/archive/advancing-precision-medicine-through-multi-omics">View the Webinar</jats:ext-link> </jats:p> </jats:list-item> </jats:list> </jats:p>

<jats:p>On this week's show: How our genes influence our microbes and a roundup of daily news stories.</jats:p>