Catálogo de publicaciones - revistas

<jats:title>Mutant protein in tumors hits the DEK</jats:title> <jats:p> Cancer genome sequencing projects have uncovered a multitude of mutations in human tumors. Understanding whether and how these mutations contribute to tumor development and progression could ultimately lead to new therapies. Theurillat <jats:italic>et al.</jats:italic> studied the protein product of a gene that is recurrently mutated in prostate cancer. Normally this protein helps attach a biochemical tag to cellular proteins that marks them for degradation. The new work shows that the tumor-associated mutant protein loses this tagging ability, which results in the stabilization of a handful of cellular proteins that would otherwise be degraded. One of the most intriguing of these proteins was DEK, which helps prostate cancer cells invade into surrounding tissue. </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="6205" page="85" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1250255">85</jats:related-article> </jats:p>

<jats:title>Excess signaling is bad for the aging brain</jats:title> <jats:p> Preventing antiviral-like responses may protect function in the aging brain. Baruch <jats:italic>et al.</jats:italic> monitored messenger RNA production in the choroid plexus, the interface between the blood and cerebrospinal fluid, in young and old mice (see the Perspective by Ransohoff). They detected an inflammatory response in older mice not present in the brain of young mice that was also seen in old aged human samples postmortem. Preventing signaling by the cytokine interferon-I, which normally helps in the antiviral response of the immune system, helped prevent the decrease in cognitive function seen in aged mice. </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="6205" page="89" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1252945">89</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="36" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1260705">36</jats:related-article> </jats:p>

<jats:title>Resident memory T cells sound the alarm</jats:title> <jats:p> Immunological memory protects against reinfection. Resident memory T cells (T <jats:sub>RM</jats:sub> ) are long-lived and remain in the tissues where they first encountered a pathogen (see the Perspective by Carbone and Gebhardt). Schenkel <jats:italic>et al.</jats:italic> and Ariotti <jats:italic>et al.</jats:italic> found that CD8 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells act like first responders in the female reproductive tissue or the skin of mice upon antigen reencounter. By secreting inflammatory proteins, T <jats:sub>RM</jats:sub> cells rapidly activated local immune cells to respond, so much so that they protected against infection with an unrelated pathogen. Iijima and Iwasaki found that CD4 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells protected mice against reinfection with intravaginal herpes simplex virus 2. </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="6205" page="98" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254536">98</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="101" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254803">101</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="93" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1257530">93</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="40" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1259925">40</jats:related-article> </jats:p>

<jats:title>Resident memory T cells sound the alarm</jats:title> <jats:p> Immunological memory protects against reinfection. Resident memory T cells (T <jats:sub>RM</jats:sub> ) are long-lived and remain in the tissues where they first encountered a pathogen (see the Perspective by Carbone and Gebhardt). Schenkel <jats:italic>et al.</jats:italic> and Ariotti <jats:italic>et al.</jats:italic> found that CD8 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells act like first responders in the female reproductive tissue or the skin of mice upon antigen reencounter. By secreting inflammatory proteins, T <jats:sub>RM</jats:sub> cells rapidly activated local immune cells to respond, so much so that they protected against infection with an unrelated pathogen. Iijima and Iwasaki found that CD4 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells protected mice against reinfection with intravaginal herpes simplex virus 2. </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="6205" page="98" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254536">98</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="101" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254803">101</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="93" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1257530">93</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="40" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1259925">40</jats:related-article> </jats:p>

<jats:title>Resident memory T cells sound the alarm</jats:title> <jats:p> Immunological memory protects against reinfection. Resident memory T cells (T <jats:sub>RM</jats:sub> ) are long-lived and remain in the tissues where they first encountered a pathogen (see the Perspective by Carbone and Gebhardt). Schenkel <jats:italic>et al.</jats:italic> and Ariotti <jats:italic>et al.</jats:italic> found that CD8 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells act like first responders in the female reproductive tissue or the skin of mice upon antigen reencounter. By secreting inflammatory proteins, T <jats:sub>RM</jats:sub> cells rapidly activated local immune cells to respond, so much so that they protected against infection with an unrelated pathogen. Iijima and Iwasaki found that CD4 <jats:sup>+</jats:sup> T <jats:sub>RM</jats:sub> cells protected mice against reinfection with intravaginal herpes simplex virus 2. </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="6205" page="98" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254536">98</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="101" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1254803">101</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="93" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1257530">93</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6205" page="40" related-article-type="in-this-issue" vol="346" xlink:href="10.1126/science.1259925">40</jats:related-article> </jats:p>

<jats:p>Until relatively recently, the power of molecular biology was at once vast and limited. Researchers who wanted to knock out specific genes to see what they did mostly had to restrict such studies to mice, and specific strains at that. Now a new class of genome- and epigenome-editing tools is reshaping the landscape. From Arabidopsis to humans to zebrafish, researchers are finding that, generally speaking, when it comes to the genome, if they can dream it, they can build it.</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>On this week's show: Mapping the bottom of the ocean and a daily news round up.</jats:p>

<jats:p>Like travel writers and diplomats, scientists have tremendous opportunities for international interactions. Researchers can train abroad and attend conferences all over the world. The academic sabbatical is a chance to experience a foreign land while maintaining domestic roots. Hosting a guest scientist from another country can bring fresh perspectives to a research group. Cross-border professional relationships require cultivation, though. This feature offers advice from experienced scientists on the whys and hows of international collaborations.</jats:p>