Catálogo de publicaciones - revistas

<jats:title>AIMing to block tissue damage</jats:title> <jats:p> Ionizing radiation kills actively dividing cells such as those in the gut and in the bone marrow. Hu <jats:italic>et al.</jats:italic> found a pathological role for the protein AIM2 in irradiation-induced tissue damage. AIM2 is best known for its role in sensing double-stranded DNA in the cytoplasm and alerting the body to infections. It seems that AIM2 also senses DNA damage caused by radiation and then triggers intestinal epithelial cells and bone marrow cells to die. Deficiency in AIM2 protected mice from irradiation-induced gastrointestinal syndrome and hematopoietic failure. </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="6313" page="765" related-article-type="in-this-issue" vol="354" xlink:href="10.1126/science.aaf7532">765</jats:related-article> </jats:p>

<jats:title>CRISPR screens illuminate enhancer function</jats:title> <jats:p> The noncoding regions around a gene that control the transcription of the protein-coding region are difficult to identify. Leveraging a CRISPR interference system (CRISPRi), Fulco <jats:italic>et al.</jats:italic> identified enhancer-promoter connections to map specific noncoding regions affecting gene regulation for the GATA1 and MYC loci (see the Perspective by Einstein and Yeo). Going forward, such CRISPRi-mapping can be used to evaluate promoter-enhancer screens functionally in an unbiased way. </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="6313" page="769" related-article-type="in-this-issue" vol="354" xlink:href="10.1126/science.aag2445">769</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6313" page="705" related-article-type="in-this-issue" vol="354" xlink:href="10.1126/science.aak9849">705</jats:related-article> </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 it is well established that DNA damage can increase the risk of cancer, changes to the epigenome or the chromatin architecture are equally important. DNA damage triggers a redistribution of DNA-binding proteins around the site of damage, resulting in localized and temporary alteration of chromatin structure. However, repeated cycles of DNA damage and repair may lead to permanent changes in the epigenome, thereby promoting the onset of pathological diseases such as cancer. This webinar will examine how we may be able to develop effective new therapeutic options for cancer treatment by targeting proteins responsible for chromatin modifications. <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/deciphering-cancer-genomic-instability-cancer">View the Webinar</jats:ext-link> </jats:p> </jats:list-item> </jats:list> </jats:p>