Catálogo de publicaciones - revistas

<jats:title>Diterpenoids inhibit lipid biosynthesis</jats:title> <jats:p> Plants make a variety of molecules that serve to protect them against hungry insects. Li <jats:italic>et al.</jats:italic> analyzed the balance between plants defending themselves and plants poisoning themselves. In wild tobacco ( <jats:italic>Nicotiana attenuata</jats:italic> ), two cytochrome P450 enzymes work within the biosynthetic pathway of 17-hydroxygeranyllinalool diterpene glycosides to help prevent the accumulation of toxic diterpene derivatives. Those same diterpene derivatives are formed in an insect herbivore after ingestion and cause toxicity by inhibiting sphingolipid biosynthesis in both plant and insect. </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="6526" page="255" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abe4713">255</jats:related-article> </jats:p>

<jats:title>α particles in stable nuclei</jats:title> <jats:p> α Decay is a common mode of radioactivity in heavy elements such as uranium that entails the loss of particles comprising two protons and two neutrons. Despite more than a century of study, when and where these α particles form in stable and unstable nuclei alike remains an open question. Tanaka <jats:italic>et al.</jats:italic> bombarded a series of stable tin isotopes with high-energy protons and detected ejected α particles at an abundance inversely correlated with mass number (see the Perspective by Hen). This observation, relating α particle accumulation to the neutron skin thickness at the nuclear surface, bears on models spanning radioactive decay to neutron star dynamics. </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="6526" page="260" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abe4688">260</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6526" page="232" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abf2427">232</jats:related-article> </jats:p>

<jats:title>Selective destruction of senescent cells</jats:title> <jats:p> Senescent cells are associated with a variety of age-related medical conditions and thus have been proposed as potential targets for therapy, but we do not yet have a full understanding of the underlying mechanisms. Johmura <jats:italic>et al.</jats:italic> used RNA interference to screen for enzymes essential to the survival of senescent cells (see the Perspective by Pan and Locasale). The authors identified a key role for glutamine metabolism, particularly the enzyme glutaminase 1, and demonstrated that inhibition of this pathway induced the death of senescent cells. Glutaminase targeting also ameliorated aging-related organ dysfunction and obesity-related disorders in mouse models, suggesting the potential therapeutic value of this approach. </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="6526" page="265" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abb5916">265</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6526" page="234" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abf6368">234</jats:related-article> </jats:p>