Catálogo de publicaciones - revistas

<jats:title>Another way for GPCRs to signal</jats:title> <jats:p> G protein–coupled receptors (GPCRs) normally transmit signals by coupling to heterotrimeric guanine nucleotide–binding proteins (G proteins) or by binding β-arrestin proteins. Smith <jats:italic>et al.</jats:italic> provide evidence for another mechanism, an approximate combination of the two. They monitored the interaction of vasopressin type 2 receptors (V2Rs) and G <jats:sub>α</jats:sub> proteins in cultured cells using bioluminescent resonance energy transfer. Even though V2Rs do not signal canonically through G <jats:sub> α <jats:sub>i</jats:sub> </jats:sub> proteins, they promoted the formation of complexes containing β-arrestin and G <jats:sub> α <jats:sub>i</jats:sub> </jats:sub> , and this led to downstream signaling to extracellular signal-regulated kinase protein kinases. </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.aay1833">eaay1833</jats:related-article> </jats:p>

<jats:title>The legacy of Tohoku-oki</jats:title> <jats:p> Ten years ago, the magnitude 9 Tohoku-oki earthquake rocked Japan and caused massive damage. The earthquake also generated a destructive tsunami, the impacts of which are still being managed today. Kodaira <jats:italic>et al.</jats:italic> review what was learned from the tremendous number of observations from the great earthquake that unexpectedly ruptured into a shallow part of the megathrust fault. Postseismic deformation is ongoing, as is the risk of another very large normal fault earthquake seaward of the Japan Trench. </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.abe1169">eabe1169</jats:related-article> </jats:p>

<jats:title>A lipid-protein autoimmunity target</jats:title> <jats:p> Several autoimmune diseases, including systemic lupus erythematosus and primary antiphospholipid syndrome, are characterized by the presence of antiphospholipid antibodies (aPLs). These molecules can activate the complement and coagulation cascades, which contributes to pathologies such as thrombosis, stroke, and pregnancy complications. Müller-Calleja <jats:italic>et al.</jats:italic> found that endothelial protein C receptor (EPCR) in complex with lysobisphosphatidic acid (LBPA) is the cell-surface target for aPL and mediates its internalization (see the Perspective by Kaplan). aPL binding to EPCR-LBPA resulted in the activation of tissue factor–mediated coagulation and interferon-α production by dendritic cells. Interferon-α, in turn, fueled the expansion of B1a cells, which secrete aPLs. The specific blockade of this target in mice inhibited the development of aPL autoimmunity, offering hope for future therapies for these conditions. </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.aay1833">eaay1833</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6534" page="1100" related-article-type="in-this-issue" vol="371" xlink:href="10.1126/science.abg6449">1100</jats:related-article> </jats:p>

<jats:title>Decrypting pathogen effector networks</jats:title> <jats:p> Many disease-causing bacteria use a molecular syringe to inject dozens of their proteins, called effectors, into intestinal cells, blocking key immune responses. Ruano-Gallego <jats:italic>et al.</jats:italic> used the mouse pathogen <jats:italic>Citrobacter rodentium</jats:italic> to model effector function in vivo. They found that effectors work together as a network, allowing the microbe great flexibility in maintaining pathogenicity. An artificial intelligence platform correctly predicted colonization outcomes of alternative networks from the in vivo data. However, the host was able to bypass the obstacles erected by different effector networks and activate complementary immune responses that cleared the pathogen and induced protective immunity. </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.abc9531">eabc9531</jats:related-article> </jats:p>

<jats:title>Transitioning lung for postnatal life</jats:title> <jats:p> The lung is a complex organ composed of multiple cell types, and its alveolus serves as the functional unit of gas exchange. The alveolar type 1 cell (AT1) serves as an active signaling hub in the developing and postnatal mouse and human lung. Zepp <jats:italic>et al.</jats:italic> generated a comprehensive single-cell atlas of the developing murine lung and identified cell differentiation and cell-to-cell communication as the lung transitions to air breathing. The AT1 cells spatially aligned with stromal progenitors and formed a signaling hub that preferentially communicated with a transient, force-exerting, myofibroblast through signaling factors including Shh and Wnts to actively remodel the alveolus after the transition to air breathing. </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.abc3172">eabc3172</jats:related-article> </jats:p>

<jats:p>As we mark the 1-year anniversary of the declaration by the World Health Organization (WHO) of COVID-19 as a global pandemic, the world has suffered a staggering and tragic human toll. During this dark time, the scientific community has been called to rise to the occasion in unprecedented ways. The intensity of the work and the sense of urgency have been unremitting and exhausting. As we sort out the triumphs and frustrations, we can begin to reflect on what we have learned.</jats:p>

<jats:p>A roundup of weekly science policy and related news.</jats:p>