Catálogo de publicaciones - revistas

<jats:title>Making the right catch</jats:title> <jats:p> Tension reveals cryptic vinculin-binding sites on α-catenin and talin at cadherin-based cell-cell and integrin-based cell-matrix adhesions, respectively. The enrichment of vinculin at cellular adhesions is thus an indicator of load-induced reinforcement of the cytoskeletal linkage. Huang <jats:italic>et al.</jats:italic> used a single-molecule optical trap assay to measure the binding lifetimes of vinculin to single actin filaments under load. The vinculin-F-actin interaction formed a directional catch bond—one that is very weak at low force but that greatly increases in lifetime with increasing force. This explains vinculin's role as a reinforcing linker at both cell-cell and cell-matrix adhesions. </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="6352" page="703" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aan2556">703</jats:related-article> </jats:p>

<jats:title>Modeling a pregnancy disorder</jats:title> <jats:p> Preeclampsia, a dangerous pregnancy disorder marked by high blood pressure, can lead to premature birth and be life-threatening to the mother and baby. Research leading to effective treatments has been hampered by a lack of informative animal models. Ho <jats:italic>et al.</jats:italic> identified ELABELA as a hormone produced by the placenta whose levels are lower in preeclampsia (see the Perspective by Wirka and Quertermous). ELABELA-deficient pregnant mice showed clinical signs of preeclampsia, including high blood pressure and elevated urine protein. A proportion of embryos lacking ELABELA displayed defective heart development, and full-term pups had low birth weights. </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="6352" page="707" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aam6607">707</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6352" page="643" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aao2642">643</jats:related-article> </jats:p>

<jats:title>Identification of a new injection system</jats:title> <jats:p> To interact with other cells, bacteria use contractile machines that function similarly to membrane-puncturing bacteriophages. The so-called type 6 secretion system (T6SS) functions from inside a bacterial cell. Böck <jats:italic>et al.</jats:italic> used modern electron microscopy methods and functional assays to resolve the structure and function of a T6SS in the cellular context. They identified three modules and showed large-scale structural changes upon firing. T6SSs are organized in multibarrel gun-like arrays and may contribute to the survival of bacteria inside their host. </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="6352" page="713" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aan7904">713</jats:related-article> </jats:p>

<jats:title>The makings of the reproductive tract</jats:title> <jats:p> Every embryo, regardless of its sex, contains both male and female primitive reproductive tracts before sexual differentiation. To establish a sex-specific reproductive system, female embryos need to remove the components of male tracts. The general consensus contends that removal of the male tracts occurs by default, a passive outcome owing to a lack of testis-derived androgens. Working in mice, Zhao <jats:italic>et al.</jats:italic> discovered that this process instead was actively promoted by the transcription factor COUP-TFII (see the Perspective by Swain). Without the action of this factor, embryos retained male reproductive tracts, independently of androgen action. These findings unveil unexpected mechanisms underlying the sexually dimorphic establishment of reproductive tracts. </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="6352" page="717" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aai9136">717</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6352" page="648" related-article-type="in-this-issue" vol="357" xlink:href="10.1126/science.aao2630">648</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>Humanized tumor xenograft mouse models are powerful experimental systems for studying in vivo interactions between human immune cells and human tumors. These models are generated by engrafting both human hematopoietic stem cells and human tumor tissue into immunodeficient mice, such as the NOD/SCID gamma (NSG) strain. In recent years, humanized tumor xenograft mouse models have been integrated into checkpoint inhibitor development programs at many pharmaceutical and biotechnology companies as an indispensable part of the drug development process. As these models have improved, they have been shown to support higher levels of human myeloid-derived cells and regulatory T cells, and have been used successfully in recent studies of anti-PD1 drugs in lung, breast, bladder, and melanoma. Join our experts to hear about the latest research developments utilizing these cutting-edge models.</jats:p>