Current policies for dealing with research misconduct emphasize the role and responsibility of individuals. Evidence from social psychology, however, shows that the environment determines personal conduct. Research misconduct policies should address these institutional factors.
Biological systems from single cells to whole organisms show emergent properties that are characteristic of complex systems. Understanding the emergence of new properties and the principles that govern it can help us to understand complex diseases and improve early diagnostic.
Many charities employ funding schemes from venture capital to accelerate research and drug development for rare diseases. Though it has yielded new treatments, venture philanthropy prompts raises criticism about the role of charities in marketing and pricing their drugs.
After a century of destruction, efforts are underway to halt the deforestation of tropical rain forests and replant lost areas. Research on ecology, biodiversity and other factors is essential to inform both policies to protect forests and measures to reclaim agricultural areas for reforestation.
This study describes the molecular architecture of the N‐type ATPase rotor ring from Burkholderia pseudomallei determined by electron cryo‐microscopy. The structure shows an unusually large c‐ring rotor with 17 subunits that is driven predominantly by protons.
Sarah Schulz, Martin Wilkes, Deryck J Mills, Werner Kühlbrandt, and Thomas Meier
p53 is a crucial regulator of cellular responses to toxic stress. This study identifies hnRNPC as a destabilizing p53 regulator. Doxorubicin treatment induces the nuclear retention and subsequent interaction of the lncRNA SNHG1 with hnRNPC, which impairs p53 destabilization.
Yuan Shen, Shanshan Liu, Jiao Fan, Yinghua Jin, Baolei Tian, Xiaofei Zheng, and Hanjiang Fu
This study shows that MYC inhibits GCLC, the rate‐limiting enzyme of glutathione synthesis, via the microRNA miR‐18a in primary tumors. Therefore, MYC‐driven liver tumors with low total tissue levels of glutathione exhibit increased sensitivity to a potent oxidant.
Brittany Anderton, Roman Camarda, Sanjeev Balakrishnan, Asha Balakrishnan, Rebecca A Kohnz, Lionel Lim, Kimberley J Evason, Olga Momcilovic, Klaus Kruttwig, Qiang Huang, Guowang Xu, Daniel K Nomura, and Andrei Goga
IL‐17 induces tissue inflammation and is involved in many autoimmune reactions. This study shows that the nuclear kinase NDR1 interacts with TRAF3 and promotes the formation of IL‐17R‐Act1‐TRAF6 complexes, which trigger downstream signal transduction and inflammation.
Chunmei Ma, Wenlong Lin, Zhiyong Liu, Wei Tang, Rahul Gautam, Hui Li, Youcun Qian, He Huang, and Xiaojian Wang
DGCR8 and DICER are required for canonical miRNA biogenesis. This study describes miRNA‐independent roles of DGCR8 that control progenitor cell expansion and neurogenesis, and promote targeting of the mRNA of the cortical transcription factor Tbr1.
Federica Marinaro, Matteo J Marzi, Nadin Hoffmann, Hayder Amin, Roberta Pelizzoli, Francesco Niola, Francesco Nicassio, and Davide De Pietri Tonelli
Increasing evidence indicates that the histone methyltransferase Ezh2 also modifies non‐histone substrates in a chromatin‐independent fashion. This study shows that Ezh2 controls immune homeostasis through such a non‐canonical mechanism by directly methylating the transcription factor PLZF.
Ajithkumar Vasanthakumar, Dakang Xu, Aaron TL Lun, Andrew J Kueh, Klaas PJM van Gisbergen, Nadia Iannarella, Xiaofang Li, Liang Yu, Die Wang, Bryan RG Williams, Stanley CW Lee, Ian J Majewski, Dale I Godfrey, Gordon K Smyth, Warren S Alexander, Marco J Herold, Axel Kallies, Stephen L Nutt, and Rhys S Allan
Deregulation of centrosome homeostasis is a feature of many human diseases. This study identifies Cep78 as an inhibitor of the HECT‐type E3 ubiquitin ligase EDD‐DYRK2‐DDB1VprBP that ubiquitinates the centriolar marker CP110 and regulates organelle homeostasis.
Delowar Hossain, Yalda Javadi Esfehani, Arindam Das, and William Y Tsang
The deacetylase SIRT1 protects against metabolic disorders in many tissues. SIRT1 also acts on the transcription factor NFATc1 in adipocytes, thereby enhancing IL‐4 expression. Sirt1 deletion lowers IL‐4 levels, reduces adipose‐resident M2 macrophages, and increases inflammation.