| | | | | Table of ContentsNews & Views Articles | Volume 34, Number 17 | News & Views | A new study shows that neutrophils recruited to a wound site enhance the proliferative activity of pre‐neoplastic cells via a paracrine mechanism, thus shedding light on the crosstalk between inflammation and cancer. Stefanie K Wculek and Ilaria Malanchi Published online 19.07.2015 | | A screen for factors modulating miRNA function in neurons identifies two new regulators of Ago2 activity and shows these to be required for neuronal plasticity. Farahnaz Sananbenesi and Andre Fischer Published online 28.07.2015 | | While it is well established that abnormal expansion of a polyQ tract in the huntingtin protein N‐terminus triggers Huntington's disease, recent findings show that C‐terminal cleavage fragments also contribute to cellular toxicity. Maria Jimenez‐Sanchez and David C Rubinsztein Published online 28.07.2015 | | At the end of the autophagic process, lysosomes need to reform via autophagic lysosome reformation. Phospholipid PI(3)P aids in this process downstream of mTOR and VPS34–UVRAG activity. Yang Chen and Li Yu Published online 28.07.2015 | Articles | Innate immune cells that are initially drawn to a wound can subsequently be attracted away to nearby cancer cells and drive their proliferation. Nicole Antonio, Marie Louise Bønnelykke‐Behrndtz, Laura Chloe Ward, John Collin, Ib Jarle Christensen, Torben Steiniche, Henrik Schmidt, Yi Feng, and Paul Martin | | The identification of two novel modulators of miRNA function reveals an additional layer of transcriptional and post‐transcriptional control of Argonaute proteins and adds further insight on the central role for miRNAs in neurogenesis. Peter H Störchel, Juliane Thümmler, Gabriele Siegel, Ayla Aksoy‐Aksel, Federico Zampa, Simon Sumer, and Gerhard Schratt Published online 23.06.2015 | | Site‐specifically controlled cleavage of the mutant huntingtin protein reveals a pathogenic mechanism induced by non‐polyQ‐containing fragments that are generated upon proteolysis during disease progression. Marie‐Thérèse El‐Daher, Emilie Hangen, Julie Bruyère, Ghislaine Poizat, Ismael Al‐Ramahi, Raul Pardo, Nicolas Bourg, Sylvie Souquere, Céline Mayet, Gérard Pierron, Sandrine Lévêque‐Fort, Juan Botas, Sandrine Humbert, and Frédéric Saudou Published online 12.07.2015 | | During starvation, VPS34 activity at the lysosomes controls autophagosome‐lysosome reformation and cell viability, illustrating a novel role for this autophagy‐initiating lipid kinase at late stages of autophagy. Michael J Munson, George FG Allen, Rachel Toth, David G Campbell, John M Lucocq, and Ian G Ganley | | Following extracellular Ca2+ influx, extended‐synaptotagmins (E‐Syts) mediate ER‐plasma membrane tethering. Tethering requires the PI(4,5)P2‐binding C2‐domains of E‐Syt1 and and is regulated by E‐Syt2. E‐Syt1 plasma membrane binding resembles the one of synaptotagmin 1, the Ca2+‐sensor mediating exocytosis. Olof Idevall‐Hagren, Alice Lü, Beichen Xie, and Pietro De Camilli Published online 22.07.2015 | | | |
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