TABLE OF CONTENTS
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January 2018 Volume 20, Issue 1 |
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| Editorial News & Views Review Articles Letters Articles | |
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Editorial | |
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Supporting the sharing of research p1 doi:10.1038/s41556-017-0025-8 |
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News & Views | |
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Review Articles | |
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Mechanoreciprocity in cell migration pp8 - 20 Sjoerd van Helvert, Cornelis Storm & Peter Friedl doi:10.1038/s41556-017-0012-0 Friedl and co-authors discuss how migrating cells sense and respond to tissue mechanics, and how cells in turn modify their surroundings. |
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Letters | |
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A Pck1-directed glycogen metabolic program regulates formation and maintenance of memory CD8+ T cells pp21 - 27 Ruihua Ma, Tiantian Ji, Huafeng Zhang, Wenqian Dong, Xinfeng Chen et al. doi:10.1038/s41556-017-0002-2 Glycogen metabolism controls memory T cells. Ma et al. show that the metabolic gene PCK1 promotes glycogen formation, which is used in the pentose phosphate pathway, generating glutathione that is important for counteraction of ROS and thus promotion of memory T-cell maintenance, and resulting in improved antitumour immunity. |
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Mechanical cues control mutant p53 stability through a mevalonate–RhoA axis pp28 - 35 Eleonora Ingallina, Giovanni Sorrentino, Rebecca Bertolio, Kamil Lisek, Alessandro Zannini et al. doi:10.1038/s41556-017-0009-8 Ingallina et al. show that mutant p53 is protected from degradation in response to matrix stiffness in a manner dependent on RhoA geranylgeranylation and actomyosin dynamics. |
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Articles | |
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A homeostatic apical microtubule network shortens cells for epithelial folding via a basal polarity shift pp36 - 45 Michiko Takeda, Mustafa M. Sami & Yu-Chiun Wang doi:10.1038/s41556-017-0001-3 Takeda et al. reveal that the shortening of epithelial cells required for dorsal fold initiation in Drosophila embryos is driven by a microtubule-based mechanism involving dynein-mediated forces and Katanin-dependent remodelling. |
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ERBB3 and NGFR mark a distinct skeletal muscle progenitor cell in human development and hPSCs pp46 - 57 Michael R. Hicks, Julia Hiserodt, Katrina Paras, Wakana Fujiwara, Ascia Eskin et al. doi:10.1038/s41556-017-0010-2 Hicks et al. compare human pluripotent stem cell (hPSC)-derived muscle progenitors to fetal muscle cells, identify ERBB3/NGFR+ populations with improved myogenic potential in vivo and enhance cell maturation by inhibiting TGF-ß signalling during directed differentiation. |
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ABIN-1 regulates RIPK1 activation by linking Met1 ubiquitylation with Lys63 deubiquitylation in TNF-RSC pp58 - 68 Slawomir A. Dziedzic, Zhenyi Su, Vica Jean Barrett, Ayaz Najafov, Adnan K. Mookhtiar et al. doi:10.1038/s41556-017-0003-1 Dziedzic et al. show that the ubiquitin-binding protein ABIN-1 is recruited into TNFR1 signalling complex in a manner dependent on Met1 -ubiquitinating complex LUBAC to regulate K63 de-ubiquitination to activate RIPK1. |
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Adhesion forces and cortical tension couple cell proliferation and differentiation to drive epidermal stratification pp69 - 80 Yekaterina A. Miroshnikova, Huy Q. Le, David Schneider, Torsten Thalheim, Matthias Rübsam et al. doi:10.1038/s41556-017-0005-z Mechanics of epidermal differentiation Miroshnikova et al. find that during embryonic development, epidermal basal layer crowding generates local changes in cell shape, cortical tension, and adhesion that initiate differentiation and delamination |
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The autophagy receptor ALLO-1 and the IKKE-1 kinase control clearance of paternal mitochondria in Caenorhabditis elegans pp81 - 91 doi:10.1038/s41556-017-0008-9 Sato et al. identify ALLO-1 as an autophagy receptor required for paternal organelle clearance in Caenorhabditis elegans, and this process is dependent on ALLO-1 phosphorylation by the TBK1 family kinase IKKE-1. |
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Unresolved recombination intermediates lead to ultra-fine anaphase bridges, chromosome breaks and aberrations pp92 - 103 Ying Wai Chan, Kasper Fugger & Stephen C. West doi:10.1038/s41556-017-0011-1 Chan et al. show that unresolved recombination intermediates form a previously unappreciated type of ultra-fine bridge. These bridges are broken upon cell division, leading to chromosome breaks and instability. |
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A PERK–miR-211 axis suppresses circadian regulators and protein synthesis to promote cancer cell survival pp104 - 115 Yiwen Bu, Akihiro Yoshida, Nilesh Chitnis, Brian J. Altman, Feven Tameire et al. doi:10.1038/s41556-017-0006-y PERK regulates tumour cell survival. Bu et al. show that the unfolded protein response protein PERK induces miR-211 repression of the circadian factor Bmal1 to regulate protein synthesis and stress responses, contributing to tumour progression. |
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