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EMBO Molecular Medicine

Cover image for Vol. 5 Issue 6

June 2013

Volume 5, Issue 6

Pages 795–965, i–ii

  1. Perspective

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have full text access to this OnlineOpen article
      Next generation therapeutics for Alzheimer's disease (pages 795–798)

      Dale E. Bredesen and Varghese John

      Article first published online: 23 MAY 2013 | DOI: 10.1002/emmm.201202307

  2. Closeups

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have full text access to this OnlineOpen article
    2. You have full text access to this OnlineOpen article
  3. Reviews

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have full text access to this OnlineOpen article
      Genetic susceptibility to Candida infections (pages 805–813)

      Sanne P. Smeekens, Frank L. van de Veerdonk, Bart Jan Kullberg and Mihai G. Netea

      Article first published online: 30 APR 2013 | DOI: 10.1002/emmm.201201678

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      This review focuses on the current knowledge of host genetic mutations and variants associated with an increased susceptibility to Candida infection in humans.

    2. You have full text access to this OnlineOpen article
      Of inflammasomes and pathogens – sensing of microbes by the inflammasome (pages 814–826)

      Franz Bauernfeind and Veit Hornung

      Article first published online: 13 MAY 2013 | DOI: 10.1002/emmm.201201771

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      Inflammasomes are multiprotein platforms that recognize pathogens and play a critical role in innate immunity. This review carefully details key discoveries on how microbes are sensed by and engage inflammasomes in the host cells.

  4. Research Articles

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have full text access to this OnlineOpen article
      Systemic ceramide accumulation leads to severe and varied pathological consequences (pages 827–842)

      Abdulfatah M. Alayoubi, James C. M. Wang, Bryan C. Y. Au, Stéphane Carpentier, Virginie Garcia, Shaalee Dworski, Samah El-Ghamrasni, Kevin N. Kirouac, Mathilde J. Exertier, Zi Jian Xiong, Gilbert G. Privé, Calogera M. Simonaro, Josefina Casas, Gemma Fabrias, Edward H. Schuchman, Patricia V. Turner, Razqallah Hakem, Thierry Levade and Jeffrey A. Medin

      Article first published online: 16 MAY 2013 | DOI: 10.1002/emmm.201202301

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      This first viable animal model of lysosomal acid ceramidase (ACDase) deficiency (Farber disease) with typical accumulation of ceramide and cellular infiltrations provides insights into the pathophysiology of the disease and development of therapy.

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      PHD2 regulates arteriogenic macrophages through TIE2 signalling (pages 843–857)

      Alexander Hamm, Lorenzo Veschini, Yukiji Takeda, Sandra Costa, Estelle Delamarre, Mario Leonardo Squadrito, Anne-Theres Henze, Mathias Wenes, Jens Serneels, Ferdinando Pucci, Carmen Roncal, Andrey Anisimov, Kari Alitalo, Michele De Palma and Massimiliano Mazzone

      Article first published online: 25 APR 2013 | DOI: 10.1002/emmm.201302695

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      TIE2-expressing macrophages switch towards an M2 phenotype following ischemia. ANG1/TIE2-signaling results in down-regulation of PHD2 and promotes arteriogenesis, suggesting new effective cell-based therapeutic approaches to treat limb ischemia.

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      TIE2-expressing monocytes/macrophages regulate revascularization of the ischemic limb (pages 858–869)

      Ashish S. Patel, Alberto Smith, Silvia Nucera, Daniela Biziato, Prakash Saha, Rizwan Q. Attia, Julia Humphries, Katherine Mattock, Steven P. Grover, Oliver T. Lyons, Luca G. Guidotti, Richard Siow, Aleksandar Ivetic, Stuart Egginton, Matthew Waltham, Luigi Naldini, Michele De Palma and Bijan Modarai

      Article first published online: 7 MAY 2013 | DOI: 10.1002/emmm.201302752

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      Tie2-expressing macrophages (TEMs) have the potential to improve revascularization of the ischemic limb and may therefore, represent an attractive novel cell therapy for promoting limb salvage in patients suffering from critical limb ischemia.

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      Defects of Vps15 in skeletal muscles lead to autophagic vacuolar myopathy and lysosomal disease (pages 870–890)

      Ivan Nemazanyy, Bert Blaauw, Cecilia Paolini, Catherine Caillaud, Feliciano Protasi, Amelie Mueller, Tassula Proikas-Cezanne, Ryan C. Russell, Kun-Liang Guan, Ichizo Nishino, Marco Sandri, Mario Pende and Ganna Panasyuk

      Article first published online: 30 APR 2013 | DOI: 10.1002/emmm.201202057

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      Mice lacking Vps15 in skeletal muscles develop the pathological features of autophagic vacuolar myopathy (AVM). Vps34/Vps15 complex activity is shown to be critical in disease conditions such as AVMs, and possibly other lysosomal storage diseases.

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      A TSPO ligand is protective in a mouse model of multiple sclerosis (pages 891–903)

      Daniel J. Daugherty, Vimal Selvaraj, Olga V. Chechneva, Xiao-Bo Liu, David E. Pleasure and Wenbin Deng

      Article first published online: 17 MAY 2013 | DOI: 10.1002/emmm.201202124

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      The Authors report on the novel neuroprotective and anti-inflammatory effect of etifoxine, a clinically available drug that is a mitochondrial TSPO ligand, against autoimmune demyelination in an experimental model of multiple sclerosis.

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      Wolfram Syndrome protein, Miner1, regulates sulphydryl redox status, the unfolded protein response, and Ca2+ homeostasis (pages 904–918)

      Sandra E. Wiley, Alexander Y. Andreyev, Ajit S. Divakaruni, Robert Karisch, Guy Perkins, Estelle A. Wall, Peter van der Geer, Yi-Fan Chen, Ting-Fen Tsai, Melvin I. Simon, Benjamin G. Neel, Jack E. Dixon and Anne N. Murphy

      Article first published online: 24 MAY 2013 | DOI: 10.1002/emmm.201201429

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      Wolfram syndrome (DIDMOAD) is an incurable metabolic disease caused by mutations in Wolframin or Miner1 genes. This study reveals Miner1 biological role in cellular redox status and proposes antioxidant as therapeutic strategy against DIDMOAD.

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      The neural crest transcription factor Brn3a is expressed in melanoma and required for cell cycle progression and survival (pages 919–934)

      Tobias Hohenauer, Carola Berking, Andreas Schmidt, Sebastian Haferkamp, Daniela Senft, Claudia Kammerbauer, Sabine Fraschka, Saskia Anna Graf, Martin Irmler, Johannes Beckers, Michael Flaig, Achim Aigner, Sabrina Höbel, Franziska Hoffmann, Heiko Hermeking, Simon Rothenfusser, Stefan Endres, Thomas Ruzicka and Robert Besch

      Article first published online: 13 MAY 2013 | DOI: 10.1002/emmm.201201862

      Thumbnail image of graphical abstract

      Brn3a, a POU family transcription factor normally involved in neuronal development, is reported here to promote melanoma survival by playing a role in cell cycle progression. Targeting Brn3a and its regulated genes could offer therapeutic value.

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      Inhibition of endotrophin, a cleavage product of collagen VI, confers cisplatin sensitivity to tumours (pages 935–948)

      Jiyoung Park, Thomas S. Morley and Philipp E. Scherer

      Article first published online: 30 APR 2013 | DOI: 10.1002/emmm.201202006

      Thumbnail image of graphical abstract

      Endotrophin, secreted from stromal adipocytes in the tumor microenvironment, confers cisplatin resistance by enhancing EMT, fibrosis and angiogenesis. Thiazolidinediones neutralize endotrophin activities and improve the therapeutic response.

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      Combined mutation of Vhl and Trp53 causes renal cysts and tumours in mice (pages 949–964)

      Joachim Albers, Michal Rajski, Désirée Schönenberger, Sabine Harlander, Peter Schraml, Adriana von Teichman, Strahil Georgiev, Peter J. Wild, Holger Moch, Wilhelm Krek and Ian J. Frew

      Article first published online: 22 APR 2013 | DOI: 10.1002/emmm.201202231

      Thumbnail image of graphical abstract

      The Authors demonstrate that secondary genetic alterations can cooperate with loss of VHL to cause kidney tumour formation and implicate TP53 mutations in the pathogenesis of a subset of clear cell renal cell carcinomas in humans.

  5. Corrigendum

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have full text access to this OnlineOpen article
      Corrigendum (page 965)

      Allan Jones, Kilian Friedrich, Maria Rohm, Michaela Schäfer, Carolyn Algire, Philipp Kulozik, Oksana Seibert, Karin Müller-Decker, Tjeerd Sijmonsma, Daniela Strzoda, Carsten Sticht, Norbert Gretz, Geesje M. Dallinga-Thie, Barbara Leuchs, Manfred Kögl, Wolfgang Stremmel, Mauricio Berriel Diaz and Stephan Herzig

      Article first published online: 4 JUN 2013 | DOI: 10.1002/emmm.201390008

      This article corrects:

      TSC22D4 is a molecular output of hepatic wasting metabolism

      Vol. 5, Issue 2, 294–308, Article first published online: 11 JAN 2013

  6. Masthead

    1. Top of page
    2. Perspective
    3. Closeups
    4. Reviews
    5. Research Articles
    6. Corrigendum
    7. Masthead
    1. You have open access to this content
      Masthead (pages i–ii)

      Article first published online: 4 JUN 2013 | DOI: 10.1002/emmm.201390009

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