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EMBO Molecular Medicine is an open access online journal published by Wiley-Blackwell on behalf of EMBO.

The quality of the journal is guaranteed by the editorial and advisory boards, consisting of leading researchers in the field of molecular medicine, together with the commitment to scientific excellence and the professionalism of EMBO Editors.

EMBO Molecular Medicine is a peer-reviewed, online open access journal dedicated to a new research discipline at the interface between clinical research and basic biology. It offers clinicians and researchers in this area the opportunity to publish their best work in a broadly distributed and highly visible forum, thereby lending a strong impetus to this important and rapidly developing field and helping to forge new links between clinicians and molecular biologists. Studies based on model organisms also fall within the scope of the journal, provided that the results presented are evidently and directly relevant to human disease.

EMBO Molecular Medicine publishes research articles as full-length research papers and short reports. In addition, the journal publishes editorials and review articles in innovative formats that target a broad and non-specialized audience.

Areas within the scope include, but are not limited to:

     Aging
     Angiogenesis
     Cancer biology
     Channelopathies
     Differentiation and development
     Endocrinology/Metabolic disease
     Genetics/epigenetics
     Genomics, transcriptomics, proteomics, metabolomics of disease, systems medicine
     Gene therapy
     Immunology and inflammation
     Infectious diseases
     Neurodegeneration, neurological diseases and myopathies, sensory defects
     Stem cells and regenerative medicine
     Vascular and cardiovascular biology

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2013-06-03•SRSF1与SRSF9 RNA结合蛋白可通过增强β连环蛋白生物合成而促进Wnt信号介导性肿瘤发生

Published 2013年6月,Volume 5,Issue 6

最新一期

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  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
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Closeups
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  Farber disease: understanding a fatal childhood disorder and dissecting ceramide biology (pages 799–801)
  Mark S. Sands
  
  Article first published online: 13 MAY 2013 | DOI: 10.1002/emmm.201302781
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  You can teach an old dog new tricks: angiopoietin-1 instructs Tie2^pos myeloid cells to promote neovascularization in ischemic limbs (pages 802–804)
  Costanza Emanueli and Nicolle Kränkel
  
  Article first published online: 4 JUN 2013 | DOI: 10.1002/emmm.201302794
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Reviews
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  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
  
  This review focuses on the current knowledge of host genetic mutations and variants associated with an increased susceptibility toCandida infection in humans.
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  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
  
  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.
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Research Articles
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  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
  
  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
  
  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
  
  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
  
  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
  
  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
  
  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
  
  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
  
  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
  
  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.
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Corrigendum
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  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
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Masthead
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  Masthead (pages i–ii)
  Article first published online: 4 JUN 2013 | DOI: 10.1002/emmm.201390009
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