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EMBO Molecular Medicine

Cover image for Vol. 6 Issue 3

March 2014

Volume 6, Issue 3

Pages 297–429

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      VEGF-B: a more balanced approach toward cardiac neovascularization? (pages 297–298)

      Christian Kupatt and Rabea Hinkel

      Article first published online: 12 FEB 2014 | DOI: 10.1002/emmm.201303730

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      A new report by Kari Alitalo's team shows that VEGF-B induces coronary artery growth that protects the heart from ischemic damage and switches myocardial metabolism from fatty acid to glucose utilization.

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      Defective minor spliceosome mRNA processing results in isolated familial growth hormone deficiency (pages 299–306)

      Jesús Argente, Raquel Flores, Armand Gutiérrez-Arumí, Bhupendra Verma, Gabriel Á Martos-Moreno, Ivon Cuscó, Ali Oghabian, Julie A Chowen, Mikko J Frilander and Luis A Pérez-Jurado

      Article first published online: 30 JAN 2014 | DOI: 10.1002/emmm.201303573

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      This is the first report of the implication of a minor spliceosome mutation in human disease. Specifically, isolated growth hormone deficiency due to a pituitary development defect affecting somatotrophs can derive from aberrant RNA splicing by RNPC3.

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    2. Closeup
    3. Report
    4. Research Articles
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      VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart (pages 307–321)

      Riikka Kivelä, Maija Bry, Marius R Robciuc, Markus Räsänen, Miia Taavitsainen, Johanna MU Silvola, Antti Saraste, Juha J Hulmi, Andrey Anisimov, Mikko I Mäyränpää, Jan H Lindeman, Lauri Eklund, Sanna Hellberg, Ruslan Hlushchuk, Zhen W Zhuang, Michael Simons, Valentin Djonov, Juhani Knuuti, Eero Mervaala and Kari Alitalo

      Article first published online: 21 JAN 2014 | DOI: 10.1002/emmm.201303147

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      Transgenic expression of VEGF-B in the rat heart leads to expansion of the coronary arterial tree and an increase in functional coronary reserve, accompanied by a shift in myocardial metabolism from fatty acid to glucose utilization.

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      Telomerase governs immunomodulatory properties of mesenchymal stem cells by regulating FAS ligand expression (pages 322–334)

      Chider Chen, Kentaro Akiyama, Takayoshi Yamaza, Yong-Ouk You, Xingtian Xu, Bei Li, Yimin Zhao and Songtao Shi

      Article first published online: 13 JAN 2014 | DOI: 10.1002/emmm.201303000

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      Bone marrow mesenchymal stem cells (BMMSC) have therapeutic properties in immune disorders. Telomerase function is shown to not only be critical for BMMSC stemness and osteogenic differentiation, but also to regulate BMMSC-mediated immune therapies.

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      Flurbiprofen ameliorated obesity by attenuating leptin resistance induced by endoplasmic reticulum stress (pages 335–346)

      Toru Hosoi, Rie Yamaguchi, Kikuko Noji, Suguru Matsuo, Sachiko Baba, Keisuke Toyoda, Takahiro Suezawa, Takaaki Kayano, Shinpei Tanaka and Koichiro Ozawa

      Article first published online: 14 JAN 2014 | DOI: 10.1002/emmm.201303227

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      Through targeting aldehyde dehydrogenase, flurbiprofen, a non-steroidal anti-inflammatory drug (NSAID), is shown to attenuate protein misfolding, endoplasmic reticulum stress and subsequent development of leptin resistance, overall reducing obesity in mice.

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      Heteropathogenic virulence and phylogeny reveal phased pathogenic metamorphosis in Escherichia coli O2:H6 (pages 347–357)

      Martina Bielaszewska, Roswitha Schiller, Lydia Lammers, Andreas Bauwens, Angelika Fruth, Barbara Middendorf, M Alexander Schmidt, Phillip I Tarr, Ulrich Dobrindt, Helge Karch and Alexander Mellmann

      Article first published online: 10 JAN 2014 | DOI: 10.1002/emmm.201303133

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      Hybrid Escherichia coli pathogens clinical significance was clearly shown during the deadly 2011 outbreak. STEC O2:H6 was diagnosed intestinal and uropathogenic in patients and is shown here as another heteropathogen that emerged via pathogroup conversion.

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      A potent anti-dengue human antibody preferentially recognizes the conformation of E protein monomers assembled on the virus surface (pages 358–371)

      Guntur Fibriansah, Joanne L Tan, Scott A Smith, Adamberage R de Alwis, Thiam-Seng Ng, Victor A Kostyuchenko, Kristie D Ibarra, Jiaqi Wang, Eva Harris, Aravinda de Silva, James E Crowe Jr and Shee-Mei Lok

      Article first published online: 14 JAN 2014 | DOI: 10.1002/emmm.201303404

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      Vaccine development against Dengue disease is complicated by the virus serotype priming to secondary infections. Structure of a potent human antibody 1F4 complexed with DENV serotype 1 highlights the hinge angle of the viral protein as critical for vaccine design.

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      Towards a new combination therapy for tuberculosis with next generation benzothiazinones (pages 372–383)

      Vadim Makarov, Benoit Lechartier, Ming Zhang, João Neres, Astrid M van der Sar, Susanne A Raadsen, Ruben C Hartkoorn, Olga B Ryabova, Anthony Vocat, Laurent A Decosterd, Nicolas Widmer, Thierry Buclin, Wilbert Bitter, Koen Andries, Florence Pojer, Paul J Dyson and Stewart T Cole

      Article first published online: 5 FEB 2014 | DOI: 10.1002/emmm.201303575

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      Tuberculosis (TB) drug resistance is still spreading worldwide, emphasizing the need for new efficient drug combinations. PBTZ169 is here presented as an optimized, potent and synergistic preclinical drug candidate for the treatment of TB in humans.

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      Triggering ubiquitination of IFNAR1 protects tissues from inflammatory injury (pages 384–397)

      Sabyasachi Bhattacharya, Kanstantsin V Katlinski, Maximilian Reichert, Shigetsugu Takano, Angela Brice, Bin Zhao, Qiujing Yu, Hui Zheng, Christopher J Carbone, Yuliya V Katlinskaya, N Adrian Leu, Kelly A McCorkell, Satish Srinivasan, Melanie Girondo, Hallgeir Rui, Michael J May, Narayan G Avadhani, Anil K Rustgi and Serge Y Fuchs

      Article first published online: 31 JAN 2014 | DOI: 10.1002/emmm.201303236

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      Inflammatory process in response to injury starts by inducing tissue damage followed by resolution of inflammation. Here, endogenous or induced IFNAR1 ubiquitination and degradation are shown to limit the extent of tissue damage and accelerate healing.

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      Pharmacological reversion of sphingomyelin-induced dendritic spine anomalies in a Niemann Pick disease type A mouse model (pages 398–413)

      Ana I Arroyo, Paola G Camoletto, Laura Morando, Marco Sassoe-Pognetto, Maurizio Giustetto, Paul P Van Veldhoven, Edward H Schuchman and Maria D Ledesma

      Article first published online: 21 JAN 2014 | DOI: 10.1002/emmm.201302649

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      A novel pathway is described in a Niemann Pick mouse model whereby elevated sphingomyelin impairs dendritic spines by modulating the actin cytoskeleton. Pharmacological activation of sphingomyelin catabolism in vivo with dexamethasone ameliorates the pathology of affected mice.

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      SIL1, a causative cochaperone gene of Marinesco-Sjögren syndrome, plays an essential role in establishing the architecture of the developing cerebral cortex (pages 414–429)

      Yutaka Inaguma, Nanako Hamada, Hidenori Tabata, Ikuko Iwamoto, Makoto Mizuno, Yoshiaki V Nishimura, Hidenori Ito, Rika Morishita, Motomasa Suzuki, Kinji Ohno, Toshiyuki Kumagai and Koh-ichi Nagata

      Article first published online: 29 JAN 2014 | DOI: 10.1002/emmm.201303069

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      SIL1 mutations cause Marinesco-Sjögren syndrome. SIL1 is shown to be involved in neuronal morphology and migration and axon network formation. SIL1 mutations may thus contribute to abnormal corticogenesis during development leading to mental retardation.

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