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EMBO Molecular Medicine

Cover image for Vol. 5 Issue 12

December 2013

Volume 5, Issue 12

Pages 1795–1934, i–ii

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      A new inducible model for t(8;21) AML (pages 1795–1797)

      James C. Mulloy

      Version of Record online: 4 NOV 2013 | DOI: 10.1002/emmm.201303483

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      New targets for old diseases: lessons from mucolipidosis type II (pages 1801–1803)

      Carmine Settembre and Andrea Ballabio

      Version of Record online: 8 NOV 2013 | DOI: 10.1002/emmm.201303496

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      Instruction of haematopoietic lineage choices, evolution of transcriptional landscapes and cancer stem cell hierarchies derived from an AML1-ETO mouse model (pages 1804–1820)

      Nina Cabezas-Wallscheid, Victoria Eichwald, Jos de Graaf, Martin Löwer, Hans-Anton Lehr, Andreas Kreft, Leonid Eshkind, Andreas Hildebrandt, Yasmin Abassi, Rosario Heck, Anna Katharina Dehof, Svetlana Ohngemach, Rolf Sprengel, Simone Wörtge, Steffen Schmitt, Johannes Lotz, Claudius Meyer, Thomas Kindler, Dong-Er Zhang, Bernd Kaina, John C. Castle, Andreas Trumpp, Ugur Sahin and Ernesto Bockamp

      Version of Record online: 4 OCT 2013 | DOI: 10.1002/emmm.201302661

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      This novel model system of AML1-ETO driven acute myeloid leukaemia addresses the concept of ‘oncogene addiction’. Better understanding of AML1-ETO need to maintain leukemia and rewire the transcriptome may help to design future therapies.

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      Combining chemotherapeutic agents and netrin-1 interference potentiates cancer cell death (pages 1821–1834)

      Andrea Paradisi, Marion Creveaux, Benjamin Gibert, Guillaume Devailly, Emeline Redoulez, David Neves, Elsa Cleyssac, Isabelle Treilleux, Christian Klein, Gerhard Niederfellner, Philippe A. Cassier, Agnès Bernet and Patrick Mehlen

      Version of Record online: 8 OCT 2013 | DOI: 10.1002/emmm.201302654

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      Conventional chemotherapeutic agents are often associated with resistance and toxicity. Interference with netrin-1/receptors interaction triggers tumor cell death. The combination of both is shown as a promising therapeutic approach.

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      An essential role for decorin in bladder cancer invasiveness (pages 1835–1851)

      Mohamed El Behi, Sophie Krumeich, Catalina Lodillinsky, Aurélie Kamoun, Lorenzo Tibaldi, Gaël Sugano, Aurélien De Reynies, Elodie Chapeaublanc, Agnès Laplanche, Thierry Lebret, Yves Allory, François Radvanyi, Olivier Lantz, Ana María Eiján, Isabelle Bernard-Pierrot and Clotilde Théry

      Version of Record online: 20 OCT 2013 | DOI: 10.1002/emmm.201302655

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      Only a small fraction of patients with non-invasive bladder cancer respond well to therapy. This study shows that the adaptive immune system cannot control invasive bladder tumors, while Decorin is found critical for this cancer progression.

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      Molecular architecture of Streptococcus pneumoniae surface thioredoxin-fold lipoproteins crucial for extracellular oxidative stress resistance and maintenance of virulence (pages 1852–1870)

      Malek Saleh, Sergio G. Bartual, Mohammed R. Abdullah, Inga Jensch, Tauseef M. Asmat, Lothar Petruschka, Thomas Pribyl, Manuela Gellert, Christopher H. Lillig, Haike Antelmann, Juan A. Hermoso and Sven Hammerschmidt

      Version of Record online: 18 OCT 2013 | DOI: 10.1002/emmm.201202435

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      Streptococcus pneumoniae can cause fatal diseases. While cytoplasmic oxidative stress-resistance is known, pneumococci thioredoxin Etrx1, -2 and SpMsrAB2 are shown here to be key for virulence and extracellular oxidative stress resistance mechanism.

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      Decreased bone formation and increased osteoclastogenesis cause bone loss in mucolipidosis II (pages 1871–1886)

      Katrin Kollmann, Jan Malte Pestka, Sonja Christin Kühn, Elisabeth Schöne, Michaela Schweizer, Kathrin Karkmann, Takanobu Otomo, Philip Catala-Lehnen, Antonio Virgilio Failla, Robert Percy Marshall, Matthias Krause, Rene Santer, Michael Amling, Thomas Braulke and Thorsten Schinke

      Version of Record online: 15 OCT 2013 | DOI: 10.1002/emmm.201302979

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      Dysfunctional osteoblasts and the Il-6-driven osteoclast increase rather than lysosomal hydrolase missorting underlie the osteoporotic phenotype in a mouse model of mucolipidosis II. Bisphosphonate treatment increased bone density and stabilization.

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      Compound loss of muscleblind-like function in myotonic dystrophy (pages 1887–1900)

      Kuang-Yung Lee, Moyi Li, Mini Manchanda, Ranjan Batra, Konstantinos Charizanis, Apoorva Mohan, Sonisha A. Warren, Christopher M. Chamberlain, Dustin Finn, Hannah Hong, Hassan Ashraf, Hideko Kasahara, Laura P. W. Ranum and Maurice S. Swanson

      Version of Record online: 8 OCT 2013 | DOI: 10.1002/emmm.201303275

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      Combined loss of Mbnl1 and Mbnl2 recapitulates myotonic dystrophy with reduced lifespan, severe myotonia and muscle weakness and wasting, cardiac conduction block and significant enhancement of myotonic dystrophy-associated RNA splicing errors.

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      A major role for RCAN1 in atherosclerosis progression (pages 1901–1917)

      Nerea Méndez-Barbero, Vanesa Esteban, Silvia Villahoz, Amelia Escolano, Katia Urso, Arantzazu Alfranca, Cristina Rodríguez, Susana A. Sánchez, Tsuyoshi Osawa, Vicente Andrés, José Martínez-González, Takashi Minami, Juan Miguel Redondo and Miguel R. Campanero

      Version of Record online: 15 OCT 2013 | DOI: 10.1002/emmm.201302842

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      Rcan1 is induced in human and mouse atherosclerotic vessels and found in lesional macrophages, endothelial and vascular smooth muscle cells. Its genetic deletion (or the transplantation of Rcan1-deficient BM-derived cells) reduces the severity of lesions.

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      Inhibition of phosphodiesterase-4 promotes oligodendrocyte precursor cell differentiation and enhances CNS remyelination (pages 1918–1934)

      Yasir A. Syed, Alexandra Baer, Matthias P. Hofer, Ginez A. González, Jon Rundle, Szymon Myrta, Jeffrey K. Huang, Chao Zhao, Moritz J. Rossner, Matthew W. B. Trotter, Gert Lubec, Robin J. M. Franklin and Mark R. Kotter

      Version of Record online: 21 OCT 2013 | DOI: 10.1002/emmm.201303123

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      Mechanisms of re-myelination failure in multiple sclerosis for example remain incompletely understood. Here, phosphodiesterase Pde4 inhibition is shown to increase OPC differentiation and remyelination via cAMP-Erk1/2/p38Mapk-Creb1 signaling axis.

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