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FEBS Journal

Cover image for Vol. 280 Issue 18

September 2013

Volume 280, Issue 18

Pages i–iii, 4337–4710

  1. Front Cover

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Front Cover (page i)

      Article first published online: 2 SEP 2013 | DOI: 10.1111/j.1742-4658.2013.08794.x

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      Schematic illustration of Stress granule (SG) assembly upon stress and recovery. SGs are RNA-protein particles that are formed transiently upon stress. In the background, SGs are shown by immunocytochemistry in HeLa cells subjected to heat stress. The possible contribution of SGs to neurodegeneration is discussed in Bentmann et al. (pp. 4348–4370)

  2. Editorial Information

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Editorial Information (pages ii–iii)

      Article first published online: 2 SEP 2013 | DOI: 10.1111/j.1742-4658.2013.08794_1.x

  3. MiniReview Series

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Neurodegeneration – from multiple sclerosis to Alzheimer's disease (page 4337)

      Wolfgang Meyerhof and Dietmar Richter

      Article first published online: 29 JUL 2013 | DOI: 10.1111/febs.12430

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      A serious public health challenge for the aging population is the increasing prevalence of neurodegenerative diseases. The 32nd Blankenese Conference, ‘Neurodegeneration: From Multiple Sclerosis to Alzheimer's Disease’, held in May 2012 (http://web.zmnh.uni-hamburg.de/blankenese_conferences/) discussed the pathogenic mechanisms, genetic risk factors and strategies in diagnosis, therapy and prevention of neurodegenerative diseases. This minireview series features as papers four highlights of the program.

  4. Minireview

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Roles of endoproteolytic α-cleavage and shedding of the prion protein in neurodegeneration (pages 4338–4347)

      Hermann C. Altmeppen, Johannes Prox, Berta Puig, Frank Dohler, Clemens Falker, Susanne Krasemann and Markus Glatzel

      Article first published online: 13 MAR 2013 | DOI: 10.1111/febs.12196

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      Besides its role in fatal and transmissible prion diseases, the cellular prion protein seems to play central roles in other neurodegenerative diseases. Here, the physiological proteolytic cleavage of this protein is reviewed with a focus on how this might influence neurodegenerative conditions, such as prion diseases and Alzheimer's disease.

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      Stress granules in neurodegeneration – lessons learnt from TAR DNA binding protein of 43 kDa and fused in sarcoma (pages 4348–4370)

      Eva Bentmann, Christian Haass and Dorothee Dormann

      Article first published online: 9 MAY 2013 | DOI: 10.1111/febs.12287

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      Stress granules (SGs) are cytoplasmic particles transiently formed in stressed cells. Recently, SG marker proteins were identified to label characteristic TDP-43- or FUS-positive inclusions found in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal lobar degeneration. This review provides an overview about SG biology in general and discusses the possible role of SGs in the pathogenesis of neurodegenerative diseases.

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      Regulatable transgenic mouse models of Alzheimer disease: onset, reversibility and spreading of Tau pathology (pages 4371–4381)

      Katja Hochgräfe, Astrid Sydow and Eva-Maria Mandelkow

      Article first published online: 22 APR 2013 | DOI: 10.1111/febs.12250

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      The review deals with the onset, reversibility and spreading of Tau pathology observed in Tau transgenic mouse models. We summarize histopathological features caused by inducible expression of pro-aggregant Tau and correlate them to behavioral deficits and impairments in synaptic transmission, which recover after removal of amyloidogenic Tau. Furthermore we discuss mechanisms of Tau spreading and transmission throughout mouse brain regions.

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      Genetic manipulations of mutant huntingtin in mice: new insights into Huntington's disease pathogenesis (pages 4382–4394)

      C. Y. Daniel Lee, Jeffrey P. Cantle and X. William Yang

      Article first published online: 31 JUL 2013 | DOI: 10.1111/febs.12418

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      Elongation of the polyglutamine repeat in huntingtin leads to selective neurodegeneration in the striatum and cortex in Huntington's disease (HD). We highlight recent findings from novel HD mouse models suggesting the role of distinct neuronal and non-neuronal cell types in eliciting cell-autonomous or non-cell-autonomous pathogenesis. We also discuss the impact of specific huntingtin cis-domains or post-translational modifications on disease pathogenesis.

  5. Minireview Series

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Post-translational modifications of CFTR: insight into protein trafficking and cystic fibrosis disease (page 4395)

      Margarida D. Amaral and Carlos M. Farinha

      Article first published online: 5 JUL 2013 | DOI: 10.1111/febs.12345

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      CFTR, which when mutated causes Cystic Fibrosis, constitutes an excellent model of regulated traffic of plasma membrane proteins. This Mini-Reviews Series covers major aspects by which post-translational modifications regulate CFTR biogenesis and trafficking, giving new insights into well-established mechanisms and covering novel aspects (such as the role of phosphorylation in the regulation of membrane stability or the relevance of signalling pathways in CF disease).

  6. Minireview

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Control of cystic fibrosis transmembrane conductance regulator membrane trafficking: not just from the endoplasmic reticulum to the Golgi (pages 4396–4406)

      Carlos M. Farinha, Paulo Matos and Margarida D. Amaral

      Article first published online: 5 JUL 2013 | DOI: 10.1111/febs.12392

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      This minireview highlights major aspects of the mechanisms of quality control that survey folding and processing of CFTR, including the role of chaperones and export machinery at the endoplasmic reticulum, as well as the different players regulating traffic and stability of CFTR at the plasma membrane. Some new developments in the field – e.g. the role of autophagy– are also discussed.

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      Structural changes of CFTR R region upon phosphorylation: a plastic platform for intramolecular and intermolecular interactions (pages 4407–4416)

      Zoltan Bozoky, Mickael Krzeminski, P. Andrew Chong and Julie D. Forman-Kay

      Article first published online: 25 JUL 2013 | DOI: 10.1111/febs.12422

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      CFTR chloride channel gating and trafficking are regulated by phosphorylation on the regulatory (R) region (red), which is intrinsically disordered in both non-phosphorylated (A) and phosphorylated (B) states. R region plays a crucial role in phosphorylation-dependent intra- and inter-molecular interactions. The dynamic conformation sampling and transient binding of R region to multiple partners enables complex control of CFTR function.

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      CFTR: a hub for kinases and crosstalk of cAMP and Ca2+ (pages 4417–4429)

      Karl Kunzelmann and Anil Mehta

      Article first published online: 27 AUG 2013 | DOI: 10.1111/febs.12457

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      The Cystic Fibrosis protein CFTR is not just a chloride channel but acts as a membrane scaffold for many other proteins linked to cell calcium and cyclic AMP. Here, we merge these themes by examining the ins and outs of signal pathways that either control CFTR or are controlled by CFTR. We focus on kinase-kinase (Figure), channel-kinase and channel-channel interactions.

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      Cystic fibrosis transmembrane conductance regulator degradation: cross-talk between the ubiquitylation and SUMOylation pathways (pages 4430–4438)

      Annette Ahner, Xiaoyan Gong and Raymond A. Frizzell

      Article first published online: 22 JUL 2013 | DOI: 10.1111/febs.12415

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      SUMOylation is a novel post-translational modification of CFTR, mediated by selective interaction of the common mutant, F508del, with the small heat shock protein, Hsp27 and the SUMO E2, Ubc9. Cross-talk with the ubiquitin pathway derives from the conjugation of F508del with SUMO-2/3 poly-chains that are recognized by the SUMO-targeted ubiquitin ligase, RNF4. Other examples of SUMO-ubiquitin pathway interactions are discussed.

  7. Original Articles

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
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      Thermodynamic characterization of five key kinetic parameters that define neuronal nitric oxide synthase catalysis (pages 4439–4453)

      Mohammad Mahfuzul Haque, Jesús Tejero, Mekki Bayachou, Zhi-Qiang Wang, Mohammed Fadlalla and Dennis J. Stuehr

      Article first published online: 15 JUL 2013 | DOI: 10.1111/febs.12404

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      Global kinetic model for NOS catalysis. NO Synthase enzymes convert L-arginine to NO in two sequential reactions. During NOS catalysis five key kinetic parameters (kcat1, kcat2, kr, kd, and kox) play major role. The interplay of these five kinetic parameters determine NOS specific activity, O2 concentration response, and pulsatile versus steady-state NO generation.

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      Consequences of proline-to-alanine substitutions for the stability and refolding of onconase (pages 4454–4462)

      Mandy Hacke, Tobias Gruber, Cindy Schulenburg, Jochen Balbach and Ulrich Arnold

      Article first published online: 12 JUL 2013 | DOI: 10.1111/febs.12406

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      Onconase contains four trans prolines. Its refolding, which includes a folding intermediate, comprises a slow phase possibly originating from a cis-to-trans peptidyl-prolyl isomerization. We substituted all four prolines individually by alanines. The slow phase was not eliminated for any of the variants, but the P43A substitution resulted in a faster formation of the intermediate and a significant increase in thermodynamic stability.

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      Characterization of Ruminococcus albus cellodextrin phosphorylase and identification of a key phenylalanine residue for acceptor specificity and affinity to the phosphate group (pages 4463–4473)

      Tatsuya Sawano, Wataru Saburi, Ken Hamura, Hirokazu Matsui and Haruhide Mori

      Article first published online: 19 JUL 2013 | DOI: 10.1111/febs.12408

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      R. albus cellodextrin phosphorylase (RaCDP), classified into glycoside hydrolase family 94, was characterized. Among the cello-oligosaccharides tested, RaCDP had the highest phosphorolytic and synthetic activities towards cellohexaose and cellopentaose, respectively. Sophorose, laminaribiose, β-1,4-xylobiose, β-1,4-mannobiose, and cellobiitol served as acceptors. Site-directed mutational study revealed that Tyr633 is responsible for low affinity to the phosphate group and synthetic activity towards β-1,4-mannobiose.

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      Morphological restriction of human coronary artery endothelial cells substantially impacts global gene expression patterns (pages 4474–4494)

      Jessica M. Stiles, Robert Pham, Rebecca K. Rowntree, Clarissa Amaya, James Battiste, Laura E. Boucheron, Dianne C. Mitchell and Brad A. Bryan

      Article first published online: 22 JUL 2013 | DOI: 10.1111/febs.12410

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      Alterations in cell shape affect endothelial cell function, yet it is unknown how morphological restriction affects the transcriptome. We cultured endothelial cells on spatially defined adhesive micropatterns and used pattern recognition algorithms, statistical analysis, and microarray data to demonstrate that the ability of endothelial cells to spread, but not necessarily their particular morphology, dictates their global gene expression patterns.

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      Mechanism of dual specificity kinase activity of DYRK1A (pages 4495–4511)

      Agnes Walte, Katharina Rüben, Ruth Birner-Gruenberger, Christian Preisinger, Simone Bamberg-Lemper, Nikolaus Hilz, Franz Bracher and Walter Becker

      Article first published online: 22 JUL 2013 | DOI: 10.1111/febs.12411

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      This study addresses the mechanism of dual specificity kinase activity in DYRK1A and related kinases. Here, present results that support a model of DYRK autoactivation in which the one-time tyrosine autophosphorylation in the activation loop stabilizes a conformation of the catalytic domain with enhanced serine/threonine kinase activity without disabling tyrosine phosphorylation by the mature kinase.

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      Effects of hyperoxia on the permeability of 16HBE14o– cell monolayers – the protective role of antioxidant vitamins E and C (pages 4512–4521)

      Hanady S. Al-Shmgani, Roy M. Moate, Peter D. Macnaughton, J. Robert Sneyd and A. John Moody

      Article first published online: 19 JUL 2013 | DOI: 10.1111/febs.12413

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      16HBE14o- cell monolayers were exposed for 24 h to normoxia, hyperoxia and hyperoxia with α-tocopherol and/or ascorbate. Decreased TER seen after hyperoxia was associated with decreased ZO-1 (immunohistochemistry, see figure), and decreased ZO-1 expression. Expression of IL-8, IL-6 and TNF-α were increased after hyperoxia and these cytokines increased in the medium. Antioxidant vitamins had a partial protective effect.

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      Downregulated adaptor protein p66Shc mitigates autophagy process by low nutrient and enhances apoptotic resistance in human lung adenocarcinoma A549 cells (pages 4522–4530)

      Zhichao Zheng, Jie Yang, Dan Zhao, Dan Gao, Xiaojie Yan, Zhi Yao, Zhe Liu and Zhenyi Ma

      Article first published online: 25 JUL 2013 | DOI: 10.1111/febs.12416

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      The adaptor protein p66Shc mediates anoikis and prevents lung cancer metastasis. Loss of p66Shc mitigates baseline level of low-nutrient induced autophagy in Ras hyperactivated A549 cancer cells and enhances apoptosis resistance. Thus, p66Shc coordinately regulates autophagy and apoptosis resistance during nutrient deprivation. Understanding of p66Shc functions is expected to be used to characterize the autophagy process in lung cancers.

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      miR-144 downregulation increases bladder cancer cell proliferation by targeting EZH2 and regulating Wnt signaling (pages 4531–4538)

      Yuwen Guo, Liang Ying, Ye Tian, Peiqian Yang, Yichen Zhu, Zhipeng Wang, Feng Qiu and Jun Lin

      Article first published online: 25 JUL 2013 | DOI: 10.1111/febs.12417

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      miR-144 level is significantly decreased in bladder cancer cell lines as well as in clinical cancer tissues. miR-144 inhibitor blocks the expression of endogenous miR-144 and promotes cancer cell proliferation, whereas miR-144 overexpression is sufficient to inhibit cell proliferation. Enhancer of zeste homolog 2 (EZH2) is a target gene of miR-144. miR-144 downregulation relieves miR-144-mediated repression of EZH2, which results in activation of Wnt/β-catenin signaling and subsequent cell proliferation.

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      The unique N-terminal region of SRMS regulates enzymatic activity and phosphorylation of its novel substrate docking protein 1 (pages 4539–4559)

      Raghuveera K. Goel, Sayem Miah, Kristin Black, Natasha Kalra, Chenlu Dai and Kiven E. Lukong

      Article first published online: 19 AUG 2013 | DOI: 10.1111/febs.12420

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      The present study pertains to the biochemical characterization of SRMS, an understudied non-receptor tyrosine kinase, and the validation of Dok1 as its first physiological substrate. Our study has identified an indispensable role of the unique N-terminus region of SRMS in regulating its kinase activity and sub-cellular localization. We have also characterized Dok1 as the first substrate of SRMS.

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      Structure of a bacterial glycoside hydrolase family 63 enzyme in complex with its glycosynthase product, and insights into the substrate specificity (pages 4560–4571)

      Takatsugu Miyazaki, Megumi Ichikawa, Gaku Yokoi, Motomitsu Kitaoka, Haruhide Mori, Yoshikazu Kitano, Atsushi Nishikawa and Takashi Tonozuka

      Article first published online: 26 JUL 2013 | DOI: 10.1111/febs.12424

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      We converted a glycoside hydrolase family 63 enzyme, Escherichia coli YgjK, to a glycosynthase to probe its substrate specificity. The reactions with β-d-glucosyl fluoride and monosaccharides showed that the largest amount of glycosynthase product accumulated when galactose was employed as an acceptor molecule. The crystal structure of E727A indicated that the disaccharide bound at the active site was 2-O-α-d-glucopyranosyl-d-galactopyranose.

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      Silibinin protects murine fibroblast L929 cells from UVB-induced apoptosis through the simultaneous inhibition of ATM-p53 pathway and autophagy (pages 4572–4584)

      Weiwei Liu, Wuxiyar Otkur, Yuning Zhang, Qiuyuan Li, Yuanchao Ye, Linghe Zang, Hao He, Toshihiko Hayashi, Shin-ichi Tashiro, Satoshi Onodera and Takashi Ikejima

      Article first published online: 2 AUG 2013 | DOI: 10.1111/febs.12426

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      UVB is a major cause of skin damages. In this study, UVB irradiation caused apoptosis in murine fibroblast L929 cells. ATM protein and p53 were activated by UVB, accompanying up-regulation of the autophagy, which synergistically promoted the cell apoptosis. Silibinin simultaneously repressed the activation of ATM-p53 and autophagy, thereby protecting UVB-irradiated L929 cells from apoptosis.

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      Plumbagin inhibits cytokinesis in Bacillus subtilis by inhibiting FtsZ assembly – a mechanistic study of its antibacterial activity (pages 4585–4599)

      Anusri Bhattacharya, Bhavya Jindal, Parminder Singh, Anindya Datta and Dulal Panda

      Article first published online: 2 AUG 2013 | DOI: 10.1111/febs.12429

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      Plumbagin was found to inhibit the proliferation of Bacillus subtilis cells apparently by perturbing Z-ring assembly. Plumbagin inhibited the assembly and GTPase activity of purified BsFtsZ. The putative plumbagin binding site on BsFtsZ was identified by docking analysis. Two BsFtsZ variants, V307R and D199A, showed resistance towards the inhibitory action of plumbagin suggesting the residues are important for plumbagin binding.

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      The interaction of gelsolin with tropomyosin modulates actin dynamics (pages 4600–4611)

      Sofia Khaitlina, Helene Fitz and Horst Hinssen

      Article first published online: 31 JUL 2013 | DOI: 10.1111/febs.12431

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      By forming a complex with gelsolin in solution, tropomyosin inhibits the actin filament severing activity of gelsolin. On the other hand, binding of tropomyosin to F-actin does not significantly protect filaments from being severed by gelsolin. Therefore, tropomyosin may be involved in the regulation of actin dynamics in vivo by binding gelsolin in solution and thereby preventing actin filament fragmentation.

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      Upregulation of heat shock protein 27 confers resistance to actinomycin D-induced apoptosis in cancer cells (pages 4612–4624)

      Wenbo Ma, Yan Teng, Hui Hua, Jinlin Hou, Ting Luo and Yangfu Jiang

      Article first published online: 31 JUL 2013 | DOI: 10.1111/febs.12432

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      The anticancer agent actinomycin D (Act D) up-regulates heat shock protein 27 (HSP27) through preventing its degradation. HSP27 knockdown leads to an increase in actinomycin D-induced caspase 3 and caspase 7 cleavage, and sensitizes Act D-induced apoptosis in rhabdosarcoma cells and breast cancer cells. Upregulation of HSP27 represents an adaptive response that compromises the anticancer activity of Act D.

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      Mitogen-activated protein kinase p38 and retinoblastoma protein signalling is required for DNA damage-mediated formation of senescence-associated heterochromatic foci in tumour cells (pages 4625–4639)

      Yu Zhang, Yanyan Gao, Li Zhao, Liping Han, Yang Lu, Pingfu Hou, Xi Shi, Xin Liu, Baoqing Tian, Xiuli Wang, Baiqu Huang and Jun Lu

      Article first published online: 1 AUG 2013 | DOI: 10.1111/febs.12435

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      DNA-damaging agents doxorubicin (Dox) and 7-ethyl-10-hydroxycamptothecin (SN-38) were able to induce SAHF in some tumor cell types, which was accompanied by activation of RB pathway. Contrarily, tumor cells in which the RB pathway could not be activated failed to form SAHF. In addition, p38 MAPK pathway was involved in tumor cell SAHF formation. Furthermore, HBP1 was required for SAHF formation.

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      Explicit consideration of topological and parameter uncertainty gives new insights into a well-established model of glycolysis (pages 4640–4651)

      Fiona Achcar, Michael P.  Barrett and Rainer Breitling

      Article first published online: 19 AUG 2013 | DOI: 10.1111/febs.12436

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      Previous models of glycolysis in the sleeping sickness parasite Trypanosoma brucei assumed that the core part of glycolysis in this parasite requires tight compartmentalization within an organelle, the glycosome. Recently, this idea was challenged when size-specific metabolite pores were discovered in the glycosomal membrane. We use a novel uncertainty-aware computational modelling approach to explore the consequences of this finding.

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      Identifying critical unrecognized sugar–protein interactions in GH10 xylanases from Geobacillus stearothermophilus using STD NMR (pages 4652–4665)

      Yael S. Balazs, Elina Lisitsin, Oshrat Carmiel, Gil Shoham, Yuval Shoham and Asher Schmidt

      Article first published online: 5 AUG 2013 | DOI: 10.1111/febs.12437

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      Saturation transfer difference 1H NMR spectroscopy epitope maps are used to compare a wild type xylanase with a non-catalytic mutant. Critical hydrophobic interactions at a highly conserved Trp pocket are exposed in the wild-type enzyme. Mutation induced anomeric specificity is revealed and interpreted in terms of looser binding. A novel subsite assignment tool based on aromatic shielding is introduced.

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      Intermediate instability at high temperature leads to low pathway efficiency for an in vitro reconstituted system of gluconeogenesis in Sulfolobus solfataricus (pages 4666–4680)

      Theresa Kouril, Dominik Esser, Julia Kort, Hans V. Westerhoff, Bettina Siebers and Jacky L. Snoep

      Article first published online: 22 AUG 2013 | DOI: 10.1111/febs.12438

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      Four enzymes of the gluconeogenic pathway in Sulfolobus solfataricus were purified, kinetically characterized and reconstituted in vitro at 70 °C to quantify the contribution of heat-unstable pathway intermediates to carbon loss from the system. A mathematical model could quantitatively predict the systems fluxes and metabolite concentrations. Approximately half the carbon in the system was lost due to degradation of thermolabile intermediates.

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      Structure of NADP+-dependent glutamate dehydrogenase from Escherichia coli – reflections on the basis of coenzyme specificity in the family of glutamate dehydrogenases (pages 4681–4692)

      Michael A. Sharkey, Tânia F. Oliveira, Paul C. Engel and Amir R. Khan

      Article first published online: 20 AUG 2013 | DOI: 10.1111/febs.12439

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      Glutamate dehydrogenases (GDHs) catalyse oxidative deamination of l-glutamate to α-ketoglutarate using NAD+ and/or NADP+. The crystal structure of E. coli GDH (EcGDH) reveals that NADP+ specificity is enabled by Asp263, which orients a positively-charged loop toward the 2′-phosphate, and Ser264, which H-bonds to the 2′-phosphate. In contrast, PyGDH exploits the equivalent acidic residue (Asp241) for direct recognition of NAD+.

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      The 5′-untranslated region regulates ATF5 mRNA stability via nonsense-mediated mRNA decay in response to environmental stress (pages 4693–4707)

      Masaya Hatano, Mariko Umemura, Natsumi Kimura, Takashi Yamazaki, Hitoshi Takeda, Haruo Nakano, Shigeru Takahashi and Yuji Takahashi

      Article first published online: 19 AUG 2013 | DOI: 10.1111/febs.12440

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      Activating transcription factor 5 (ATF5) mRNA increases in response to environmental stress and this increase is dependent on mRNA stabilization. We show that ATF5 mRNA is a naturally-occurring normal mRNA target of NMD, and provide evidence of linkage between stress-regulated translational regulation and the mRNA decay pathway, which constitutes a mechanism regulating expression of stress response genes.

  8. Author index

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
    1. You have free access to this content
      Author index (page 4708)

      Article first published online: 2 SEP 2013 | DOI: 10.1111/j.1742-4658.2013.08793.x

  9. Table of Contents

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. MiniReview Series
    5. Minireview
    6. Minireview Series
    7. Minireview
    8. Original Articles
    9. Author index
    10. Table of Contents
    1. You have free access to this content
      Table of Contents (pages 4709–4710)

      Article first published online: 2 SEP 2013 | DOI: 10.1111/febs.12492

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