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The FEBS Journal

Cover image for Vol. 280 Issue 21

Special Issue: Frontiers in Cell Signalling, and Ca2+-Signalling and Transport in Health and Disease

November 2013

Volume 280, Issue 21

Pages i–iii, 5163–5568

  1. Front Cover

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Special Issue
    5. Author index
    6. Table of Contents
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      Front Cover (page i)

      Version of Record online: 15 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08800.x

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      Signalling and regulation of sphingosine kinase 2 by H.A. Neubauer & S.M. Pitson (pp. 5317–5336).

  2. Editorial Information

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Special Issue
    5. Author index
    6. Table of Contents
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      Editorial Information (pages ii–iii)

      Version of Record online: 15 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08800_1.x

  3. Special Issue

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Special Issue
    5. Author index
    6. Table of Contents
    1. You have free access to this content
      Special Issue – Signalling. Introduction: Frontiers in cell signalling (page 5163)

      Roger Daly and Tony Tiganis

      Version of Record online: 23 SEP 2013 | DOI: 10.1111/febs.12508

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      This series of articles in the FEBS Journal Special Issue on Signalling is based on the 6th Garvan Signalling Symposium, 2012. Articles focused on understanding the spatial and temporal contexts for signalling, the complexities of signalling networks in biology, and the translational opportunities afforded by delineating the role of signalling in human disease are featured. An accompanying series is based on an international symposium ‘Ca2+ Signalling and Transport in Health and Disease’, Aarhus, 2012.

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      Do signalling endosomes play a role in T cell activation? (pages 5164–5176)

      Carola Benzing, Jérémie Rossy and Katharina Gaus

      Version of Record online: 26 JUL 2013 | DOI: 10.1111/febs.12427

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      Signalling endosomes are a mechanism to modulate and compartmentalize cell signalling. In T cell, the spatial distribution of signalling proteins within the plasma membrane and between membranes is central to T cell activation. Here, we review the mechanisms by which endosomes regulate signalling and asked whether signalling endosomes and other signalling vesicles play a role in T cell signalling.

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      Advanced intravital subcellular imaging reveals vital three-dimensional signalling events driving cancer cell behaviour and drug responses in live tissue (pages 5177–5197)

      Max Nobis, Neil O. Carragher, Ewan J. McGhee, Jennifer P. Morton, Owen J. Sansom, Kurt I. Anderson and Paul Timpson

      Version of Record online: 28 JUN 2013 | DOI: 10.1111/febs.12348

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      Intravital imaging offers a new approach to study disease in living tissue with greater fidelity and biological complexity than can be achieved in many 2D-settings. Here we highlight how 3D or live intravital imaging has uncovered biological mechanisms or modes of drug action and we offer a view of how this may be integrated into the early drug discovery process.

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      Syndapin – a membrane remodelling and endocytic F-BAR protein (pages 5198–5212)

      Annie Quan and Phillip J. Robinson

      Version of Record online: 5 JUL 2013 | DOI: 10.1111/febs.12343

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      Syndapin (PACSIN), an F-BAR protein, functions in different endocytic and vesicle trafficking pathways and provide critical links between the cytoskeletal network in different cellular processes. The membrane remodelling activity of the F-BAR domain is important to syndapin function. Signalling pathways regulating syndapin function by phosphorylation are now contributing to our understanding of the broader functions of this family of proteins.

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      Glycogen synthase kinase 3 substrates in mood disorders and schizophrenia (pages 5213–5227)

      Adam R. Cole

      Version of Record online: 15 JUL 2013 | DOI: 10.1111/febs.12407

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      Glycogen synthase kinase 3 (GSK3) and its upstream regulators are strongly implicated in mood disorders and Schizophrenia. However, relatively little progress has been made on identifying its pathogenic targets in these disorders. These could become next generation therapeutic targets that are more potent and specific than current drugs. Possible candidates and their connection to mood disorders and Schizophrenia are discussed.

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      Specific inhibition of PI3K p110δ inhibits CSF-1-induced macrophage spreading and invasive capacity (pages 5228–5236)

      Kellie A. Mouchemore, Natalia G. Sampaio, Michael W. Murrey, E. Richard Stanley, Brian J. Lannutti and Fiona J. Pixley

      Version of Record online: 5 JUN 2013 | DOI: 10.1111/febs.12316

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      CSF-1-induced phosphorylation of CSF-1R Y721 mediates association of PI3K to trigger PIP3 production and spreading and invasive capacity in macrophages. These activities are mediated solely by the p110™ isoform in a macrophage cell line, M−/−.WT, and in primary macrophages. GS-1101, a potent and selective p110™ inhibitor, inhibits macrophage invasion and matrix degradation.

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      Global characterization of signalling networks associated with tamoxifen resistance in breast cancer (pages 5237–5257)

      Brigid C. Browne, Falko Hochgräfe, Jianmin Wu, Ewan K. A. Millar, Jane Barraclough, Andrew Stone, Rachael A. McCloy, Christine S. Lee, Caroline Roberts, Naveid A. Ali, Alice Boulghourjian, Fabian Schmich, Rune Linding, Lynn Farrow, Julia M. W. Gee, Robert I. Nicholson, Sandra A. O'Toole, Robert L. Sutherland, Elizabeth A. Musgrove, Alison J. Butt and Roger J. Daly

      Version of Record online: 19 AUG 2013 | DOI: 10.1111/febs.12441

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      In this study, tamoxifen-resistant MCF7 breast cancer cells (TamR) were characterized using proteomics and phosphoproteomics. Phosphorylation of Yes kinase and expression of actin-binding protein MARCKS were significantly elevated in TamR cells, and each were found to contribute to TamR cell motility. In primary breast cancers, MARCKS was independently predictive of poor survival in the whole cohort and in ER-positive patients.

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      Unravelling the molecular complexity of GPCR-mediated EGFR transactivation using functional genomics approaches (pages 5258–5268)

      Amee J. George, Ross D. Hannan and Walter G. Thomas

      Version of Record online: 23 SEP 2013 | DOI: 10.1111/febs.12509

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      Cross-talk between G protein-coupled receptors (GPCRs) and the epidermal growth factor receptor (EGFR) facilitate many important cellular activities. However, the molecular mechanism still remains poorly understood. In this review, we discuss the current view of GPCR-EGFR transactivation, and propose that functional genomics approaches will allow a renewed concentration of our efforts to further investigate the mechanism underlying this process.

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      Phosphoproteomic analysis of anaplastic lymphoma kinase (ALK) downstream signaling pathways identifies signal transducer and activator of transcription 3 as a functional target of activated ALK in neuroblastoma cells (pages 5269–5282)

      Kamaraj Sattu, Falko Hochgräfe, Jianmin Wu, Ganesh Umapathy, Christina Schönherr, Kristina Ruuth, Damini Chand, Barbara Witek, James Fuchs, Pui-Kai Li, Fredrik Hugosson, Roger J. Daly, Ruth H. Palmer and Bengt Hallberg

      Version of Record online: 22 AUG 2013 | DOI: 10.1111/febs.12453

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      In this study, mass spectrometry-based phosphotyrosine profiling has been employed to characterize signaling events associated with the full-length ALK RTK. Both novel and previously known targets, such as STAT3, were identified. Loss of STAT3 function resulted in decreased MYCN protein levels downstream of ALK signalling. These observations suggest that activation of STAT3 is important for ALK signaling activity in neuroblastoma.

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      Lymphotoxin α induces apoptosis, necroptosis and inflammatory signals with the same potency as tumour necrosis factor (pages 5283–5297)

      Nima Etemadi, Jessica K. Holien, Diep Chau, Grant Dewson, James M. Murphy, Warren S. Alexander, Michael W. Parker, John Silke and Ueli Nachbur

      Version of Record online: 2 AUG 2013 | DOI: 10.1111/febs.12419

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      The cytokine TNF induces inflammatory responses through the activation of transcription factor NFκB and MAPK signalling and, in some circumstances, triggers cell death. The paralogue of TNF, lymphotoxin α3, had been assumed to be a less potent ligand for the identical receptors, TNFR1 and TNFR2. Here, we showed that both TNF and lymphotoxin α bind similarly to TNFR1 and signal with the same potency.

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      Conserved systems and functional genomic assessment of nociception (pages 5298–5306)

      Thang M. Khuong and Graham Greg Neely

      Version of Record online: 27 AUG 2013 | DOI: 10.1111/febs.12464

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      Current therapies do not adequately address the needs of patients with chronic pain. Human genetics has revealed causal relationships between a handful of genes and chronic pain which may help instruct development of next generation analgesics. In this paper, we discuss our efforts in providing additional insight into pain genetics using fruit fly systems biology combined with mammalian genetics.

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      AKT signalling is required for ribosomal RNA synthesis and progression of Eμ-Myc B-cell lymphoma in vivo (pages 5307–5316)

      Jennifer R. Devlin, Katherine M. Hannan, Pui Y. Ng, Megan J. Bywater, Jake Shortt, Carleen Cullinane, Grant A. McArthur, Ricky W. Johnstone, Ross D. Hannan and Richard B. Pearson

      Version of Record online: 13 FEB 2013 | DOI: 10.1111/febs.12135

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      Hyperactivation of PI3K/AKT and/or MYC signalling activity is observed in many cancers and results in increased ribosome biogenesis thought to be critical for oncogenesis. We show that AKT inhibition antagonizes rDNA transcription in Eμ-Myc lymphoma and this is associated with delayed disease progression in vivo. Thus cancers characterized by unrestrained ribosome biogenesis may be vulnerable to therapies targeting PI3K/AKT signalling.

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      Roles, regulation and inhibitors of sphingosine kinase 2 (pages 5317–5336)

      Heidi A. Neubauer and Stuart M. Pitson

      Version of Record online: 7 JUN 2013 | DOI: 10.1111/febs.12314

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      The sphingosine kinases (SKs), SK1 and SK2, catalyse the production of the bioactive phospholipid sphingosine-1-phosphate. SK1 functions to promote cell survival, proliferation and neoplastic transformation, however, the roles of SK2 appear more complex and are somewhat conflicting. Here, we review the functions of SK2, the current knowledge of its regulation, and developments in targeting this enzyme.

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      Extended treatment with selective phosphatidylinositol 3-kinase and mTOR inhibitors has effects on metabolism, growth, behaviour and bone strength (pages 5337–5349)

      Greg C. Smith, Wee-Kiat Ong, Jessica L. Costa, Maureen Watson, Jillian Cornish, Andrew Grey, Greg D. Gamble, Michelle Dickinson, Sophie Leung, Gordon W. Rewcastle, Weiping Han and Peter R. Shepherd

      Version of Record online: 12 AUG 2013 | DOI: 10.1111/febs.12428

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      A number of small molecule PI 3-kinase inhibitors have been developed. We investigated the effects of extended treatment of mice with eight such inhibitors. Surprisingly, defects in glucose metabolism were minimal. However, there were deleterious effects on growth, behaviour and bone health. These studies identify a range of possible side effects of long term use of PI 3-kinase inhibitors.

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      The epidermal growth factor receptor variant III (EGFRvIII): where wild things are altered (pages 5350–5370)

      Hui K. Gan, Anna N. Cvrljevic and Terrance G. Johns

      Version of Record online: 8 JUL 2013 | DOI: 10.1111/febs.12393

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      Tumors with EGFR gene amplification frequently contain EGFR gene rearrangements, with the most common extracellular domain mutation being EGFRvIII. This EGFR deletion mutation is incapable of binding ligand, yet EGFRvIII displays low-level constitutive signaling augmented by reduced internalization. We analyze the evidence for EGFRvIII expression in different tumor types and discuss recent findings regarding its tumorigenic properties in brain cancer.

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      The tail wagging the dog – regulation of lipid metabolism by protein kinase C (pages 5371–5383)

      Carsten Schmitz-Peiffer

      Version of Record online: 3 MAY 2013 | DOI: 10.1111/febs.12285

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      PKC isoforms are associated with the inhibitory effects of lipids on insulin action. It is now evident that these enzymes also play key roles in the modulation of lipid metabolism, regulating the supply of lipids between tissues such as adipose and liver. These kinases are not merely effectors of lipid accumulation, but in fact control the fate of fatty acids.

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      Special Issue – Signalling. Introduction – Ca2+ signalling and transport in health and disease (page 5384)

      Henning Tidow and Poul Nissen

      Version of Record online: 23 SEP 2013 | DOI: 10.1111/febs.12507

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      This series of articles in the FEBS Journal Special Issue on Signalling is based on the international symposium ‘Ca2+ Signalling and Transport in Health and Disease’, Aarhus, 2012. A mixture of research articles and reviews cover a broad range of calcium signalling and transport-related topics. An accompanying series entitled Frontiers in Cell Signalling is based on the 6th Garvan Signalling Symposium, Sydney, 2012.

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      The plasma membrane calcium pump in health and disease (pages 5385–5397)

      Marisa Brini, Tito Calì, Denis Ottolini and Ernesto Carafoli

      Version of Record online: 11 MAR 2013 | DOI: 10.1111/febs.12193

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      Plasma membrane Ca2+ pumps (PMCAs 1-4) extrude Ca2+ from eukaryotic cells. Molecular modeling shows that their structure repeats that of that of the SERCA pump, except for the presence of a long C-terminal tail that binds calmodulin. PMCA defects (mostly genetic) impair Ca2+ homeostasis and generate various disease phenotypes. PMCA2 mutations produce deafness, PMCA3 mutations a cerebellar X-linked ataxia.

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      Conformational changes of recombinant Ca2+–ATPase studied by reaction-induced infrared difference spectroscopy (pages 5398–5407)

      Saroj Kumar, Chenge Li, Cédric Montigny, Marc le Maire and Andreas Barth

      Version of Record online: 13 FEB 2013 | DOI: 10.1111/febs.12131

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      Recombinant Ca2+-ATPase was expressed in Saccharomyces cerevisiae and conformational changes upon formation of its phosphoenzyme intermediates were followed with time-resolved infrared spectroscopy. The results show that the recombinant enzyme has similar structural and dynamical properties as native rabbit SERCA1a. It is now possible to apply this expression system together with infrared spectroscopy to investigate the role of individual amino acids.

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      Modulation of endoplasmic reticulum calcium pump expression during lung cancer cell differentiation (pages 5408–5418)

      Atousa Arbabian, Jean-Philippe Brouland, Ágota Apáti, Katalin Pászty, Luca Hegedűs, Ágnes Enyedi, Christine Chomienne and Béla Papp

      Version of Record online: 11 DEC 2012 | DOI: 10.1111/febs.12064

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      Calcium is accumulated in the endoplasmic reticulum by SERCA-type calcium pumps. Induction of differentiation in lung adenocarcinoma cells leads to the induction of the expression of the SERCA3 isoform, which is abundantly expressed in normal bronchial epithelium. Thus, SERCA3, a new marker of lung epithelial differentiation, may be useful for the investigation of normal versus tumoral calcium homeostasis and signaling.

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      Antimalarial screening via large-scale purification of Plasmodium falciparum Ca2+-ATPase 6 and in vitro studies (pages 5419–5429)

      Stéphanie David-Bosne, Isabelle Florent, Anne-Marie Lund- Winther, John B. Hansen, Morten Buch-Pedersen, Paul Machillot, Marc le Maire and Christine Jaxel

      Version of Record online: 8 APR 2013 | DOI: 10.1111/febs.12244

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      PfATP6, the P. falciparum SERCA, was investigated as an antimalarial drug target. It was expressed in yeast and large-scale purified, a chemical library of 1680 molecules was screened on its calcium-dependent ATPase activity and eight compounds were chosen for their effect on P. falciparum in vitro growth. This study describes a multidisciplinary approach allowing the selection of new potential antimalarials.

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      Differential effects of thapsigargin analogues on apoptosis of prostate cancer cells : Complex regulation by intracellular calcium (pages 5430–5440)

      Charlotte Dubois, Fabien Vanden Abeele, Pankaj Sehgal, Claus Olesen, Steffen Junker, Søren B. Christensen, Natalia Prevarskaya and Jesper V. Møller

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12475

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      Inhibition of sarcoplasmic reticulum Ca2+-ATPase (SERCA) by thapsigargin (Tg) and Tg analogues is considered to trigger cell death by activation of calcium mediated apoptotic pathways. The present study evaluates the effect of thapsigargin analogues on prostate cancer cells and among a number of surprising findings demonstrate that an early cytosolic increase of Ca2+ concentration is not involved in apoptosis induction.

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      Probing determinants of cyclopiazonic acid sensitivity of bacterial Ca2+-ATPases (pages 5441–5449)

      Aljona Kotšubei, Manuela Gorgel, Jens P. Morth, Poul Nissen and Jacob L. Andersen

      Version of Record online: 28 MAY 2013 | DOI: 10.1111/febs.12310

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      Listeria monocytogenes Ca2+-ATPase 1 (LMCA1) is despite high sequence similarity to SERCA1a, not inhibited by the inhibitor cyclopiazonic acid (CPA). To test whether a CPA binding site could be created while maintaining functionality, we targeted four amino acid positions in LMCA1 for mutational studies. The identification of CPA sensitive gain-of-function mutants pinpointed key determinants of the CPA binding site.

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      Calcium oscillations triggered by cardiotonic steroids (pages 5450–5455)

      Jacopo M. Fontana, Ievgeniia Burlaka, Georgiy Khodus, Hjalmar Brismar and Anita Aperia

      Version of Record online: 2 SEP 2013 | DOI: 10.1111/febs.12448

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      In addition to its pumping role, Na+, K+–ATPase (NKA) functions as a signal transducer. In this review we describe how cardiotonic steroids (CTS), which are highly specific NKA ligands, trigger slow Ca2+ oscillations by promoting the interaction between NKA and IP3R, and how this Ca2+ signal activates the NF-κB subunit p65 increasing the expression of the antiapoptotic factor Bcl-xL.

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      Ryanodine receptor calcium release channels: lessons from structure–function studies (pages 5456–5470)

      Fernando J. Amador, Peter B. Stathopulos, Masahiro Enomoto and Mitsuhiko Ikura

      Version of Record online: 18 MAR 2013 | DOI: 10.1111/febs.12194

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      Ryanodine Receptors (RyRs) and inositol 1,4,5-trisphospate receptors (IP3Rs) are large tetrameric Ca2+ release channels that are typically found in excitable and non-excitable cells, respectively. This review focuses on recent high-resolution structural studies of both receptors, with an emphasis on the N-terminal region. The conserved structural architecture in this domain suggests both receptors evolved from an ancestral unicellular RyR/IP3R.

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      What do we know about the transient receptor potential vanilloid 2 (TRPV2) ion channel? (pages 5471–5487)

      Alex Perálvarez-Marín, Pau Doñate-Macian and Rachelle Gaudet

      Version of Record online: 28 MAY 2013 | DOI: 10.1111/febs.12302

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      Here we outline the current knowledge on transient receptor potential vanilloid 2 (TRPV2) ion channel. Although initially described as a noxious heat thermosensor, its molecular mechanism and regulation has been revealed as much more complex and still to be fully elucidated. The present work attempts to highlight the most relevant structural features and physiological roles for TRPV2.

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      Vascular smooth muscle cell phenotype is defined by Ca2+-dependent transcription factors (pages 5488–5499)

      Olga Kudryavtseva, Christian Aalkjær and Vladimir V. Matchkov

      Version of Record online: 19 JUL 2013 | DOI: 10.1111/febs.12414

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      Ca2+ in VSMCs is important for contraction and it can activate multiple transcriptional factors (CREB, NFAT, SRF), moreover C-terminus of L-type Ca2+ channels can also serve as a transcriptional regulator. Interplay between Ca2+ signalling events, transcriptional factors recruitment and selective gene activation is important for defining VSMCs phenotype in health and disease.

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      Targeting apoptosis by the remodelling of calcium-transporting proteins in cancerogenesis (pages 5500–5510)

      Charlotte Dubois, Fabien Vanden Abeele and Natacha Prevarskaya

      Version of Record online: 12 APR 2013 | DOI: 10.1111/febs.12246

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      In physiopathological conditions such as cancer, apoptotic processes become deregulated, leading to apoptosis-resistant phenotypes. Recently, perturbations of cellular calcium homeostasis have been described to be implicated in this phenomenon. In this review, we present the calcium-transporting protein-dependent pathways involved in apoptosis resistance, molecular actors involved in the deregulation of apoptosis and those chemotherapies which target them.

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      Calmodulin in a Heartbeat (pages 5511–5532)

      Anders B. Sorensen, Mads T. Søndergaard and Michael T. Overgaard

      Version of Record online: 18 JUN 2013 | DOI: 10.1111/febs.12337

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      Calmodulin is intimately involved in cardiomyocyte Ca2+ signalling and plays a pivotal role in the regulation of cardiac contraction. Recent studies have identified the first human calmodulin mutations and linked these to severe cardiac arrhythmias. Here we aim to give an overview of calmodulin modulated components in the cardiac contraction cycle and the potential disease mechanisms associated with calmodulin mutations.

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      Structural and functional diversity in the activity and regulation of DAPK-related protein kinases (pages 5533–5550)

      Koen Temmerman, Bertrand Simon and Matthias Wilmanns

      Version of Record online: 5 JUL 2013 | DOI: 10.1111/febs.12384

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      The calcium/calmodulin-dependent protein kinase family harbours a distinct subfamily of highly related kinases, including death-associated protein-related kinases; myosin light chain-related kinases and triple functional domain protein-related kinases. This subfamily displays unique structural features stabilizing their catalytic domains in a constitutively active conformation. Concordantly, the mode of kinetic activity regulation is shifted towards additional autoregulatory domains.

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      Structural diversity of calmodulin binding to its target sites (pages 5551–5565)

      Henning Tidow and Poul Nissen

      Version of Record online: 13 MAY 2013 | DOI: 10.1111/febs.12296

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      Canonical binding mode observed in selected CaM-complex structures. (A) Myosin light chain kinase. (B) CaM-dependent protein kinase II. (C) CaM-dependent protein kinase kinase. (D) Ryanodine receptor. (E) Vacuolar Ca2+-ATPase. (F) Nitric oxide synthase. The spacing of hydrophobic anchor residues is indicated. CaM is coloured cyan with residues forming hydrophobic pocket in olive. The target peptides are coloured grey with anchor residues in red.

  4. Author index

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Special Issue
    5. Author index
    6. Table of Contents
    1. You have free access to this content
      Author index (page 5566)

      Version of Record online: 15 OCT 2013 | DOI: 10.1111/j.1742-4658.2013.08799.x

  5. Table of Contents

    1. Top of page
    2. Front Cover
    3. Editorial Information
    4. Special Issue
    5. Author index
    6. Table of Contents
    1. You have free access to this content
      Table of Contents (pages 5567–5568)

      Version of Record online: 15 OCT 2013 | DOI: 10.1111/febs.12557

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