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  • SOS1 and Ras regulate epithelial tight junction formation in the human airway through EMP1
    1. Joanne Durgan15,
    2. Guangbo Tao1,,
    3. Matthew S Walters2,,
    4. Oliver Florey15,
    5. Anja Schmidt3,
    6. Vanessa Arbelaez2,
    7. Neal Rosen4,
    8. Ronald G Crystal2 and
    9. Alan Hall*,1
    1. 1Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    2. 2Department of Genetic Medicine, Weill Cornell Medical College, New York, NY, USA
    3. 3MRC Laboratory for Molecular Cell Biology, University College London, London, UK
    4. 4Molecular Pharmacology & Chemistry Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    5. 5The Babraham Institute, Cambridge, UK
    1. *Corresponding author. Tel: +1 212 639 2387; Fax: +1 212 717 3604; E‐mail: halla{at}mskcc.org
    1. These authors contributed equally to the work

    SOS1 and Ras promote the assembly of tight junctions in human bronchial epithelial cells by signaling through MEK and ERK. This controls the expression of EMP1, which is essential for tight junction formation and function in human airway epithelia.

    Synopsis

    SOS1 and Ras promote the assembly of tight junctions in human bronchial epithelial cells by signaling through MEK and ERK. This controls the expression of EMP1, which is essential for tight junction formation and function in human airway epithelia.

    • SOS1, Ras, MEK and ERK are required for proper tight junction assembly in bronchial epithelial cells.

    • The ERK MAPK pathway controls the expression of multiple bronchial genes, including EMP1.

    • EMP1 localises to tight junctions and is essential for their formation and function.

    • EMP1
    • lung
    • Ras
    • SOS1
    • tight junctions
    • Received June 25, 2014.
    • Revision received October 23, 2014.
    • Accepted October 24, 2014.
    Joanne Durgan, Guangbo Tao, Matthew S Walters, Oliver Florey, Anja Schmidt, Vanessa Arbelaez, Neal Rosen, Ronald G Crystal, Alan Hall
  • Tyrosine phosphorylation of LRP6 by Src and Fer inhibits Wnt/β‐catenin signalling
    Qing Chen, Yi Su, Janine Wesslowski, Anja I Hagemann, Mirana Ramialison, Joachim Wittbrodt, Steffen Scholpp, Gary Davidson
  • Closing the MCM cycle at replication termination sites
    1. Armelle Lengronne1 and
    2. Philippe Pasero (philippe.pasero{at}igh.cnrs.fr) 1
    1. 1Institute of Human Genetics CNRS, Montpellier, France

    The initiation of eukaryotic DNA replication is a highly regulated process conserved from yeast to human. The past decade has seen significant advances in understanding how the CMG (Cdc45‐MCM‐GINS) replicative helicase is loaded onto DNA. However, very little was known on how this complex is removed from chromatin at the end of S phase. Two papers in a recent issue of Science [1], [2] show that in yeast and in Xenopus, the CMG complex is unloaded at replication termination sites by an active mechanism involving the polyubiquitylation of Mcm7.

    See also: M Maric et al and

    SP Moreno et al (October 2014)

    The termination of eukaryotic DNA replication is a poorly understood process. Two recent papers show that the CMG replicative helicase is unloaded at replication termination sites after Mcm7 ubiquitylation by Cdc48/p97‐mediated extraction.

    Armelle Lengronne, Philippe Pasero
  • Scientometrics in a changing research landscapeBibliometrics has become an integral part of research quality evaluation and has been changing the practice of research

    Bibliometrics has become an integral part of research quality evaluation and has been changing the practice of research

    1. Lutz Bornmann (bornmann{at}gv.mpg.de) 1 and
    2. Loet Leydesdorff (loet{at}leydesdorff.net) 2
    1. 1Division for Science and Innovation Studies, Administrative Headquarters of the Max Planck Society, Munich, Germany
    2. 2Amsterdam School of Communication Research (ASCoR) University of Amsterdam, Amsterdam, The Netherlands

    Bibliometrics has become an integral component of quality assessment for science and funding decisions. The next challenge for scientometrics is to develop similarly reliable indicators for the social impact of research.

    Lutz Bornmann, Loet Leydesdorff
  • The extracellular matrix modulates the hallmarks of cancer
    1. Michael W Pickup1,
    2. Janna K Mouw1 and
    3. Valerie M Weaver*,1,2,3,4
    1. 1Department of Surgery, Center for Bioengineering and Tissue Regeneration UCSF, San Francisco, CA, USA
    2. 2Departments of Anatomy, Bioengineering and Therapeutic Sciences, UCSF, San Francisco, CA, USA
    3. 3Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research UCSF, San Francisco, CA, USA
    4. 4UCSF Helen Diller Comprehensive Cancer Center UCSF, San Francisco, CA, USA
    1. *Corresponding author. Tel: +(415) 476‐3826; Fax: +(415) 476‐3985; E‐mail: Valerie.Weaver{at}ucsfmedctr.org

    This review discusses how the biochemical and biophysical properties of the extracellular matrix evolve during tumor progression and how they critically impact the behavior of tumor and stromal cells.

    • ECM
    • hallmarks of cancer
    • mechanotransduction
    • Received July 1, 2014.
    • Revision received October 20, 2014.
    • Accepted October 20, 2014.
    Michael W Pickup, Janna K Mouw, Valerie M Weaver
  • Lifestyle in the spermThere is growing evidence that epigenetic marks can be inherited. But what is the nature of the information they store and over how many generations do they prevail?

    There is growing evidence that epigenetic marks can be inherited. But what is the nature of the information they store and over how many generations do they prevail?

    1. Katrin Weigmann, Freelance Journalist (mail{at}k-weigmann.de) 1
    1. 1Oldenburg, Germany

    Observations of epigenetic inheritance challenge classical genetics and imply that Lamarck might have been right—sort of. The jury is still out, as the mechanisms and scope of epigenetic inheritance are not yet fully understood.

    Katrin Weigmann
  • Foxd3 suppresses NFAT‐mediated differentiation to maintain self‐renewal of embryonic stem cells
    1. Lili Zhu1,,
    2. Shiyue Zhang1,2, and
    3. Ying Jin*,1,3
    1. 1Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes of Biological Sciences Chinese Academy of Sciences/Shanghai JiaoTong University School of Medicine, Shanghai, China
    2. 2University of Chinese Academy of Sciences, Beijing, China
    3. 3Shanghai Stem Cell Institute, Shanghai JiaoTong University School of Medicine, Shanghai, China
    1. *Corresponding author. Tel: +86 21 5492 3342; E‐mail: yjin{at}sibs.ac.cn
    1. These authors contributed equally to this study

    This study shows that Foxd3, a pluripotency‐associated transcription factor, interacts with and represses NFAT transcriptional activities by recruiting the co‐repressor Tle4. Thus, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes to maintain the balance between self‐renewal and differentiation in mouse embryonic stem cells.

    Synopsis

    This study shows that Foxd3, a pluripotency‐associated transcription factor, interacts with and represses NFAT transcriptional activities by recruiting the co‐repressor Tle4. Thus, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes to maintain the balance between self‐renewal and differentiation in mouse embryonic stem cells.

    • Foxd3 suppresses NFATc3‐induced differentiation in embryonic stem cells by recruiting the co‐repressor Tle4.

    • Globally, Foxd3 represses, while NFATc3 activates, a set of differentiation‐associated genes in mESCs.

    • embryonic stem cells
    • Foxd3
    • NFAT
    • Received February 17, 2014.
    • Revision received September 30, 2014.
    • Accepted October 6, 2014.
    Lili Zhu, Shiyue Zhang, Ying Jin