Ticket #388: Feed.atom

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  <title>PLoS ONE Alerts: PLoS ONE Journal</title>
  <link rel="self" href="/" />
  <author>
    <name>Public Library of Science</name>
    <uri>http://plosone.org</uri>
    <email>gen@plos.org</email>
  </author>
  <subtitle>Publishing science, accelerating research</subtitle>
  <id>/</id>
  <rights>This work is licensed under a Creative Commons Attribution-Share Alike 3.0 License, http://creativecommons.org/licenses/by-sa/3.0/</rights>
  <updated>2007-06-15T00:25:05Z</updated>
  <entry>
    <title>Simulation Modifies Prehension: Evidence for a Conjoined Representation of the Graspable Features of an Object and the Action of Grasping It</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000311" />
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    <category term="Neuroscience" label="Neuroscience" />
    <category term="Behavioral Neuroscience (Subcategory)" label="Behavioral Neuroscience (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Cognitive Neuroscience (Subcategory)" label="Cognitive Neuroscience (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Motor Systems (Subcategory)" label="Motor Systems (Subcategory)" />
    <author>
      <name>Victor Frak</name>
    </author>
    <author>
      <name>Isabelle Croteau</name>
    </author>
    <author>
      <name>Daniel Bourbonnais</name>
    </author>
    <author>
      <name>Christian Duval</name>
    </author>
    <author>
      <name>Cyril Duclos</name>
    </author>
    <author>
      <name>Henri Cohen</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000311</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Movement formulas, engrams, kinesthetic images and internal models of the body in action are notions derived mostly from clinical observations of brain-damaged subjects. They also suggest that the prehensile geometry of an object is integrated in the neural circuits and includes the object's graspable characteristics as well as its semantic properties. In order to determine whether there is a conjoined representation of the graspable characteristics of an object in relation to the actual grasping, it is necessary to separate the graspable (low-level) from the semantic (high-level) properties of the object. Right-handed subjects were asked to grasp and lift a smooth 300-g cylinder with one hand, before and after judging the level of difficulty of a “grasping for pouring” action, involving a smaller cylinder and using the opposite hand. The results showed that simulated grasps with the right hand exert a direct influence on actual motor acts with the left hand. These observations add to the evidence that there is a conjoined representation of the graspable characteristics of the object and the biomechanical constraints of the arm.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Genes Involved in the Balance between Neuronal Survival and Death during Inflammation</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000310" />
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    <category term="Neuroscience" label="Neuroscience" />
    <category term="Neuronal and Glial Cell Biology (Subcategory)" label="Neuronal and Glial Cell Biology (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Gene Expression (Subcategory)" label="Gene Expression (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Neurobiology of Disease and Regeneration (Subcategory)" label="Neurobiology of Disease and Regeneration (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Innate Immunity (Subcategory)" label="Innate Immunity (Subcategory)" />
    <author>
      <name>Isaias Glezer</name>
    </author>
    <author>
      <name>Ariel Chernomoretz</name>
    </author>
    <author>
      <name>Samuel David</name>
    </author>
    <author>
      <name>Marie-Michèle Plante</name>
    </author>
    <author>
      <name>Serge Rivest</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000310</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Glucocorticoids are potent regulators of the innate immune response, and alteration in this inhibitory feedback has detrimental consequences for the neural tissue. This study profiled and investigated functionally candidate genes mediating this switch between cell survival and death during an acute inflammatory reaction subsequent to the absence of glucocorticoid signaling. Oligonucleotide microarray analysis revealed that following lipopolysaccharide (LPS) intracerebral administration at striatum level, more modulated genes presented transcription impairment than exacerbation upon glucocorticoid receptor blockage. Among impaired genes we identified ceruloplasmin (Cp), which plays a key role in iron metabolism and is implicated in a neurodegenative disease. Microglial and endothelial induction of Cp is a natural neuroprotective mechanism during inflammation, because Cp-deficient mice exhibited increased iron accumulation and demyelination when exposed to LPS and neurovascular reactivity to pneumococcal meningitis. This study has identified genes that can play a critical role in programming the innate immune response, helping to clarify the mechanisms leading to protection or damage during inflammatory conditions in the CNS.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Sharing Detailed Research Data Is Associated with Increased Citation Rate</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000308" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000308" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000308" />
    <category term="Evidence-Based Healthcare" label="Evidence-Based Healthcare" />
    <category term="Statistical Methodologies and Health Informatics (Subcategory)" label="Statistical Methodologies and Health Informatics (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Bioinformatics (Subcategory)" label="Bioinformatics (Subcategory)" />
    <category term="Science Policy" label="Science Policy" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Gene Expression (Subcategory)" label="Gene Expression (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Cancer Genetics (Subcategory)" label="Cancer Genetics (Subcategory)" />
    <author>
      <name>Heather A. Piwowar</name>
    </author>
    <author>
      <name>Roger S. Day</name>
    </author>
    <author>
      <name>Douglas B. Fridsma</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000308</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Sharing research data provides benefit to the general scientific community, but the benefit is less obvious for the investigator who makes his or her data available.&lt;/p&gt;Principal Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;We examined the citation history of 85 cancer microarray clinical trial publications with respect to the availability of their data. The 48% of trials with publicly available microarray data received 85% of the aggregate citations. Publicly available data was significantly (p = 0.006) associated with a 69% increase in citations, independently of journal impact factor, date of publication, and author country of origin using linear regression.&lt;/p&gt;Significance
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;This correlation between publicly available data and increased literature impact may further motivate investigators to share their detailed research data.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Multiple Antimicrobial Resistance in Plague: An Emerging Public Health Risk</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000309" />
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    <category term="Infectious Diseases" label="Infectious Diseases" />
    <category term="Antimicrobials and Drug Resistance (Subcategory)" label="Antimicrobials and Drug Resistance (Subcategory)" />
    <category term="Public Health and Epidemiology" label="Public Health and Epidemiology" />
    <category term="Infectious Diseases (Subcategory)" label="Infectious Diseases (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Microbial Evolution and Genomics (Subcategory)" label="Microbial Evolution and Genomics (Subcategory)" />
    <category term="Microbiology" label="Microbiology" />
    <category term="Applied Microbiology (Subcategory)" label="Applied Microbiology (Subcategory)" />
    <category term="Microbiology" label="Microbiology" />
    <category term="Applied Microbiology (Subcategory)" label="Applied Microbiology (Subcategory)" />
    <category term="Infectious Diseases" label="Infectious Diseases" />
    <category term="Antimicrobials and Drug Resistance (Subcategory)" label="Antimicrobials and Drug Resistance (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Microbial Evolution and Genomics (Subcategory)" label="Microbial Evolution and Genomics (Subcategory)" />
    <category term="Public Health and Epidemiology" label="Public Health and Epidemiology" />
    <category term="Infectious Diseases (Subcategory)" label="Infectious Diseases (Subcategory)" />
    <author>
      <name>Timothy J. Welch</name>
    </author>
    <author>
      <name>W. Florian Fricke</name>
    </author>
    <author>
      <name>Patrick F. McDermott</name>
    </author>
    <author>
      <name>David G. White</name>
    </author>
    <author>
      <name>Marie-Laure Rosso</name>
    </author>
    <author>
      <name>David A. Rasko</name>
    </author>
    <author>
      <name>Mark K. Mammel</name>
    </author>
    <author>
      <name>Mark Eppinger</name>
    </author>
    <author>
      <name>M.J. Rosovitz</name>
    </author>
    <author>
      <name>David Wagner</name>
    </author>
    <author>
      <name>Lila Rahalison</name>
    </author>
    <author>
      <name>J. Eugene LeClerc</name>
    </author>
    <author>
      <name>Jeffrey M. Hinshaw</name>
    </author>
    <author>
      <name>Luther E. Lindler</name>
    </author>
    <author>
      <name>Thomas A. Cebula</name>
    </author>
    <author>
      <name>Elisabeth Carniel</name>
    </author>
    <author>
      <name>Jacques Ravel</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000309</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Antimicrobial resistance in &lt;i&gt;Yersinia pestis&lt;/i&gt; is rare, yet constitutes a significant international public health and biodefense threat. In 1995, the first multidrug resistant (MDR) isolate of &lt;i&gt;Y. pestis&lt;/i&gt; (strain IP275) was identified, and was shown to contain a self-transmissible plasmid (pIP1202) that conferred resistance to many of the antimicrobials recommended for plague treatment and prophylaxis. Comparative analysis of the DNA sequence of &lt;i&gt;Y. pestis&lt;/i&gt; plasmid pIP1202 revealed a near identical IncA/C plasmid backbone that is shared by MDR plasmids isolated from &lt;i&gt;Salmonella enterica&lt;/i&gt; serotype Newport SL254 and the fish pathogen &lt;i&gt;Yersinia ruckeri&lt;/i&gt; YR71. The high degree of sequence identity and gene synteny between the plasmid backbones suggests recent acquisition of these plasmids from a common ancestor. In addition, the &lt;i&gt;Y. pestis&lt;/i&gt; pIP1202-like plasmid backbone was detected in numerous MDR enterobacterial pathogens isolated from retail meat samples collected between 2002 and 2005 in the United States. Plasmid-positive strains were isolated from beef, chicken, turkey and pork, and were found in samples from the following states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York and Oregon. Our studies reveal that this common plasmid backbone is broadly disseminated among MDR zoonotic pathogens associated with agriculture. This reservoir of mobile resistance determinants has the potential to disseminate to &lt;i&gt;Y. pestis&lt;/i&gt; and other human and zoonotic bacterial pathogens and therefore represents a significant public health concern.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>LPS Responsiveness and Neutrophil Chemotaxis In Vivo Require PMN MMP-8 Activity</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000312" />
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    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000312" />
    <category term="Immunology" label="Immunology" />
    <category term="Innate Immunity (Subcategory)" label="Innate Immunity (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Immune Response (Subcategory)" label="Immune Response (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Innate Immunity (Subcategory)" label="Innate Immunity (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Immune Response (Subcategory)" label="Immune Response (Subcategory)" />
    <author>
      <name>Angus M. Tester</name>
    </author>
    <author>
      <name>Jennifer H. Cox</name>
    </author>
    <author>
      <name>Andrea R. Connor</name>
    </author>
    <author>
      <name>Amanda E. Starr</name>
    </author>
    <author>
      <name>Richard A. Dean</name>
    </author>
    <author>
      <name>Xose S. Puente</name>
    </author>
    <author>
      <name>Carlos López-Otín</name>
    </author>
    <author>
      <name>Christopher M. Overall</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000312</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;We identify matrix metalloproteinase (MMP)-8, the polymorphonuclear (PMN) leukocyte collagenase, as a critical mediator initiating lipopolysaccharide (LPS)-responsiveness &lt;i&gt;in vivo&lt;/i&gt;. PMN infiltration towards LPS is abrogated in &lt;i&gt;Mmp8&lt;/i&gt;-null mice. MMP-8 cleaves LPS-induced CXC chemokine (LIX) at Ser&lt;sup&gt;4&lt;/sup&gt;~Val&lt;sup&gt;5&lt;/sup&gt; and Lys&lt;sup&gt;79&lt;/sup&gt;~Arg&lt;sup&gt;80&lt;/sup&gt;. LIX bioactivity is increased upon N-terminal cleavage, enhancing intracellular calcium mobilization and chemotaxis upon binding its cognate receptor, CXCR2. As there is no difference in PMN chemotaxis in &lt;i&gt;Mmp8&lt;/i&gt;-null mice compared with wild-type mice towards synthetic analogues of MMP-8-cleaved LIX, MMP-8 is not essential for extravasation or cell migration in collagenous matrices &lt;i&gt;in vivo&lt;/i&gt;. However, with biochemical redundancy between MMPs 1, 2, 9, and 13, which also cleave LIX at position 4~5, it was surprising to observe such a markedly reduced PMN infiltration towards LPS and LIX in &lt;i&gt;Mmp8&lt;/i&gt;-/- mice. This lack of physiological redundancy &lt;i&gt;in vivo&lt;/i&gt; identifies MMP-8 as a key mediator in the regulation of innate immunity. Comparable results were found with CXCL8/IL-8 and CXCL5/ENA-78, the human orthologues of LIX. MMP-8 cleaves CXCL8 at Arg&lt;sup&gt;5&lt;/sup&gt;-Ser&lt;sup&gt;6&lt;/sup&gt; and at Val&lt;sup&gt;7&lt;/sup&gt;-Leu&lt;sup&gt;8&lt;/sup&gt; in CXCL5 to activate respective chemokines. Hence, rather than collagen, these PMN chemoattractants are important MMP-8 substrates &lt;i&gt;in vivo&lt;/i&gt;; PMN-derived MMP-8 cleaves and activates LIX to execute an &lt;i&gt;in cis&lt;/i&gt; PMN-controlled feed-forward mechanism to orchestrate the initial inflammatory response and promote LPS responsiveness in tissue.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Ribonuclease Activity of Dis3 Is Required for Mitotic Progression and Provides a Possible Link between Heterochromatin and Kinetochore Function</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000317" />
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    <category term="Cell Biology" label="Cell Biology" />
    <category term="Cell Growth and Division (Subcategory)" label="Cell Growth and Division (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Chromosome Structure (Subcategory)" label="Chromosome Structure (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Chromosome Biology (Subcategory)" label="Chromosome Biology (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Chromatin Structure (Subcategory)" label="Chromatin Structure (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Centromeres (Subcategory)" label="Centromeres (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Epigenetics (Subcategory)" label="Epigenetics (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Histone Modification (Subcategory)" label="Histone Modification (Subcategory)" />
    <category term="Cell Biology" label="Cell Biology" />
    <category term="Gene Expression (Subcategory)" label="Gene Expression (Subcategory)" />
    <author>
      <name>Hiroaki Murakami</name>
    </author>
    <author>
      <name>Derek B. Goto</name>
    </author>
    <author>
      <name>Takashi Toda</name>
    </author>
    <author>
      <name>Ee Sin Chen</name>
    </author>
    <author>
      <name>Shiv I. Grewal</name>
    </author>
    <author>
      <name>Robert A. Martienssen</name>
    </author>
    <author>
      <name>Mitsuhiro Yanagida</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000317</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Cellular RNA metabolism has a broad range of functional aspects in cell growth and division, but its role in chromosome segregation during mitosis is only poorly understood. The Dis3 ribonuclease is a key component of the RNA-processing exosome complex. Previous isolation of the &lt;i&gt;dis3-54&lt;/i&gt; cold-sensitive mutant of fission yeast &lt;i&gt;Schizosaccharomyces pombe&lt;/i&gt; suggested that Dis3 is also required for correct chromosome segregation.&lt;/p&gt;Methodology/Principal Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;We show here that the progression of mitosis is arrested in &lt;i&gt;dis3-54&lt;/i&gt;, and that segregation of the chromosomes is blocked by activation of the mitotic checkpoint control. This block is dependent on the Mad2 checkpoint protein. Double mutant and inhibitor analyses revealed that Dis3 is required for correct kinetochore formation and function, and that this activity is monitored by the Mad2 checkpoint. Dis3 is a member of the highly conserved RNase II family and is known to be an essential subunit of the exosome complex. The &lt;i&gt;dis3-54&lt;/i&gt; mutation was found to alter the RNaseII domain of Dis3, which caused a reduction in ribonuclease activity &lt;i&gt;in vitro&lt;/i&gt;. This was associated with loss of silencing of an &lt;i&gt;ura4&lt;sup&gt;+&lt;/sup&gt;&lt;/i&gt; reporter gene inserted into the outer repeats (&lt;i&gt;otr&lt;/i&gt;) and central core (&lt;i&gt;cnt&lt;/i&gt; and &lt;i&gt;imr&lt;/i&gt;) regions of the centromere. On the other hand, centromeric siRNA maturation and formation of the RITS RNAi effector complex was normal in the &lt;i&gt;dis3-54&lt;/i&gt; mutant. Micrococcal nuclease assay also suggested the overall chromatin structure of the centromere was not affected in &lt;i&gt;dis3-54&lt;/i&gt; mutant.&lt;/p&gt;Conclusions/Significance
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;RNase activity of Dis3, a core subunit of exosome, was found to be required for proper kinetochore formation and establishment of kinetochore-microtubule interactions. Moreover, Dis3 was suggested to contribute to kinetochore formation through an involvement in heterochromatic silencing at both outer centromeric repeats and within the central core region. This activity is likely monitored by the mitotic checkpoint, and distinct from that of RNAi-mediated heterochromatin formation directly targeting outer centromeric repeats.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Identification of a Small TAF Complex and Its Role in the Assembly of TAF-Containing Complexes</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000316" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000316" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000316" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Transcription Initiation and Activation (Subcategory)" label="Transcription Initiation and Activation (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <author>
      <name>Màté A. Demény</name>
    </author>
    <author>
      <name>Evi Soutoglou</name>
    </author>
    <author>
      <name>Zita Nagy</name>
    </author>
    <author>
      <name>Elisabeth Scheer</name>
    </author>
    <author>
      <name>Àgnes Jànoshàzi</name>
    </author>
    <author>
      <name>Magalie Richardot</name>
    </author>
    <author>
      <name>Manuela Argentini</name>
    </author>
    <author>
      <name>Pascal Kessler</name>
    </author>
    <author>
      <name>Laszlo Tora</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000316</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;TFIID plays a role in nucleating RNA polymerase II preinitiation complex assembly on protein-coding genes. TFIID is a multisubunit complex comprised of the TATA box binding protein (TBP) and 14 TBP-associated factors (TAFs). Another class of multiprotein transcriptional regulatory complexes having histone acetyl transferase (HAT) activity, and containing TAFs, includes TFTC, STAGA and the PCAF/GCN5 complex. Looking for as yet undiscovered subunits by a proteomic approach, we had identified TAF8 and SPT7L in human TFTC preparations. Subsequently, however, we demonstrated that TAF8 was not a stable component of TFTC, but that it is present in a small TAF complex (SMAT), containing TAF8, TAF10 and SPT7L, that co-purified with TFTC. Thus, TAF8 is a subunit of both TFIID and SMAT. The latter has to be involved in a pathway of complex formation distinct from the other known TAF complexes, since these three histone fold (HF)-containing proteins (TAF8, TAF10 and SPT7L) can never be found together either in TFIID or in STAGA/TFTC HAT complexes. Here we show that TAF8 is absolutely necessary for the integration of TAF10 in a higher order TFIID core complex containing seven TAFs. TAF8 forms a heterodimer with TAF10 through its HF and proline rich domains, and also interacts with SPT7L through its C-terminal region, and the three proteins form a complex &lt;i&gt;in vitro&lt;/i&gt; and &lt;i&gt;in vivo&lt;/i&gt;. Thus, the TAF8-TAF10 and TAF10-SPT7L HF pairs, and also the SMAT complex, seem to be important regulators of the composition of different TFIID and/or STAGA/TFTC complexes in the nucleus and consequently may play a role in gene regulation.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>XIAP Protection of Photoreceptors in Animal Models of Retinitis Pigmentosa</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000314" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000314" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000314" />
    <category term="Ophthalmology" label="Ophthalmology" />
    <category term="Inherited Eye Disorders (Subcategory)" label="Inherited Eye Disorders (Subcategory)" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <category term="Gene Therapy (Subcategory)" label="Gene Therapy (Subcategory)" />
    <category term="Ophthalmology" label="Ophthalmology" />
    <category term="Retinal Disorders (Subcategory)" label="Retinal Disorders (Subcategory)" />
    <author>
      <name>Kevin C. Leonard</name>
    </author>
    <author>
      <name>Dino Petrin</name>
    </author>
    <author>
      <name>Stuart G. Coupland</name>
    </author>
    <author>
      <name>Adam N. Baker</name>
    </author>
    <author>
      <name>Brian C. Leonard</name>
    </author>
    <author>
      <name>Eric C. LaCasse</name>
    </author>
    <author>
      <name>William W. Hauswirth</name>
    </author>
    <author>
      <name>Robert G. Korneluk</name>
    </author>
    <author>
      <name>Catherine Tsilfidis</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000314</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Retinitis pigmentosa (RP) is a blinding genetic disorder that is caused by the death of photoreceptors in the outer nuclear layer of the retina. To date, 39 different genetic loci have been associated with the disease, and 28 mutated genes have been identified. Despite the complexity of the underlying genetic basis for RP, the final common pathway is photoreceptor cell death via apoptosis.&lt;/p&gt;Methodology/Principal Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;In this study, P23H and S334ter rhodopsin transgenic rat models of RP were used to test the neuroprotective effects of anti-apoptotic gene therapy. Adeno-associated viruses (AAV) carrying the X-linked inhibitor of apoptosis (XIAP) or green fluorescent protein (GFP) were delivered subretinally into the eye of transgenic rat pups. Histological and functional measures were used to assess neuroprotection. XIAP is known to block apoptosis by inhibiting the action of caspases-3, -7 and -9. The results show that XIAP gene therapy provides long-term neuroprotection of photoreceptors at both structural and functional levels.&lt;/p&gt;Conclusions/Significance
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Our gene therapy strategy targets the apoptotic cascade, which is the final common pathway in all forms of retinitis pigmentosa. This strategy holds great promise for the treatment of RP, as it allows for the broad protection of photoreceptors, regardless of the initial disease causing mutation.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>A Glimpse of Streptococcal Toxic Shock Syndrome from Comparative Genomics of &lt;italic&gt;S. suis&lt;/italic&gt; 2 Chinese Isolates</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000315" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000315" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000315" />
    <category term="Microbiology" label="Microbiology" />
    <category term="Infectious Diseases" label="Infectious Diseases" />
    <category term="Genetics and Genomics" label="Genetics and Genomics" />
    <author>
      <name>Chen Chen</name>
    </author>
    <author>
      <name>Jiaqi Tang</name>
    </author>
    <author>
      <name>Wei Dong</name>
    </author>
    <author>
      <name>Changjun Wang</name>
    </author>
    <author>
      <name>Youjun Feng</name>
    </author>
    <author>
      <name>Jing Wang</name>
    </author>
    <author>
      <name>Feng Zheng</name>
    </author>
    <author>
      <name>Xiuzhen Pan</name>
    </author>
    <author>
      <name>Di Liu</name>
    </author>
    <author>
      <name>Ming Li</name>
    </author>
    <author>
      <name>Yajun Song</name>
    </author>
    <author>
      <name>Xinxing Zhu</name>
    </author>
    <author>
      <name>Haibo Sun</name>
    </author>
    <author>
      <name>Tao Feng</name>
    </author>
    <author>
      <name>Zhaobiao Guo</name>
    </author>
    <author>
      <name>Aiping Ju</name>
    </author>
    <author>
      <name>Junchao Ge</name>
    </author>
    <author>
      <name>Yaqing Dong</name>
    </author>
    <author>
      <name>Wen Sun</name>
    </author>
    <author>
      <name>Yongqiang Jiang</name>
    </author>
    <author>
      <name>Jun Wang</name>
    </author>
    <author>
      <name>Jinghua Yan</name>
    </author>
    <author>
      <name>Huanming Yang</name>
    </author>
    <author>
      <name>Xiaoning Wang</name>
    </author>
    <author>
      <name>George F. Gao</name>
    </author>
    <author>
      <name>Ruifu Yang</name>
    </author>
    <author>
      <name>Jian Wang</name>
    </author>
    <author>
      <name>Jun Yu</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000315</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;
            &lt;i&gt;Streptococcus suis&lt;/i&gt; serotype 2 (SS2) is an important zoonotic pathogen, causing more than 200 cases of severe human infection worldwide, with the hallmarks of meningitis, septicemia, arthritis, etc. Very recently, SS2 has been recognized as an etiological agent for streptococcal toxic shock syndrome (STSS), which was originally associated with &lt;i&gt;Streptococcus pyogenes&lt;/i&gt; (GAS) in &lt;i&gt;Streptococci&lt;/i&gt;. However, the molecular mechanisms underlying STSS are poorly understood.&lt;/p&gt;Methods and Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;To elucidate the genetic determinants of STSS caused by SS2, whole genome sequencing of 3 different Chinese SS2 strains was undertaken. Comparative genomics accompanied by several lines of experiments, including experimental animal infection, PCR assay, and expression analysis, were utilized to further dissect a candidate pathogenicity island (PAI). Here we show, for the first time, a novel molecular insight into Chinese isolates of highly invasive SS2, which caused two large-scale human STSS outbreaks in China. A candidate PAI of ~89 kb in length, which is designated 89K and specific for Chinese SS2 virulent isolates, was investigated at the genomic level. It shares the universal properties of PAIs such as distinct GC content, consistent with its pivotal role in STSS and high virulence.&lt;/p&gt;Conclusions
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;To our knowledge, this is the first PAI candidate from &lt;i&gt;S. suis&lt;/i&gt; worldwide. Our finding thus sheds light on STSS triggered by SS2 at the genomic level, facilitates further understanding of its pathogenesis and points to directions of development on some effective strategies to combat highly pathogenic SS2 infections.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>A Key Role of Dendritic Cells in Probiotic Functionality</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000313" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000313" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000313" />
    <category term="Microbiology" label="Microbiology" />
    <author>
      <name>Benoit Foligne</name>
    </author>
    <author>
      <name>Georgia Zoumpopoulou</name>
    </author>
    <author>
      <name>Joelle Dewulf</name>
    </author>
    <author>
      <name>Amena Ben Younes</name>
    </author>
    <author>
      <name>Fabrice Chareyre</name>
    </author>
    <author>
      <name>Jean-Claude Sirard</name>
    </author>
    <author>
      <name>Bruno Pot</name>
    </author>
    <author>
      <name>Corinne Grangette</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000313</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Disruption of the intestinal homeostasis and tolerance towards the resident microbiota is a major mechanism involved in the development of inflammatory bowel disease. While some bacteria are inducers of disease, others, known as probiotics, are able to reduce inflammation. Because dendritic cells (DCs) play a central role in regulating immune responses and in inducing tolerance, we investigated their role in the anti-inflammatory potential of probiotic lactic acid bacteria.&lt;/p&gt;Methodology/Principal Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Selected LAB strains, while efficiently taken up by DCs &lt;i&gt;in vitro&lt;/i&gt;, induced a partial maturation of the cells. Transfer of probiotic-treated DCs conferred protection against 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Protection was associated with a reduction of inflammatory scores and colonic expression of pro-inflammatory genes, while a high local expression of the immunoregulatory enzyme indolamine 2, 3 dioxgenase (IDO) was observed. The preventive effect of probiotic-pulsed DCs required not only MyD88-, TLR2- and NOD2-dependent signaling but also the induction of CD4+ CD25+ regulatory cells in an IL-10-independent pathway.&lt;/p&gt;Conclusions/Significance
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Altogether, these results suggest that selected probiotics can stimulate DC regulatory functions by targeting specific pattern-recognition receptors and pathways. The results not only emphasize the role of DCs in probiotic immune interactions, but indicate a possible role in immune-intervention therapy for IBD.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>MLN51 Stimulates the RNA-Helicase Activity of eIF4AIII</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000303" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000303" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000303" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="RNA-Protein Interactions (Subcategory)" label="RNA-Protein Interactions (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="Post-Translational Regulation of Gene Expression (Subcategory)" label="Post-Translational Regulation of Gene Expression (Subcategory)" />
    <category term="Molecular Biology" label="Molecular Biology" />
    <category term="mRNA Stability (Subcategory)" label="mRNA Stability (Subcategory)" />
    <author>
      <name>Christian G. Noble</name>
    </author>
    <author>
      <name>Haiwei Song</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000303</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;The core of the exon-junction complex consists of Y14, Magoh, MLN51 and eIF4AIII, a DEAD-box RNA helicase. MLN51 stimulates the ATPase activity of eIF4AIII, whilst the Y14-Magoh complex inhibits it. We show that the MLN51-dependent stimulation increases both the affinity of eIF4AIII for ATP and the rate of enzyme turnover; the &lt;i&gt;K&lt;/i&gt;&lt;sub&gt;M&lt;/sub&gt; is decreased by an order of magnitude and &lt;i&gt;k&lt;/i&gt;&lt;sub&gt;cat&lt;/sub&gt; increases 30 fold. Y14-Magoh do inhibit the MLN51-stimulated ATPase activity, but not back to background levels. The ATP-bound form of the eIF4AIII-MLN51 complex has a 100-fold higher affinity for RNA than the unbound form and ATP hydrolysis reduces this affinity. MLN51 stimulates the RNA-helicase activity of eIF4AIII, suggesting that this activity may be functionally important.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>A Positive Regulatory Loop between &lt;italic&gt;foxi3a&lt;/italic&gt; and &lt;italic&gt;foxi3b&lt;/italic&gt; Is Essential for Specification and Differentiation of Zebrafish Epidermal Ionocytes</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000302" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000302" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000302" />
    <category term="Developmental Biology" label="Developmental Biology" />
    <category term="Cell Differentiation (Subcategory)" label="Cell Differentiation (Subcategory)" />
    <category term="Developmental Biology" label="Developmental Biology" />
    <category term="Embryology (Subcategory)" label="Embryology (Subcategory)" />
    <category term="Developmental Biology" label="Developmental Biology" />
    <category term="Molecular Development (Subcategory)" label="Molecular Development (Subcategory)" />
    <author>
      <name>Chung-Der Hsiao</name>
    </author>
    <author>
      <name>May-Su You</name>
    </author>
    <author>
      <name>Ying-Jey Guh</name>
    </author>
    <author>
      <name>Ming Ma</name>
    </author>
    <author>
      <name>Yun-Jin Jiang</name>
    </author>
    <author>
      <name>Pung-Pung Hwang</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000302</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Epidermal ionocytes play essential roles in the transepithelial transportation of ions, water, and acid-base balance in fish embryos before their branchial counterparts are fully functional. However, the mechanism controlling epidermal ionocyte specification and differentiation remains unknown.&lt;/p&gt;Methodology/Principal Findings
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;In zebrafish, we demonstrated that Delta-Notch-mediated lateral inhibition plays a vital role in singling out epidermal ionocyte progenitors from epidermal stem cells. The entire epidermal ionocyte domain of genetic mutants and morphants, which failed to transmit the DeltaC-Notch1a/Notch3 signal from sending cells (epidermal ionocytes) to receiving cells (epidermal stem cells), differentiates into epidermal ionocytes. The low Notch activity in epidermal ionocyte progenitors is permissive for activating winged helix/forkhead box transcription factors of foxi3a and foxi3b. Through gain- and loss-of-function assays, we show that the foxi3a-foxi3b regulatory loop functions as a master regulator to mediate a dual role of specifying epidermal ionocyte progenitors as well as of subsequently promoting differentiation of Na&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;-ATPase-rich cells and H&lt;sup&gt;+&lt;/sup&gt;-ATPase-rich cells in a concentration-dependent manner.&lt;/p&gt;Conclusions/Significance
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;This study provides a framework to show the molecular mechanism controlling epidermal ionocyte specification and differentiation in a low vertebrate for the first time. We propose that the positive regulatory loop between foxi3a and foxi3b not only drives early ionocyte differentiation but also prevents the complete blockage of ionocyte differentiation when the master regulator of foxi3 function is unilaterally compromised.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Multiple-Color Optical Activation, Silencing, and Desynchronization of Neural Activity, with Single-Spike Temporal Resolution</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000299" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000299" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000299" />
    <category term="Biophysics" label="Biophysics" />
    <category term="Physiology" label="Physiology" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Animal Cognition (Subcategory)" label="Animal Cognition (Subcategory)" />
    <category term="Pharmacology" label="Pharmacology" />
    <category term="Drug Development (Subcategory)" label="Drug Development (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Physiology" label="Physiology" />
    <category term="Neuronal Signaling Mechanisms (Subcategory)" label="Neuronal Signaling Mechanisms (Subcategory)" />
    <category term="Cell Biology" label="Cell Biology" />
    <category term="Neuronal Signaling Mechanisms (Subcategory)" label="Neuronal Signaling Mechanisms (Subcategory)" />
    <category term="Biotechnology" label="Biotechnology" />
    <category term="Neurological Disorders" label="Neurological Disorders" />
    <category term="Biophysics" label="Biophysics" />
    <category term="Experimental Biophysical Methods (Subcategory)" label="Experimental Biophysical Methods (Subcategory)" />
    <category term="Anesthesiology and Pain Management" label="Anesthesiology and Pain Management" />
    <category term="Anesthetic Mechanisms (Subcategory)" label="Anesthetic Mechanisms (Subcategory)" />
    <category term="Cell Biology" label="Cell Biology" />
    <category term="Neuronal and Glial Cell Biology (Subcategory)" label="Neuronal and Glial Cell Biology (Subcategory)" />
    <category term="Biophysics" label="Biophysics" />
    <category term="Membrane Proteins and Energy Transduction (Subcategory)" label="Membrane Proteins and Energy Transduction (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Cognitive Neuroscience (Subcategory)" label="Cognitive Neuroscience (Subcategory)" />
    <category term="Neuroscience" label="Neuroscience" />
    <category term="Theoretical Neuroscience (Subcategory)" label="Theoretical Neuroscience (Subcategory)" />
    <author>
      <name>Xue Han</name>
    </author>
    <author>
      <name>Edward S. Boyden</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000299</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;The quest to determine how precise neural activity patterns mediate computation, behavior, and pathology would be greatly aided by a set of tools for reliably activating and inactivating genetically targeted neurons, in a temporally precise and rapidly reversible fashion. Having earlier adapted a light-activated cation channel, channelrhodopsin-2 (ChR2), for allowing neurons to be stimulated by blue light, we searched for a complementary tool that would enable optical neuronal inhibition, driven by light of a second color. Here we report that targeting the codon-optimized form of the light-driven chloride pump halorhodopsin from the archaebacterium &lt;i&gt;Natronomas pharaonis&lt;/i&gt; (hereafter abbreviated Halo) to genetically-specified neurons enables them to be silenced reliably, and reversibly, by millisecond-timescale pulses of yellow light. We show that trains of yellow and blue light pulses can drive high-fidelity sequences of hyperpolarizations and depolarizations in neurons simultaneously expressing yellow light-driven Halo and blue light-driven ChR2, allowing for the first time manipulations of neural synchrony without perturbation of other parameters such as spiking rates. The Halo/ChR2 system thus constitutes a powerful toolbox for multichannel photoinhibition and photostimulation of virally or transgenically targeted neural circuits without need for exogenous chemicals, enabling systematic analysis and engineering of the brain, and quantitative bioengineering of excitable cells.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Breakage-Reunion Domain of &lt;italic&gt;Streptococcus pneumoniae&lt;/italic&gt; Topoisomerase IV: Crystal Structure of a Gram-Positive Quinolone Target</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000301" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000301" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000301" />
    <category term="Biophysics" label="Biophysics" />
    <category term="Biomacromolecule-Ligand Interactions (Subcategory)" label="Biomacromolecule-Ligand Interactions (Subcategory)" />
    <category term="Biophysics" label="Biophysics" />
    <category term="Computational Biology" label="Computational Biology" />
    <category term="Macromolecular Structure Analysis (Subcategory)" label="Macromolecular Structure Analysis (Subcategory)" />
    <category term="Biochemistry" label="Biochemistry" />
    <category term="Macromolecular Chemistry (Subcategory)" label="Macromolecular Chemistry (Subcategory)" />
    <author>
      <name>Ivan Laponogov</name>
    </author>
    <author>
      <name>Dennis A. Veselkov</name>
    </author>
    <author>
      <name>Maninder K. Sohi</name>
    </author>
    <author>
      <name>Xiao-Su Pan</name>
    </author>
    <author>
      <name>Aniruddha Achari</name>
    </author>
    <author>
      <name>Cheng Yang</name>
    </author>
    <author>
      <name>Joseph D. Ferrara</name>
    </author>
    <author>
      <name>L. Mark Fisher</name>
    </author>
    <author>
      <name>Mark R. Sanderson</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000301</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;The 2.7 Å crystal structure of the 55-kDa N-terminal breakage-reunion domain of topoisomerase (topo) IV subunit A (ParC) from &lt;i&gt;Streptococcus pneumoniae&lt;/i&gt;, the first for the quinolone targets from a gram-positive bacterium, has been solved and reveals a ‘closed’ dimer similar in fold to &lt;i&gt;Escherichia coli&lt;/i&gt; DNA gyrase subunit A (GyrA), but distinct from the ‘open’ gate structure of &lt;i&gt;Escherichia coli&lt;/i&gt; ParC. Unlike GyrA whose DNA binding groove is largely positively charged, the DNA binding site of ParC exhibits a distinct pattern of alternating positively and negatively charged regions coincident with the predicted positions of the grooves and phosphate backbone of DNA. Based on the ParC structure, a new induced-fit model for sequence-specific recognition of the gate (G) segment by ParC has been proposed. These features may account for the unique DNA recognition and quinolone targeting properties of pneumococcal type II topoisomerases compared to their gram-negative counterparts.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>The Role of Cytokines which Signal through the Common γ Chain Cytokine Receptor in the Reversal of HIV Specific CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; T Cell Anergy</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000300" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000300" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000300" />
    <category term="Infectious Diseases" label="Infectious Diseases" />
    <category term="HIV Infection and AIDS (Subcategory)" label="HIV Infection and AIDS (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Immune Response (Subcategory)" label="Immune Response (Subcategory)" />
    <category term="Immunology" label="Immunology" />
    <category term="Immunity to Infections (Subcategory)" label="Immunity to Infections (Subcategory)" />
    <category term="Virology" label="Virology" />
    <category term="Immunodeficiency Viruses (Subcategory)" label="Immunodeficiency Viruses (Subcategory)" />
    <category term="Virology" label="Virology" />
    <category term="Host Antiviral Responses (Subcategory)" label="Host Antiviral Responses (Subcategory)" />
    <author>
      <name>Xiao Xiao Jenny Gu</name>
    </author>
    <author>
      <name>Feng Yun Yue</name>
    </author>
    <author>
      <name>Colin M. Kovacs</name>
    </author>
    <author>
      <name>Mario A. Ostrowski</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000300</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">Background
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;HIV specific T cells are putatively anergic &lt;i&gt;in vivo&lt;/i&gt;. IL-2, a member of a class of cytokines that binds to receptors containing the common gamma chain (γc) has been shown to reverse anergy. We examined the role of γc cytokines in reversing HIV specific T cell anergy.&lt;/p&gt;Methods
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;PBMC from untreated HIV-infected individuals were briefly exposed to a panel of γc cytokines, and frequencies of &lt;i&gt;gag&lt;/i&gt; specific T cells were enumerated by intracellular IFN-γ flow cytometry.&lt;/p&gt;Results
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Of the γc cytokines, brief exposure to IL-2, IL-15, or combined IL-15/IL-7 significantly enhanced (range 2–7 fold) the CD4&lt;sup&gt;+&lt;/sup&gt; and CD8&lt;sup&gt;+&lt;/sup&gt; T cell IFN-γ responses to HIV &lt;i&gt;gag&lt;/i&gt;, with IL-15 giving the greatest enhancement. The effects of cytokines were not due to enhanced proliferation of pre-existing antigen specific cells, but were due to a combination of enhanced cytokine production from antigen specific T cells plus activation of non-epitope specific T cells.&lt;/p&gt;Conclusions
&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;These observations support the notion that a significant number of HIV specific T cells are circulating in an anergic state. IL-2, IL-7 and particularly IL-15 as an immune modulator to reverse HIV-1 specific T cell anergy should be investigated, with the caveat that non-specific activation of T cells may also be induced.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Transcriptional Repressor Gfi1 Integrates Cytokine-Receptor Signals Controlling B-Cell Differentiation</title>
    <link rel="alternate" href="http://localhost:8080/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000306" />
    <link rel="alternate" type="application/pdf" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=PDF&amp;uri=info:doi/10.1371/journal.pone.0000306" />
    <link rel="alternate" type="text/xml" href="http://localhost:8080/article/fetchObjectAttachment.action?representation=XML&amp;uri=info:doi/10.1371/journal.pone.0000306" />
    <category term="Hematology" label="Hematology" />
    <category term="Immunology" label="Immunology" />
    <author>
      <name>Chozhavendan Rathinam</name>
    </author>
    <author>
      <name>Christoph Klein</name>
    </author>
    <id>info:doi/10.1371/journal.pone.0000306</id>
    <updated>2007-03-21T07:00:00Z</updated>
    <published>2007-03-21T07:00:00Z</published>
    <content type="html">&lt;p xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:fn="http://www.w3.org/2005/xpath-functions" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:util="http://dtd.nlm.nih.gov/xsl/util" xmlns:mml="http://www.w3.org/1998/Math/MathML"&gt;Hematopoietic stem cell differentiation is specified by cytokines and transcription factors, but the mechanisms controlling instructive and permissive signalling networks are poorly understood. We provide evidence that CLP1-dependent IL7-receptor mediated B cell differentiation is critically controlled by the transcriptional repressor Gfi1. Gfi1-deficient progenitor B cells show global defects in IL7Rα-dependent signal cascades. Consequently, IL7-dependent trophic, proliferative and differentiation-inducing responses of progenitor B cells are perturbed. Gfi1 directly regulates expression levels of IL7Rα and indirectly controls STAT5 signalling via expression of SOCS3. Thus, Gfi1 selectively specifies IL7-dependent development of B cells from CLP1 progenitors, providing clues to the transcriptional networks integrating cytokine signals and lymphoid differentiation.&lt;/p&gt;</content>
  </entry>
  <entry>
    <title>Response Properties of Human Amygdala Subregions: Evidence Based on Functional MRI Combined with Probabilistic Anatomical Maps</title>
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&nb