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<pubDate>Thu, 21 Aug 2008 11:03:17 BST</pubDate>


	<title>CiteULike: wsjames' Wu</title>
	<description>CiteULike: wsjames' Wu</description>


	<link>http://www.citeulike.org/user/wsjames/author/Wu</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2932569"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2805568"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2520243"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2499829"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2320259"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/wsjames/article/2079748"/>

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<item rdf:about="http://www.citeulike.org/user/wsjames/article/2932569">
    <title>Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors</title>
    <link>http://www.citeulike.org/user/wsjames/article/2932569</link>
    <description>&lt;i&gt;Nature (29 June 2008)&lt;/i&gt;</description>
    <dc:title>Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors</dc:title>

    <dc:creator>Jeong Kim</dc:creator>
    <dc:creator>Holm Zaehres</dc:creator>
    <dc:creator>Guangming Wu</dc:creator>
    <dc:creator>Luca Gentile</dc:creator>
    <dc:creator>Kinarm Ko</dc:creator>
    <dc:creator>Vittorio Sebastiano</dc:creator>
    <dc:creator>Marcos Araúzo-Bravo</dc:creator>
    <dc:creator>David Ruau</dc:creator>
    <dc:creator>Dong Han</dc:creator>
    <dc:creator>Martin Zenke</dc:creator>
    <dc:creator>Hans Schöler</dc:creator>
    <dc:identifier>doi:10.1038/nature07061</dc:identifier>
    <dc:source>Nature (29 June 2008)</dc:source>
    <dc:date>2008-06-27T04:54:04-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>stemcells</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2805568">
    <title>Productive infection of human immunodeficiency virus type 1 in dendritic cells requires fusion-mediated viral entry</title>
    <link>http://www.citeulike.org/user/wsjames/article/2805568</link>
    <description>&lt;i&gt;Virology, Vol. 375, No. 2. (5 June 2008), pp. 442-451.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Human immunodeficiency virus type 1 (HIV-1) enters dendritic cells (DCs) through endocytosis and viral receptor-mediated fusion. Although endocytosis-mediated HIV-1 entry can generate productive infection in certain cell types, including human monocyte-derived macrophages, productive HIV-1 infection in DCs appears to be dependent on fusion-mediated viral entry. It remains to be defined whether endocytosed HIV-1 in DCs can initiate productive infection. Using HIV-1 infection and cellular fractionation assays to measure productive viral infection and entry, here we show that HIV-1 enters monocyte-derived DCs predominately through endocytosis; however, endocytosed HIV-1 cannot initiate productive HIV-1 infection in DCs. In contrast, productive HIV-1 infection in DCs requires fusion-mediated viral entry. Together, these results provide functional evidence in understanding HIV-1 cis-infection of DCs, suggesting that different pathways of HIV-1 entry into DCs determine the outcome of viral infection.</description>
    <dc:title>Productive infection of human immunodeficiency virus type 1 in dendritic cells requires fusion-mediated viral entry</dc:title>

    <dc:creator>Alicia Janas</dc:creator>
    <dc:creator>Chunsheng Dong</dc:creator>
    <dc:creator>Jian-Hua Wang</dc:creator>
    <dc:creator>Li Wu</dc:creator>
    <dc:identifier>doi:10.1016/j.virol.2008.01.044</dc:identifier>
    <dc:source>Virology, Vol. 375, No. 2. (5 June 2008), pp. 442-451.</dc:source>
    <dc:date>2008-05-16T16:51:45-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Virology</prism:publicationName>
    <prism:volume>375</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>442</prism:startingPage>
    <prism:endingPage>451</prism:endingPage>
    <prism:category>entry</prism:category>
    <prism:category>fusion</prism:category>
    <prism:category>hiv</prism:category>
    <prism:category>macrophage</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2520243">
    <title>Nucleoprotein structure of the CD4 locus: Implications for the mechanisms underlying CD4 regulation during T cell development</title>
    <link>http://www.citeulike.org/user/wsjames/article/2520243</link>
    <description>&lt;i&gt;Proceedings of the National Academy of Sciences, Vol. 105, No. 10. (11 March 2008), pp. 3873-3878.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The CD4 gene is regulated in a stage-specific manner during T cell development, being repressed in CD4CD8 double-negative (DN) and CD8 cells, but expressed in CD4+CD8+ double-positive (DP) and CD4 cells. Furthermore, the expression/repression pattern is reversible in developing (DN and DP) thymocytes, but irreversible in mature (CD4 and CD8) T cells. Here, we explored the molecular mechanisms underlying this complex mode of regulation by examining the nucleoprotein structure of the CD4 locus throughout T cell development and in DN cells lacking the CD4 silencer. In DN cells, the CD4 enhancer is preloaded with multiple transcription activators, but p300 recruitment is impaired by the silencer that is associated with the repressor Runx1. DP cells achieve high-level CD4 expression via a combination of CD4 derepression and true activation, but Runx1 remains bound to the silencer that retains an open chromatin configuration. In CD4 cells, Runx1 dissociates from the silencer that has become less accessible, and CD4 transcription appears to be achieved via a mechanism distinct from that operating in DP cells. In CD8 cells, the CD4 promoter becomes incorporated into heterochromatin-like structure. Our data shed light on the molecular basis of CD4 regulation and provide a conceptual framework for understanding how the same regulatory elements can mediate both reversible and irreversible CD4 regulation. 10.1073/pnas.0800810105</description>
    <dc:title>Nucleoprotein structure of the CD4 locus: Implications for the mechanisms underlying CD4 regulation during T cell development</dc:title>

    <dc:creator>Ming Yu</dc:creator>
    <dc:creator>Mimi Wan</dc:creator>
    <dc:creator>Jianmin Zhang</dc:creator>
    <dc:creator>Jie Wu</dc:creator>
    <dc:creator>Rohini Khatri</dc:creator>
    <dc:creator>Tian Chi</dc:creator>
    <dc:identifier>doi:10.1073/pnas.0800810105</dc:identifier>
    <dc:source>Proceedings of the National Academy of Sciences, Vol. 105, No. 10. (11 March 2008), pp. 3873-3878.</dc:source>
    <dc:date>2008-03-12T13:21:25-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Proceedings of the National Academy of Sciences</prism:publicationName>
    <prism:volume>105</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>3873</prism:startingPage>
    <prism:endingPage>3878</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2499829">
    <title>Human macrophages support persistent transcription from unintegrated HIV-1 DNA</title>
    <link>http://www.citeulike.org/user/wsjames/article/2499829</link>
    <description>&lt;i&gt;Virology, Vol. 372, No. 2. (15 March 2008), pp. 300-312.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Retroviruses require integration of their RNA genomes for both stability and productive viral replication. In HIV infection of non-dividing, resting CD4 T cells, where integration is greatly impeded, the reverse transcribed HIV DNA has limited biological activity and a short half-life. In metabolically active and proliferating T cells, unintegrated DNA rapidly diminishes with cell division. HIV also infects the non-dividing but metabolically active macrophage population. In an in vitro examination of HIV infection of macrophages, we find that unintegrated viral DNA not only has an unusual stability, but also maintains biological activity. The unintegrated linear DNA, 1-LTR, and 2-LTR circles are stable for at least 30 days. Additionally, there is persistent viral gene transcription, which is selective and skewed towards viral early genes such as nef and tat with highly diminished rev and vif. One viral early gene product Nef was measurably synthesized. We also find that independent of integration, the HIV infection process in macrophages leads to generation of numerous chemokines.</description>
    <dc:title>Human macrophages support persistent transcription from unintegrated HIV-1 DNA</dc:title>

    <dc:creator>Jeremy Kelly</dc:creator>
    <dc:creator>Margaret Beddall</dc:creator>
    <dc:creator>Dongyang Yu</dc:creator>
    <dc:creator>Subashini Iyer</dc:creator>
    <dc:creator>Jon Marsh</dc:creator>
    <dc:creator>Yuntao Wu</dc:creator>
    <dc:identifier>doi:10.1016/j.virol.2007.11.007</dc:identifier>
    <dc:source>Virology, Vol. 372, No. 2. (15 March 2008), pp. 300-312.</dc:source>
    <dc:date>2008-03-10T09:46:33-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Virology</prism:publicationName>
    <prism:volume>372</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>300</prism:startingPage>
    <prism:endingPage>312</prism:endingPage>
    <prism:category>hiv</prism:category>
    <prism:category>macrophage</prism:category>
    <prism:category>replication</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2320259">
    <title>Antigenic Profile of Avian H5N1 Viruses in Asia from 2002 to 2007</title>
    <link>http://www.citeulike.org/user/wsjames/article/2320259</link>
    <description>&lt;i&gt;J. Virol., Vol. 82, No. 4. (15 February 2008), pp. 1798-1807.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Antigenic profiles of post-2002 H5N1 viruses representing major genetic clades and various geographic sources were investigated using a panel of 17 monoclonal antibodies raised from five H5N1 strains. Four antigenic groups from seven clades of H5N1 virus were distinguished and characterized based on their cross-reactivity to the monoclonal antibodies in hemagglutination inhibition and cell-based neutralization assays. Genetic polymorphisms associated with the variation of antigenicity of H5N1 strains were identified and further verified in antigenic analysis with recombinant H5N1 viruses carrying specific mutations in the hemagglutinin protein. Modification of some of these genetic variations produced marked improvement to the immunogenicity and cross-reactivity of H5N1 strains in assays utilizing monoclonal antibodies and ferret antisera raised against clade 1 and 2 H5N1 viruses, suggesting that these sites represent antigenically significant amino acids. These results provide a comprehensive antigenic profile for H5N1 virus strains circulating in recent years and will facilitate the recognition of emerging antigenic variants of H5N1 virus and aid in the selection of vaccine strains. 10.1128/JVI.02256-07</description>
    <dc:title>Antigenic Profile of Avian H5N1 Viruses in Asia from 2002 to 2007</dc:title>

    <dc:creator>Wai Wu</dc:creator>
    <dc:creator>Yixin Chen</dc:creator>
    <dc:creator>Pui Wang</dc:creator>
    <dc:creator>Wenjun Song</dc:creator>
    <dc:creator>Siu-Ying Lau</dc:creator>
    <dc:creator>Jane Rayner</dc:creator>
    <dc:creator>Gavin Smith</dc:creator>
    <dc:creator>Robert Webster</dc:creator>
    <dc:creator>Malik Peiris</dc:creator>
    <dc:creator>Tianwei Lin</dc:creator>
    <dc:creator>Ningshao Xia</dc:creator>
    <dc:creator>Yi Guan</dc:creator>
    <dc:creator>Honglin Chen</dc:creator>
    <dc:identifier>doi:10.1128/JVI.02256-07</dc:identifier>
    <dc:source>J. Virol., Vol. 82, No. 4. (15 February 2008), pp. 1798-1807.</dc:source>
    <dc:date>2008-02-01T18:27:58-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>J. Virol.</prism:publicationName>
    <prism:volume>82</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1798</prism:startingPage>
    <prism:endingPage>1807</prism:endingPage>
    <prism:category>influenza</prism:category>
    <prism:category>neutralization</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/wsjames/article/2079748">
    <title>Treatment of Sickle Cell Anemia Mouse Model with iPS Cells Generated from Autologous Skin</title>
    <link>http://www.citeulike.org/user/wsjames/article/2079748</link>
    <description>&lt;i&gt;Science (6 December 2007), 1152092.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;It has recently been demonstrated that mouse and human fibroblasts can be reprogrammed into an embryonic stem celllike state by introducing combinations of four transcription factors. However, the therapeutic potential of such induced pluripotent stem (iPS) cells remained undefined. By using a humanized sickle cell anemia mouse model, we show that mice can be rescued after transplantation with hematopoietic progenitors obtained in vitro from autologous iPS cells. This was achieved after correction of the human sickle hemoglobin allele by gene-specific targeting. Our results provide proof of principle for using transcription factorinduced reprogramming combined with gene and cell therapy for disease treatment in mice. The problems associated with using retroviruses and oncogenes for reprogramming need to be resolved before iPS cells can be considered for human therapy. 10.1126/science.1152092</description>
    <dc:title>Treatment of Sickle Cell Anemia Mouse Model with iPS Cells Generated from Autologous Skin</dc:title>

    <dc:creator>Jacob Hanna</dc:creator>
    <dc:creator>Marius Wernig</dc:creator>
    <dc:creator>Styliani Markoulaki</dc:creator>
    <dc:creator>Chiao-Wang Sun</dc:creator>
    <dc:creator>Alexander Meissner</dc:creator>
    <dc:creator>John Cassady</dc:creator>
    <dc:creator>Caroline Beard</dc:creator>
    <dc:creator>Tobias Brambrink</dc:creator>
    <dc:creator>Li-Chen Wu</dc:creator>
    <dc:creator>Tim Townes</dc:creator>
    <dc:creator>Rudolf Jaenisch</dc:creator>
    <dc:identifier>doi:10.1126/science.1152092</dc:identifier>
    <dc:source>Science (6 December 2007), 1152092.</dc:source>
    <dc:date>2007-12-08T17:56:55-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:startingPage>1152092</prism:startingPage>
    <prism:category>stemcells</prism:category>
</item>



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