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  • Cell Research
    State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China Correspondence Xiaolong Liu Tel 86 21 54921178 E mail 86 21 54921178 The roles of the reprogramming factors Oct4 Sox2 c Myc and Klf4 in early T cell development are incompletely defined Here we show that Klf4 is the only reprogramming factor whose expression is downregulated when early thymic progenitors ETPs differentiate into T cells Enforced expression of Klf4 in uncommitted progenitors severely impaired T cell development mainly at the DN2 to DN3 transition when T cell lineage commitment occurs and affected the transcription of a variety of genes with crucial functions in early T cell development including genes involved in microenvironmental signaling IL 7R α Notch target genes Deltex1 and essential T cell lineage regulatory or inhibitory genes Bcl11a SpiB and Id1 The survival of thymocytes and the rearrangement at the Tcrb locus were impaired in the presence of enforced Klf4 expression The defects in the DN1 to DN2 and DN2 to DN3 transitions in Klf4 transgenic mice could not be rescued by the introduction of a TCR transgene but was partially

    Original URL path: http://www.cell-research.com/arts.asp?id=258 (2016-02-14)
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  • Cell Research
    4 Division of Integrative Biosciences and Biotechnology Pohang University of Science and Technology Pohang Korea Correspondence ř í Friml Tel 32 0 9 33 13 800 E mail jiri friml psb vib ugent be Subcellular trafficking is required for a multitude of functions in eukaryotic cells It involves regulation of cargo sorting vesicle formation trafficking and fusion processes at multiple levels Adaptor protein AP complexes are key regulators of cargo sorting into vesicles in yeast and mammals but their existence and function in plants have not been demonstrated Here we report the identification of the protein affected trafficking 4 pat4 mutant defective in the putative δ subunit of the AP 3 complex pat4 and pat2 a mutant isolated from the same GFP imaging based forward genetic screen that lacks a functional putative AP 3 β as well as dominant negative AP 3 μ transgenic lines display undistinguishable phenotypes characterized by largely normal morphology and development but strong intracellular accumulation of membrane proteins in aberrant vacuolar structures All mutants are defective in morphology and function of lytic and protein storage vacuoles PSVs but show normal sorting of reserve proteins to PSVs Immunoprecipitation experiments and genetic studies revealed tight functional and physical

    Original URL path: http://www.cell-research.com/arts.asp?id=259 (2016-02-14)
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  • Cell Research
    Baylor College of Medicine Houston TX77030 USA 3 Riken Research Center for Allergy and Immunology 1 7 22 Suehiro Tsurumi ku Yokohama 230 0045 Japan Correspondence Jiemin Wong E mail jmweng bio ecnu edu cn Recent studies demonstrate that UHRF1 is required for DNA methylation maintenance by targeting DNMT1 to DNA replication foci presumably through its unique hemi methylated DNA binding activity and interaction with DNMT1 UHRF2 another member of the UHRF family proteins is highly similar to UHRF1 in both sequence and structure raising questions about its role in DNA methylation In this study we demonstrate that like UHRF1 UHRF2 also binds preferentially to methylated histone H3 lysine 9 H3K9 through its conserved tudor domain and hemi methylated DNA through the SET and Ring associated domain Like UHRF1 UHRF2 is enriched in pericentric heterochromatin The heterochromatin localization depends to large extent on its methylated H3K9 binding activity and to less extent on its methylated DNA binding activity Coimmunoprecipitation experiments demonstrate that both UHRF1 and UHRF2 interact with DNMT1 DNMT3a DNMT3b and G9a Despite all these conserved functions we find that UHRF2 is not able to rescue the DNA methylation defect in Uhrf1 null mouse embryonic stem cells This can

    Original URL path: http://www.cell-research.com/arts.asp?id=260 (2016-02-14)
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  • Cell Research
    causing mutations by homologous recombination in integration free patient iPSCs Mo Li 1 Keiichiro Suzuki 1 Jing Qu 1 Preeti Saini 1 Ilir Dubova 1 Fei Yi 1 Jungmin Lee 1 Ignacio Sancho Martinez 1 Guang Hui Liu 1 and Juan Carlos I 1 Salk Institute for Biological Studies 10010 N Torrey Pines Rd La Jolla CA 92037 USA 2 Center of Regenerative Medicine in Barcelona Dr Aiguader 88 08003

    Original URL path: http://www.cell-research.com/arts.asp?id=261 (2016-02-14)
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  • Cell Research
    Hui Zhang 1 Tatiana Ecoiffier 1 Bronislaw Pytowski 4 and Lu Chen 1 5 6 1 Center for Eye Disease and Development Program in Vision Science University of California Berkeley CA 94720 USA 2 School of Medicine Shanghai Jiao Tong University China 3 Department of Molecular and Cell Biology Helen Wills Neuroscience Institute University of California Berkeley USA 4 Cell Biology and Bioimaging ImClone Systems Eli Lilly and Company New

    Original URL path: http://www.cell-research.com/arts.asp?id=262 (2016-02-14)
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  • Cell Research
    1 Ge Li 1 4 Zhen Chao Zhang 1 Jian Yong Wang 1 Yong Wen Qin 2 and Qing Jing 1 2 1 Key Laboratory of Stem Cell Biology and Laboratory of Nucleic Acid and Molecular Medicine Institute of Health Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine Shanghai 200025 China 2 Department of Cardiology Changhai Hospital Shanghai 200433 China

    Original URL path: http://www.cell-research.com/arts.asp?id=263 (2016-02-14)
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  • Cell Research

    (No additional info available in detailed archive for this subpage)
    Original URL path: /artsmore1.asp?id=18 (2016-02-14)


  • Cell Research
    526 Thomson Reuters 2013 Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 22 ISSUE 1 1 2012 1 2 A special issue on cell signaling disease and stem cells Dangsheng Li Deputy Editor in Chief Cell Research Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China E mail dsli sibs ac cn Cell Research 2012 22 1 2 doi 10 1038 cr 2012

    Original URL path: http://www.cell-research.com/arts.asp?id=225 (2016-02-14)
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