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  • Cell Research
    304 Neural crest stem cells discovery properties and potential for therapy Annita Achilleos 1 and Paul A Trainor 1 2 1 Stowers Institute for Medical Research 1000 East 50th Street Kansas City MO 64110 USA 2 Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City KS 66160 USA Correspondence Paul A Trainor Tel 1 816 926 4414 E mail pat stowers org Cell Research 2012 22

    Original URL path: http://www.cell-research.com/arts.asp?id=212 (2016-02-14)
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  • Cell Research
    David O Ferguson 3 Jean Yves Masson 2 and St閜han 1 Terry Fox Molecular Oncology Group Bloomfield Center for Research on Aging Lady Davis Institute for Medical Research Sir Mortimer B Davis Jewish General Hospital and Departments of Oncology and Medicine McGill University Montreal Quebec Canada H3T 1E2 2 Genome Stability Laboratory Laval University Cancer Research Center H魌el Dieu de Qu閎ec CHUQ Quebec city Quebec Canada G1R 2J6 3 Department of Pathology University of Michigan Medical School Ann Arbor MI 48109 USA 4 Leukemia Cell Bank of Quebec and Division of Hematology Maisonneuve Rosemont Hospital Montreal Quebec Canada 5 Department of Medicine Universit de Montr閍l Montreal Quebec Canada H1T 2M4 Correspondence Stéphane Richard Tel 514 340 8260 E mail stephane richard mcgill ca The MRE11 RAD50 NBS1 complex is the primary sensor rapidly recruited to DNA double strand breaks DSBs MRE11 is known to be arginine methylated by PRMT1 within its glycine arginine rich GAR motif In this study we report a mouse knock in allele of Mre11 that substitutes the arginines with lysines in the GAR motif and generates the MRE11 RK protein devoid of methylated arginines The Mre11 RK RK mice were hypersensitive to γ irradiation IR and the cells from these mice displayed cell cycle checkpoint defects and chromosome instability Moreover the Mre11 RK RK MEFs exhibited ATR CHK1 signaling defects and impairment in the recruitment of RPA and RAD51 to the damaged sites The M RK RN complex formed and localized to the sites of DNA damage and normally activated the ATM pathway in response to IR The M RK RN complex exhibited exonuclease and DNA binding defects in vitro responsible for the impaired DNA end resection and ATR activation observed in vivo in response to IR Our findings provide genetic evidence for the critical role

    Original URL path: http://www.cell-research.com/arts.asp?id=213 (2016-02-14)
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  • Cell Research
    of Colorado School of Medicine Aurora CO 80045 USA 2 Shanghai First People s Hospital School of Medicine Shanghai Jiaotong University Shanghai 201620 China 3 Department of Pharmacology University of Colorado School of Medicine Aurora CO 80045 USA 4 Department of Neurology University of Colorado School of Medicine Aurora CO 80045 USA 5 Third Military Medical University Chongqing 400038 China 6 School of Life Science and Biotechnology Shanghai Jiaotong University Shanghai 200240 China 7 Department of Pediatrics University of Colorado School of Medicine Aurora CO 80045 USA 8 Charles Gates Center for Stem Cell and Regenerative Medicine University of Colorado School of Medicine Aurora CO 80045 USA 9 Current address Department of Dermatology Box 3135 Duke University Medical Center Durham NC 27710 USA Correspondence Chuan Yuan Li Tel 1 919 613 8754 E mail Chuan Li duke edu Transplantation of exogenous dopaminergic neuron DA neurons is a promising approach for treating Parkinson s disease PD However a major stumbling block has been the lack of a reliable source of donor DA neurons Here we show that a combination of five transcriptional factors Mash1 Ngn2 Sox2 Nurr1 and Pitx3 can directly and effectively reprogram human fibroblasts into DA neuron like cells

    Original URL path: http://www.cell-research.com/arts.asp?id=280 (2016-02-14)
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  • Cell Research
    and Regenerative Medicine Guangzhou Institutes of Biomedicine and Health Chinese Academy of Sciences Guangzhou 510530 China 2 School of Life Sciences University of Science and Technology of China Hefei 230027 China 3 Key Laboratory of Chemical Genomics School of Chemical Biology and Biotechnology Shenzhen Graduate School of Peking University Shenzhen 518055 China Correspondence Xiaodong Shu Duanqing Pei E mail shu xiaodong gibh ac cn pei duanqing gibh ac cn Sorting nexins SNXs are phosphoinositide binding proteins implicated in the sorting of various membrane proteins in vitro but the in vivo functions of them remain largely unknown We reported previously that SNX10 is a unique member of the SNX family genes in that it has vacuolation activity in cells We investigate the biological function of SNX10 by loss of function assay in this study and demonstrate that SNX10 is required for the formation of primary cilia in cultured cells In zebrafish SNX10 is involved in ciliogenesis in the Kupffer s vesicle and essential for left right patterning of visceral organs Mechanistically SNX10 interacts with V ATPase complex and targets it to the centrosome where ciliogenesis is initiated Like SNX10 V ATPase regulates ciliogenesis in vitro and in vivo and does so

    Original URL path: http://www.cell-research.com/arts.asp?id=214 (2016-02-14)
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  • Cell Research
    of Molecular Biology National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health Bethesda MD 20892 USA Correspondence Yihong Ye Tel 301 5940845 E mail yihongy mail nih gov The AAA ATPase associated with various cellular activities ATPase p97 acts on diverse substrate proteins to partake in various cellular processes such as membrane fusion and endoplasmic reticulum associated degradation ERAD In membrane fusion p97 is thought to function in analogy to the related ATPase NSF N ethylmaleimide sensitive fusion protein which promotes membrane fusion by disassembling a SNARE complex In ERAD p97 dislocates misfolded proteins from the ER membrane to facilitate their turnover by the proteasome Here we identify a novel function of p97 in endocytic trafficking by establishing the early endosomal autoantigen 1 EEA1 as a new p97 substrate We demonstrate that a fraction of p97 is localized to the early endosome membrane where it binds EEA1 via the N terminal C2H2 zinc finger domain Inhibition of p97 either by siRNA or a pharmacological inhibitor results in clustering and enlargement of early endosomes which is associated with an altered trafficking pattern for an endocytic cargo Mechanistically we show that p97 inhibition causes increased EEA1 self association

    Original URL path: http://www.cell-research.com/arts.asp?id=215 (2016-02-14)
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  • Cell Research
    McManus 1 and Honglin Luo 1 1 James Hogg iCAPTURE Centre Providence Heart Lung Institute St Paul s Hospital and Department of Pathology and Laboratory Medicine University of British Columbia 1081 Burrard Street Vancouver BC V6Z 1Y Canada 2 Center for Molecular Development and Disease Institute of Biosciences and Technology Texas A M Health Science Center Houston TX 77030 USA Correspondence Honglin Luo Tel 1 604 682 2344 ext 62847 E mail honglin luo hli ubc ca Enteroviral infection can lead to dilated cardiomyopathy DCM which is a major cause of cardiovascular mortality worldwide However the pathogenetic mechanisms have not been fully elucidated Serum response factor SRF is a cardiac enriched transcription regulator controlling the expression of a variety of target genes including those involved in the contractile apparatus and immediate early response as well as microRNAs that silence the expression of cardiac regulatory factors Knockout of SRF in the heart results in downregulation of cardiac contractile gene expression and development of DCM The goal of this study is to understand the role of SRF in enterovirus induced cardiac dysfunction and progression to DCM Here we report that SRF is cleaved following enteroviral infection of mouse heart and cultured cardiomyocytes This cleavage is accompanied by impaired cardiac function and downregulation of cardiac specific contractile and regulatory genes Further investigation by antibody epitope mapping and site directed mutagenesis demonstrates that SRF cleavage occurs at the region of its transactivation domain through the action of virus encoded protease 2A Moreover we demonstrate that cleavage of SRF dissociates its transactivation domain from DNA binding domain resulting in the disruption of SRF mediated gene transactivation In addition to loss of functional SRF finally we report that the N terminal fragment of SRF cleavage products can also act as a dominant negative transcription factor which

    Original URL path: http://www.cell-research.com/arts.asp?id=216 (2016-02-14)
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  • Cell Research
    Xiaoshan Shi 1 3 Yuan Gao 1 2 Jing Zhou 1 2 Ping Xu 1 1 State Key Laboratory of Microbial Metabolism and School of Life Sciences Biotechnology Shanghai Jiao Tong University Shanghai 200240 China 2 Key Laboratory of MOE for Developmental Genetics and Neuropsychiatric Diseases Shanghai Jiao Tong University Shanghai 200240 China 3 Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 4 Department of Pathophysiology Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education Shanghai Jiao Tong University School of Medicine SJTU SM Shanghai 200025 China Correspondence Geng Wu Kui Lin Jian Zhang E mail geng wu sjtu edu cn klin sjtu edu cn bjian zhang sjtu edu jian zhang sjtu edu cn Adenomatous polyposis coli APC regulates cell cell adhesion and cell migration through activating the APC stimulated guanine nucleotide exchange factor GEF Asef which is usually autoinhibited through the binding between its Src homology 3 SH3 and Dbl homology DH domains The APC activated Asef stimulates the small GTPase Cdc42 which leads to decreased cell cell adherence and enhanced cell migration In colorectal cancers truncated APC constitutively activates Asef and promotes cancer cell migration and angiogenesis Here we report crystal structures of the human APC Asef complex We find that the armadillo repeat domain of APC uses a highly conserved surface groove to recognize the APC binding region ABR of Asef conformation of which changes dramatically upon binding to APC Key residues on APC and Asef for the complex formation were mutated and their importance was demonstrated by binding and activity assays Structural superimposition of the APC Asef complex with autoinhibited Asef suggests that the binding between APC and Asef might create a steric clash between Asef DH domain and APC which possibly leads

    Original URL path: http://www.cell-research.com/arts.asp?id=217 (2016-02-14)
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  • Cell Research
    1 Hui Xiong 1 Jiong Tao 2 and Zhi Qi Xiong 1 1 Institute of Neuroscience and State Key Laboratory of Neuroscience Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Yueyang Road 320 ION building Room 426 Shanghai 200031 China 2 Xinhua Hospital School of Medicine Shanghai Jiao Tong University Shanghai 200092 China Correspondence Zhi Qi Xiong Tel 86 21 54921716 E mail xiongzhiqi ion ac cn Serum inducible kinase SNK also known as p olo l ike k inase 2 PLK2 is a known regulator of mitosis synaptogenesis and synaptic homeostasis However its role in early cortical development is unknown Herein we show that snk is expressed in the cortical plate from embryonic day 14 but not in the ventricular subventricular zones VZ SVZ and SNK protein localizes to the soma and dendrites of cultured immature cortical neurons Loss of SNK impaired dendritic but not axonal arborization in a dose dependent manner and overexpression had opposite effects both in vitro and in vivo Overexpression of SNK also caused abnormal branching of the leading process of migrating cortical neurons in electroporated cortices The kinase activity was necessary for these effects Extracellular signal regulated kinase ERK pathway activity downstream of

    Original URL path: http://www.cell-research.com/arts.asp?id=218 (2016-02-14)
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