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  • Cell Research
    Yuanheng Ning 1 Lei Huang 1 Hong Zhang 2 Xiang Gao 3 Li Yu 1 and Ye Guang Chen 1 1 State Key Laboratory of Biomembrane and Membrane Biotechnology Tsinghua Peking Center for Life Sciences School of Life Sciences Tsinghua University Beijing 100084 China 2 State Key Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China 3 Key Laboratory of Model Animal for Disease Study of Ministry of Education Model Animal Research Center Nanjing University Nanjing Jiangsu 210061 China 4 Current address CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety National Center for Nanoscience and Technology Beijing 100190 China Correspondence Ye Guang Chen Tel 86 10 6279 5184 Fax 86 10 6279 4376 E mail ygchen tsinghua edu cn Autophagy is an intracellular degradation process to clear up aggregated proteins or aged and damaged organelles The Beclin1 Vps34 Atg14L complex is essential for autophagosome formation However how the complex formation is regulated is unclear Here we show that Dapper1 Dpr1 acts as a critical regulator of the Beclin1 Vps34 Atg14L complex to promote autophagy Dpr1 ablation in the central nervous system results in motor coordination defect and accumulation of p62 and ubiquitinated proteins Dpr1

    Original URL path: http://www.cell-research.com/arts.asp?id=1968 (2016-02-14)
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  • Cell Research
    Lin 1 Lei Li 1 Hongmei Wang 1 Yan ling Wang 1 Bing Li 3 Qi Chen 1 Enkui Duan 1 and Haibin Wang 1 1 State Key Laboratory of Reproductive Biology Institute of Zoology Chinese Academy of Sciences Beijing 100101 China 2 University of Chinese Academy of Sciences Beijing 100101 China 3 Reproductive Medical Center The Third Affiliated Hospital of Guangzhou Medical College Key Laboratory for Major Obstetric Diseases of Guangdong Province Guangzhou Guangdong China 4 Department of Molecular and Cellular Biology Baylor College of Medicine Houston TX 77030 USA 5 Department of Pathology Perelman School of Medicine University of Pennsylvania Philadelphia PA 19104 USA 6 Department of Dermatology Xijing Hospital Fourth Military Medical University Xi an Shanxi 710032 China 7 State Key Laboratory of Cancer Biology Department of Medical Genetics and Developmental Biology Fourth Military Medical University Xi an Shanxi 710032 China Correspondence Haibin Wang Tel 86 01 64807868 E mail hbwang ioz ac cn Enkui Duan Tel 86 01 64807182 E mail duane ioz ac cn Qi Chen Tel 86 01 64807182 E mail chenqi ioz ac cn Coordinated uterine embryonic axis formation and decidual remodeling are hallmarks of mammalian post implantation embryo development Embryonic uterine orientation is determined at initial implantation and synchronized with decidual development However the molecular mechanisms controlling these events remain elusive despite its discovery a long time ago In the present study we found that uterine specific deletion of Rbpj the nuclear transducer of Notch signaling resulted in abnormal embryonic uterine orientation and decidual patterning at post implantation stages leading to substantial embryo loss We further revealed that prior to embryo attachment Rbpj confers on time uterine lumen shape transformation via physically interacting with uterine estrogen receptor ERα in a Notch pathway independent manner which is essential for the initial establishment of

    Original URL path: http://www.cell-research.com/arts.asp?id=1969 (2016-02-14)
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  • Cell Research
    1 2 Shuo Wang 1 Guanling Huang 1 2 Ying Du 1 Pingping Zhu 1 Man Li 1 2 and Zusen Fan 1 1 Key Laboratory of Infection and Immunity of CAS Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China 2 University of Chinese Academy of Sciences Beijing 100049 China Correspondence Zusen Fan Tel 86 10 64888457 Fax 86 10 64871293 E mail fanz moon ibp ac cn WASH Wiskott Aldrich syndrome protein WASP and SCAR homolog was identified to function in endosomal sorting via Arp2 3 activation We previously demonstrated that WASH is a new interactor of BECN1 and present in the BECN1 PIK3C3 complex with AMBRA1 The AMBRA1 DDB1 CUL4A complex is an E3 ligase for K63 linked ubiquitination of BECN1 which is required for starvation induced autophagy WASH suppresses autophagy by inhibition of BECN1 ubiquitination However how AMBRA1 is regulated during autophagy remains elusive Here we found that RNF2 associates with AMBRA1 to act as an E3 ligase to ubiquitinate AMBRA1 via K48 linkage RNF2 mediates ubiquitination of AMBRA1 at lysine 45 Notably RNF2 deficiency enhances autophagy induction Upon autophagy induction RNF2 potentiates AMBRA1 degradation with the help of WASH WASH deficiency impairs the association

    Original URL path: http://www.cell-research.com/arts.asp?id=1970 (2016-02-14)
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  • Cell Research
    China 2 State Key Laboratory of Electroanalytical Chemistry Changchun Institute of Applied Chemistry Chinese Academy of Sciences Changchun Jilin 130022 China 3 National Center for Protein Science Shanghai State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yueyang Road Shanghai 200031 China 4 Department of Thoracic Surgery The Second Hospital of Jilin University Changchun Jilin 130041 China 5 School of Computer Science and Information Technology Northeast Normal University Changchun Jilin 130117 China 6 University of Chinese Academy of Sciences Beijing 100049 China 7 Department of Oncology Changhai Hospital Second Military Medical University Shanghai 200433 China Correspondence Hongda Wang E mail hdwang ciac ac cn Hongbin Ji E mail hbji sibcb ac cn Chenqi Xu E mail cqxu sibcb ac cn The abnormal activation of epidermal growth factor receptor EGFR is strongly associated with a variety of human cancers but the underlying molecular mechanism is not fully understood By using direct stochastic optical reconstruction microscopy dSTORM we find that EGFR proteins form nanoclusters in the cell membrane of both normal lung epithelial cells and lung cancer cells but the number and size of clusters significantly increase in lung

    Original URL path: http://www.cell-research.com/arts.asp?id=1971 (2016-02-14)
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  • Cell Research
    Jinjin Chen 1 3 Liang Xu 1 2 Hong Zhang 1 2 Jiangchuan Ye 1 3 Fei Lv 1 3 Jian Huang 1 3 Luying Peng 4 and Yi Han Chen 1 2 3 4 1 Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China 2 Institute of Medical Genetics Tongji University Shanghai 200092 China 3 Department of Cardiology East Hospital Tongji University School of Medicine Shanghai 200120 China 4 Department of Pathology and Pathophysiology Tongji University School of Medicine Shanghai 200092 China Correspondence Yi Han Chen Tel 86 21 65989086 Fax 86 21 65989086 E mail yihanchen tongji edu cn Pathological cardiac hypertrophy is an inevitable forerunner of heart failure Regardless of the etiology of cardiac hypertrophy cardiomyocyte mitochondrial alterations are always observed in this context The translocases of mitochondrial outer membrane Tom complex governs the import of mitochondrial precursor proteins to maintain mitochondrial function under pathophysiological conditions however its role in the development of pathological cardiac hypertrophy remains unclear Here we showed that Tom70 was downregulated in pathological hypertrophic hearts from humans and experimental animals The reduction in Tom70 expression produced distinct pathological

    Original URL path: http://www.cell-research.com/arts.asp?id=1972 (2016-02-14)
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  • Cell Research
    The University of Tokyo Meguro ku 153 8904 Japan 3 Department of Respiratory Medicine Graduate School of Medicine The University of Tokyo Bunkyo ku Tokyo 113 0033 Japan 4 Department of Biochemistry Interdisciplinary Graduate School of Medicine and Engineering University of Yamanashi 1110 Shimokato Chuo Yamanashi 409 3898 Japan Correspondence Kohei Miyazono Tel 81 3 5841 3345 Fax 81 3 5841 3354 E mail miyazono m u tokyo ac jp Daizo Koinuma Tel 81 3 5841 3345 Fax 81 3 5841 3354 E mail koinuma m u tokyo ac jp Thyroid transcription factor 1 TTF 1 also known as NKX2 1 is a tissue specific transcription factor in lung epithelial cells Although TTF 1 inhibits the epithelial to mesenchymal transition induced by transforming growth factor β TGF β in lung adenocarcinoma cells the mechanism through which TTF 1 inhibits the functions of TGF β is unknown Here we show that TTF 1 disrupts the nuclear Smad3 Smad4 complex without affecting the nuclear localization of phospho Smad3 Genome wide analysis by chromatin immunoprecipitation followed by sequencing revealed that TTF 1 colocalizes with Smad3 on chromatin and alters Smad3 binding patterns throughout the genome while TTF 1 generally inhibits Smad4 binding to

    Original URL path: http://www.cell-research.com/arts.asp?id=1973 (2016-02-14)
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  • Cell Research
    8 8 2014 1009 1012 Genome wide identification of CRISPR Cas9 off targets in human genome FREE Jinzhi Duan 1 2 Guangqing Lu 1 2 Zhan Xie 2 Mingliang Lou 2 Jiao Luo 2 Lei Guo 2 and Yu Zhang 1 2 1 Graduate Program Peking Union Medical College and Chinese Academy of Medical Sciences Beijing 100730 China 2 National Institute of Biological Sciences Beijing 102206 China Correspondence Yu Zhang E mail zhangyu nibs ac cn Genome editing techniques have been rapidly developing in recent decades1 Among them site specific cleavage of genomic loci in various organisms by homing endonucleases HEases 2 Zinc finger nucleases ZFNs 3 transcription activator like effector nucleases TALENs 4 and most recently the CRISPR clustered regularly interspersed short palindromic repeats Cas9 system5 has been utilized widely not only in laboratories but also for translational studies The central issue of genome editing is how to achieve specific and robust recognition of particular genomic sequences In the case of HEases ZFNs and TALENs this is achieved by specific intermolecular interactions between nucleotides and protein motifs while for CRISPR Cas9 the specificity is due to Watson Crick base pairing between CRISPR RNA crRNA and its recognition sequences The

    Original URL path: http://www.cell-research.com/arts.asp?id=1974 (2016-02-14)
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  • Cell Research
    1 Haifeng Liu 1 Xiang Sun 1 Mujun Zhao 2 and Xiaolong Liu 1 1 State Key Laboratory of Cell Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 2 State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Correspondence Xiaolong Liu E mail liux sibs ac cn Hematopoietic stem cells HSCs are responsible for the lifelong production of all blood cells1 Like many other tissues and organs the hematopoietic system develops during embryogenesis2 One of the challenges of this developing process is to generate a functional HSC pool which is a prerequisite for seeding bone marrow and thereafter lifelong hematopoiesis3 HSC expansion is critical for the establishment of such HSC pool2 To accomplish the expansion the fetal liver HSCs FL HSCs are continuously undergoing symmetric cell division which requires precise collaboration of multiple cellular processes2 especially those that serve to maintain the genomic stability of the dividing HSCs Many factors have been shown to be involved in FL HSC expansion Growth factors such as insulin like growth factor 2 IGF2 and stem cell factor

    Original URL path: http://www.cell-research.com/arts.asp?id=1975 (2016-02-14)
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