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  • Cell Research
    2013 Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 25 ISSUE 6 6 2015 653 654 AChE for DNA degradation FREE María Sánchez Osuna 1 and Victor J Yuste 1 1 Cell Death Senescence and Survival group Departament de Bioquímica i Biologia Molecular Unitat de Medicina Institut de Neurociències Facultat de Medicina Universitat Autònoma de Barcelona 08193 Barcelona Spain Correspondence Victor J Yuste E mail victor

    Original URL path: http://www.cell-research.com/arts.asp?id=2112 (2016-02-14)
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  • Cell Research
    Bao Ting Zhang 6 Chun Sheng 7 Hongyan Wang 2 and Ping Hu 1 1 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 2 Key Laboratory of Systems Biology Innovation Center for Cell Signaling Network Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China 3 CAS Key Laboratory of Computational Biology CAS MPG Partner Institute for Computational Biology 320 Yueyang Road Shanghai 200031 China 4 Department of Chemical Pathology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Hong Kong SAR China 5 Department of Orthopaedics and Traumatology Li Ka Shing Institute of Health Sciences The Chinese University of Hong Kong Hong Kong SAR China 6 School of Chinese Medicine The Chinese University of Hong Kong Hong Kong SAR China 7 Shanghai Normal University Guilin Road Shanghai 200234 China Correspondence Ping Hu Hongyan Wang Tel 86 021 5492 1254 86 021 5492 1086 E mail hup sibcb ac cn hongyanwang sibcb ac cn Muscle stem cells MuSCs satellite cells are the major contributor to muscle regeneration Like most adult stem cells long term expansion of MuSCs in vitro is difficult The in vivo muscle regeneration abilities of MuSCs are quickly lost after culturing in vitro which prevents the potential applications of MuSCs in cell based therapies Here we establish a system to serially expand MuSCs in vitro for over 20 passages by mimicking the endogenous microenvironment We identified that the combination of four pro inflammatory cytokines IL 1α IL 13 TNF α and IFN γ secreted by T cells was able to stimulate MuSC proliferation in vivo upon injury and promote serial expansion of MuSCs in vitro The

    Original URL path: http://www.cell-research.com/arts.asp?id=2113 (2016-02-14)
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  • Cell Research
    Ahmed 1 Ying Mei Lu 3 Zhi Rong Liu 4 Wei Xing Shi 5 En Yin Lai 6 Christopher S Wilcox 7 and Feng Han 1 1 Institute of Pharmacology and Toxicology College of Pharmaceutical Sciences Zhejiang University Hangzhou Zhejiang 310058 China 2 Key Laboratory of Carbohydrate and Lipid Metabolism Research College of Life Science and Technology Dalian University Dalian Liaoning 116622 China 3 School of Medicine Zhejiang University City College Hangzhou Zhejiang 310015 China 4 Department of Neurology Second Affiliated Hospital of Zhejiang University School of Medicine Hangzhou Zhejiang 310009 China 5 Department of Basic Sciences Loma Linda University Health Schools of Medicine Pharmacy and Behavioral Health Loma Linda CA 92350 USA 6 Department of Physiology Zhejiang University School of Medicine Hangzhou Zhejiang 310058 China 7 Hypertension Kidney and Vascular Research Center Georgetown University Medical Center Washington DC 20007 USA Correspondence Feng Han Tel 86 571 88208402 E mail changhuahan zju edu cn Septic encephalopathy SE is a critical factor determining sepsis mortality Vascular inflammation is known to be involved in SE but the molecular events that lead to the development of encephalopathy remain unclear Using time lapse in vivo two photon laser scanning microscopy we provide the first direct evidence that cecal ligation and puncture in septic mice induces microglial trafficking to sites adjacent to leukocyte adhesion on inflamed cerebral microvessels Our data further demonstrate that septic injury increased the chemokine CXCL1 level in brain endothelial cells by activating endothelial P2RX7 and eventually enhanced the binding of Mac 1 CD11b CD18 expressing leukocytes to endothelial ICAM 1 In turn leukocyte adhesion upregulated endothelial CX3CL1 thereby triggering microglia trafficking to the injured site The sepsis induced increase in endothelial CX3CL1 was abolished in CD18 hypomorphic mutant mice Inhibition of the P2RX7 pathway not only decreased endothelial ICAM 1 expression

    Original URL path: http://www.cell-research.com/arts.asp?id=2114 (2016-02-14)
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  • Cell Research
    Yankai Wen 1 Xiaoni Kong 1 and Wei Qiang Gao 1 1 State Key Laboratory for Oncogenes and Related Genes Renji Med X Clinical Stem Cell Research Center Ren Ji Hospital School of Biomedical Engineering Shanghai Jiao Tong University Shanghai 200030 China Correspondence Xiaoni Kong Tel 86 21 34206284 E mail xiaonikong sjtu edu cn xiaonikong gmail com Inappropriate inflammation responses contribute to mortality during sepsis Through Toll like receptors TLRs reactive oxygen species ROS produced by NADPH oxidase could modulate the inflammation responses Parkinson disease autosomal recessive early onset 7 Park7 has a cytoprotective role by eliminating ROS However whether Park7 could modulate inflammation responses and mortality in sepsis is unclear Here we show that compared with wild type mice Park7 mice had significantly increased mortality and bacterial burdens in sepsis model along with markedly decreased systemic and local inflammation and drastically impaired macrophage phagocytosis and bacterial killing abilities Surprisingly LPS and phorbol 12 myristate 13 acetate stimulation failed to induce ROS and proinflammatory cytokine production in Park7 macrophages and Park7 deficient RAW264 7 cells Through its C terminus Park7 binds to p47phox a subunit of the NADPH oxidase to promote NADPH oxidase dependent production of ROS Restoration of

    Original URL path: http://www.cell-research.com/arts.asp?id=2115 (2016-02-14)
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  • Cell Research
    Hong 6 Jean M Mulcahy Levy 7 Daniel A Pollyea 8 Craig T Jordan 8 Pearlly Yan 9 David Frankhouser 9 Deedra Nicolet 9 10 Kati Maharry 9 10 Guido Marcucci 9 Kyeong Sook Choi 1 2 Hyeseong Cho 1 2 Andrew Thorburn 3 and You Sun Kim 1 2 1 Department of Biochemistry Ajou University School of Medicine Suwon 443 380 Korea 2 Department of Biomedical Sciences Graduate School Ajou University Suwon 443 380 Korea 3 Department of Pharmacology University of Colorado School of Medicine Aurora CO 80045 USA 4 Department of Pathology Yonsei University College of Medicine Seoul 120 752 Korea 5 Department of Surgery Yonsei University College of Medicine Seoul 120 752 Korea 6 Department of Biomedical Sciences College of Medicine Inha University Incheon 402 751 Korea 7 Department of Pediatrics University of Colorado Denver Aurora 80045 CO 80045 USA 8 Division of Hematology Hematologic Malignancies and Stem Cell Transplantation University of Colorado School of Medicine Aurora CO USA 9 Ohio State University Comprehensive Cancer Center Columbus OH 43210 USA 10 Alliance for Clinical Trials in Oncology Statistics and Data Center Mayo Clinic Rochester MN 55905 USA Correspondence You Sun Kim Tel 82 31 219 4509 E mail yousunkim ajou ac kr Receptor interacting protein kinase 3 RIP3 or RIPK3 is an essential part of the cellular machinery that executes programmed or regulated necrosis Here we show that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy induced cell death However we show that RIP3 expression is often silenced in cancer cells due to genomic methylation near its transcriptional start site thus RIP3 dependent activation of MLKL and downstream programmed necrosis during chemotherapeutic death is largely repressed Nevertheless treatment with hypomethylating agents restores RIP3 expression and thereby promotes sensitivity to chemotherapeutics in

    Original URL path: http://www.cell-research.com/arts.asp?id=2116 (2016-02-14)
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  • Cell Research
    China 2 Center for Structural Biology School of Life Sciences Tsinghua University Beijing 100084 China 3 State Key Laboratory of Protein and Plant Genetic Engineering College of Life Sciences Peking University Beijing 100871 China 4 Key Laboratory of Phycology of CAS Institute of Hydrobiology Chinese Academy of Sciences Wuhan Hubei 430072 China 5 Current address MRC Laboratory of Molecular Biology Cambridge CB2 0QH UK Correspondence Jindong Zhao E mail jzhao pku edu cn Phycobilisomes PBSs are light harvesting antennae that transfer energy to photosynthetic reaction centers in cyanobacteria and red algae PBSs are supermolecular complexes composed of phycobiliproteins PBPs that bear chromophores for energy absorption and linker proteins Although the structures of some individual components have been determined using crystallography the three dimensional structure of an entire PBS complex which is critical for understanding the energy transfer mechanism remains unknown Here we report the structures of an intact PBS and a PBS in complex with photosystem II PSII from Anabaena sp strain PCC 7120 using single particle electron microscopy in combination with biochemical and molecular analyses In the PBS structure all PBP trimers and the conserved linker protein domains were unambiguously located and the global distribution of all chromophores was

    Original URL path: http://www.cell-research.com/arts.asp?id=2117 (2016-02-14)
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  • Cell Research
    Xiaohong Fang 1 Youyi Zhang 2 and Ye Guang Chen 3 1 Beijing National Laboratory for Molecular Sciences Key Laboratory of Molecular Nanostructures and Nanotechnology Institute of Chemistry Chinese Academy of Sciences Beijing 100190 China 2 Institute of Vascular Medicine Peking University Third Hospital and Academy for Advanced Interdisciplinary Studies Peking University Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides Ministry of Health Key Laboratory of Molecular Cardiovascular Sciences Ministry of Education and Beijing Key Laboratory of Cardiovascular Receptors Research Beijing 100191 China 3 State Key Laboratory of Biomembrane and Membrane Biotechnology Tsinghua Peking Center for Life Sciences School of Life Sciences Tsinghua University Beijing 100084 China Correspondence Xiaohong Fang Tel 86 10 6265 3083 E mail xfang iccas ac cn Endocytosis and intracellular sorting of transforming growth factor β TGF β receptors play an important regulatory role in TGF β signaling Two major endocytic pathways clathrin and caveolae mediated endocytosis have been reported to independently mediate the internalization of TGF β receptors In this study we demonstrate that the clathrin and caveolae mediated endocytic pathways can converge during TGF β receptor endocytic trafficking By tracking the intracellular dynamics of fluorescently labeled TGF β type I receptor TβRI we found that after mediating TβRI internalization certain clathrin coated vesicles and caveolar vesicles are fused underneath the plasma membrane forming a novel type of caveolin 1 and clathrin double positive vesicles Under the regulation of Rab5 the fused vesicles are targeted to early endosomes and thus deliver the internalized TβRI to the caveolin 1 and EEA1 double positive early endosomes caveolin 1 positive early endosomes We further showed that the caveolin 1 positive early endosomes are positive for Smad3 SARA Rab11 and Smad7 Smurf2 and may act as a multifunctional device for TGF β signaling and TGF β receptor recycling

    Original URL path: http://www.cell-research.com/arts.asp?id=2118 (2016-02-14)
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  • Cell Research
    Peng 4 Aiping Wu 2 F Xiao Feng Qin 1 Genhong Cheng 1 5 and Taijiao Jiang 1 2 1 Center for Systems Medicine Institute of Basic Medical Sciences Chinese Academy of Medical Sciences Peking Union Medical College Beijing 100005 Suzhou Institute of Systems Medicine Suzhou Jiangsu 215123 China 2 Key Laboratory of Protein and Peptide Pharmaceuticals Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China 3 University of

    Original URL path: http://www.cell-research.com/arts.asp?id=2119 (2016-02-14)
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