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  • Cell Research
    Sciences Texas A M Health Science Center Baylor College of Dentistry Dallas TX 75246 USA Correspondence Jianming Xu E mail jxu bcm edu This article reviews the molecular structure expression pattern physiological function pathological roles and molecular mechanisms of Twist1 in development genetic disease and cancer Twist1 is a basic helix loop helix domain containing transcription factor It forms homo or hetero dimers in order to bind the Nde1 E box element and activate or repress its target genes During development Twist1 is essential for mesoderm specification and differentiation Heterozygous loss of function mutations of the human Twist1 gene cause several diseases including the Saethre Chotzen syndrome The Twist1 null mouse embryos die with unclosed cranial neural tubes and defective head mesenchyme somites and limb buds Twist1 is expressed in breast liver prostate gastric and other types of cancers and its expression is usually associated with invasive and metastatic cancer phenotypes In cancer cells Twist1 is upregulated by multiple factors including SRC 1 STAT3 MSX2 HIF 1 α integrin linked kinase and NF κB Twist1 significantly enhances epithelial mesenchymal transition EMT and cancer cell migration and invasion hence promoting cancer metastasis Twist1 promotes EMT in part by directly repressing E

    Original URL path: http://www.cell-research.com/arts.asp?id=235 (2016-02-14)
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  • Cell Research
    by microRNA Lin Zhang 1 Dongxia Hou 1 Xi Chen 1 Donghai Li 1 Lingyun Zhu 1 2 Yujing Zhang 1 Jing Li 1 Zhen Bian 1 Xiangying Liang 1 Xing Cai 1 Y 1 Jiangsu Engineering Research Center for microRNA Biology and Biotechnology State Key Laboratory of Pharmaceutical Biotechnology School of Life Sciences Nanjing University 22 Hankou Road Nanjing 210093 China 2 Department of Chemistry and Biology School of

    Original URL path: http://www.cell-research.com/arts.asp?id=236 (2016-02-14)
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  • Cell Research
    of Apoptosis and Cancer Biology The National Key Laboratory of Biomembrane and Membrane Biotechnology Chinese Academy of Sciences Beijing 100101 China 2 College of Life Sciences Nankai University Tianjin 300071 China 3 Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China Correspondence Quan Chen Jianxin Xu Tel 86 22 2350 2962 86 10 6487 1293 E mail chenquan nankai edu cn xujx sun5 ibp ac cn Mitochondrial catastrophe can be the cause or consequence of apoptosis and is associated with a number of pathophysiological conditions The exact relationship between mitochondrial catastrophe and caspase activation is not completely understood Here we addressed the underlying mechanism explaining how activated caspase could feedback to attack mitochondria to amplify further cytochrome c cyto c release We discovered that cytochrome c1 cyto c1 in the bc1 complex of the mitochondrial respiration chain was a novel substrate of caspase 3 casp 3 We found that cyto c1 was cleaved at the site of D106 which is critical for binding with cyto c following apoptotic stresses or targeted expression of casp 3 into the mitochondrial intermembrane space We demonstrated that this cleavage was closely linked with further cyto c release and mitochondrial catastrophe These mitochondrial events

    Original URL path: http://www.cell-research.com/arts.asp?id=238 (2016-02-14)
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  • Cell Research
    Alyssa K Riley 1 Cardiovascular Research Center Massachusetts General Hospital Charles River Plaza CPZN 3208 185 Cambridge Street Boston MA 02114 USA 2 Harvard Stem Cell Institute 3 Department of Stem Cell and Regenerative Biology Harvard University 7 Divinity Avenue Cambridge MA 02138 USA 4 Broad Institute Cambridge MA 02142 USA 5 Cardiac Biology HF Discovery Performance Unit Metabolic and Cardiovascular Therapeutic Area Unit GlaxoSmithKline Pharmaceuticals 709 Swedeland Road King of Prussia PA 19406 USA Correspondence Kenneth R Chien E mail krchien partners org Cardiomyocytes derived from pluripotent stem cells can be applied in drug testing disease modeling and cell based therapy However without procardiogenic growth factors the efficiency of cardiomyogenesis from pluripotent stem cells is usually low and the resulting cardiomyocyte population is heterogeneous Here we demonstrate that induced pluripotent stem cells iPSCs can be derived from murine ventricular myocytes VMs and consistent with other reports of iPSCs derived from various somatic cell types VM derived iPSCs ViPSCs exhibit a markedly higher propensity to spontaneously differentiate into beating cardiomyocytes as compared to genetically matched embryonic stem cells ESCs or iPSCs derived from tail tip fibroblasts Strikingly the majority of ViPSC derived cardiomyocytes display a ventricular phenotype The enhanced ventricular

    Original URL path: http://www.cell-research.com/arts.asp?id=239 (2016-02-14)
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  • Cell Research
    to the pluripotency network Junjun Ding 1 Huilei Xu 2 Francesco Faiola 1 Avi Ma ayan 2 and Jianlong Wang 1 1 Department of Developmental and Regenerative Biology Black Family Stem Cell Institute Mount Sinai School of Medicine New York NY 10029 USA 2 Department of Pharmacology and Systems Therapeutics Mount Sinai School of Medicine New York NY 10029 USA Correspondence Jianlong Wang Tel 1 212 241 7425 E mail jianlong wang mssm edu Oct4 is a well known transcription factor that plays fundamental roles in stem cell self renewal pluripotency and somatic cell reprogramming However limited information is available on Oct4 associated protein complexes and their intrinsic protein protein interactions that dictate Oct4 s critical regulatory activities Here we employed an improved affinity purification approach combined with mass spectrometry to purify Oct4 protein complexes in mouse embryonic stem cells mESCs and discovered many novel Oct4 partners important for self renewal and pluripotency of mESCs Notably we found that Oct4 is associated with multiple chromatin modifying complexes with documented as well as newly proved functional significance in stem cell maintenance and somatic cell reprogramming Our study establishes a solid biochemical basis for genetic and epigenetic regulation of stem cell pluripotency

    Original URL path: http://www.cell-research.com/arts.asp?id=240 (2016-02-14)
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  • Cell Research
    M Batchelder 1 Nongluk Plon 1 Gene Expression Laboratory The Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA 2 Departments of Chemistry and Molecular Biology and Scripps Center for Metabolomics and Mass Spectrometry The Scripps Research Institute La Jolla CA 92037 USA 3 Metabolomics Platform of the Spanish Biomedical Research Center in Diabetes and Associated Metabolic Disorders CIBERDEM University Rovira i Virgili 43007 Tarragona Spain 4 Bioinformatics and Systems Biology Graduate Program University of California at San Diego La Jolla CA 92093 USA 5 Center of Regenerative Medicine in Barcelona Dr Aiguader 88 08003 Barcelona Spain 6 Department of Bioengineering Institute for Genomic Medicine and Institute of Engineering in Medicine University of California at San Diego La Jolla CA 92093 USA 7 Stem Cell Core The Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA 8 Howard Hughes Medical Institute The Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA Correspondence Gary Siuzdak Juan Carlos Izpisua Belmonte E mail siuzdak scripps edu belmonte salk edu izpisua cmrb eu Metabolism is vital to every aspect of cell function yet the metabolome of induced pluripotent stem cells iPSCs remains largely unexplored Here we report using an untargeted metabolomics approach that human iPSCs share a pluripotent metabolomic signature with embryonic stem cells ESCs that is distinct from their parental cells and that is characterized by changes in metabolites involved in cellular respiration Examination of cellular bioenergetics corroborated with our metabolomic analysis and demonstrated that somatic cells convert from an oxidative state to a glycolytic state in pluripotency Interestingly the bioenergetics of various somatic cells correlated with their reprogramming efficiencies We further identified metabolites that differ between iPSCs and ESCs which revealed novel metabolic pathways

    Original URL path: http://www.cell-research.com/arts.asp?id=241 (2016-02-14)
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  • Cell Research
    Cancer Center University of California Los Angeles Los Angeles CA 90095 USA 3 Eli and Edythe Broad Center for Stem Cell Research University of California Los Angeles Los Angeles CA 90095 USA 4 Molecular Biology Institute University of California Los Angeles Los Angeles CA 90095 USA Correspondence William E Lowry Tel 1 310 794 5175 E mail blowry ucla edu While it is clear that human pluripotent stem cells hPSCs can differentiate to generate a panoply of various cell types it is unknown how closely in vitro development mirrors that which occurs in vivo To determine whether human embryonic stem cells hESCs and human induced pluripotent stem cells hiPSCs make equivalent progeny and whether either makes cells that are analogous to tissue derived cells we performed comprehensive transcriptome profiling of purified PSC derivatives and their tissue derived counterparts Expression profiling demonstrated that hESCs and hiPSCs make nearly identical progeny for the neural hepatic and mesenchymal lineages and an absence of re expression from exogenous reprogramming factors in hiPSC progeny However when compared to a tissue derived counterpart the progeny of both hESCs and hiPSCs maintained expression of a subset of genes normally associated with early mammalian development regardless of the

    Original URL path: http://www.cell-research.com/arts.asp?id=242 (2016-02-14)
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  • Cell Research
    Zhenchuan Miao 1 Yaxin Lv 1 Yanlei Yang 1 Huidan Zhang 1 Pengbo Zhang 1 Yang Liu 1 2 Liying Du 1 Department of Cell Biology The MOE Key Laboratory of Cell Proliferation and Differentiation College of Life Sciences Peking University Beijing 100871 China 2 Laboratory of Chemical Genomics Shenzhen Graduate School of Peking University The University Town Shenzhen 518055 China Correspondence Hongkui Deng Tel 86 10 6275 6954 E mail hongkui deng pku edu cn Embryonic hematopoiesis is a complex process Elucidating the mechanism regulating hematopoietic differentiation from pluripotent stem cells would allow us to establish a strategy to efficiently generate hematopoietic cells However the mechanism governing the generation of hematopoietic progenitors from human embryonic stem cells hESCs remains unknown Here on the basis of the emergence of CD43 hematopoietic cells from hemogenic endothelial HE cells we demonstrated that VEGF was essential and sufficient and that bFGF was synergistic with VEGF to specify the HE cells and the subsequent transition into CD43 hematopoietic cells Significantly we identified TGFβ as a novel signal to regulate hematopoietic development as the TGFβ inhibitor SB 431542 significantly promoted the transition from HE cells into CD43 hematopoietic progenitor cells HPCs during hESC differentiation By

    Original URL path: http://www.cell-research.com/arts.asp?id=243 (2016-02-14)
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