Now showing items 1-11 of 11

    • Comprehensive analysis of promoter-proximal RNA polymerase II pausing across mammalian cell types 

      Day, Daniel S.; Zhang, Bing; Stevens, Sean M.; Ferrari, Francesco; Larschan, Erica N.; Park, Peter J.; Pu, William T. (BioMed Central, 2016)
      Background: For many genes, RNA polymerase II stably pauses before transitioning to productive elongation. Although polymerase II pausing has been shown to be a mechanism for regulating transcriptional activation, the ...
    • Congenital Heart Disease–Causing Gata4 Mutation Displays Functional Deficits In Vivo 

      Misra, Chaitali; Sachan, Nita; McNally, Caryn Rothrock; Koenig, Sara N.; Nichols, Haley A.; Guggilam, Anuradha; Lucchesi, Pamela A.; Pu, William T.; Srivastava, Deepak; Garg, Vidu (Public Library of Science, 2012)
      Defects of atrial and ventricular septation are the most frequent form of congenital heart disease, accounting for almost 50% of all cases. We previously reported that a heterozygous G296S missense mutation of GATA4 caused ...
    • Dissecting Spatio-Temporal Protein Networks Driving Human Heart Development and Related Disorders 

      Lage, Kasper; Møllgård, Kjeld; Greenway, Steven; Workman, Christopher T; Bendsen, Eske; Hansen, Niclas T; Rigina, Olga; Roque, Francisco S; Wiese, Cornelia; Christoffels, Vincent M; Tommerup, Niels; Brunak, Søren; Larsen, Lars A; Wakimoto, Hiroko; Gorham, Josh McClean; Roberts, Amy Elizabeth; Smoot, Leslie; Pu, William T.; Donahoe, Patricia; Seidman, Christine Edry; Seidman, Jonathan G. (Nature Publishing Group, 2010)
      Aberrant organ development is associated with a wide spectrum of disorders, from schizophrenia to congenital heart disease, but systems-level insight into the underlying processes is very limited. Using heart morphogenesis ...
    • Modeling the mitochondrial cardiomyopathy of Barth syndrome with iPSC and heart-on-chip technologies 

      Wang, Gang; McCain, Megan L.; Yang, Luhan; He, Aibin; Pasqualini, Francesco Silvio; Agarwal, Ashutosh; Yuan, Hongyan; Jiang, Dawei; Zhang, Donghui; Zangi, Lior; Geva, Judith; Roberts, Amy E.; Ma, Qing; Ding, Jian; Chen, Jinghai; Wang, Da-zhi; Li, Kai; Wang, Jiwu; Wanders, Ronald J. A.; Kulik, Wim; Vaz, Frédéric M.; Laflamme, Michael A.; Murry, Charles E.; Chien, Kenneth R.; Kelley, Richard I.; Church, George M.; Parker, Kevin Kit; Pu, William T. (2014)
      Studying monogenic mitochondrial cardiomyopathies may yield insights into mitochondrial roles in cardiac development and disease. Here, we combine patient-derived and genetically engineered iPSCs with tissue engineering ...
    • Modified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarction 

      Zangi, Lior; Lui, Kathy O; von Gise, Alexander; Ma, Qing; Ebina, Wataru; Ptaszek, Leon M.; Später, Daniela; Xu, Huansheng; Tabebordbar, Mohammadsharif; Gorbatov, Rostic; Sena, Brena; Nahrendorf, Matthias; Briscoe, David Michael; Li, Ronald A; Wagers, Amy Jo; Rossi, Derrick J; Pu, William T.; Chien, Kenneth R (Nature Publishing Group, 2013)
      In a cell-free approach to regenerative therapeutics, transient application of paracrine factors in vivo could be used to alter the behavior and fate of progenitor cells to achieve sustained clinical benefits. Here we show ...
    • Optimization of Genome Engineering Approaches with the CRISPR/Cas9 System 

      Li, Kai; Wang, Gang; Andersen, Troels; Zhou, Pingzhu; Pu, William T. (Public Library of Science, 2014)
      Designer nucleases such as TALENS and Cas9 have opened new opportunities to scarlessly edit the mammalian genome. Here we explored several parameters that influence Cas9-mediated scarless genome editing efficiency in murine ...
    • Regional differences in WT-1 and Tcf21 expression during ventricular development: implications for myocardial compaction 

      Vicente-Steijn, Rebecca; Scherptong, Roderick W. C.; Kruithof, Boudewijn P. T.; Duim, Sjoerd N.; Goumans, Marie Jose T. H.; Wisse, Lambertus J.; Zhou, Bin; Pu, William T.; Poelmann, Robert E.; Schalij, Martin J.; Tallquist, Michelle D.; Gittenberger-de Groot, Adriana C.; Jongbloed, Monique RM (Public Library of Science, 2015)
      Background: Morphological and functional differences of the right and left ventricle are apparent in the adult human heart. A differential contribution of cardiac fibroblasts and smooth muscle cells (populations of ...
    • A simple method for deriving functional MSCs and applied for osteogenesis in 3D scaffolds 

      Zou, Lijin; Luo, Yonglun; Chen, Muwan; Wang, Gang; Ding, Ming; Petersen, Charlotte Christie; Kang, Ran; Dagnaes-Hansen, Frederik; Zeng, Yuanlin; Lv, Nonghua; Ma, Qing; Le, Dang Q. S.; Besenbacher, Flemming; Bolund, Lars; Jensen, Thomas G.; Kjems, Jørgen; Pu, William T.; Bünger, Cody (Nature Publishing Group, 2013)
      We describe a simple method for bone engineering using biodegradable scaffolds with mesenchymal stem cells derived from human induced-pluripotent stem cells (hiPS-MSCs). The hiPS-MSCs expressed mesenchymal markers (CD90, ...
    • SOCS3 in retinal neurons and glial cells suppresses VEGF signaling to prevent pathological neovascular growth 

      Sun, Ye; Ju, Meihua; Lin, Zhiqiang; Fredrick, T. W.; Evans, L. P.; Tian, Katherine; Saba, N. J.; Morss, P. C.; Pu, William T.; Chen, Jing; Stahl, A.; Joyal, Jean; Smith, Lois Elaine Hodgson (American Association for the Advancement of Science (AAAS), 2015)
      Accumulating evidence indicates that retinal neuroglia and neural cells contribute to neovascularization in proliferative retinopathy, but the controlling molecular interactions are not well known. We identified a mechanism ...
    • Trbp regulates heart function through miRNA-mediated Sox6 repression 

      Ding, Jian; Chen, Jinghai; Wang, Yanqun; Kataoka, Masaharu; Ma, Lixin; Zhou, Pingzhu; Hu, Xiaoyun; Lin, Zhiqiang; Nie, Mao; Deng, Zhong-Liang; Pu, William T; Wang, Da-Zhi (2015)
      Cardiomyopathy is associated with altered expression of genes encoding contractile proteins. Here we show that Trbp (Tarbp2), an RNA binding protein, is required for normal heart function. Cardiac-specific inactivation of ...