Induction of functional hepatocyte-like cells from mouse fibroblasts by defined factors

[1]  L. Hui,et al.  Hepatoblast-like progenitor cells derived from embryonic stem cells can repopulate livers of mice. , 2010, Gastroenterology.

[2]  A. Schnerch,et al.  Direct conversion of human fibroblasts to multilineage blood progenitors , 2010, Nature.

[3]  V. Vedantham,et al.  Direct Reprogramming of Fibroblasts into Functional Cardiomyocytes by Defined Factors , 2010, Cell.

[4]  Thomas Vierbuchen,et al.  Direct conversion of fibroblasts to functional neurons by defined factors , 2010, Nature.

[5]  Stephen Dalton,et al.  Highly efficient generation of human hepatocyte–like cells from induced pluripotent stem cells , 2010, Hepatology.

[6]  Jehyuk Lee,et al.  Generation of functional human hepatic endoderm from human induced pluripotent stem cells , 2009, Hepatology.

[7]  M. Blasco,et al.  The Ink4/Arf locus is a barrier for iPS cell reprogramming , 2009, Nature.

[8]  M. Zern Cell transplantation to replace whole liver transplantation. , 2009, Gastroenterology.

[9]  Alejandro Soto-Gutiérrez,et al.  Differentiation and transplantation of human embryonic stem cell-derived hepatocytes. , 2009, Gastroenterology.

[10]  Douglas A. Melton,et al.  In vivo reprogramming of adult pancreatic exocrine cells to β-cells , 2008, Nature.

[11]  K. Zaret Genetic programming of liver and pancreas progenitors: lessons for stem-cell differentiation , 2008, Nature Reviews Genetics.

[12]  T. Graf,et al.  PU.1 and C/EBPα/β convert fibroblasts into macrophage-like cells , 2008, Proceedings of the National Academy of Sciences.

[13]  Ying Meng,et al.  Differentiation and Enrichment of Hepatocyte‐Like Cells from Human Embryonic Stem Cells In Vitro and In Vivo , 2007, Stem cells.

[14]  Christian Haslinger,et al.  p38α suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathway , 2007, Nature Genetics.

[15]  Gordon Keller,et al.  BMP-4 is required for hepatic specification of mouse embryonic stem cell–derived definitive endoderm , 2006, Nature Biotechnology.

[16]  N. Kobayashi,et al.  Reversal of mouse hepatic failure using an implanted liver-assist device containing ES cell–derived hepatocytes , 2006, Nature Biotechnology.

[17]  F. Tronche,et al.  Plasticity and expanding complexity of the hepatic transcription factor network during liver development. , 2006, Genes & development.

[18]  H. Schrem,et al.  Liver-Enriched Transcription Factors in Liver Function and Development. Part II: the C/EBPs and D Site-Binding Protein in Cell Cycle Control, Carcinogenesis, Circadian Gene Regulation, Liver Regeneration, Apoptosis, and Liver-Specific Gene Regulation , 2004, Pharmacological Reviews.

[19]  T. Graf,et al.  Stepwise Reprogramming of B Cells into Macrophages , 2004, Cell.

[20]  R. Schulte‐Hermann,et al.  Immortalized p19ARF null hepatocytes restore liver injury and generate hepatic progenitors after transplantation , 2004, Hepatology.

[21]  Nicola J. Rinaldi,et al.  Control of Pancreas and Liver Gene Expression by HNF Transcription Factors , 2004, Science.

[22]  Xin Wang,et al.  The origin and liver repopulating capacity of murine oval cells , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[23]  H. Schrem,et al.  Liver-Enriched Transcription Factors in Liver Function and Development. Part I: The Hepatocyte Nuclear Factor Network and Liver-Specific Gene Expression , 2002, Pharmacological Reviews.

[24]  Frank R. Lin,et al.  Opening of compacted chromatin by early developmental transcription factors HNF3 (FoxA) and GATA-4. , 2002, Molecular cell.

[25]  David Tosh,et al.  Molecular basis of transdifferentiation of pancreas to liver , 2000, Nature Cell Biology.

[26]  M. Grompe,et al.  Hepatocytes corrected by gene therapy are selected in vivo in a murine model of hereditary tyrosinaemia type I , 1996, Nature Genetics.

[27]  S. Lindstedt,et al.  Pharmacological correction of neonatal lethal hepatic dysfunction in a murine model of hereditary tyrosinaemia type I , 1995, Nature Genetics.

[28]  Philippe Soriano,et al.  Loss of fumarylacetoacetate hydrolase is responsible for the neonatal hepatic dysfunction phenotype of lethal albino mice. , 1993, Genes & development.

[29]  Jian Xu,et al.  Pioneer factors, genetic competence, and inductive signaling: programming liver and pancreas progenitors from the endoderm. , 2008, Cold Spring Harbor symposia on quantitative biology.