Cell, ISSN 0092-8674, 03/2018, Volume 173, Issue 1, pp. 104 - 116.e12
Human diseases are often caused by loss of somatic cells that are incapable of re-entering the cell cycle for regenerative repair. Here, we report a...
heart failure | cyclin | proliferation | cell cycle | regeneration | cytokinesis | cardiomyocyte | cell division | CDK | heart | HYPERTROPHY | INFARCTION | EXPRESSION ANALYSIS | AMPLIFICATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICE | ZEBRAFISH HEART REGENERATION | FAILURE | CANCER | FIBROBLASTS | PROGRAM | CELL BIOLOGY | Cyclin D1 - metabolism | Cell Proliferation | Protein-Tyrosine Kinases - metabolism | Cyclin-Dependent Kinase 4 - genetics | Heart - physiology | Humans | Myosin Heavy Chains - genetics | Cyclin B1 - metabolism | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Myocardial Infarction - pathology | Transforming Growth Factor beta - antagonists & inhibitors | Myocardial Infarction - veterinary | Induced Pluripotent Stem Cells - cytology | Induced Pluripotent Stem Cells - metabolism | CDC2 Protein Kinase - genetics | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cyclin B1 - genetics | Rats | Mice, Transgenic | Nuclear Proteins - metabolism | Myocardial Infarction - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Cytokinesis | Regeneration | Animals | Cyclin D1 - genetics | Nuclear Proteins - antagonists & inhibitors | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Heart | Bone morphogenetic proteins | Transforming growth factors | Cell cycle | Stem cells | Cell Cycle | Cardiomyocyte | Cell Division | Cyclin
heart failure | cyclin | proliferation | cell cycle | regeneration | cytokinesis | cardiomyocyte | cell division | CDK | heart | HYPERTROPHY | INFARCTION | EXPRESSION ANALYSIS | AMPLIFICATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICE | ZEBRAFISH HEART REGENERATION | FAILURE | CANCER | FIBROBLASTS | PROGRAM | CELL BIOLOGY | Cyclin D1 - metabolism | Cell Proliferation | Protein-Tyrosine Kinases - metabolism | Cyclin-Dependent Kinase 4 - genetics | Heart - physiology | Humans | Myosin Heavy Chains - genetics | Cyclin B1 - metabolism | CDC2 Protein Kinase - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Myocardial Infarction - pathology | Transforming Growth Factor beta - antagonists & inhibitors | Myocardial Infarction - veterinary | Induced Pluripotent Stem Cells - cytology | Induced Pluripotent Stem Cells - metabolism | CDC2 Protein Kinase - genetics | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Cyclin B1 - genetics | Rats | Mice, Transgenic | Nuclear Proteins - metabolism | Myocardial Infarction - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Cytokinesis | Regeneration | Animals | Cyclin D1 - genetics | Nuclear Proteins - antagonists & inhibitors | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Heart | Bone morphogenetic proteins | Transforming growth factors | Cell cycle | Stem cells | Cell Cycle | Cardiomyocyte | Cell Division | Cyclin
Journal Article
Cell, ISSN 0092-8674, 2006, Volume 126, Issue 6, pp. 1203 - 1217
We present , a method for identifying microRNA binding sites and their corresponding heteroduplexes. does not rely upon cross-species conservation, is...
RNA INTERFERENCE | CAENORHABDITIS-ELEGANS | FAMILIES | BIOCHEMISTRY & MOLECULAR BIOLOGY | INSULIN-SECRETION | GENES | NETWORKS | DISCOVERY | TARGET PREDICTIONS | CELL BIOLOGY | Cell Line | Computational Biology - methods | Nucleic Acid Heteroduplexes - genetics | Humans | RNA, Messenger - genetics | Genome - genetics | MicroRNAs - metabolism | Binding Sites - genetics | Open Reading Frames - genetics | RNA, Messenger - metabolism | Molecular Biology - methods | Nucleic Acid Heteroduplexes - metabolism | Heteroduplex Analysis - methods | Algorithms | Animals | Caenorhabditis - genetics | Mice | MicroRNAs - genetics | Protein Biosynthesis - genetics | Software Design | Untranslated Regions - genetics | Drosophila - genetics | Amino acids | Research | RNA | Protein binding | Animal genetics | Stem cell research | Developmental biology | Analysis | Stem cells | Chemical properties | Methods
RNA INTERFERENCE | CAENORHABDITIS-ELEGANS | FAMILIES | BIOCHEMISTRY & MOLECULAR BIOLOGY | INSULIN-SECRETION | GENES | NETWORKS | DISCOVERY | TARGET PREDICTIONS | CELL BIOLOGY | Cell Line | Computational Biology - methods | Nucleic Acid Heteroduplexes - genetics | Humans | RNA, Messenger - genetics | Genome - genetics | MicroRNAs - metabolism | Binding Sites - genetics | Open Reading Frames - genetics | RNA, Messenger - metabolism | Molecular Biology - methods | Nucleic Acid Heteroduplexes - metabolism | Heteroduplex Analysis - methods | Algorithms | Animals | Caenorhabditis - genetics | Mice | MicroRNAs - genetics | Protein Biosynthesis - genetics | Software Design | Untranslated Regions - genetics | Drosophila - genetics | Amino acids | Research | RNA | Protein binding | Animal genetics | Stem cell research | Developmental biology | Analysis | Stem cells | Chemical properties | Methods
Journal Article
Cell, ISSN 0092-8674, 2011, Volume 145, Issue 2, pp. 183 - 197
The embryonic stem (ES) cell transcriptional and chromatin-modifying networks are critical for self-renewal maintenance. However, it remains unclear whether...
METHYLATION | DEVELOPMENTAL REGULATORS | CHROMATIN-STRUCTURE | RECOGNITION | HISTONE H3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENES | POLYCOMB | BINDING | GENOME | PLURIPOTENT | CELL BIOLOGY | Embryonic Stem Cells - metabolism | Myeloid-Lymphoid Leukemia Protein - metabolism | Embryonic Stem Cells - cytology | Histone-Lysine N-Methyltransferase | Transcriptional Activation | Gene Regulatory Networks | Sequence Analysis, DNA | Animals | Proteins - metabolism | Chromatin Immunoprecipitation | Octamer Transcription Factor-3 - metabolism | Mice | Histones - metabolism | Methylation | Medical colleges | Genetic aspects | Embryonic stem cells | Genomics | Analysis | reprogramming | embryonic stem | histone methylation | Oct4 | wdr5 | transcriptional network | induced pluripotent stem | chromatin | trithorax
METHYLATION | DEVELOPMENTAL REGULATORS | CHROMATIN-STRUCTURE | RECOGNITION | HISTONE H3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENES | POLYCOMB | BINDING | GENOME | PLURIPOTENT | CELL BIOLOGY | Embryonic Stem Cells - metabolism | Myeloid-Lymphoid Leukemia Protein - metabolism | Embryonic Stem Cells - cytology | Histone-Lysine N-Methyltransferase | Transcriptional Activation | Gene Regulatory Networks | Sequence Analysis, DNA | Animals | Proteins - metabolism | Chromatin Immunoprecipitation | Octamer Transcription Factor-3 - metabolism | Mice | Histones - metabolism | Methylation | Medical colleges | Genetic aspects | Embryonic stem cells | Genomics | Analysis | reprogramming | embryonic stem | histone methylation | Oct4 | wdr5 | transcriptional network | induced pluripotent stem | chromatin | trithorax
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2015, Volume 112, Issue 41, pp. 12705 - 12710
Single cardiomyocytes contain myofibrils that harbor the sarcomerebased contractile machinery of the myocardium. Cardiomyocytes differentiated from human...
Single cell | Cardiomyocyte | Stem cell | Sarcomeres | Contractility | MATRIX | ISOFORMS | MYOSIN | contractility | MULTIDISCIPLINARY SCIENCES | TENSION | MYOCYTE SHAPE | sarcomeres | CULTURE | ADULT CARDIOMYOCYTES | STRESS FIBERS | single cell | stem cell | CARDIAC TROPONIN-T | cardiomyocyte | CALCIUM | Myocardial Contraction | Pluripotent Stem Cells - metabolism | Pluripotent Stem Cells - cytology | Myocytes, Cardiac - cytology | Models, Biological | Cell Shape | Humans | Cells, Cultured | Mitochondria, Heart | Myocytes, Cardiac - metabolism | Cell Differentiation | Calcium Signaling | Genotype | Genetic aspects | Muscle contraction | Identification and classification | Heart cells | Biological Sciences
Single cell | Cardiomyocyte | Stem cell | Sarcomeres | Contractility | MATRIX | ISOFORMS | MYOSIN | contractility | MULTIDISCIPLINARY SCIENCES | TENSION | MYOCYTE SHAPE | sarcomeres | CULTURE | ADULT CARDIOMYOCYTES | STRESS FIBERS | single cell | stem cell | CARDIAC TROPONIN-T | cardiomyocyte | CALCIUM | Myocardial Contraction | Pluripotent Stem Cells - metabolism | Pluripotent Stem Cells - cytology | Myocytes, Cardiac - cytology | Models, Biological | Cell Shape | Humans | Cells, Cultured | Mitochondria, Heart | Myocytes, Cardiac - metabolism | Cell Differentiation | Calcium Signaling | Genotype | Genetic aspects | Muscle contraction | Identification and classification | Heart cells | Biological Sciences
Journal Article
Circulation, ISSN 0009-7322, 03/2017, Volume 135, Issue 10, pp. 978 - 995
BACKGROUND:Reprogramming of cardiac fibroblasts into induced cardiomyocyte-like cells in situ represents a promising strategy for cardiac regeneration. A...
Heart | Regeneration | Transcription factors | Cell differentiation | MOUSE FIBROBLASTS | cell differentiation | DEXAMETHASONE | CARDIAC & CARDIOVASCULAR SYSTEMS | EXPRESSION ANALYSIS | regeneration | transcription factors | HEART-FAILURE | CATENIN | heart | PLURIPOTENT STEM-CELLS | GROWTH-FACTOR-BETA | INHIBITION | AMPLIFICATION | FUNCTIONAL CARDIOMYOCYTES | PERIPHERAL VASCULAR DISEASE | Dioxoles - therapeutic use | MEF2 Transcription Factors - genetics | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Wnt Proteins - metabolism | Benzamides - therapeutic use | Dioxoles - pharmacology | Transforming Growth Factor beta - antagonists & inhibitors | Benzamides - pharmacology | Fibroblasts - metabolism | GATA4 Transcription Factor - metabolism | Myocytes, Cardiac - cytology | Cells, Cultured | GATA4 Transcription Factor - genetics | Myocardium - pathology | Transcription Factors - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Heart - diagnostic imaging | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Magnetic Resonance Imaging | Animals | Myocardial Infarction - drug therapy | Fibroblasts - drug effects | Heterocyclic Compounds, 3-Ring - therapeutic use | MEF2 Transcription Factors - metabolism | Myocytes, Cardiac - metabolism | Fibroblasts - cytology | Mice | Wnt Proteins - antagonists & inhibitors | Transforming Growth Factor beta - metabolism | Care and treatment | Heart cells | Dosage and administration | Research | Transforming growth factors | Heart diseases | reprogramming | cardiac differentiation | calcium | heart regeneration
Heart | Regeneration | Transcription factors | Cell differentiation | MOUSE FIBROBLASTS | cell differentiation | DEXAMETHASONE | CARDIAC & CARDIOVASCULAR SYSTEMS | EXPRESSION ANALYSIS | regeneration | transcription factors | HEART-FAILURE | CATENIN | heart | PLURIPOTENT STEM-CELLS | GROWTH-FACTOR-BETA | INHIBITION | AMPLIFICATION | FUNCTIONAL CARDIOMYOCYTES | PERIPHERAL VASCULAR DISEASE | Dioxoles - therapeutic use | MEF2 Transcription Factors - genetics | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Wnt Proteins - metabolism | Benzamides - therapeutic use | Dioxoles - pharmacology | Transforming Growth Factor beta - antagonists & inhibitors | Benzamides - pharmacology | Fibroblasts - metabolism | GATA4 Transcription Factor - metabolism | Myocytes, Cardiac - cytology | Cells, Cultured | GATA4 Transcription Factor - genetics | Myocardium - pathology | Transcription Factors - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Heart - diagnostic imaging | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Magnetic Resonance Imaging | Animals | Myocardial Infarction - drug therapy | Fibroblasts - drug effects | Heterocyclic Compounds, 3-Ring - therapeutic use | MEF2 Transcription Factors - metabolism | Myocytes, Cardiac - metabolism | Fibroblasts - cytology | Mice | Wnt Proteins - antagonists & inhibitors | Transforming Growth Factor beta - metabolism | Care and treatment | Heart cells | Dosage and administration | Research | Transforming growth factors | Heart diseases | reprogramming | cardiac differentiation | calcium | heart regeneration
Journal Article
Nature, ISSN 0028-0836, 06/2010, Volume 465, Issue 7299, pp. 808 - 812
The generation of reprogrammed induced pluripotent stem cells (iPSCs) from patients with defined genetic disorders holds the promise of increased understanding...
SOMATIC PTPN11 MUTATIONS | SHP2 MUTATIONS | HUMAN ES | HEMATOPOIESIS | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | DISEASE | LEUKEMOGENESIS | DIFFERENTIATION | LEUKEMIA | FIBROBLASTS | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Embryonic Stem Cells - metabolism | Humans | Male | Gene Expression Profiling | LEOPARD Syndrome - drug therapy | Octamer Transcription Factor-3 - genetics | Phosphoproteins - analysis | SOXB1 Transcription Factors - genetics | Polymerase Chain Reaction | Adult | Female | Cell Differentiation | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Precision Medicine | Induced Pluripotent Stem Cells - pathology | Cell Line | Induced Pluripotent Stem Cells - enzymology | Nanog Homeobox Protein | LEOPARD Syndrome - metabolism | NFATC Transcription Factors - metabolism | Cells, Cultured | Fibroblasts - pathology | Homeodomain Proteins - genetics | Cell Lineage | Myocytes, Cardiac - pathology | Models, Biological | LEOPARD Syndrome - pathology | Myocytes, Cardiac - metabolism | Enzyme Activation | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Mitogen-Activated Protein Kinases - metabolism | NFATC Transcription Factors - genetics | Proteins | Signal transduction | Insects | Genes | Cardiomyocytes | Mutation | Kinases
SOMATIC PTPN11 MUTATIONS | SHP2 MUTATIONS | HUMAN ES | HEMATOPOIESIS | MULTIDISCIPLINARY SCIENCES | CARDIAC-HYPERTROPHY | DISEASE | LEUKEMOGENESIS | DIFFERENTIATION | LEUKEMIA | FIBROBLASTS | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Embryonic Stem Cells - metabolism | Humans | Male | Gene Expression Profiling | LEOPARD Syndrome - drug therapy | Octamer Transcription Factor-3 - genetics | Phosphoproteins - analysis | SOXB1 Transcription Factors - genetics | Polymerase Chain Reaction | Adult | Female | Cell Differentiation | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Precision Medicine | Induced Pluripotent Stem Cells - pathology | Cell Line | Induced Pluripotent Stem Cells - enzymology | Nanog Homeobox Protein | LEOPARD Syndrome - metabolism | NFATC Transcription Factors - metabolism | Cells, Cultured | Fibroblasts - pathology | Homeodomain Proteins - genetics | Cell Lineage | Myocytes, Cardiac - pathology | Models, Biological | LEOPARD Syndrome - pathology | Myocytes, Cardiac - metabolism | Enzyme Activation | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Mitogen-Activated Protein Kinases - metabolism | NFATC Transcription Factors - genetics | Proteins | Signal transduction | Insects | Genes | Cardiomyocytes | Mutation | Kinases
Journal Article
Nature Medicine, ISSN 1078-8956, 10/2016, Volume 22, Issue 10, pp. 1131 - 1139
Epigenetic reprogramming is a critical process of pathological gene induction during cardiac hypertrophy and remodeling, but the underlying regulatory...
MEDICINE, RESEARCH & EXPERIMENTAL | CARDIOMYOCYTE HYPERTROPHY | PRESSURE-OVERLOAD | PATHOLOGICAL HYPERTROPHY | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | HISTONE METHYLATION | MTOR | CELL BIOLOGY | RAPTOR | GENE-EXPRESSION | BINDING | EZH2 | TOR Serine-Threonine Kinases - metabolism | Humans | Immunoblotting | Gene Expression Profiling | Gene Knockdown Techniques | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - metabolism | Chromatin Immunoprecipitation | Computer Simulation | Myocardium - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Rats | In Situ Hybridization, Fluorescence | RNA, Long Noncoding - genetics | Reverse Transcriptase Polymerase Chain Reaction | Heart - diagnostic imaging | Mice, Knockout | Blotting, Northern | Animals | Epigenesis, Genetic - genetics | Myocytes, Cardiac - metabolism | Mice | Cardiomegaly - genetics | In Vitro Techniques | Methylation | Polycomb Repressive Complex 2 - metabolism | Induced Pluripotent Stem Cells | Histone Code - genetics | Cardiomegaly - metabolism | Genetic aspects | Research | RNA | Heart enlargement | Heart | Epigenetic inheritance | Antisense RNA | Genes | TOR protein | Chromatin | Rapamycin | Gene expression | Ribonucleic acid--RNA | Polycomb group proteins | Lysine | Regulatory mechanisms (biology) | DNA methylation | Epigenetics | Catalysis | Inhibition | Histone H3 | Hypertrophy
MEDICINE, RESEARCH & EXPERIMENTAL | CARDIOMYOCYTE HYPERTROPHY | PRESSURE-OVERLOAD | PATHOLOGICAL HYPERTROPHY | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | HISTONE METHYLATION | MTOR | CELL BIOLOGY | RAPTOR | GENE-EXPRESSION | BINDING | EZH2 | TOR Serine-Threonine Kinases - metabolism | Humans | Immunoblotting | Gene Expression Profiling | Gene Knockdown Techniques | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - metabolism | Chromatin Immunoprecipitation | Computer Simulation | Myocardium - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Rats | In Situ Hybridization, Fluorescence | RNA, Long Noncoding - genetics | Reverse Transcriptase Polymerase Chain Reaction | Heart - diagnostic imaging | Mice, Knockout | Blotting, Northern | Animals | Epigenesis, Genetic - genetics | Myocytes, Cardiac - metabolism | Mice | Cardiomegaly - genetics | In Vitro Techniques | Methylation | Polycomb Repressive Complex 2 - metabolism | Induced Pluripotent Stem Cells | Histone Code - genetics | Cardiomegaly - metabolism | Genetic aspects | Research | RNA | Heart enlargement | Heart | Epigenetic inheritance | Antisense RNA | Genes | TOR protein | Chromatin | Rapamycin | Gene expression | Ribonucleic acid--RNA | Polycomb group proteins | Lysine | Regulatory mechanisms (biology) | DNA methylation | Epigenetics | Catalysis | Inhibition | Histone H3 | Hypertrophy
Journal Article
Circulation Research, ISSN 0009-7330, 10/2014, Volume 115, Issue 10, pp. 824 - 825
Journal Article
Cell, ISSN 0092-8674, 12/2016, Volume 167, Issue 7, pp. 1734 - 1749.e22
Mutation of highly conserved residues in transcription factors may affect protein-protein or protein-DNA interactions, leading to gene network dysregulation...
systems biology | heart development | gene regulation | disease modeling | birth defect | GATA4 | TBX5 | cardiomyopathy | epigenetics | congenital heart defects | PLURIPOTENT STEM-CELLS | VENTRAL MORPHOGENESIS | CHROMATIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | ATRIAL SEPTATION | HEART TUBE FORMATION | GENE-EXPRESSION | CARDIOMYOCYTES | DIFFERENTIATION | CARDIAC DEVELOPMENT | CELL BIOLOGY | Chromatin | Signal Transduction | Heart - growth & development | Humans | Heart Defects, Congenital - pathology | GATA4 Transcription Factor - genetics | Male | Phosphatidylinositol 3-Kinases - metabolism | Mutation, Missense | T-Box Domain Proteins - genetics | Heart Defects, Congenital - genetics | Myocytes, Cardiac - pathology | Enhancer Elements, Genetic | Myocytes, Cardiac - metabolism | Female | Induced Pluripotent Stem Cells | Pharmacogenetics | Genes | Stem cells | Genetic aspects | Models | DNA binding proteins | Mechanical engineering | Epigenetic inheritance | Genetic disorders | Developmental biology | Congenital heart disease | Anopheles | Analysis | birth defects
systems biology | heart development | gene regulation | disease modeling | birth defect | GATA4 | TBX5 | cardiomyopathy | epigenetics | congenital heart defects | PLURIPOTENT STEM-CELLS | VENTRAL MORPHOGENESIS | CHROMATIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | ATRIAL SEPTATION | HEART TUBE FORMATION | GENE-EXPRESSION | CARDIOMYOCYTES | DIFFERENTIATION | CARDIAC DEVELOPMENT | CELL BIOLOGY | Chromatin | Signal Transduction | Heart - growth & development | Humans | Heart Defects, Congenital - pathology | GATA4 Transcription Factor - genetics | Male | Phosphatidylinositol 3-Kinases - metabolism | Mutation, Missense | T-Box Domain Proteins - genetics | Heart Defects, Congenital - genetics | Myocytes, Cardiac - pathology | Enhancer Elements, Genetic | Myocytes, Cardiac - metabolism | Female | Induced Pluripotent Stem Cells | Pharmacogenetics | Genes | Stem cells | Genetic aspects | Models | DNA binding proteins | Mechanical engineering | Epigenetic inheritance | Genetic disorders | Developmental biology | Congenital heart disease | Anopheles | Analysis | birth defects
Journal Article
PLoS Computational Biology, ISSN 1553-734X, 08/2014, Volume 10, Issue 8, p. e1003777
A 30-node signed and directed network responsible for self-renewal and pluripotency of mouse embryonic stem cells (mESCs) was extracted from several ChIP-Seq...
OCT4 | CIRCUITRY | GENES | BIOCHEMICAL RESEARCH METHODS | MATHEMATICAL & COMPUTATIONAL BIOLOGY | STATE | NANOG | DIFFERENTIATION | TCF3 | FATE | EXPRESSION | OCT-3/4 | Cell Line | Reproducibility of Results | Animals | Gene Regulatory Networks - genetics | Computer Simulation | Pluripotent Stem Cells - physiology | Gene Expression Profiling | Mice | Gene Regulatory Networks - physiology | Systems Biology | Embryonic Stem Cells - physiology | Gene Knockdown Techniques | Stem cell research | Genetic research | Genetic aspects | Research | Nucleotide sequencing | Embryonic stem cells | Gene expression | DNA sequencing | Studies | Datasets | Stem cells | Ordinary differential equations | Agreements | Experiments | Binding sites
OCT4 | CIRCUITRY | GENES | BIOCHEMICAL RESEARCH METHODS | MATHEMATICAL & COMPUTATIONAL BIOLOGY | STATE | NANOG | DIFFERENTIATION | TCF3 | FATE | EXPRESSION | OCT-3/4 | Cell Line | Reproducibility of Results | Animals | Gene Regulatory Networks - genetics | Computer Simulation | Pluripotent Stem Cells - physiology | Gene Expression Profiling | Mice | Gene Regulatory Networks - physiology | Systems Biology | Embryonic Stem Cells - physiology | Gene Knockdown Techniques | Stem cell research | Genetic research | Genetic aspects | Research | Nucleotide sequencing | Embryonic stem cells | Gene expression | DNA sequencing | Studies | Datasets | Stem cells | Ordinary differential equations | Agreements | Experiments | Binding sites
Journal Article
Circulation, ISSN 0009-7322, 11/2014, Volume 130, Issue 22
Journal Article
STEM CELLS, ISSN 1066-5099, 02/2010, Volume 28, Issue 2, pp. 221 - 228
Direct reprogramming of somatic cells into induced pluripotent stem (iPS) cells by only four transcription factors (Oct4, Sox2, Klf4, and c‐Myc) has great...
Hair follicle | Reprogramming | Dermal papilla | Cell fate | Induced pluripotent stem cells | MOUSE | INDUCTION | CELL & TISSUE ENGINEERING | CELL BIOLOGY | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | MYC | HUMAN FIBROBLASTS | GENERATION | HEMATOLOGY | Dermis - metabolism | Humans | Cells, Cultured | Male | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Octamer Transcription Factor-3 - genetics | Animals | Kruppel-Like Transcription Factors - metabolism | Mice, Mutant Strains | Octamer Transcription Factor-3 - metabolism | Female | Fibroblasts - cytology | Mice | Dermis - cytology | Induced Pluripotent Stem Cells - cytology | SOXB1 Transcription Factors | Cellular Reprogramming - genetics | Gonadotropins, Equine | Kruppel-Like Transcription Factors - genetics | Cellular Reprogramming - physiology
Hair follicle | Reprogramming | Dermal papilla | Cell fate | Induced pluripotent stem cells | MOUSE | INDUCTION | CELL & TISSUE ENGINEERING | CELL BIOLOGY | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | MYC | HUMAN FIBROBLASTS | GENERATION | HEMATOLOGY | Dermis - metabolism | Humans | Cells, Cultured | Male | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Octamer Transcription Factor-3 - genetics | Animals | Kruppel-Like Transcription Factors - metabolism | Mice, Mutant Strains | Octamer Transcription Factor-3 - metabolism | Female | Fibroblasts - cytology | Mice | Dermis - cytology | Induced Pluripotent Stem Cells - cytology | SOXB1 Transcription Factors | Cellular Reprogramming - genetics | Gonadotropins, Equine | Kruppel-Like Transcription Factors - genetics | Cellular Reprogramming - physiology
Journal Article
Trends in Pharmacological Sciences, ISSN 0165-6147, 2011, Volume 32, Issue 7, pp. 394 - 401
Increasing evidence suggests that epigenetic regulation is key to the maintenance of the stem cell state. Chromatin is the physiological form of eukaryotic...
Advanced Basic Science | LINEAGE COMMITMENT | DEFINED FACTORS | X-CHROMOSOME | CHROMATIN-STRUCTURE | TRANSCRIPTIONAL NETWORK | SELF-RENEWAL | PHARMACOLOGY & PHARMACY | PLURIPOTENCY | EARLY EMBRYOGENESIS | ES CELLS | RNAI SCREEN | Embryonic Stem Cells - metabolism | Animals | Epigenomics | Gene Expression Regulation, Developmental | Humans | Embryonic Development - genetics | Chromatin - genetics | Embryonic Stem Cells - physiology | Histones | Chromatin | DNA binding proteins | Embryonic stem cells | Methylation | Analysis
Advanced Basic Science | LINEAGE COMMITMENT | DEFINED FACTORS | X-CHROMOSOME | CHROMATIN-STRUCTURE | TRANSCRIPTIONAL NETWORK | SELF-RENEWAL | PHARMACOLOGY & PHARMACY | PLURIPOTENCY | EARLY EMBRYOGENESIS | ES CELLS | RNAI SCREEN | Embryonic Stem Cells - metabolism | Animals | Epigenomics | Gene Expression Regulation, Developmental | Humans | Embryonic Development - genetics | Chromatin - genetics | Embryonic Stem Cells - physiology | Histones | Chromatin | DNA binding proteins | Embryonic stem cells | Methylation | Analysis
Journal Article