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  • 1
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    Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-03
    Description: Reprogramming of somatic cells is a valuable tool to understand the mechanisms of regaining pluripotency and further opens up the possibility of generating patient-specific pluripotent stem cells. Reprogramming of mouse and human somatic cells into pluripotent stem cells, designated as induced pluripotent stem (iPS) cells, has been possible with the expression of the transcription factor quartet Oct4 (also known as Pou5f1), Sox2, c-Myc and Klf4 (refs 1-11). Considering that ectopic expression of c-Myc causes tumorigenicity in offspring and that retroviruses themselves can cause insertional mutagenesis, the generation of iPS cells with a minimal number of factors may hasten the clinical application of this approach. Here we show that adult mouse neural stem cells express higher endogenous levels of Sox2 and c-Myc than embryonic stem cells, and that exogenous Oct4 together with either Klf4 or c-Myc is sufficient to generate iPS cells from neural stem cells. These two-factor iPS cells are similar to embryonic stem cells at the molecular level, contribute to development of the germ line, and form chimaeras. We propose that, in inducing pluripotency, the number of reprogramming factors can be reduced when using somatic cells that endogenously express appropriate levels of complementing factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jeong Beom -- Zaehres, Holm -- Wu, Guangming -- Gentile, Luca -- Ko, Kinarm -- Sebastiano, Vittorio -- Arauzo-Bravo, Marcos J -- Ruau, David -- Han, Dong Wook -- Zenke, Martin -- Scholer, Hans R -- England -- Nature. 2008 Jul 31;454(7204):646-50. doi: 10.1038/nature07061. Epub 2008 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Rontgenstrasse 20, 48149 Munster, NRW, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18594515" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology/metabolism ; Animals ; Cell Differentiation/genetics ; Cells, Cultured ; *Cellular Reprogramming ; Chimera ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Expression Profiling ; Genes, myc/genetics ; HMGB Proteins/genetics/metabolism ; Homeodomain Proteins/genetics ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Nude ; Mice, Transgenic ; Neurons/*cytology ; Octamer Transcription Factor-3/genetics/metabolism ; Pluripotent Stem Cells/*cytology/*metabolism ; Proteins/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Untranslated ; SOXB1 Transcription Factors ; Transcription Factors/genetics/metabolism ; Transduction, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Direct reprogramming of human neural stem cells by OCT4 (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-09-01
    Description: Induced pluripotent stem (iPS) cells have been generated from mouse and human somatic cells by ectopic expression of four transcription factors (OCT4 (also called POU5F1), SOX2, c-Myc and KLF4). We previously reported that Oct4 alone is sufficient to reprogram directly adult mouse neural stem cells to iPS cells. Here we report the generation of one-factor human iPS cells from human fetal neural stem cells (one-factor (1F) human NiPS cells) by ectopic expression of OCT4 alone. One-factor human NiPS cells resemble human embryonic stem cells in global gene expression profiles, epigenetic status, as well as pluripotency in vitro and in vivo. These findings demonstrate that the transcription factor OCT4 is sufficient to reprogram human neural stem cells to pluripotency. One-factor iPS cell generation will advance the field further towards understanding reprogramming and generating patient-specific pluripotent stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jeong Beom -- Greber, Boris -- Arauzo-Bravo, Marcos J -- Meyer, Johann -- Park, Kook In -- Zaehres, Holm -- Scholer, Hans R -- England -- Nature. 2009 Oct 1;461(7264):649-3. doi: 10.1038/nature08436.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Rontgenstrasse 20, 48149 Munster, NRW, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19718018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; *Cell Dedifferentiation ; Cell Differentiation ; Cell Line ; *Cellular Reprogramming ; DNA Methylation ; Embryonic Stem Cells/cytology/metabolism ; Epigenesis, Genetic ; Fetus/*cytology ; Gene Expression Profiling ; Germ Layers/cytology/metabolism ; Humans ; Mice ; Neurons/*cytology/metabolism ; Octamer Transcription Factor-3/genetics/*metabolism ; Pluripotent Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Endochondral ossification is required for haematopoietic stem-cell niche formation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-12-17
    Description: Little is known about the formation of niches, local micro-environments required for stem-cell maintenance. Here we develop an in vivo assay for adult haematopoietic stem-cell (HSC) niche formation. With this assay, we identified a population of progenitor cells with surface markers CD45(-)Tie2(-)alpha(V)(+)CD105(+)Thy1.1(-) (CD105(+)Thy1(-)) that, when sorted from 15.5 days post-coitum fetal bones and transplanted under the adult mouse kidney capsule, could recruit host-derived blood vessels, produce donor-derived ectopic bones through a cartilage intermediate and generate a marrow cavity populated by host-derived long-term reconstituting HSC (LT-HSC). In contrast, CD45(-)Tie2(-)alpha(V)(+)CD105(+)Thy1(+) (CD105(+)Thy1(+)) fetal bone progenitors form bone that does not contain a marrow cavity. Suppressing expression of factors involved in endochondral ossification, such as osterix and vascular endothelial growth factor (VEGF), inhibited niche generation. CD105(+)Thy1(-) progenitor populations derived from regions of the fetal mandible or calvaria that do not undergo endochondral ossification formed only bone without marrow in our assay. Collectively, our data implicate endochondral ossification, bone formation that proceeds through a cartilage intermediate, as a requirement for adult HSC niche formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648141/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Charles K F -- Chen, Ching-Cheng -- Luppen, Cynthia A -- Kim, Jae-Beom -- DeBoer, Anthony T -- Wei, Kevin -- Helms, Jill A -- Kuo, Calvin J -- Kraft, Daniel L -- Weissman, Irving L -- 1R01HL074267-01/HL/NHLBI NIH HHS/ -- 1R01NS052830-01/NS/NINDS NIH HHS/ -- 2R01HL058770-08/HL/NHLBI NIH HHS/ -- 5K99HL087936-02/HL/NHLBI NIH HHS/ -- 5R01CA086065-09/CA/NCI NIH HHS/ -- K08-HL076335/HL/NHLBI NIH HHS/ -- K99 HL087936/HL/NHLBI NIH HHS/ -- K99 HL087936-01/HL/NHLBI NIH HHS/ -- K99 HL087936-02/HL/NHLBI NIH HHS/ -- R00 HL087936/HL/NHLBI NIH HHS/ -- R00 HL087936-03/HL/NHLBI NIH HHS/ -- R00 HL087936-04/HL/NHLBI NIH HHS/ -- R00 HL087936-05/HL/NHLBI NIH HHS/ -- R01 CA086065/CA/NCI NIH HHS/ -- R01 CA086065-09/CA/NCI NIH HHS/ -- R01 HL058770/HL/NHLBI NIH HHS/ -- R01 HL058770-08/HL/NHLBI NIH HHS/ -- England -- Nature. 2009 Jan 22;457(7228):490-4. doi: 10.1038/nature07547. Epub 2008 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Developmental Biology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, California, USA. chazchan@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19078959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Antigens, Thy-1/metabolism ; Cartilage/*cytology/embryology ; Choristoma ; Fetus/cytology ; Hematopoietic Stem Cells/*cytology/metabolism ; Mandible/cytology/embryology ; Mice ; Mice, Inbred C57BL ; Osteogenesis/*physiology ; Skull/cytology/embryology ; Stem Cell Niche/*cytology/*physiology ; Transcription Factors/antagonists & inhibitors/metabolism ; Vascular Endothelial Growth Factor A/antagonists & inhibitors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Polony multiplex analysis of gene expression (PMAGE) in mouse hypertrophic cardiomyopathy (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-09
    Description: We describe a sensitive mRNA profiling technology, PMAGE (for "polony multiplex analysis of gene expression"), which detects messenger RNAs (mRNAs) as rare as one transcript per three cells. PMAGE incorporates an improved ligation-based method to sequence 14-nucleotide tags derived from individual mRNA molecules. One sequence tag from each mRNA molecule is amplified onto a separate 1-micrometer bead, denoted as a polymerase colony or polony, and about 5 million polonies are arrayed in a flow cell for parallel sequencing. Using PMAGE, we identified early transcriptional changes that preceded pathological manifestations of hypertrophic cardiomyopathy in mice carrying a disease-causing mutation. PMAGE provided a comprehensive profile of cardiac mRNAs, including low-abundance mRNAs encoding signaling molecules and transcription factors that are likely to participate in disease pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jae Bum -- Porreca, Gregory J -- Song, Lei -- Greenway, Steven C -- Gorham, Joshua M -- Church, George M -- Seidman, Christine E -- Seidman, J G -- New York, N.Y. -- Science. 2007 Jun 8;316(5830):1481-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Division, Brigham and Women's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17556586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Hypertrophic/*genetics/pathology/physiopathology ; DNA, Complementary ; Fibrosis/genetics/pathology ; Gene Expression Profiling/*methods ; *Gene Expression Regulation ; Gene Library ; Heart Ventricles/metabolism ; Mice ; Mutation ; Myocardial Contraction ; Myocardium/*metabolism ; Myosin Heavy Chains/genetics ; RNA, Messenger/genetics/metabolism ; Reproducibility of Results ; Sensitivity and Specificity ; Sequence Analysis, DNA ; Templates, Genetic ; Transcription Factors/genetics ; *Transcription, Genetic ; Ventricular Myosins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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