ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Telomere shortening and loss of self-renewal in dyskeratosis congenita induced pluripotent stem cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-05-24
    Description: The differentiation of patient-derived induced pluripotent stem cells (iPSCs) to committed fates such as neurons, muscle and liver is a powerful approach for understanding key parameters of human development and disease. Whether undifferentiated iPSCs themselves can be used to probe disease mechanisms is uncertain. Dyskeratosis congenita is characterized by defective maintenance of blood, pulmonary tissue and epidermal tissues and is caused by mutations in genes controlling telomere homeostasis. Short telomeres, a hallmark of dyskeratosis congenita, impair tissue stem cell function in mouse models, indicating that a tissue stem cell defect may underlie the pathophysiology of dyskeratosis congenita. Here we show that even in the undifferentiated state, iPSCs from dyskeratosis congenita patients harbour the precise biochemical defects characteristic of each form of the disease and that the magnitude of the telomere maintenance defect in iPSCs correlates with clinical severity. In iPSCs from patients with heterozygous mutations in TERT, the telomerase reverse transcriptase, a 50% reduction in telomerase levels blunts the natural telomere elongation that accompanies reprogramming. In contrast, mutation of dyskerin (DKC1) in X-linked dyskeratosis congenita severely impairs telomerase activity by blocking telomerase assembly and disrupts telomere elongation during reprogramming. In iPSCs from a form of dyskeratosis congenita caused by mutations in TCAB1 (also known as WRAP53), telomerase catalytic activity is unperturbed, yet the ability of telomerase to lengthen telomeres is abrogated, because telomerase mislocalizes from Cajal bodies to nucleoli within the iPSCs. Extended culture of DKC1-mutant iPSCs leads to progressive telomere shortening and eventual loss of self-renewal, indicating that a similar process occurs in tissue stem cells in dyskeratosis congenita patients. These findings in iPSCs from dyskeratosis congenita patients reveal that undifferentiated iPSCs accurately recapitulate features of a human stem cell disease and may serve as a cell-culture-based system for the development of targeted therapeutics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155806/" 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/PMC3155806/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Batista, Luis F Z -- Pech, Matthew F -- Zhong, Franklin L -- Nguyen, Ha Nam -- Xie, Kathleen T -- Zaug, Arthur J -- Crary, Sharon M -- Choi, Jinkuk -- Sebastiano, Vittorio -- Cherry, Athena -- Giri, Neelam -- Wernig, Marius -- Alter, Blanche P -- Cech, Thomas R -- Savage, Sharon A -- Reijo Pera, Renee A -- Artandi, Steven E -- R01 AG033747/AG/NIA NIH HHS/ -- R01 AG033747-02/AG/NIA NIH HHS/ -- R01 CA111691/CA/NCI NIH HHS/ -- R01 CA111691-05/CA/NCI NIH HHS/ -- R01 CA125453/CA/NCI NIH HHS/ -- R01 CA125453-05/CA/NCI NIH HHS/ -- RC1 HL100361/HL/NHLBI NIH HHS/ -- RC1 HL100361-01/HL/NHLBI NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2011 May 22;474(7351):399-402. doi: 10.1038/nature10084.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21602826" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle Proteins/genetics/metabolism ; Cell Division ; Cellular Reprogramming ; Dyskeratosis Congenita/*genetics/*pathology ; Fibroblasts ; Gene Expression Regulation ; Humans ; Induced Pluripotent Stem Cells/*metabolism/*pathology ; Nuclear Proteins/genetics/metabolism ; RNA/genetics ; Telomerase/genetics/metabolism ; Telomere/enzymology/genetics/metabolism/*pathology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Induction of human neuronal cells by defined transcription factors (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-05-28
    Description: Somatic cell nuclear transfer, cell fusion, or expression of lineage-specific factors have been shown to induce cell-fate changes in diverse somatic cell types. We recently observed that forced expression of a combination of three transcription factors, Brn2 (also known as Pou3f2), Ascl1 and Myt1l, can efficiently convert mouse fibroblasts into functional induced neuronal (iN) cells. Here we show that the same three factors can generate functional neurons from human pluripotent stem cells as early as 6 days after transgene activation. When combined with the basic helix-loop-helix transcription factor NeuroD1, these factors could also convert fetal and postnatal human fibroblasts into iN cells showing typical neuronal morphologies and expressing multiple neuronal markers, even after downregulation of the exogenous transcription factors. Importantly, the vast majority of human iN cells were able to generate action potentials and many matured to receive synaptic contacts when co-cultured with primary mouse cortical neurons. Our data demonstrate that non-neural human somatic cells, as well as pluripotent stem cells, can be converted directly into neurons by lineage-determining transcription factors. These methods may facilitate robust generation of patient-specific human neurons for in vitro disease modelling or future applications in regenerative medicine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159048/" 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/PMC3159048/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pang, Zhiping P -- Yang, Nan -- Vierbuchen, Thomas -- Ostermeier, Austin -- Fuentes, Daniel R -- Yang, Troy Q -- Citri, Ami -- Sebastiano, Vittorio -- Marro, Samuele -- Sudhof, Thomas C -- Wernig, Marius -- 1R01MH092931/MH/NIMH NIH HHS/ -- R01 MH092931/MH/NIMH NIH HHS/ -- R01 MH092931-01/MH/NIMH NIH HHS/ -- RC4 NS073015/NS/NINDS NIH HHS/ -- RC4 NS073015-01/NS/NINDS NIH HHS/ -- RC4NS073015/NS/NINDS NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 May 26;476(7359):220-3. doi: 10.1038/nature10202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 265 Campus Drive, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21617644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; *Cellular Reprogramming/genetics/physiology ; Cerebral Cortex/cytology ; Coculture Techniques ; DNA-Binding Proteins/genetics/metabolism ; Electric Conductivity ; Fibroblasts/cytology/metabolism ; Humans ; Membrane Potentials ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*cytology/*metabolism ; POU Domain Factors/genetics/metabolism ; Pluripotent Stem Cells/cytology/metabolism ; Regenerative Medicine ; Synapses/metabolism ; Transcription Factors/genetics/*metabolism ; Transgenes
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-10-18
    Description: Phelan-McDermid syndrome (PMDS) is a complex neurodevelopmental disorder characterized by global developmental delay, severely impaired speech, intellectual disability, and an increased risk of autism spectrum disorders (ASDs). PMDS is caused by heterozygous deletions of chromosome 22q13.3. Among the genes in the deleted region is SHANK3, which encodes a protein in the postsynaptic density (PSD). Rare mutations in SHANK3 have been associated with idiopathic ASDs, non-syndromic intellectual disability, and schizophrenia. Although SHANK3 is considered to be the most likely candidate gene for the neurological abnormalities in PMDS patients, the cellular and molecular phenotypes associated with this syndrome in human neurons are unknown. We generated induced pluripotent stem (iPS) cells from individuals with PMDS and autism and used them to produce functional neurons. We show that PMDS neurons have reduced SHANK3 expression and major defects in excitatory, but not inhibitory, synaptic transmission. Excitatory synaptic transmission in PMDS neurons can be corrected by restoring SHANK3 expression or by treating neurons with insulin-like growth factor 1 (IGF1). IGF1 treatment promotes formation of mature excitatory synapses that lack SHANK3 but contain PSD95 and N-methyl-D-aspartate (NMDA) receptors with fast deactivation kinetics. Our findings provide direct evidence for a disruption in the ratio of cellular excitation and inhibition in PMDS neurons, and point to a molecular pathway that can be recruited to restore it.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shcheglovitov, Aleksandr -- Shcheglovitova, Olesya -- Yazawa, Masayuki -- Portmann, Thomas -- Shu, Rui -- Sebastiano, Vittorio -- Krawisz, Anna -- Froehlich, Wendy -- Bernstein, Jonathan A -- Hallmayer, Joachim F -- Dolmetsch, Ricardo E -- 5DP1OD3889/OD/NIH HHS/ -- DP1 OD003889/OD/NIH HHS/ -- R33MH087898/MH/NIMH NIH HHS/ -- England -- Nature. 2013 Nov 14;503(7475):267-71. doi: 10.1038/nature12618. Epub 2013 Oct 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24132240" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Child ; Chromosome Deletion ; Chromosome Disorders/genetics/*physiopathology ; Chromosomes, Human, Pair 22/genetics ; Female ; GABA Agents/pharmacology ; Gene Expression Regulation/drug effects ; Humans ; Insulin-Like Growth Factor I/*pharmacology ; Lentivirus/genetics ; Male ; Nerve Tissue Proteins/*genetics/*metabolism ; Neurons/cytology/drug effects/*physiology ; Pluripotent Stem Cells/cytology ; Receptors, Glutamate/genetics ; Sequence Deletion ; Synapses/*drug effects/genetics/*physiology ; Synaptic Transmission/drug effects/genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Lift NIH restrictions on chimera research (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Arun -- Sebastiano, Vittorio -- Scott, Christopher T -- Magnus, David -- Koyano-Nakagawa, Naoko -- Garry, Daniel J -- Witte, Owen N -- Nakauchi, Hiromitsu -- Wu, Joseph C -- Weissman, Irving L -- Wu, Sean M -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):640. doi: 10.1126/science.350.6261.640-a. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Center for Biomedical Ethics, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA. ; Lillehei Heart Institute, University of Minnesota, Minneapolis, MN 55455, USA. Stem Cell Institute and Paul and Sheila Wellstone Muscular Dystrophy Center, University of Minnesota, Minneapolis, MN 55455, USA. Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA. ; Broad Stem Cell Research Center and Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA. Center for Stem Cell Biology and Regenerative Medicine, The University of Tokyo, Tokyo, Japan. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Radiology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. irv@stanford.edu smwu@stanford.edu. ; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. irv@stanford.edu smwu@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bioethical Issues ; Blastocyst ; *Chimera ; Financial Management/ethics ; Humans ; Mice ; National Institutes of Health (U.S.)/economics/ethics ; Pluripotent Stem Cells/*transplantation ; Stem Cell Research/economics/*ethics ; United States
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Characterization of the human ESC transcriptome by hybrid sequencing (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-11-26
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Hybrid sequencing of hESC transcriptome [Statistics] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-12-11
    Description: Although transcriptional and posttranscriptional events are detected in RNA-Seq data from second-generation sequencing, full-length mRNA isoforms are not captured. On the other hand, third-generation sequencing, which yields much longer reads, has current limitations of lower raw accuracy and throughput. Here, we combine second-generation sequencing and third-generation sequencing with a custom-designed...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...