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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)
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    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
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  • 2
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    Superconductivity at 43 K in SmFeAsO1-xFx (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-27
    Description: Since the discovery of high-transition-temperature (high-T(c)) superconductivity in layered copper oxides, extensive effort has been devoted to exploring the origins of this phenomenon. A T(c) higher than 40 K (about the theoretical maximum predicted from Bardeen-Cooper-Schrieffer theory), however, has been obtained only in the copper oxide superconductors. The highest reported value for non-copper-oxide bulk superconductivity is T(c) = 39 K in MgB(2) (ref. 2). The layered rare-earth metal oxypnictides LnOFeAs (where Ln is La-Nd, Sm and Gd) are now attracting attention following the discovery of superconductivity at 26 K in the iron-based LaO(1-x)F(x)FeAs (ref. 3). Here we report the discovery of bulk superconductivity in the related compound SmFeAsO(1-x)F(x), which has a ZrCuSiAs-type structure. Resistivity and magnetization measurements reveal a transition temperature as high as 43 K. This provides a new material base for studying the origin of high-temperature superconductivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, X H -- Wu, T -- Wu, G -- Liu, R H -- Chen, H -- Fang, D F -- England -- Nature. 2008 Jun 5;453(7196):761-2. doi: 10.1038/nature07045. Epub 2008 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hefei National Laboratory for Physical Sciences at Microscale and Department of Physics, University of Science and Technology of China, Hefei, Anhui 230026, China. chenxh@ustc.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18500328" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Compound vesicle fusion increases quantal size and potentiates synaptic transmission (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-13
    Description: Exocytosis at synapses involves fusion between vesicles and the plasma membrane. Although compound fusion between vesicles was proposed to occur at ribbon-type synapses, whether it exists, how it is mediated, and what role it plays at conventional synapses remain unclear. Here we report the existence of compound fusion, its underlying mechanism, and its role at a nerve terminal containing conventional active zones in rats and mice. We found that high potassium application and high frequency firing induced giant capacitance up-steps, reflecting exocytosis of vesicles larger than regular ones, followed by giant down-steps, reflecting bulk endocytosis. These intense stimuli also induced giant vesicle-like structures, as observed with electron microscopy, and giant miniature excitatory postsynaptic currents (mEPSCs), reflecting more transmitter release. Calcium and its sensor for vesicle fusion, synaptotagmin, were required for these giant events. After high frequency firing, calcium/synaptotagmin-dependent mEPSC size increase was paralleled by calcium/synaptotagmin-dependent post-tetanic potentiation. These results suggest a new route of exocytosis and endocytosis composed of three steps. First, calcium/synaptotagmin mediates compound fusion between vesicles. Second, exocytosis of compound vesicles increases quantal size, which increases synaptic strength and contributes to the generation of post-tetanic potentiation. Third, exocytosed compound vesicles are retrieved via bulk endocytosis. We suggest that this vesicle cycling route be included in models of synapses in which only vesicle fusion with the plasma membrane is considered.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768540/" 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/PMC2768540/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Liming -- Xue, Lei -- Xu, Jianhua -- McNeil, Benjamin D -- Bai, Li -- Melicoff, Ernestina -- Adachi, Roberto -- Wu, Ling-Gang -- Z99 NS999999/Intramural NIH HHS/ -- England -- Nature. 2009 May 7;459(7243):93-7. doi: 10.1038/nature07860.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Disorders and Stroke, 35 Convent Drive, Building 35, Room 2B-1012, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19279571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Excitatory Postsynaptic Potentials ; Exocytosis/physiology ; Mice ; Rats ; Rats, Wistar ; Synaptic Transmission/*physiology ; Synaptic Vesicles/metabolism/*physiology ; Synaptotagmin II/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    A large iron isotope effect in SmFeAsO(1 - x)F(x) and Ba(1 - x)K(x)Fe(2)As(2) (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-05-09
    Description: The recent discovery of superconductivity in oxypnictides with a critical transition temperature (T(C)) higher than the McMillan limit of 39 K (the theoretical maximum predicted by Bardeen-Cooper-Schrieffer theory) has generated great excitement. Theoretical calculations indicate that the electron-phonon interaction is not strong enough to give rise to such high transition temperatures, but strong ferromagnetic/antiferromagnetic fluctuations have been proposed to be responsible. Superconductivity and magnetism in pnictide superconductors, however, show a strong sensitivity to the crystal lattice, suggesting the possibility of unconventional electron-phonon coupling. Here we report the effect of oxygen and iron isotope substitution on T(C) and the spin-density wave (SDW) transition temperature (T(SDW)) in the SmFeAsO(1 - x)F(x) and Ba(1 - x)K(x)Fe(2)As(2) systems. The oxygen isotope effect on T(C) and T(SDW) is very small, while the iron isotope exponent alpha(C) = -dlnT(C)/dlnM is about 0.35 (0.5 corresponds to the full isotope effect). Surprisingly, the iron isotope exchange shows the same effect on T(SDW) as T(C). This indicates that electron-phonon interaction plays some role in the superconducting mechanism, but a simple electron-phonon coupling mechanism seems unlikely because a strong magnon-phonon coupling is included.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, R H -- Wu, T -- Wu, G -- Chen, H -- Wang, X F -- Xie, Y L -- Ying, J J -- Yan, Y J -- Li, Q J -- Shi, B C -- Chu, W S -- Wu, Z Y -- Chen, X H -- England -- Nature. 2009 May 7;459(7243):64-7. doi: 10.1038/nature07981.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hefei National Laboratory for Physical Sciences at Microscale and Department of Physics, University of Science and Technology of China, Hefei, Anhui 230026, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19424151" target="_blank"〉PubMed〈/a〉
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Global risks: Pool knowledge to stem losses from disasters (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cutter, Susan L -- Ismail-Zadeh, Alik -- Alcantara-Ayala, Irasema -- Altan, Orhan -- Baker, Daniel N -- Briceno, Salvano -- Gupta, Harsh -- Holloway, Ailsa -- Johnston, David -- McBean, Gordon A -- Ogawa, Yujiro -- Paton, Douglas -- Porio, Emma -- Silbereisen, Rainer K -- Takeuchi, Kuniyoshi -- Valsecchi, Giovanni B -- Vogel, Coleen -- Wu, Guoxiong -- England -- Nature. 2015 Jun 18;522(7556):277-9. doi: 10.1038/522277a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hazards and Vulnerability Research Institute at the University of South Carolina, Columbia, USA. ; Karlsruhe Institute of Technology, Karlsruhe, Germany, and at the Institute of Earthquake Prediction, Russian Academy of Sciences, Moscow, Russia. ; Institute of Geography, National Autonomous University of Mexico, Mexico City, Mexico. ; Istanbul Technical University, Istanbul, Turkey. ; Laboratory for Atmospheric and Space Physics, University of Colorado at Boulder, Colorado, USA. ; United Nations Office for Disaster Risk Reduction, Divonne-les-Bains, France. ; National Geophysical Research Institute, Hyderabad, India, and a former member of the National Disaster Management Authority, Government of India, Delhi, India. ; Research Alliance for Disaster and Risk Reduction, Stellenbosch University, Stellenbosch, South Africa. ; Joint Centre for Disaster Research at Massey University and Senior Scientist at GNS Science, Wellington, New Zealand. ; Centre for Environment and Sustainability, and director of policy studies at the Institute for Catastrophic Loss Reduction, University of Western Ontario, London, Canada. ; Institute of Geosciences at the University of Tsukuba, Tsukuba, Japan. ; School of Psychological and Clinical Sciences, Charles Darwin University, Australia. ; Department of Sociology and Anthropology at Ateneo de Manila University, Quezon City, the Philippines. ; Center for Applied Developmental Science, University of Jena, Jena, Germany. ; Civil and Environmental Engineering Department, University of Yamanashi, Kofu, Japan, and founding director of the International Centre for Water Hazard Risk Management, Tsukuba, Japan. ; National Institute for Astrophysics, Rome, Italy, and at the National Research Council, Sesto Fiorentino, Italy. ; University of the Witwatersrand, Johannesburg, South Africa. ; Institute of Atmospheric Physics of the Chinese Academy of Sciences, Beijing, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26085255" target="_blank"〉PubMed〈/a〉
    Keywords: Building Codes ; Disaster Planning/economics/*methods ; Disasters/economics/*prevention & control/statistics & numerical data ; Earthquakes/mortality ; Humans ; International Cooperation/legislation & jurisprudence ; Nepal/epidemiology ; *Policy Making ; Risk Management/economics/*methods ; Risk Reduction Behavior
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  • 6
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    RAF inhibitors that evade paradoxical MAPK pathway activation (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-10-16
    Description: Oncogenic activation of BRAF fuels cancer growth by constitutively promoting RAS-independent mitogen-activated protein kinase (MAPK) pathway signalling. Accordingly, RAF inhibitors have brought substantially improved personalized treatment of metastatic melanoma. However, these targeted agents have also revealed an unexpected consequence: stimulated growth of certain cancers. Structurally diverse ATP-competitive RAF inhibitors can either inhibit or paradoxically activate the MAPK pathway, depending whether activation is by BRAF mutation or by an upstream event, such as RAS mutation or receptor tyrosine kinase activation. Here we have identified next-generation RAF inhibitors (dubbed 'paradox breakers') that suppress mutant BRAF cells without activating the MAPK pathway in cells bearing upstream activation. In cells that express the same HRAS mutation prevalent in squamous tumours from patients treated with RAF inhibitors, the first-generation RAF inhibitor vemurafenib stimulated in vitro and in vivo growth and induced expression of MAPK pathway response genes; by contrast the paradox breakers PLX7904 and PLX8394 had no effect. Paradox breakers also overcame several known mechanisms of resistance to first-generation RAF inhibitors. Dissociating MAPK pathway inhibition from paradoxical activation might yield both improved safety and more durable efficacy than first-generation RAF inhibitors, a concept currently undergoing human clinical evaluation with PLX8394.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Chao -- Spevak, Wayne -- Zhang, Ying -- Burton, Elizabeth A -- Ma, Yan -- Habets, Gaston -- Zhang, Jiazhong -- Lin, Jack -- Ewing, Todd -- Matusow, Bernice -- Tsang, Garson -- Marimuthu, Adhirai -- Cho, Hanna -- Wu, Guoxian -- Wang, Weiru -- Fong, Daniel -- Nguyen, Hoa -- Shi, Songyuan -- Womack, Patrick -- Nespi, Marika -- Shellooe, Rafe -- Carias, Heidi -- Powell, Ben -- Light, Emily -- Sanftner, Laura -- Walters, Jason -- Tsai, James -- West, Brian L -- Visor, Gary -- Rezaei, Hamid -- Lin, Paul S -- Nolop, Keith -- Ibrahim, Prabha N -- Hirth, Peter -- Bollag, Gideon -- England -- Nature. 2015 Oct 22;526(7574):583-6. doi: 10.1038/nature14982. Epub 2015 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plexxikon Inc., 91 Bolivar Drive, Berkeley, California 94710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26466569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Enzyme Activation/drug effects ; Female ; Genes, ras/genetics ; Heterocyclic Compounds, 2-Ring/adverse effects/pharmacology ; Humans ; Indoles/adverse effects/pharmacology ; MAP Kinase Signaling System/*drug effects/genetics ; Mice ; Mitogen-Activated Protein Kinases/*metabolism ; Models, Biological ; Mutation/genetics ; Protein Kinase Inhibitors/adverse effects/*pharmacology ; Proto-Oncogene Proteins B-raf/*antagonists & inhibitors/genetics ; Sulfonamides/adverse effects/pharmacology
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Unusual base pairing during the decoding of a stop codon by the ribosome (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-07-03
    Description: During normal translation, the binding of a release factor to one of the three stop codons (UGA, UAA or UAG) results in the termination of protein synthesis. However, modification of the initial uridine to a pseudouridine (Psi) allows efficient recognition and read-through of these stop codons by a transfer RNA (tRNA), although it requires the formation of two normally forbidden purine-purine base pairs. Here we determined the crystal structure at 3.1 A resolution of the 30S ribosomal subunit in complex with the anticodon stem loop of tRNA(Ser) bound to the PsiAG stop codon in the A site. The PsiA base pair at the first position is accompanied by the formation of purine-purine base pairs at the second and third positions of the codon, which show an unusual Watson-Crick/Hoogsteen geometry. The structure shows a previously unsuspected ability of the ribosomal decoding centre to accommodate non-canonical base pairs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732562/" 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/PMC3732562/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez, Israel S -- Ng, Chyan Leong -- Kelley, Ann C -- Wu, Guowei -- Yu, Yi-Tao -- Ramakrishnan, V -- 096570/Wellcome Trust/United Kingdom -- GM104077/GM/NIGMS NIH HHS/ -- MC_U105184332/Medical Research Council/United Kingdom -- R01 GM104077/GM/NIGMS NIH HHS/ -- R21 AG039559/AG/NIA NIH HHS/ -- U105184332/Medical Research Council/United Kingdom -- England -- Nature. 2013 Aug 1;500(7460):107-10. doi: 10.1038/nature12302. Epub 2013 Jun 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812587" target="_blank"〉PubMed〈/a〉
    Keywords: Anticodon/chemistry/genetics/metabolism ; *Base Pairing ; Base Sequence ; Codon, Terminator/chemistry/*genetics/*metabolism ; Crystallography, X-Ray ; Models, Molecular ; Nucleic Acid Conformation ; Protein Conformation ; Pseudouridine/chemistry/genetics/metabolism ; RNA, Transfer, Ser/chemistry/genetics/metabolism ; Ribosome Subunits, Small, Bacterial/chemistry/genetics/metabolism ; Ribosomes/*chemistry/genetics/*metabolism
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  • 8
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    A central role for TFIID in the pluripotent transcription circuitry (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-19
    Description: Embryonic stem (ES) cells are pluripotent and characterized by open chromatin and high transcription levels, achieved through auto-regulatory and feed-forward transcription factor loops. ES-cell identity is maintained by a core of factors including Oct4 (also known as Pou5f1), Sox2, Klf4, c-Myc (OSKM) and Nanog, and forced expression of the OSKM factors can reprogram somatic cells into induced pluripotent stem cells (iPSCs) resembling ES cells. These gene-specific factors for RNA-polymerase-II-mediated transcription recruit transcriptional cofactors and chromatin regulators that control access to and activity of the basal transcription machinery on gene promoters. How the basal transcription machinery is involved in setting and maintaining the pluripotent state is unclear. Here we show that knockdown of the transcription factor IID (TFIID) complex affects the pluripotent circuitry in mouse ES cells and inhibits reprogramming of fibroblasts. TFIID subunits and the OSKM factors form a feed-forward loop to induce and maintain a stable transcription state. Notably, transient expression of TFIID subunits greatly enhanced reprogramming. These results show that TFIID is critical for transcription-factor-mediated reprogramming. We anticipate that, by creating plasticity in gene expression programs, transcription complexes such as TFIID assist reprogramming into different cellular states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pijnappel, W W M Pim -- Esch, Daniel -- Baltissen, Marijke P A -- Wu, Guangming -- Mischerikow, Nikolai -- Bergsma, Atze J -- van der Wal, Erik -- Han, Dong Wook -- Bruch, Hermann vom -- Moritz, Soren -- Lijnzaad, Phillip -- Altelaar, A F Maarten -- Sameith, Katrin -- Zaehres, Holm -- Heck, Albert J R -- Holstege, Frank C P -- Scholer, Hans R -- Timmers, H T Marc -- England -- Nature. 2013 Mar 28;495(7442):516-9. doi: 10.1038/nature11970. Epub 2013 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cancer Research, University Medical Center Utrecht, 3584 CG Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23503660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/genetics ; Chromatin/genetics/metabolism ; Embryonic Stem Cells/cytology/metabolism ; Female ; Fibroblasts/cytology/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Male ; Mice ; Pluripotent Stem Cells/cytology/*metabolism ; Promoter Regions, Genetic/genetics ; RNA Polymerase II/metabolism ; TATA-Binding Protein Associated Factors/deficiency/genetics/metabolism ; TATA-Box Binding Protein/metabolism ; Transcription Factor TFIID/deficiency/genetics/*metabolism ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic
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  • 9
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    Nuclear reprogramming by interphase cytoplasm of two-cell mouse embryos (2014)
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    Publication Date: 2014-03-29
    Description: Successful mammalian cloning using somatic cell nuclear transfer (SCNT) into unfertilized, metaphase II (MII)-arrested oocytes attests to the cytoplasmic presence of reprogramming factors capable of inducing totipotency in somatic cell nuclei. However, these poorly defined maternal factors presumably decline sharply after fertilization, as the cytoplasm of pronuclear-stage zygotes is reportedly inactive. Recent evidence suggests that zygotic cytoplasm, if maintained at metaphase, can also support derivation of embryonic stem (ES) cells after SCNT, albeit at low efficiency. This led to the conclusion that critical oocyte reprogramming factors present in the metaphase but not in the interphase cytoplasm are 'trapped' inside the nucleus during interphase and effectively removed during enucleation. Here we investigated the presence of reprogramming activity in the cytoplasm of interphase two-cell mouse embryos (I2C). First, the presence of candidate reprogramming factors was documented in both intact and enucleated metaphase and interphase zygotes and two-cell embryos. Consequently, enucleation did not provide a likely explanation for the inability of interphase cytoplasm to induce reprogramming. Second, when we carefully synchronized the cell cycle stage between the transplanted nucleus (ES cell, fetal fibroblast or terminally differentiated cumulus cell) and the recipient I2C cytoplasm, the reconstructed SCNT embryos developed into blastocysts and ES cells capable of contributing to traditional germline and tetraploid chimaeras. Last, direct transfer of cloned embryos, reconstructed with ES cell nuclei, into recipients resulted in live offspring. Thus, the cytoplasm of I2C supports efficient reprogramming, with cell cycle synchronization between the donor nucleus and recipient cytoplasm as the most critical parameter determining success. The ability to use interphase cytoplasm in SCNT could aid efforts to generate autologous human ES cells for regenerative applications, as donated or discarded embryos are more accessible than unfertilized MII oocytes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124901/" 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/PMC4124901/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Eunju -- Wu, Guangming -- Ma, Hong -- Li, Ying -- Tippner-Hedges, Rebecca -- Tachibana, Masahito -- Sparman, Michelle -- Wolf, Don P -- Scholer, Hans R -- Mitalipov, Shoukhrat -- P51 OD011092/OD/NIH HHS/ -- P51OD011092/OD/NIH HHS/ -- R01 EY021214/EY/NEI NIH HHS/ -- R01 HD057121/HD/NICHD NIH HHS/ -- R01 HD059946/HD/NICHD NIH HHS/ -- R01 HD063276/HD/NICHD NIH HHS/ -- R01EY021214/EY/NEI NIH HHS/ -- R01HD057121/HD/NICHD NIH HHS/ -- R01HD059946/HD/NICHD NIH HHS/ -- R01HD063276/HD/NICHD NIH HHS/ -- England -- Nature. 2014 May 1;509(7498):101-4. doi: 10.1038/nature13134. Epub 2014 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97006, USA. ; Max Planck Institute for Molecular Biomedicine, Munster 48149, Germany. ; 1] Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97006, USA [2] South Miyagi Medical Center, Miyagi 989-1253, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; *Cellular Reprogramming ; Cloning, Organism ; Cytoplasm/*metabolism ; Embryo, Mammalian/*cytology ; Embryonic Stem Cells/*cytology ; Female ; Induced Pluripotent Stem Cells/*cytology ; *Interphase ; Male ; Metaphase ; Mice ; *Nuclear Transfer Techniques
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    The genetic basis of early T-cell precursor acute lymphoblastic leukaemia (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-01-13
    Description: Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267575/" 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/PMC3267575/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jinghui -- Ding, Li -- Holmfeldt, Linda -- Wu, Gang -- Heatley, Sue L -- Payne-Turner, Debbie -- Easton, John -- Chen, Xiang -- Wang, Jianmin -- Rusch, Michael -- Lu, Charles -- Chen, Shann-Ching -- Wei, Lei -- Collins-Underwood, J Racquel -- Ma, Jing -- Roberts, Kathryn G -- Pounds, Stanley B -- Ulyanov, Anatoly -- Becksfort, Jared -- Gupta, Pankaj -- Huether, Robert -- Kriwacki, Richard W -- Parker, Matthew -- McGoldrick, Daniel J -- Zhao, David -- Alford, Daniel -- Espy, Stephen -- Bobba, Kiran Chand -- Song, Guangchun -- Pei, Deqing -- Cheng, Cheng -- Roberts, Stefan -- Barbato, Michael I -- Campana, Dario -- Coustan-Smith, Elaine -- Shurtleff, Sheila A -- Raimondi, Susana C -- Kleppe, Maria -- Cools, Jan -- Shimano, Kristin A -- Hermiston, Michelle L -- Doulatov, Sergei -- Eppert, Kolja -- Laurenti, Elisa -- Notta, Faiyaz -- Dick, John E -- Basso, Giuseppe -- Hunger, Stephen P -- Loh, Mignon L -- Devidas, Meenakshi -- Wood, Brent -- Winter, Stuart -- Dunsmore, Kimberley P -- Fulton, Robert S -- Fulton, Lucinda L -- Hong, Xin -- Harris, Christopher C -- Dooling, David J -- Ochoa, Kerri -- Johnson, Kimberly J -- Obenauer, John C -- Evans, William E -- Pui, Ching-Hon -- Naeve, Clayton W -- Ley, Timothy J -- Mardis, Elaine R -- Wilson, Richard K -- Downing, James R -- Mullighan, Charles G -- CA114766/CA/NCI NIH HHS/ -- CA98413/CA/NCI NIH HHS/ -- CA98543/CA/NCI NIH HHS/ -- P30 CA021765/CA/NCI NIH HHS/ -- P30 CA021765-33/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- U01GM92666/GM/NIGMS NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Jan 11;481(7380):157-63. doi: 10.1038/nature10725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237106" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Child ; DNA Copy Number Variations/genetics ; Genes, ras/genetics ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genomics ; Hematopoiesis/genetics ; Histones/metabolism ; Humans ; Janus Kinases/genetics/metabolism ; Leukemia, Myeloid, Acute/drug therapy/genetics/pathology ; Molecular Sequence Data ; Mutation/*genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/*genetics/pathology ; Receptors, Interleukin-7/genetics ; Sequence Analysis, DNA ; Signal Transduction/genetics ; Stem Cells/metabolism/pathology ; T-Lymphocytes/metabolism/pathology ; Translocation, Genetic/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)
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