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  • Condensed Matter: Electronic Properties, etc.  (8)
  • Cells, Cultured  (4)
  • Male  (4)
  • Mice, Inbred C57BL  (3)
  • 1
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    Transport Inefficiency in Branched-Out Mesoscopic Networks: An Analog of the Braess Paradox (2012)
    American Physical Society (APS)
    Details
    Publication Date: 2012-02-14
    Description: Author(s): M. G. Pala, S. Baltazar, P. Liu, H. Sellier, B. Hackens, F. Martins, V. Bayot, X. Wallart, L. Desplanque, and S. Huant We present evidence for a counterintuitive behavior of semiconductor mesoscopic networks that is the analog of the Braess paradox encountered in classical networks. A numerical simulation of quantum transport in a two-branch mesoscopic network reveals that adding a third branch can paradoxically ind... [Phys. Rev. Lett. 108, 076802] Published Mon Feb 13, 2012
    Keywords: Condensed Matter: Electronic Properties, etc.
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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  • 2
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    Essential roles of PI(3)K-p110beta in cell growth, metabolism and tumorigenesis (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-03
    Description: On activation by receptors, the ubiquitously expressed class IA isoforms (p110alpha and p110beta) of phosphatidylinositol-3-OH kinase (PI(3)K) generate lipid second messengers, which initiate multiple signal transduction cascades. Recent studies have demonstrated specific functions for p110alpha in growth factor and insulin signalling. To probe for distinct functions of p110beta, we constructed conditional knockout mice. Here we show that ablation of p110beta in the livers of the resulting mice leads to impaired insulin sensitivity and glucose homeostasis, while having little effect on phosphorylation of Akt, suggesting the involvement of a kinase-independent role of p110beta in insulin metabolic action. Using established mouse embryonic fibroblasts, we found that removal of p110beta also had little effect on Akt phosphorylation in response to stimulation by insulin and epidermal growth factor, but resulted in retarded cell proliferation. Reconstitution of p110beta-null cells with a wild-type or kinase-dead allele of p110beta demonstrated that p110beta possesses kinase-independent functions in regulating cell proliferation and trafficking. However, the kinase activity of p110beta was required for G-protein-coupled receptor signalling triggered by lysophosphatidic acid and had a function in oncogenic transformation. Most strikingly, in an animal model of prostate tumour formation induced by Pten loss, ablation of p110beta (also known as Pik3cb), but not that of p110alpha (also known as Pik3ca), impeded tumorigenesis with a concomitant diminution of Akt phosphorylation. Taken together, our findings demonstrate both kinase-dependent and kinase-independent functions for p110beta, and strongly indicate the kinase-dependent functions of p110beta as a promising target in cancer therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750091/" 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/PMC2750091/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jia, Shidong -- Liu, Zhenning -- Zhang, Sen -- Liu, Pixu -- Zhang, Lei -- Lee, Sang Hyun -- Zhang, Jing -- Signoretti, Sabina -- Loda, Massimo -- Roberts, Thomas M -- Zhao, Jean J -- P01 CA050661/CA/NCI NIH HHS/ -- P01 CA050661-200001/CA/NCI NIH HHS/ -- P01 CA089021/CA/NCI NIH HHS/ -- P01 CA089021-06A1/CA/NCI NIH HHS/ -- P50 CA089393/CA/NCI NIH HHS/ -- P50 CA089393-08S1/CA/NCI NIH HHS/ -- P50 CA090381/CA/NCI NIH HHS/ -- P50 CA090381-05/CA/NCI NIH HHS/ -- R01 CA030002/CA/NCI NIH HHS/ -- R01 CA030002-27/CA/NCI NIH HHS/ -- R01 CA134502/CA/NCI NIH HHS/ -- R01 CA134502-01/CA/NCI NIH HHS/ -- England -- Nature. 2008 Aug 7;454(7205):776-9. doi: 10.1038/nature07091. Epub 2008 Jun 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18594509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Proliferation/drug effects ; *Cell Transformation, Neoplastic ; Epidermal Growth Factor/pharmacology ; Fibroblasts/cytology ; Glucose/*metabolism ; Glucose Intolerance/enzymology/genetics ; Homeostasis ; Humans ; Insulin/*metabolism/pharmacology ; Insulin Resistance/genetics ; Liver/enzymology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; PTEN Phosphohydrolase/deficiency/genetics ; Phosphatidylinositol 3-Kinases/deficiency/genetics/*metabolism ; Phosphorylation/drug effects ; Prostatic Neoplasms/enzymology/genetics/pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    piggyBac transposition reprograms fibroblasts to induced pluripotent stem cells (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-03-03
    Description: Transgenic expression of just four defined transcription factors (c-Myc, Klf4, Oct4 and Sox2) is sufficient to reprogram somatic cells to a pluripotent state. The resulting induced pluripotent stem (iPS) cells resemble embryonic stem cells in their properties and potential to differentiate into a spectrum of adult cell types. Current reprogramming strategies involve retroviral, lentiviral, adenoviral and plasmid transfection to deliver reprogramming factor transgenes. Although the latter two methods are transient and minimize the potential for insertion mutagenesis, they are currently limited by diminished reprogramming efficiencies. piggyBac (PB) transposition is host-factor independent, and has recently been demonstrated to be functional in various human and mouse cell lines. The PB transposon/transposase system requires only the inverted terminal repeats flanking a transgene and transient expression of the transposase enzyme to catalyse insertion or excision events. Here we demonstrate successful and efficient reprogramming of murine and human embryonic fibroblasts using doxycycline-inducible transcription factors delivered by PB transposition. Stable iPS cells thus generated express characteristic pluripotency markers and succeed in a series of rigorous differentiation assays. By taking advantage of the natural propensity of the PB system for seamless excision, we show that the individual PB insertions can be removed from established iPS cell lines, providing an invaluable tool for discovery. In addition, we have demonstrated the traceless removal of reprogramming factors joined with viral 2A sequences delivered by a single transposon from murine iPS lines. We anticipate that the unique properties of this virus-independent simplification of iPS cell production will accelerate this field further towards full exploration of the reprogramming process and future cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3758996/" 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/PMC3758996/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woltjen, Knut -- Michael, Iacovos P -- Mohseni, Paria -- Desai, Ridham -- Mileikovsky, Maria -- Hamalainen, Riikka -- Cowling, Rebecca -- Wang, Wei -- Liu, Pentao -- Gertsenstein, Marina -- Kaji, Keisuke -- Sung, Hoon-Ki -- Nagy, Andras -- 077186/Wellcome Trust/United Kingdom -- G0700672/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Apr 9;458(7239):766-70. doi: 10.1038/nature07863. Epub 2009 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19252478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/*genetics ; DNA Transposable Elements ; Fibroblasts/*cytology/*physiology/virology ; Gene Order ; Gene Transfer Techniques ; Genetic Vectors/*genetics ; Humans ; Mice ; Mice, Nude ; Pluripotent Stem Cells/*physiology ; Sequence Alignment ; Transcription Factors/genetics ; Transgenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Loss of delta-catenin function in severe autism (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-26
    Description: Autism is a multifactorial neurodevelopmental disorder affecting more males than females; consequently, under a multifactorial genetic hypothesis, females are affected only when they cross a higher biological threshold. We hypothesize that deleterious variants at conserved residues are enriched in severely affected patients arising from female-enriched multiplex families with severe disease, enhancing the detection of key autism genes in modest numbers of cases. Here we show the use of this strategy by identifying missense and dosage sequence variants in the gene encoding the adhesive junction-associated delta-catenin protein (CTNND2) in female-enriched multiplex families and demonstrating their loss-of-function effect by functional analyses in zebrafish embryos and cultured hippocampal neurons from wild-type and Ctnnd2 null mouse embryos. Finally, through gene expression and network analyses, we highlight a critical role for CTNND2 in neuronal development and an intimate connection to chromatin biology. Our data contribute to the understanding of the genetic architecture of autism and suggest that genetic analyses of phenotypic extremes, such as female-enriched multiplex families, are of innate value in multifactorial disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383723/" 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/PMC4383723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turner, Tychele N -- Sharma, Kamal -- Oh, Edwin C -- Liu, Yangfan P -- Collins, Ryan L -- Sosa, Maria X -- Auer, Dallas R -- Brand, Harrison -- Sanders, Stephan J -- Moreno-De-Luca, Daniel -- Pihur, Vasyl -- Plona, Teri -- Pike, Kristen -- Soppet, Daniel R -- Smith, Michael W -- Cheung, Sau Wai -- Martin, Christa Lese -- State, Matthew W -- Talkowski, Michael E -- Cook, Edwin -- Huganir, Richard -- Katsanis, Nicholas -- Chakravarti, Aravinda -- 1U24MH081810/MH/NIMH NIH HHS/ -- 5R25MH071584-07/MH/NIMH NIH HHS/ -- MH095867/MH/NIMH NIH HHS/ -- MH19961-14/MH/NIMH NIH HHS/ -- R00 MH095867/MH/NIMH NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 MH060007/MH/NIMH NIH HHS/ -- R01 MH074090/MH/NIMH NIH HHS/ -- R01MH074090/MH/NIMH NIH HHS/ -- R01MH081754/MH/NIMH NIH HHS/ -- England -- Nature. 2015 Apr 2;520(7545):51-6. doi: 10.1038/nature14186. Epub 2015 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Complex Disease Genomics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] Predoctoral Training Program in Human Genetics and Molecular Biology, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [3] National Institute of Mental Health (NIMH) Autism Centers of Excellence (ACE) Genetics Consortium at the University of California, Los Angeles, Los Angeles, California 90095, USA. ; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. ; Center for Human Disease Modeling, Duke University, Durham, North Carolina 27710, USA. ; Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; 1] Center for Complex Disease Genomics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA [2] National Institute of Mental Health (NIMH) Autism Centers of Excellence (ACE) Genetics Consortium at the University of California, Los Angeles, Los Angeles, California 90095, USA. ; 1] Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA [2] Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 USA. ; 1] National Institute of Mental Health (NIMH) Autism Centers of Excellence (ACE) Genetics Consortium at the University of California, Los Angeles, Los Angeles, California 90095, USA [2] Department of Psychiatry, University of California, San Francisco, San Francisco, California 94158, USA. ; 1] National Institute of Mental Health (NIMH) Autism Centers of Excellence (ACE) Genetics Consortium at the University of California, Los Angeles, Los Angeles, California 90095, USA [2] Department of Psychiatry, Yale University, New Haven, Connecticut 06511, USA. ; Leidos Biomedical Research, Inc., Frederick, Maryland 21702, USA. ; National Human Genome Research Institute, Bethesda, Maryland 20892, USA. ; Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] National Institute of Mental Health (NIMH) Autism Centers of Excellence (ACE) Genetics Consortium at the University of California, Los Angeles, Los Angeles, California 90095, USA [2] Autism &Developmental Medicine Institute, Geisinger Health System, Lewisburg, Pennsylvania 17837, USA. ; University of Illinois at Chicago, Chicago, Illinois 60608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25807484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*genetics/*metabolism ; Brain/embryology/*metabolism ; Catenins/*deficiency/*genetics/metabolism ; Cells, Cultured ; Chromatin/genetics/metabolism ; DNA Copy Number Variations/genetics ; Embryo, Mammalian/cytology/metabolism ; Exome/genetics ; Female ; Gene Expression ; Gene Expression Regulation, Developmental ; Hippocampus/pathology ; Humans ; Male ; Mice ; Models, Genetic ; Multifactorial Inheritance/genetics ; Mutation, Missense ; Nerve Net ; Neurons/cytology/metabolism ; Sex Characteristics ; Zebrafish/embryology/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-03-29
    Description: Akt, also known as protein kinase B, plays key roles in cell proliferation, survival and metabolism. Akt hyperactivation contributes to many pathophysiological conditions, including human cancers, and is closely associated with poor prognosis and chemo- or radiotherapeutic resistance. Phosphorylation of Akt at S473 (ref. 5) and T308 (ref. 6) activates Akt. However, it remains unclear whether further mechanisms account for full Akt activation, and whether Akt hyperactivation is linked to misregulated cell cycle progression, another cancer hallmark. Here we report that Akt activity fluctuates across the cell cycle, mirroring cyclin A expression. Mechanistically, phosphorylation of S477 and T479 at the Akt extreme carboxy terminus by cyclin-dependent kinase 2 (Cdk2)/cyclin A or mTORC2, under distinct physiological conditions, promotes Akt activation through facilitating, or functionally compensating for, S473 phosphorylation. Furthermore, deletion of the cyclin A2 allele in the mouse olfactory bulb leads to reduced S477/T479 phosphorylation and elevated cellular apoptosis. Notably, cyclin A2-deletion-induced cellular apoptosis in mouse embryonic stem cells is partly rescued by S477D/T479E-Akt1, supporting a physiological role for cyclin A2 in governing Akt activation. Together, the results of our study show Akt S477/T479 phosphorylation to be an essential layer of the Akt activation mechanism to regulate its physiological functions, thereby providing a new mechanistic link between aberrant cell cycle progression and Akt hyperactivation in cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076493/" 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/PMC4076493/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Pengda -- Begley, Michael -- Michowski, Wojciech -- Inuzuka, Hiroyuki -- Ginzberg, Miriam -- Gao, Daming -- Tsou, Peiling -- Gan, Wenjian -- Papa, Antonella -- Kim, Byeong Mo -- Wan, Lixin -- Singh, Amrik -- Zhai, Bo -- Yuan, Min -- Wang, Zhiwei -- Gygi, Steven P -- Lee, Tae Ho -- Lu, Kun-Ping -- Toker, Alex -- Pandolfi, Pier Paolo -- Asara, John M -- Kirschner, Marc W -- Sicinski, Piotr -- Cantley, Lewis -- Wei, Wenyi -- 2P01CA120964/CA/NCI NIH HHS/ -- 5T32HL007893/HL/NHLBI NIH HHS/ -- CA177910/CA/NCI NIH HHS/ -- GM089763/GM/NIGMS NIH HHS/ -- GM094777/GM/NIGMS NIH HHS/ -- P01 CA120964/CA/NCI NIH HHS/ -- R01 CA132740/CA/NCI NIH HHS/ -- R01 CA167677/CA/NCI NIH HHS/ -- R01 CA177910/CA/NCI NIH HHS/ -- R01 GM041890/GM/NIGMS NIH HHS/ -- R01 GM089763/GM/NIGMS NIH HHS/ -- R01 GM094777/GM/NIGMS NIH HHS/ -- R01 HL111430/HL/NHLBI NIH HHS/ -- R01CA132740/CA/NCI NIH HHS/ -- S10 OD010612/OD/NIH HHS/ -- T32 HL007893/HL/NHLBI NIH HHS/ -- England -- Nature. 2014 Apr 24;508(7497):541-5. doi: 10.1038/nature13079. Epub 2014 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; 1] Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA [2] Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Cancer Biology, Dana-Farber Cancer Institute and Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA [3] Cancer Genetics Program and Division of Genetics, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA. ; Division of Gerontology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. ; Cell Signaling Technology, Danvers, Massachusetts 01923, USA. ; Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. ; 1] Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] The Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, the First Affiliated Hospital, Soochow University, Suzhou 215123, China (Z.W.); Cancer Center at Weill Cornell Medical College and NewYork-Presbyterian Hospital, New York, New York 10065, USA (L.C.). ; Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA [2] Department of Systems Biology, Harvard Medical School, Boston, Massachusetts 02115, USA [3] The Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, the First Affiliated Hospital, Soochow University, Suzhou 215123, China (Z.W.); Cancer Center at Weill Cornell Medical College and NewYork-Presbyterian Hospital, New York, New York 10065, USA (L.C.).〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670654" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics ; Cell Cycle/*physiology ; Cell Proliferation ; Cyclin A2/metabolism ; Cyclin-Dependent Kinase 2/metabolism ; Embryonic Stem Cells/cytology/metabolism ; Enzyme Activation ; Male ; Mice ; Multiprotein Complexes/metabolism ; Neoplasms/enzymology/pathology ; Olfactory Bulb/cytology/enzymology/metabolism ; Oncogene Protein v-akt/chemistry/metabolism ; Phosphorylation ; Phosphoserine/metabolism ; Phosphothreonine/metabolism ; Proto-Oncogene Proteins c-akt/*chemistry/*metabolism ; TOR Serine-Threonine Kinases/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    The DNA methylation landscape of human early embryos (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-08-01
    Description: DNA methylation is a crucial element in the epigenetic regulation of mammalian embryonic development. However, its dynamic patterns have not been analysed at the genome scale in human pre-implantation embryos due to technical difficulties and the scarcity of required materials. Here we systematically profile the methylome of human early embryos from the zygotic stage through to post-implantation by reduced representation bisulphite sequencing and whole-genome bisulphite sequencing. We show that the major wave of genome-wide demethylation is complete at the 2-cell stage, contrary to previous observations in mice. Moreover, the demethylation of the paternal genome is much faster than that of the maternal genome, and by the end of the zygotic stage the genome-wide methylation level in male pronuclei is already lower than that in female pronuclei. The inverse correlation between promoter methylation and gene expression gradually strengthens during early embryonic development, reaching its peak at the post-implantation stage. Furthermore, we show that active genes, with the trimethylation of histone H3 at lysine 4 (H3K4me3) mark at the promoter regions in pluripotent human embryonic stem cells, are essentially devoid of DNA methylation in both mature gametes and throughout pre-implantation development. Finally, we also show that long interspersed nuclear elements or short interspersed nuclear elements that are evolutionarily young are demethylated to a milder extent compared to older elements in the same family and have higher abundance of transcripts, indicating that early embryos tend to retain higher residual methylation at the evolutionarily younger and more active transposable elements. Our work provides insights into the critical features of the methylome of human early embryos, as well as its functional relation to the regulation of gene expression and the repression of transposable elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Hongshan -- Zhu, Ping -- Yan, Liying -- Li, Rong -- Hu, Boqiang -- Lian, Ying -- Yan, Jie -- Ren, Xiulian -- Lin, Shengli -- Li, Junsheng -- Jin, Xiaohu -- Shi, Xiaodan -- Liu, Ping -- Wang, Xiaoye -- Wang, Wei -- Wei, Yuan -- Li, Xianlong -- Guo, Fan -- Wu, Xinglong -- Fan, Xiaoying -- Yong, Jun -- Wen, Lu -- Xie, Sunney X -- Tang, Fuchou -- Qiao, Jie -- England -- Nature. 2014 Jul 31;511(7511):606-10. doi: 10.1038/nature13544. Epub 2014 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2]. ; 1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2] Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China [3]. ; 1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2] Key Laboratory of Assisted Reproduction, Ministry of Education, Beijing 100191, China [3]. ; Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China. ; 1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2] Key Laboratory of Assisted Reproduction, Ministry of Education, Beijing 100191, China. ; Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China. ; 1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2] Department of Chemistry and Chemical Biology, Harvard University, Cambridge, Massachusetts 02138, USA. ; 1] Biodynamic Optical Imaging Center &Center for Reproductive Medicine, College of Life Sciences, Third Hospital, Peking University, Beijing 100871, China [2] Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, Beijing 100871, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079557" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Methylation ; DNA Transposable Elements/genetics ; Embryo, Mammalian ; Embryonic Stem Cells/physiology ; *Epigenesis, Genetic ; Female ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Germ Cells/metabolism ; Histones/metabolism ; Humans ; Long Interspersed Nucleotide Elements/genetics ; Male ; Mice ; Promoter Regions, Genetic/genetics ; Short Interspersed Nucleotide Elements/genetics
    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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    Broadband Terahertz Generation via the Interface Inverse Rashba-Edelstein Effect (2018)
    American Physical Society (APS)
    Details
    Publication Date: 2018-08-21
    Description: Author(s): C. Zhou, Y. P. Liu, Z. Wang, S. J. Ma, M. W. Jia, R. Q. Wu, L. Zhou, W. Zhang, M. K. Liu, Y. Z. Wu, and J. Qi Novel mechanisms for electromagnetic wave emission in the terahertz frequency regime emerging at the nanometer scale have recently attracted intense attention for the purpose of searching next-generation broadband THz emitters. Here, we report broadband THz emission, utilizing the interface inverse ... [Phys. Rev. Lett. 121, 086801] Published Mon Aug 20, 2018
    Keywords: Condensed Matter: Electronic Properties, etc.
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
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  • 8
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    Reprogramming of T cells to natural killer-like cells upon Bcl11b deletion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-12
    Description: T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628452/" 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/PMC3628452/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Burke, Shannon -- Wang, Juexuan -- Chen, Xiongfeng -- Ortiz, Mariaestela -- Lee, Song-Choon -- Lu, Dong -- Campos, Lia -- Goulding, David -- Ng, Bee Ling -- Dougan, Gordon -- Huntly, Brian -- Gottgens, Bertie -- Jenkins, Nancy A -- Copeland, Neal G -- Colucci, Francesco -- Liu, Pentao -- 076962/Wellcome Trust/United Kingdom -- 077186/Wellcome Trust/United Kingdom -- G0501150/Medical Research Council/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- G116/187/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):85-9. doi: 10.1126/science.1188063. Epub 2010 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20538915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; *Cell Lineage ; Cells, Cultured ; Coculture Techniques ; Cytotoxicity, Immunologic ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genes, T-Cell Receptor beta ; Killer Cells, Natural/cytology/immunology/*physiology ; *Lymphopoiesis/genetics ; Melanoma, Experimental/immunology/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; Precursor Cells, T-Lymphoid/cytology/physiology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Repressor Proteins/*genetics/*metabolism ; Signal Transduction ; Stromal Cells/cytology/physiology ; T-Lymphocytes/cytology/immunology/*physiology/transplantation ; Tamoxifen/analogs & derivatives/pharmacology ; Tumor Suppressor Proteins/*genetics/*metabolism
    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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  • 9
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    PiggyBac transposon mutagenesis: a tool for cancer gene discovery in mice (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Transposons are mobile DNA segments that can disrupt gene function by inserting in or near genes. Here, we show that insertional mutagenesis by the PiggyBac transposon can be used for cancer gene discovery in mice. PiggyBac transposition in genetically engineered transposon-transposase mice induced cancers whose type (hematopoietic versus solid) and latency were dependent on the regulatory elements introduced into transposons. Analysis of 63 hematopoietic tumors revealed that PiggyBac is capable of genome-wide mutagenesis. The PiggyBac screen uncovered many cancer genes not identified in previous retroviral or Sleeping Beauty transposon screens, including Spic, which encodes a PU.1-related transcription factor, and Hdac7, a histone deacetylase gene. PiggyBac and Sleeping Beauty have different integration preferences. To maximize the utility of the tool, we engineered 21 mouse lines to be compatible with both transposon systems in constitutive, tissue- or temporal-specific mutagenesis. Mice with different transposon types, copy numbers, and chromosomal locations support wide applicability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719098/" 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/PMC3719098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rad, Roland -- Rad, Lena -- Wang, Wei -- Cadinanos, Juan -- Vassiliou, George -- Rice, Stephen -- Campos, Lia S -- Yusa, Kosuke -- Banerjee, Ruby -- Li, Meng Amy -- de la Rosa, Jorge -- Strong, Alexander -- Lu, Dong -- Ellis, Peter -- Conte, Nathalie -- Yang, Fang Tang -- Liu, Pentao -- Bradley, Allan -- 077186/Wellcome Trust/United Kingdom -- 079643/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1104-7. doi: 10.1126/science.1193004. Epub 2010 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Genome Campus, Hinxton-Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Transposable Elements ; *Genes, Neoplasm ; Genetic Testing/*methods ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Mutagenesis, Insertional ; Neoplasms/genetics ; Oncogenes ; Promoter Regions, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Fragment spanning the SV40 replication origin is the only DNA sequence required in cis for viral excision (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-12-17
    Description: A 311-base pair fragment containing the SV40 origin of replication was linked to the chicken thymidine kinase gene on a recombinant plasmid. This molecule was transfected into human 143 thymidine kinase-deficient (TK-) cells, and colonies positive for thymidine kinase were selected. When cell lines derived from these colonies were fused to permissive simian cells that produce SV40 T antigen, the recombinant plasmid excised itself from the human cellular genome and replicated with a high copy number per cell. These results show that this segment of the viral genome is the only sequence required in cis to mediate SV40 excision and replication upon fusion to permissive cells. In addition, we have shown that excised plasmids apparently identical to the input DNA can be efficiently rescued in Escherichia coli. SV40 excision and replication may therefore be useful for the recovery of cloned genes from eukaryotic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conrad, S E -- Liu, C P -- Botchan, M R -- CA 30490/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1982 Dec 17;218(4578):1223-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6293055" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Chickens ; *DNA Replication ; DNA, Viral/*genetics ; Gene Expression Regulation ; Genes, Viral ; Humans ; Recombination, Genetic ; Simian virus 40/*genetics ; *Virus Replication
    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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