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  • 1
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    Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta) (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-02
    Description: Glucose homeostasis depends on insulin responsiveness in target tissues, most importantly, muscle and liver. The critical initial steps in insulin action include phosphorylation of scaffolding proteins and activation of phosphatidylinositol 3-kinase. These early events lead to activation of the serine-threonine protein kinase Akt, also known as protein kinase B. We show that mice deficient in Akt2 are impaired in the ability of insulin to lower blood glucose because of defects in the action of the hormone on liver and skeletal muscle. These data establish Akt2 as an essential gene in the maintenance of normal glucose homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, H -- Mu, J -- Kim, J K -- Thorvaldsen, J L -- Chu, Q -- Crenshaw, E B 3rd -- Kaestner, K H -- Bartolomei, M S -- Shulman, G I -- Birnbaum, M J -- GM07229/GM/NIGMS NIH HHS/ -- P30 19525/PHS HHS/ -- P30 DK50306/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R01 DK56886/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 1;292(5522):1728-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11387480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Deoxyglucose/metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Female ; Gene Targeting ; Glucose/*metabolism ; Glucose Clamp Technique ; Glucose Tolerance Test ; Homeostasis ; Insulin/administration & dosage/blood/*metabolism ; *Insulin Resistance/genetics/physiology ; Islets of Langerhans/cytology/physiology ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle, Skeletal/enzymology/metabolism ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Signal Transduction
    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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  • 2
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    Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: During pregnancy, maternal pancreatic islets grow to match dynamic physiological demands, but the mechanisms regulating adaptive islet growth in this setting are poorly understood. Here we show that menin, a protein previously characterized as an endocrine tumor suppressor and transcriptional regulator, controls islet growth in pregnant mice. Pregnancy stimulated proliferation of maternal pancreatic islet beta-cells that was accompanied by reduced islet levels of menin and its targets. Transgenic expression of menin in maternal beta-cells prevented islet expansion and led to hyperglycemia and impaired glucose tolerance, hallmark features of gestational diabetes. Prolactin, a hormonal regulator of pregnancy, repressed islet menin levels and stimulated beta-cell proliferation. These results expand our understanding of mechanisms underlying diabetes pathogenesis and reveal potential targets for therapy in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karnik, Satyajit K -- Chen, Hainan -- McLean, Graeme W -- Heit, Jeremy J -- Gu, Xueying -- Zhang, Andrew Y -- Fontaine, Magali -- Yen, Michael H -- Kim, Seung K -- T32DK007217-32/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975067" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Diabetes, Gestational/*etiology/metabolism ; Female ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Obesity/metabolism ; Pregnancy ; Prolactin/metabolism ; Proto-Oncogene Proteins/*physiology ; Tumor Cells, Cultured
    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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  • 3
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    Gender disparity in liver cancer due to sex differences in MyD88-dependent IL-6 production (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: Hepatocellular carcinoma (HCC), the most common liver cancer, occurs mainly in men. Similar gender disparity is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN). DEN administration caused greater increases in serum interleukin-6 (IL-6) concentration in males than it did in females. Furthermore, ablation of IL-6 abolished the gender differences in hepatocarcinogenesis in mice. DEN exposure promoted production of IL-6 in Kupffer cells (KCs) in a manner dependent on the Toll-like receptor adaptor protein MyD88, ablation of which also protected male mice from DEN-induced hepatocarcinogenesis. Estrogen inhibited secretion of IL-6 from KCs exposed to necrotic hepatocytes and reduced circulating concentrations of IL-6 in DEN-treated male mice. We propose that estrogen-mediated inhibition of IL-6 production by KCs reduces liver cancer risk in females, and these findings may be used to prevent HCC in males.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naugler, Willscott E -- Sakurai, Toshiharu -- Kim, Sunhwa -- Maeda, Shin -- Kim, Kyounghyun -- Elsharkawy, Ahmed M -- Karin, Michael -- CA118165/CA/NCI NIH HHS/ -- DK007202/DK/NIDDK NIH HHS/ -- ES004151/ES/NIEHS NIH HHS/ -- ES006376/ES/NIEHS NIH HHS/ -- R01 CA118165/CA/NCI NIH HHS/ -- R01 ES006376/ES/NIEHS NIH HHS/ -- T32 CA121938/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 6;317(5834):121-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology and Cancer Center, University of California, San Diego, CA 93093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Tetrachloride/administration & dosage ; Diethylnitrosamine/administration & dosage/metabolism ; Estradiol/pharmacology ; Female ; Hepatocytes ; Interleukin-6/blood/genetics/*metabolism ; Kupffer Cells/*metabolism ; Liver/metabolism/pathology ; Liver Neoplasms, Experimental/chemically induced/immunology/*physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88/*physiology ; Necrosis ; Ovariectomy ; RNA, Messenger/genetics/metabolism ; *Sex Characteristics
    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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  • 4
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    Histocompatible embryonic stem cells by parthenogenesis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: Genetically matched pluripotent embryonic stem (ES) cells generated via nuclear transfer or parthenogenesis (pES cells) are a potential source of histocompatible cells and tissues for transplantation. After parthenogenetic activation of murine oocytes and interruption of meiosis I or II, we isolated and genotyped pES cells and characterized those that carried the full complement of major histocompatibility complex (MHC) antigens of the oocyte donor. Differentiated tissues from these pES cells engrafted in immunocompetent MHC-matched mouse recipients, demonstrating that selected pES cells can serve as a source of histocompatible tissues for transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kitai -- Lerou, Paul -- Yabuuchi, Akiko -- Lengerke, Claudia -- Ng, Kitwa -- West, Jason -- Kirby, Andrew -- Daly, Mark J -- Daley, George Q -- T32: HD07466/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Jan 26;315(5811):482-6. Epub 2006 Dec 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Hematology/Oncology, Children's Hospital Boston and Dana Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Line ; Chromosome Segregation ; Embryonic Stem Cells/cytology/*immunology/physiology ; Female ; Genotype ; H-2 Antigens/*genetics/*immunology ; Heterozygote ; *Histocompatibility ; Histocompatibility Antigens Class II/genetics/immunology ; *Major Histocompatibility Complex ; Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Oocytes/cytology/immunology ; *Parthenogenesis ; Pluripotent Stem Cells/cytology/*immunology/physiology ; Polymerase Chain Reaction ; Recombination, Genetic ; Stem Cell Transplantation
    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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  • 5
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    Transcriptional architecture and chromatin landscape of the core circadian clock in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: The mammalian circadian clock involves a transcriptional feed back loop in which CLOCK and BMAL1 activate the Period and Cryptochrome genes, which then feedback and repress their own transcription. We have interrogated the transcriptional architecture of the circadian transcriptional regulatory loop on a genome scale in mouse liver and find a stereotyped, time-dependent pattern of transcription factor binding, RNA polymerase II (RNAPII) recruitment, RNA expression, and chromatin states. We find that the circadian transcriptional cycle of the clock consists of three distinct phases: a poised state, a coordinated de novo transcriptional activation state, and a repressed state. Only 22% of messenger RNA (mRNA) cycling genes are driven by de novo transcription, suggesting that both transcriptional and posttranscriptional mechanisms underlie the mammalian circadian clock. We also find that circadian modulation of RNAPII recruitment and chromatin remodeling occurs on a genome-wide scale far greater than that seen previously by gene expression profiling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694775/" 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/PMC3694775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koike, Nobuya -- Yoo, Seung-Hee -- Huang, Hung-Chung -- Kumar, Vivek -- Lee, Choogon -- Kim, Tae-Kyung -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- R01 NS053616/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 19;338(6105):349-54. doi: 10.1126/science.1226339. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936566" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Chromatin/*metabolism ; Chromatin Assembly and Disassembly/genetics ; Circadian Clocks/*genetics ; Cryptochromes/*genetics ; DNA, Intergenic ; Enhancer Elements, Genetic ; *Epigenesis, Genetic ; Gene Expression Profiling ; Genetic Loci ; Histones/metabolism ; Liver/metabolism/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Period Circadian Proteins/genetics ; RNA Polymerase II/metabolism ; RNA, Messenger/genetics ; *Transcription, Genetic ; *Transcriptional Activation
    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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  • 6
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    C57BL/6N mutation in cytoplasmic FMRP interacting protein 2 regulates cocaine response (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The inbred mouse C57BL/6J is the reference strain for genome sequence and for most behavioral and physiological phenotypes. However, the International Knockout Mouse Consortium uses an embryonic stem cell line derived from a related C57BL/6N substrain. We found that C57BL/6N has a lower acute and sensitized response to cocaine and methamphetamine. We mapped a single causative locus and identified a nonsynonymous mutation of serine to phenylalanine (S968F) in Cytoplasmic FMRP interacting protein 2 (Cyfip2) as the causative variant. The S968F mutation destabilizes CYFIP2, and deletion of the C57BL/6N mutant allele leads to acute and sensitized cocaine-response phenotypes. We propose that CYFIP2 is a key regulator of cocaine response in mammals and present a framework to use mouse substrains to identify previously unknown genes and alleles regulating behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4500108/" 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/PMC4500108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Vivek -- Kim, Kyungin -- Joseph, Chryshanthi -- Kourrich, Said -- Yoo, Seung-Hee -- Huang, Hung Chung -- Vitaterna, Martha H -- de Villena, Fernando Pardo-Manuel -- Churchill, Gary -- Bonci, Antonello -- Takahashi, Joseph S -- F32 DA024556/DA/NIDA NIH HHS/ -- F32DA024556/DA/NIDA NIH HHS/ -- U01 MH061915/MH/NIMH NIH HHS/ -- U01MH61915/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1508-12. doi: 10.1126/science.1245503.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357318" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Central Nervous System Stimulants/administration & dosage ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*genetics/*psychology ; *Drug-Seeking Behavior ; Methamphetamine/administration & dosage ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Mutation ; Nerve Tissue Proteins/genetics/*physiology ; Phenylalanine/genetics ; Polymorphism, Single Nucleotide ; Psychomotor Performance/drug effects ; Quantitative Trait Loci ; Serine/genetics
    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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  • 7
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    A directional switch of integrin signalling and a new anti-thrombotic strategy (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-10-29
    Description: Integrins have a critical role in thrombosis and haemostasis. Antagonists of the platelet integrin alphaIIbbeta3 are potent anti-thrombotic drugs, but also have the life-threatening adverse effect of causing bleeding. It is therefore desirable to develop new antagonists that do not cause bleeding. Integrins transmit signals bidirectionally. Inside-out signalling activates integrins through a talin-dependent mechanism. Integrin ligation mediates thrombus formation and outside-in signalling, which requires Galpha13 and greatly expands thrombi. Here we show that Galpha13 and talin bind to mutually exclusive but distinct sites within the integrin beta3 cytoplasmic domain in opposing waves. The first talin-binding wave mediates inside-out signalling and also ligand-induced integrin activation, but is not required for outside-in signalling. Integrin ligation induces transient talin dissociation and Galpha13 binding to an EXE motif (in which X denotes any residue), which selectively mediates outside-in signalling and platelet spreading. The second talin-binding wave is associated with clot retraction. An EXE-motif-based inhibitor of Galpha13-integrin interaction selectively abolishes outside-in signalling without affecting integrin ligation, and suppresses occlusive arterial thrombosis without affecting bleeding time. Thus, we have discovered a new mechanism for the directional switch of integrin signalling and, on the basis of this mechanism, designed a potent new anti-thrombotic drug that does not cause bleeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823815/" 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/PMC3823815/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Bo -- Zhao, Xiaojuan -- O'Brien, Kelly A -- Stojanovic-Terpo, Aleksandra -- Delaney, M Keegan -- Kim, Kyungho -- Cho, Jaehyung -- Lam, Stephen C-T -- Du, Xiaoping -- HL062350/HL/NHLBI NIH HHS/ -- HL080264/HL/NHLBI NIH HHS/ -- HL109439/HL/NHLBI NIH HHS/ -- R01 HL080264/HL/NHLBI NIH HHS/ -- R01 HL109439/HL/NHLBI NIH HHS/ -- T32 HL007829/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Nov 7;503(7474):131-5. doi: 10.1038/nature12613. Epub 2013 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, Illinois 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24162846" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Antithrombins/adverse effects/*pharmacology/therapeutic use ; Binding Sites ; Bleeding Time ; *Cell Polarity ; Cytoplasm/metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/metabolism ; Hemorrhage/chemically induced ; Humans ; Integrin beta3/chemistry/genetics/metabolism ; Integrins/chemistry/deficiency/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Signal Transduction/*drug effects ; Talin/metabolism ; Thrombosis/*drug therapy/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)
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  • 8
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    PDGF signalling controls age-dependent proliferation in pancreatic beta-cells (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-14
    Description: Determining the signalling pathways that direct tissue expansion is a principal goal of regenerative biology. Vigorous pancreatic beta-cell replication in juvenile mice and humans declines with age, and elucidating the basis for this decay may reveal strategies for inducing beta-cell expansion, a long-sought goal for diabetes therapy. Here we show that platelet-derived growth factor receptor (Pdgfr) signalling controls age-dependent beta-cell proliferation in mouse and human pancreatic islets. With age, declining beta-cell Pdgfr levels were accompanied by reductions in beta-cell enhancer of zeste homologue 2 (Ezh2) levels and beta-cell replication. Conditional inactivation of the Pdgfra gene in beta-cells accelerated these changes, preventing mouse neonatal beta-cell expansion and adult beta-cell regeneration. Targeted human PDGFR-alpha activation in mouse beta-cells stimulated Erk1/2 phosphorylation, leading to Ezh2-dependent expansion of adult beta-cells. Adult human islets lack PDGF signalling competence, but exposure of juvenile human islets to PDGF-AA stimulated beta-cell proliferation. The discovery of a conserved pathway controlling age-dependent beta-cell proliferation indicates new strategies for beta-cell expansion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3503246/" 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/PMC3503246/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Hainan -- Gu, Xueying -- Liu, Yinghua -- Wang, Jing -- Wirt, Stacey E -- Bottino, Rita -- Schorle, Hubert -- Sage, Julien -- Kim, Seung K -- R01 CA114102/CA/NCI NIH HHS/ -- R01 DK056709/DK/NIDDK NIH HHS/ -- R01 DK072184/DK/NIDDK NIH HHS/ -- R01 DK075919/DK/NIDDK NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- U01 DK089532/DK/NIDDK NIH HHS/ -- U01 DK89532/DK/NIDDK NIH HHS/ -- U01 DK89572/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Oct 12;478(7369):349-55. doi: 10.1038/nature10502.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, 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/21993628" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Proliferation ; Cells, Cultured ; Diabetes Mellitus, Experimental/pathology ; E2F Transcription Factors/metabolism ; Female ; Gene Expression Regulation, Enzymologic ; Gene Knockout Techniques ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Insulin-Secreting Cells/*cytology/enzymology/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Polycomb Repressive Complex 2 ; Receptors, Platelet-Derived Growth Factor/*metabolism ; Retinoblastoma Protein/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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  • 9
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    Epigenetic memory in induced pluripotent stem cells (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-07-21
    Description: Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150836/" 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/PMC3150836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, K -- Doi, A -- Wen, B -- Ng, K -- Zhao, R -- Cahan, P -- Kim, J -- Aryee, M J -- Ji, H -- Ehrlich, L I R -- Yabuuchi, A -- Takeuchi, A -- Cunniff, K C -- Hongguang, H -- McKinney-Freeman, S -- Naveiras, O -- Yoon, T J -- Irizarry, R A -- Jung, N -- Seita, J -- Hanna, J -- Murakami, P -- Jaenisch, R -- Weissleder, R -- Orkin, S H -- Weissman, I L -- Feinberg, A P -- Daley, G Q -- CA86065/CA/NCI NIH HHS/ -- DP1 OD000256/OD/NIH HHS/ -- DP1 OD000256-01/OD/NIH HHS/ -- HL099999/HL/NHLBI NIH HHS/ -- K99 HL093212/HL/NHLBI NIH HHS/ -- K99 HL093212-01/HL/NHLBI NIH HHS/ -- K99 HL093212-02/HL/NHLBI NIH HHS/ -- K99HL093212-01/HL/NHLBI NIH HHS/ -- P50HG003233/HG/NHGRI NIH HHS/ -- R01 CA086065/CA/NCI NIH HHS/ -- R01 DK059279/DK/NIDDK NIH HHS/ -- R01 DK059279-02/DK/NIDDK NIH HHS/ -- R01 DK059279-10/DK/NIDDK NIH HHS/ -- R01 DK070055/DK/NIDDK NIH HHS/ -- R01 DK070055-01/DK/NIDDK NIH HHS/ -- R01 GM083084/GM/NIGMS NIH HHS/ -- R01 GM083084-04/GM/NIGMS NIH HHS/ -- R01-DK59279/DK/NIDDK NIH HHS/ -- R01-DK70055/DK/NIDDK NIH HHS/ -- R01AI047457/AI/NIAID NIH HHS/ -- R01AI047458/AI/NIAID NIH HHS/ -- R37 HD045022/HD/NICHD NIH HHS/ -- R37CA054358/CA/NCI NIH HHS/ -- RC2 HL102815/HL/NHLBI NIH HHS/ -- RC2 HL102815-01/HL/NHLBI NIH HHS/ -- RC2-HL102815/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 16;467(7313):285-90. doi: 10.1038/nature09342.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Transplantation Program, Division of Pediatric Hematology/Oncology, Manton Center for Orphan Disease Research, Howard Hughes Medical Institute, Children's Hospital Boston and 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/20644535" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Cellular Reprogramming/genetics ; DNA Methylation/genetics ; Embryonic Stem Cells/cytology/metabolism ; *Epigenesis, Genetic ; Genome/genetics ; Hematopoietic Stem Cells/cytology/metabolism ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Nuclear Transfer Techniques ; Transcription Factors/genetics/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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  • 10
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    Widespread transcription at neuronal activity-regulated enhancers (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-16
    Description: We used genome-wide sequencing methods to study stimulus-dependent enhancer function in mouse cortical neurons. We identified approximately 12,000 neuronal activity-regulated enhancers that are bound by the general transcriptional co-activator CBP in an activity-dependent manner. A function of CBP at enhancers may be to recruit RNA polymerase II (RNAPII), as we also observed activity-regulated RNAPII binding to thousands of enhancers. Notably, RNAPII at enhancers transcribes bi-directionally a novel class of enhancer RNAs (eRNAs) within enhancer domains defined by the presence of histone H3 monomethylated at lysine 4. The level of eRNA expression at neuronal enhancers positively correlates with the level of messenger RNA synthesis at nearby genes, suggesting that eRNA synthesis occurs specifically at enhancers that are actively engaged in promoting mRNA synthesis. These findings reveal that a widespread mechanism of enhancer activation involves RNAPII binding and eRNA synthesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020079/" 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/PMC3020079/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Tae-Kyung -- Hemberg, Martin -- Gray, Jesse M -- Costa, Allen M -- Bear, Daniel M -- Wu, Jing -- Harmin, David A -- Laptewicz, Mike -- Barbara-Haley, Kellie -- Kuersten, Scott -- Markenscoff-Papadimitriou, Eirene -- Kuhl, Dietmar -- Bito, Haruhiko -- Worley, Paul F -- Kreiman, Gabriel -- Greenberg, Michael E -- DP2OD006461/OD/NIH HHS/ -- MH-053608/MH/NIMH NIH HHS/ -- NS028829/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P30 HD018655-25/HD/NICHD NIH HHS/ -- P30 HD018655-26/HD/NICHD NIH HHS/ -- P30 HD018655-27/HD/NICHD NIH HHS/ -- R01 NS028829/NS/NINDS NIH HHS/ -- R21EY019710/EY/NEI NIH HHS/ -- R37 NS028829/NS/NINDS NIH HHS/ -- R37 NS028829-12/NS/NINDS NIH HHS/ -- R37 NS028829-13/NS/NINDS NIH HHS/ -- R37 NS028829-14/NS/NINDS NIH HHS/ -- R37 NS028829-15/NS/NINDS NIH HHS/ -- R37 NS028829-16/NS/NINDS NIH HHS/ -- R37 NS028829-17/NS/NINDS NIH HHS/ -- England -- Nature. 2010 May 13;465(7295):182-7. doi: 10.1038/nature09033. Epub 2010 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; CREB-Binding Protein/metabolism ; Consensus Sequence/genetics ; Cytoskeletal Proteins/genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/*genetics ; Genes, Reporter ; Genes, fos/genetics ; Histones/metabolism ; Methylation ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/genetics ; Neurons/*metabolism ; RNA Polymerase II/metabolism ; RNA, Untranslated/biosynthesis/genetics ; Transcription, 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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