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  • 1
    Publication Date: 2008-04-11
    Description: Energy and glucose homeostasis are regulated by food intake and liver glucose production, respectively. The upper intestine has a critical role in nutrient digestion and absorption. However, studies indicate that upper intestinal lipids inhibit food intake as well in rodents and humans by the activation of an intestine-brain axis. In parallel, a brain-liver axis has recently been proposed to detect blood lipids to inhibit glucose production in rodents. Thus, we tested the hypothesis that upper intestinal lipids activate an intestine-brain-liver neural axis to regulate glucose homeostasis. Here we demonstrate that direct administration of lipids into the upper intestine increased upper intestinal long-chain fatty acyl-coenzyme A (LCFA-CoA) levels and suppressed glucose production. Co-infusion of the acyl-CoA synthase inhibitor triacsin C or the anaesthetic tetracaine with duodenal lipids abolished the inhibition of glucose production, indicating that upper intestinal LCFA-CoAs regulate glucose production in the preabsorptive state. Subdiaphragmatic vagotomy or gut vagal deafferentation interrupts the neural connection between the gut and the brain, and blocks the ability of upper intestinal lipids to inhibit glucose production. Direct administration of the N-methyl-d-aspartate ion channel blocker MK-801 into the fourth ventricle or the nucleus of the solitary tract where gut sensory fibres terminate abolished the upper-intestinal-lipid-induced inhibition of glucose production. Finally, hepatic vagotomy negated the inhibitory effects of upper intestinal lipids on glucose production. These findings indicate that upper intestinal lipids activate an intestine-brain-liver neural axis to inhibit glucose production, and thereby reveal a previously unappreciated pathway that regulates glucose homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Penny Y T -- Caspi, Liora -- Lam, Carol K L -- Chari, Madhu -- Li, Xiaosong -- Light, Peter E -- Gutierrez-Juarez, Roger -- Ang, Michelle -- Schwartz, Gary J -- Lam, Tony K T -- DK45024/DK/NIDDK NIH HHS/ -- DK47208/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):1012-6. doi: 10.1038/nature06852. Epub 2008 Apr 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Toronto General Hospital Research Institute, University Health Network, Toronto M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18401341" target="_blank"〉PubMed〈/a〉
    Keywords: Acyl Coenzyme A/biosynthesis/metabolism ; Animals ; Brain/drug effects/*metabolism ; Dietary Fats/administration & dosage/metabolism/*pharmacology ; Fatty Acids/chemistry/metabolism ; Glucose/*biosynthesis/metabolism ; Homeostasis/drug effects ; Insulin/metabolism ; Intestines/drug effects/innervation/*metabolism ; *Lipid Metabolism ; Liver/drug effects/innervation/*metabolism ; Rats ; Satiety Response/drug effects ; Tetracaine/pharmacology ; Triazenes/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2008-06-20
    Description: Lancelets ('amphioxus') are the modern survivors of an ancient chordate lineage, with a fossil record dating back to the Cambrian period. Here we describe the structure and gene content of the highly polymorphic approximately 520-megabase genome of the Florida lancelet Branchiostoma floridae, and analyse it in the context of chordate evolution. Whole-genome comparisons illuminate the murky relationships among the three chordate groups (tunicates, lancelets and vertebrates), and allow not only reconstruction of the gene complement of the last common chordate ancestor but also partial reconstruction of its genomic organization, as well as a description of two genome-wide duplications and subsequent reorganizations in the vertebrate lineage. These genome-scale events shaped the vertebrate genome and provided additional genetic variation for exploitation during vertebrate evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putnam, Nicholas H -- Butts, Thomas -- Ferrier, David E K -- Furlong, Rebecca F -- Hellsten, Uffe -- Kawashima, Takeshi -- Robinson-Rechavi, Marc -- Shoguchi, Eiichi -- Terry, Astrid -- Yu, Jr-Kai -- Benito-Gutierrez, E Lia -- Dubchak, Inna -- Garcia-Fernandez, Jordi -- Gibson-Brown, Jeremy J -- Grigoriev, Igor V -- Horton, Amy C -- de Jong, Pieter J -- Jurka, Jerzy -- Kapitonov, Vladimir V -- Kohara, Yuji -- Kuroki, Yoko -- Lindquist, Erika -- Lucas, Susan -- Osoegawa, Kazutoyo -- Pennacchio, Len A -- Salamov, Asaf A -- Satou, Yutaka -- Sauka-Spengler, Tatjana -- Schmutz, Jeremy -- Shin-I, Tadasu -- Toyoda, Atsushi -- Bronner-Fraser, Marianne -- Fujiyama, Asao -- Holland, Linda Z -- Holland, Peter W H -- Satoh, Nori -- Rokhsar, Daniel S -- BBS/B/12067/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/12067/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Jun 19;453(7198):1064-71. doi: 10.1038/nature06967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18563158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chordata/classification/*genetics ; Conserved Sequence ; DNA Transposable Elements/genetics ; *Evolution, Molecular ; Gene Duplication ; Genes/genetics ; Genetic Linkage ; Genome/*genetics ; Humans ; Introns/genetics ; Karyotyping ; Multigene Family ; Phylogeny ; Polymorphism, Genetic/genetics ; Proteins/genetics ; Synteny ; Time Factors ; Vertebrates/classification/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-12-17
    Description: To provide context for the diversification of archosaurs--the group that includes crocodilians, dinosaurs, and birds--we generated draft genomes of three crocodilians: Alligator mississippiensis (the American alligator), Crocodylus porosus (the saltwater crocodile), and Gavialis gangeticus (the Indian gharial). We observed an exceptionally slow rate of genome evolution within crocodilians at all levels, including nucleotide substitutions, indels, transposable element content and movement, gene family evolution, and chromosomal synteny. When placed within the context of related taxa including birds and turtles, this suggests that the common ancestor of all of these taxa also exhibited slow genome evolution and that the comparatively rapid evolution is derived in birds. The data also provided the opportunity to analyze heterozygosity in crocodilians, which indicates a likely reduction in population size for all three taxa through the Pleistocene. Finally, these data combined with newly published bird genomes allowed us to reconstruct the partial genome of the common ancestor of archosaurs, thereby providing a tool to investigate the genetic starting material of crocodilians, birds, and dinosaurs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4386873/" 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/PMC4386873/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Richard E -- Braun, Edward L -- Armstrong, Joel -- Earl, Dent -- Nguyen, Ngan -- Hickey, Glenn -- Vandewege, Michael W -- St John, John A -- Capella-Gutierrez, Salvador -- Castoe, Todd A -- Kern, Colin -- Fujita, Matthew K -- Opazo, Juan C -- Jurka, Jerzy -- Kojima, Kenji K -- Caballero, Juan -- Hubley, Robert M -- Smit, Arian F -- Platt, Roy N -- Lavoie, Christine A -- Ramakodi, Meganathan P -- Finger, John W Jr -- Suh, Alexander -- Isberg, Sally R -- Miles, Lee -- Chong, Amanda Y -- Jaratlerdsiri, Weerachai -- Gongora, Jaime -- Moran, Christopher -- Iriarte, Andres -- McCormack, John -- Burgess, Shane C -- Edwards, Scott V -- Lyons, Eric -- Williams, Christina -- Breen, Matthew -- Howard, Jason T -- Gresham, Cathy R -- Peterson, Daniel G -- Schmitz, Jurgen -- Pollock, David D -- Haussler, David -- Triplett, Eric W -- Zhang, Guojie -- Irie, Naoki -- Jarvis, Erich D -- Brochu, Christopher A -- Schmidt, Carl J -- McCarthy, Fiona M -- Faircloth, Brant C -- Hoffmann, Federico G -- Glenn, Travis C -- Gabaldon, Toni -- Paten, Benedict -- Ray, David A -- 1U41HG006992-2/HG/NHGRI NIH HHS/ -- 1U41HG007234-01/HG/NHGRI NIH HHS/ -- 5U01HG004695/HG/NHGRI NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- U41 HG006992/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1254449. doi: 10.1126/science.1254449. Epub 2014 Dec 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ed@soe.ucsc.edu david.a.ray@ttu.edu. ; Department of Biology and Genetics Institute, University of Florida, Gainesville, FL 32611, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. Center for Biomolecular Science and Engineering, University of California, Santa Cruz, CA 95064, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Biomolecular Engineering, University of California, Santa Cruz, CA 95064, USA. ; Bioinformatics and Genomics Programme, Centre for Genomic Regulation, 08003 Barcelona, Spain. Universitat Pompeu Fabra, 08003 Barcelona, Spain. ; Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, CO 80045, USA. Department of Biology, University of Texas, Arlington, TX 76019, USA. ; Department of Computer and Information Sciences, University of Delaware, Newark, DE 19717, USA. ; Department of Biology, University of Texas, Arlington, TX 76019, USA. ; Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. ; Genetic Information Research Institute, Mountain View, CA 94043, USA. ; Institute for Systems Biology, Seattle, WA 98109, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Department of Environmental Health Science, University of Georgia, Athens, GA 30602, USA. ; Institute of Experimental Pathology (ZMBE), University of Munster, D-48149 Munster, Germany. Department of Evolutionary Biology (EBC), Uppsala University, SE-752 36 Uppsala, Sweden. ; Porosus Pty. Ltd., Palmerston, NT 0831, Australia. Faculty of Veterinary Science, University of Sydney, Sydney, NSW 2006, Australia. Centre for Crocodile Research, Noonamah, NT 0837, Australia. ; Faculty of Veterinary Science, University of Sydney, Sydney, NSW 2006, Australia. ; Departamento de Desarrollo Biotecnologico, Instituto de Higiene, Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay. ; Moore Laboratory of Zoology, Occidental College, Los Angeles, CA 90041, USA. ; College of Agriculture and Life Sciences, University of Arizona, Tucson, AZ 85721, USA. ; Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. ; School of Plant Sciences, University of Arizona, Tucson, AZ 85721, USA. ; Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC 27607, USA. ; Howard Hughes Medical Institute, Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. ; Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. Department of Plant and Soil Sciences, Mississippi State University, Mississippi State, MS 39762, USA. ; Institute of Experimental Pathology (ZMBE), University of Munster, D-48149 Munster, Germany. ; Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, CO 80045, USA. ; Center for Biomolecular Science and Engineering, University of California, Santa Cruz, CA 95064, USA. Howard Hughes Medical Institute, Bethesda, MD 20814, USA. ; Department of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA. ; China National GeneBank, BGI-Shenzhen, Shenzhen, China. Center for Social Evolution, Department of Biology, University of Copenhagen, Copenhagen, Denmark. ; Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo, Japan. ; Department of Earth and Environmental Sciences, University of Iowa, Iowa City, IA 52242, USA. ; Department of Animal and Food Sciences, University of Delaware, Newark, DE 19717, USA. ; School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ 85721, USA. ; Department of Ecology and Evolutionary Biology, University of California, Los Angeles, CA 90019, USA. Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. ; Bioinformatics and Genomics Programme, Centre for Genomic Regulation, 08003 Barcelona, Spain. Universitat Pompeu Fabra, 08003 Barcelona, Spain. Institucio Catalana de Recerca i Estudis Avancats, 08010 Barcelona, Spain. ; Center for Biomolecular Science and Engineering, University of California, Santa Cruz, CA 95064, USA. ; Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, MS 39762, USA. Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University, Mississippi State, MS 39762, USA. Department of Biological Sciences, Texas Tech University, Lubbock, TX 79409, USA. ed@soe.ucsc.edu david.a.ray@ttu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504731" target="_blank"〉PubMed〈/a〉
    Keywords: Alligators and Crocodiles/classification/*genetics ; Animals ; Biological Evolution ; Birds/classification/*genetics ; Conserved Sequence ; DNA Transposable Elements ; Dinosaurs/classification/*genetics ; *Evolution, Molecular ; Genetic Variation ; *Genome ; Molecular Sequence Annotation ; Molecular Sequence Data ; Phylogeny ; Reptiles/classification/genetics ; Sequence Alignment ; Sequence Analysis, DNA ; Transcriptome
    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
    Publication Date: 2005-08-06
    Description: The brain keenly depends on glucose for energy, and mammalians have redundant systems to control glucose production. An increase in circulating glucose inhibits glucose production in the liver, but this negative feedback is impaired in type 2 diabetes. Here we report that a primary increase in hypothalamic glucose levels lowers blood glucose through inhibition of glucose production in rats. The effect of glucose requires its conversion to lactate followed by stimulation of pyruvate metabolism, which leads to activation of adenosine triphosphate (ATP)-sensitive potassium channels. Thus, interventions designed to enhance the hypothalamic sensing of glucose may improve glucose homeostasis in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Tony K T -- Gutierrez-Juarez, Roger -- Pocai, Alessandro -- Rossetti, Luciano -- AG 21654/AG/NIA NIH HHS/ -- DK 20541/DK/NIDDK NIH HHS/ -- DK 45024/DK/NIDDK NIH HHS/ -- DK 48321/DK/NIDDK NIH HHS/ -- T32-AG023475/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/metabolism ; Blood Glucose/*metabolism ; Citric Acid Cycle ; Feedback, Physiological ; Glucose/administration & dosage/*metabolism ; Glucose-6-Phosphatase/metabolism ; Hypothalamus/*metabolism ; Injections, Intraventricular ; Lactic Acid/metabolism ; Liver/*metabolism ; Male ; Neurons/metabolism ; Potassium Channels/metabolism ; Pyruvates/*metabolism ; Rats ; Rats, Sprague-Dawley
    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
    Publication Date: 2005-01-18
    Description: In mammals, hair cell loss causes irreversible hearing and balance impairment because hair cells are terminally differentiated and do not regenerate spontaneously. By profiling gene expression in developing mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of cell cycle exit in hair cells. Differentiated and functional mouse hair cells with a targeted deletion of Rb1 undergo mitosis, divide, and cycle, yet continue to become highly differentiated and functional. Moreover, acute loss of Rb1 in postnatal hair cells caused cell cycle reentry. Manipulation of the pRb pathway may ultimately lead to mammalian hair cell regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sage, Cyrille -- Huang, Mingqian -- Karimi, Kambiz -- Gutierrez, Gabriel -- Vollrath, Melissa A -- Zhang, Duan-Sun -- Garcia-Anoveros, Jaime -- Hinds, Philip W -- Corwin, Jeffrey T -- Corey, David P -- Chen, Zheng-Yi -- DC-00200/DC/NIDCD NIH HHS/ -- DC-04546/DC/NIDCD NIH HHS/ -- DC-AG20208/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1114-8. Epub 2005 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Service, MGH-HMS Center for Nervous System Repair, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653467" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Count ; Cell Cycle ; Cell Differentiation ; *Cell Proliferation ; Cell Shape ; Cochlea/cytology/embryology ; Female ; Gene Deletion ; Gene Expression Profiling ; Genes, Retinoblastoma ; Hair Cells, Auditory, Inner/*cytology/*physiology ; Mice ; Mice, Knockout ; Mitosis ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Pyridinium Compounds/metabolism ; Quaternary Ammonium Compounds/metabolism ; Regeneration ; Retinoblastoma Protein/genetics/*physiology ; Saccule and Utricle/embryology/metabolism ; Stem Cells/cytology/physiology
    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
    Publication Date: 2011-03-04
    Description: The effective use of targeted therapy is highly dependent on the identification of responder patient populations. Loss of FBW7, which encodes a tumour-suppressor protein, is frequently found in various types of human cancer, including breast cancer, colon cancer and T-cell acute lymphoblastic leukaemia (T-ALL). In line with these genomic data, engineered deletion of Fbw7 in mouse T cells results in T-ALL, validating FBW7 as a T-ALL tumour suppressor. Determining the precise molecular mechanisms by which FBW7 exerts antitumour activity is an area of intensive investigation. These mechanisms are thought to relate in part to FBW7-mediated destruction of key proteins relevant to cancer, including Jun, Myc, cyclin E and notch 1 (ref. 9), all of which have oncoprotein activity and are overexpressed in various human cancers, including leukaemia. In addition to accelerating cell growth, overexpression of Jun, Myc or notch 1 can also induce programmed cell death. Thus, considerable uncertainty surrounds how FBW7-deficient cells evade cell death in the setting of upregulated Jun, Myc and/or notch 1. Here we show that the E3 ubiquitin ligase SCF(FBW7) (a SKP1-cullin-1-F-box complex that contains FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family member, for ubiquitylation and destruction in a manner that depends on phosphorylation by glycogen synthase kinase 3. Human T-ALL cell lines showed a close relationship between FBW7 loss and MCL1 overexpression. Correspondingly, T-ALL cell lines with defective FBW7 are particularly sensitive to the multi-kinase inhibitor sorafenib but resistant to the BCL2 antagonist ABT-737. On the genetic level, FBW7 reconstitution or MCL1 depletion restores sensitivity to ABT-737, establishing MCL1 as a therapeutically relevant bypass survival mechanism that enables FBW7-deficient cells to evade apoptosis. Therefore, our work provides insight into the molecular mechanism of direct tumour suppression by FBW7 and has implications for the targeted treatment of patients with FBW7-deficient T-ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076007/" 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/PMC3076007/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inuzuka, Hiroyuki -- Shaik, Shavali -- Onoyama, Ichiro -- Gao, Daming -- Tseng, Alan -- Maser, Richard S -- Zhai, Bo -- Wan, Lixin -- Gutierrez, Alejandro -- Lau, Alan W -- Xiao, Yonghong -- Christie, Amanda L -- Aster, Jon -- Settleman, Jeffrey -- Gygi, Steven P -- Kung, Andrew L -- Look, Thomas -- Nakayama, Keiichi I -- DePinho, Ronald A -- Wei, Wenyi -- GM089763/GM/NIGMS NIH HHS/ -- R01 GM089763/GM/NIGMS NIH HHS/ -- R01 GM089763-01/GM/NIGMS NIH HHS/ -- R01 GM089763-02/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Mar 3;471(7336):104-9. doi: 10.1038/nature09732.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368833" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Apoptosis/drug effects ; Benzenesulfonates/pharmacology ; Biphenyl Compounds/pharmacology ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line, Tumor ; F-Box Proteins/genetics/*metabolism ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Myeloid Cell Leukemia Sequence 1 Protein ; Niacinamide/analogs & derivatives ; Nitrophenols/pharmacology ; Phenylurea Compounds ; Phosphorylation ; Piperazines/pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors/*chemistry/*metabolism ; Pyridines/pharmacology ; SKP Cullin F-Box Protein Ligases/*chemistry/*metabolism ; Sulfonamides/pharmacology ; Tumor Suppressor Proteins/deficiency/genetics/metabolism ; Ubiquitin-Protein Ligases/deficiency/genetics/*metabolism ; *Ubiquitination/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2012-10-30
    Description: Mutations in mitochondrial DNA (mtDNA) are associated with severe human diseases and are maternally inherited through the egg's cytoplasm. Here we investigated the feasibility of mtDNA replacement in human oocytes by spindle transfer (ST; also called spindle-chromosomal complex transfer). Of 106 human oocytes donated for research, 65 were subjected to reciprocal ST and 33 served as controls. Fertilization rate in ST oocytes (73%) was similar to controls (75%); however, a significant portion of ST zygotes (52%) showed abnormal fertilization as determined by an irregular number of pronuclei. Among normally fertilized ST zygotes, blastocyst development (62%) and embryonic stem cell isolation (38%) rates were comparable to controls. All embryonic stem cell lines derived from ST zygotes had normal euploid karyotypes and contained exclusively donor mtDNA. The mtDNA can be efficiently replaced in human oocytes. Although some ST oocytes displayed abnormal fertilization, remaining embryos were capable of developing to blastocysts and producing embryonic stem cells similar to controls.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561483/" 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/PMC3561483/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tachibana, Masahito -- Amato, Paula -- Sparman, Michelle -- Woodward, Joy -- Sanchis, Dario Melguizo -- Ma, Hong -- Gutierrez, Nuria Marti -- Tippner-Hedges, Rebecca -- Kang, Eunju -- Lee, Hyo-Sang -- Ramsey, Cathy -- Masterson, Keith -- Battaglia, David -- Lee, David -- Wu, Diana -- Jensen, Jeffrey -- Patton, Phillip -- Gokhale, Sumita -- Stouffer, Richard -- Mitalipov, Shoukhrat -- 8P51OD011092/OD/NIH HHS/ -- EY021214/EY/NEI NIH HHS/ -- HD057121/HD/NICHD NIH HHS/ -- HD059946/HD/NICHD NIH HHS/ -- HD063276/HD/NICHD NIH HHS/ -- P51 OD011092/OD/NIH HHS/ -- P51 RR000163/RR/NCRR 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/ -- England -- Nature. 2013 Jan 31;493(7434):627-31. doi: 10.1038/nature11647. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive & Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, Oregon 97006, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103867" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Nucleus/genetics ; Cryopreservation ; Cytoplasm/genetics ; DNA, Mitochondrial/analysis/genetics ; Embryo, Mammalian/embryology ; Embryonic Stem Cells/cytology ; Female ; Fertilization ; *Genetic Therapy ; Humans ; Macaca mulatta/genetics/growth & development ; Microsatellite Repeats/genetics ; Mitochondrial Diseases/*genetics/*therapy ; Nuclear Transfer Techniques/*standards ; Oocytes/cytology ; Pregnancy ; Young Adult ; Zygote/cytology/pathology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-07-11
    Description: Human pluripotent stem cells hold potential for regenerative medicine, but available cell types have significant limitations. Although embryonic stem cells (ES cells) from in vitro fertilized embryos (IVF ES cells) represent the 'gold standard', they are allogeneic to patients. Autologous induced pluripotent stem cells (iPS cells) are prone to epigenetic and transcriptional aberrations. To determine whether such abnormalities are intrinsic to somatic cell reprogramming or secondary to the reprogramming method, genetically matched sets of human IVF ES cells, iPS cells and nuclear transfer ES cells (NT ES cells) derived by somatic cell nuclear transfer (SCNT) were subjected to genome-wide analyses. Both NT ES cells and iPS cells derived from the same somatic cells contained comparable numbers of de novo copy number variations. In contrast, DNA methylation and transcriptome profiles of NT ES cells corresponded closely to those of IVF ES cells, whereas iPS cells differed and retained residual DNA methylation patterns typical of parental somatic cells. Thus, human somatic cells can be faithfully reprogrammed to pluripotency by SCNT and are therefore ideal for cell replacement therapies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Hong -- Morey, Robert -- O'Neil, Ryan C -- He, Yupeng -- Daughtry, Brittany -- Schultz, Matthew D -- Hariharan, Manoj -- Nery, Joseph R -- Castanon, Rosa -- Sabatini, Karen -- Thiagarajan, Rathi D -- Tachibana, Masahito -- Kang, Eunju -- Tippner-Hedges, Rebecca -- Ahmed, Riffat -- Gutierrez, Nuria Marti -- Van Dyken, Crystal -- Polat, Alim -- Sugawara, Atsushi -- Sparman, Michelle -- Gokhale, Sumita -- Amato, Paula -- Wolf, Don P -- Ecker, Joseph R -- Laurent, Louise C -- Mitalipov, Shoukhrat -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jul 10;511(7508):177-83. doi: 10.1038/nature13551. Epub 2014 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Embryonic Cell and Gene Therapy, Oregon Health & Science University, 3303 Southwest Bond Avenue, Portland, Oregon 97239, USA [2] Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA [3]. ; 1] Department of Reproductive Medicine, University of California, San Diego, Sanford Consortium for Regenerative Medicine, 2880 Torrey Pines Scenic Drive, La Jolla, California 92037, USA [2]. ; 1] Genomic Analysis Laboratory, the Salk Institute for Biological Studies, La Jolla, California 92037, USA [2] Bioinformatics Program, University of California at San Diego, La Jolla, California 92093, USA. ; 1] Center for Embryonic Cell and Gene Therapy, Oregon Health & Science University, 3303 Southwest Bond Avenue, Portland, Oregon 97239, USA [2] Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA. ; Genomic Analysis Laboratory, the Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Department of Reproductive Medicine, University of California, San Diego, Sanford Consortium for Regenerative Medicine, 2880 Torrey Pines Scenic Drive, La Jolla, California 92037, USA. ; 1] Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA [2] Department of Obstetrics and Gynecology, South Miyagi Medical Center, Shibata-gun, Miyagi 989-1253, Japan (M.T.); Department of Cell and Molecular Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden (A.P.). ; Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA. ; University Pathologists LLC, Boston University School of Medicine, Roger Williams Medical Center, Providence, Rhode Island 02118, USA. ; Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA. ; 1] Genomic Analysis Laboratory, the Salk Institute for Biological Studies, La Jolla, California 92037, USA [2] Howard Hughes Medical Institute, the Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; 1] Center for Embryonic Cell and Gene Therapy, Oregon Health & Science University, 3303 Southwest Bond Avenue, Portland, Oregon 97239, USA [2] Division of Reproductive and Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA [3] Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25008523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cellular Reprogramming ; Chromosome Aberrations ; Chromosomes, Human, X/genetics/metabolism ; DNA Copy Number Variations ; DNA Methylation ; Genome-Wide Association Study ; Genomic Imprinting ; Humans ; Nuclear Transfer Techniques/standards ; Pluripotent Stem Cells/cytology/*metabolism ; Transcriptome
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2012-07-06
    Description: Most leukocytes can roll along the walls of venules at low shear stress (1 dyn cm-2), but neutrophils have the ability to roll at tenfold higher shear stress in microvessels in vivo. The mechanisms involved in this shear-resistant rolling are known to involve cell flattening and pulling of long membrane tethers at the rear. Here we show that these long tethers do not retract as postulated, but instead persist and appear as 'slings' at the front of rolling cells. We demonstrate slings in a model of acute inflammation in vivo and on P-selectin in vitro, where P-selectin-glycoprotein-ligand-1 (PSGL-1) is found in discrete sticky patches whereas LFA-1 is expressed over the entire length on slings. As neutrophils roll forward, slings wrap around the rolling cells and undergo a step-wise peeling from the P-selectin substrate enabled by the failure of PSGL-1 patches under hydrodynamic forces. The 'step-wise peeling of slings' is distinct from the 'pulling of tethers' reported previously. Each sling effectively lays out a cell-autonomous adhesive substrate in front of neutrophils rolling at high shear stress during inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3433404/" 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/PMC3433404/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sundd, Prithu -- Gutierrez, Edgar -- Koltsova, Ekaterina K -- Kuwano, Yoshihiro -- Fukuda, Satoru -- Pospieszalska, Maria K -- Groisman, Alex -- Ley, Klaus -- EB02185/EB/NIBIB NIH HHS/ -- R01 EB002185/EB/NIBIB NIH HHS/ -- England -- Nature. 2012 Aug 16;488(7411):399-403. doi: 10.1038/nature11248.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22763437" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesiveness ; Animals ; Antigens, CD/metabolism ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; E-Selectin/metabolism ; Inflammation/immunology/metabolism/pathology ; Intercellular Adhesion Molecule-1/metabolism ; *Leukocyte Rolling ; Lymphocyte Function-Associated Antigen-1/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Microvessels/metabolism ; Neutrophils/*cytology/immunology/*metabolism ; P-Selectin/metabolism ; *Shear Strength ; Th1 Cells/cytology/immunology ; Venules/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2013-03-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gutierrez, Eliecer E -- Helgen, Kristofer M -- England -- Nature. 2013 Mar 21;495(7441):314. doi: 10.1038/495314e.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23518556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Classification/*methods ; Conservation of Natural Resources/*methods ; *Phylogeny
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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