ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Female  (135)
  • Cell Line  (73)
  • Instrumentation and Photography
  • American Association for the Advancement of Science (AAAS)  (200)
  • 2000-2004  (200)
  • 2004  (76)
  • 2001  (71)
  • 2000  (53)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (200)
Years
  • 2000-2004  (200)
Year
  • 2004  (76)
  • 2001  (71)
  • 2000  (53)
  • 2003  (68)
  • 2002  (69)
  • 11
    facet.materialart.
    Unknown
    T cell activation by lipopeptide antigens (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-24
    Description: Unlike major histocompatibility proteins, which bind peptides, CD1 proteins display lipid antigens to T cells. Here, we report that CD1a presents a family of previously unknown lipopeptides from Mycobacterium tuberculosis, named didehydroxymycobactins because of their structural relation to mycobactin siderophores. T cell activation was mediated by the alphabeta T cell receptors and was specific for structure of the acyl and peptidic components of these antigens. These studies identify a means of intracellular pathogen detection and identify lipopeptides as a biochemical class of antigens for T cells, which, like conventional peptides, have a potential for marked structural diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, D Branch -- Young, David C -- Cheng, Tan-Yun -- Rosat, Jean-Pierre -- Roura-Mir, Carme -- O'Connor, Peter B -- Zajonc, Dirk M -- Walz, Andrew -- Miller, Marvin J -- Levery, Steven B -- Wilson, Ian A -- Costello, Catherine E -- Brenner, Michael B -- AI30988/AI/NIAID NIH HHS/ -- AI50216/AI/NIAID NIH HHS/ -- AR48632/AR/NIAMS NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- GM25845/GM/NIGMS NIH HHS/ -- GM62116/GM/NIGMS NIH HHS/ -- P20 RR16459/RR/NCRR NIH HHS/ -- P41-RR10888/RR/NCRR NIH HHS/ -- S10-RR10493/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 23;303(5657):527-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Smith Building Room 514, 1 Jimmy Fund Way, Boston, MA 02115, USA. bmoody@rics.bwh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14739458" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigen Presentation ; Antigens, Bacterial/chemistry/*immunology/metabolism ; Antigens, CD1/chemistry/immunology/metabolism ; Cell Line ; Chromatography, High Pressure Liquid ; Humans ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Hydroxylation ; Lipoproteins/chemistry/*immunology/metabolism ; *Lymphocyte Activation ; Models, Molecular ; Mycobacterium tuberculosis/growth & development/*immunology ; Oxazoles/chemistry/*immunology/metabolism ; Protein Conformation ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 12
    facet.materialart.
    Unknown
    Breast cancer risks for BRCA1/2 carriers (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Easton, Douglas F -- Hopper, John L -- Thomas, Duncan C -- Antoniou, Antonis -- Pharoah, Paul D P -- Whittemore, Alice S -- Haile, Robert W -- New York, N.Y. -- Science. 2004 Dec 24;306(5705):2187-91; author reply 2187-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15622557" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Neoplasms/epidemiology/*genetics ; Female ; *Genes, BRCA1 ; *Genes, BRCA2 ; *Genetic Predisposition to Disease ; Heterozygote ; Humans ; Jews/genetics ; Middle Aged ; Mutation ; Penetrance ; Risk ; Selection Bias
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 13
    facet.materialart.
    Unknown
    Effects of environment on compensatory mutations to ameliorate costs of antibiotic resistance (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; *Antiporters ; Carrier Proteins/genetics ; Culture Media ; Drug Resistance, Microbial/*genetics ; Escherichia coli Proteins ; Evolution, Molecular ; Female ; Fusidic Acid/pharmacology ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; *Mutation ; Peptide Elongation Factor G/genetics ; Ribosomal Proteins/genetics ; Salmonella typhimurium/*drug effects/*genetics/growth & development/metabolism ; Selection, Genetic ; Serial Passage ; Streptomycin/pharmacology ; Suppression, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 14
    facet.materialart.
    Unknown
    Insect population control using a dominant, repressible, lethal genetic system (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: A major modification to the sterile insect technique is described, in which transgenic insects homozygous for a dominant, repressible, female-specific lethal gene system are used. We demonstrate two methods that give the required genetic characteristics in an otherwise wild-type genetic background. The first system uses a sex-specific promoter or enhancer to drive the expression of a repressible transcription factor, which in turn controls the expression of a toxic gene product. The second system uses non-sex-specific expression of the repressible transcription factor to regulate a selectively lethal gene product. Both methods work efficiently in Drosophila melanogaster, and we expect these principles to be widely applicable to more economically important organisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomas, D D -- Donnelly, C A -- Wood, R J -- Alphey, L S -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2474-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Wellcome Trust Centre for the Epidemiology of Infectious Disease, Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741964" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Crosses, Genetic ; DNA-Binding Proteins ; *Drosophila Proteins ; Drosophila melanogaster/*genetics ; Egg Proteins/genetics ; Enhancer Elements, Genetic ; Fat Body/metabolism ; Female ; Gene Expression Regulation ; *Genes, Dominant ; *Genes, Insect ; *Genes, Lethal ; Genes, ras ; Homozygote ; Male ; Models, Biological ; Nuclear Proteins/genetics ; *Pest Control, Biological ; Promoter Regions, Genetic ; Tetracycline/pharmacology ; Trans-Activators/genetics ; Transcription Factors/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 15
    facet.materialart.
    Unknown
    Requirement of the inositol trisphosphate receptor for activation of store-operated Ca2+ channels (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-04
    Description: The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+ signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rs mediate both SOC and TRP channel opening and that the InsP3R is essential for maintaining coupling between store emptying and physiological activation of SOCs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, H T -- Patterson, R L -- van Rossum, D B -- Birnbaumer, L -- Mikoshiba, K -- Gill, D L -- AR07592/AR/NIAMS NIH HHS/ -- HL55426/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 3;287(5458):1647-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10698739" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Boron Compounds/pharmacology ; Calcium/*metabolism ; Calcium Channels/chemistry/*metabolism ; *Calcium Signaling ; Carbachol/pharmacology ; Cell Line ; Cell Membrane/metabolism ; Diglycerides/metabolism/pharmacology ; Endoplasmic Reticulum/*metabolism ; Enzyme Inhibitors/pharmacology ; Humans ; Inositol 1,4,5-Trisphosphate Receptors ; Ionomycin/pharmacology ; Macrocyclic Compounds ; Oxazoles/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/*metabolism ; Strontium/metabolism ; TRPC Cation Channels ; Thapsigargin/pharmacology ; Transfection ; Type C Phospholipases/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 16
    facet.materialart.
    Unknown
    An fMRI investigation of emotional engagement in moral judgment (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-15
    Description: The long-standing rationalist tradition in moral psychology emphasizes the role of reason in moral judgment. A more recent trend places increased emphasis on emotion. Although both reason and emotion are likely to play important roles in moral judgment, relatively little is known about their neural correlates, the nature of their interaction, and the factors that modulate their respective behavioral influences in the context of moral judgment. In two functional magnetic resonance imaging (fMRI) studies using moral dilemmas as probes, we apply the methods of cognitive neuroscience to the study of moral judgment. We argue that moral dilemmas vary systematically in the extent to which they engage emotional processing and that these variations in emotional engagement influence moral judgment. These results may shed light on some puzzling patterns in moral judgment observed by contemporary philosophers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, J D -- Sommerville, R B -- Nystrom, L E -- Darley, J M -- Cohen, J D -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2105-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Brain, Mind, and Behavior, Department of Philosophy, 1879 Hall, Princeton University, Princeton, NJ 08544, USA. jdgreene@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557895" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiology ; Brain Mapping ; *Emotions ; Female ; Humans ; *Judgment ; *Magnetic Resonance Imaging ; Male ; Mental Processes ; *Morals ; Reaction Time
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 17
    facet.materialart.
    Unknown
    Negative regulation of neural stem/progenitor cell proliferation by the Pten tumor suppressor gene in vivo (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-11-03
    Description: The mechanisms controlling neural stem cell proliferation are poorly understood. Here we demonstrate that the PTEN tumor suppressor plays an important role in regulating neural stem/progenitor cells in vivo and in vitro. Mice lacking PTEN exhibited enlarged, histoarchitecturally abnormal brains, which resulted from increased cell proliferation, decreased cell death, and enlarged cell size. Neurosphere cultures revealed a greater proliferation capacity for tripotent Pten-/- central nervous system stem/progenitor cells, which can be attributed, at least in part, to a shortened cell cycle. However, cell fate commitments of the progenitors were largely undisturbed. Our results suggest that PTEN negatively regulates neural stem cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groszer, M -- Erickson, R -- Scripture-Adams, D D -- Lesche, R -- Trumpp, A -- Zack, J A -- Kornblum, H I -- Liu, X -- Wu, H -- MH062800-01/MH/NIMH NIH HHS/ -- NS38489/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 7;294(5549):2186-9. Epub 2001 Nov 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Medical Pharmacology, UCLA School of Medicine, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11691952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Astrocytes/cytology ; Brain/abnormalities/*cytology/embryology ; Cell Count ; Cell Differentiation ; *Cell Division ; Cell Lineage ; Cell Size ; Cells, Cultured ; Female ; Flow Cytometry ; Fluoresceins/metabolism ; Gene Deletion ; Intermediate Filament Proteins/metabolism ; Male ; Mice ; Mice, Knockout ; *Nerve Tissue Proteins ; Nestin ; Neurons/*cytology ; PTEN Phosphohydrolase ; Phosphoric Monoester Hydrolases/*genetics/*physiology ; Stem Cells/*cytology ; Succinimides/metabolism ; Tumor Suppressor Proteins/*genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 18
    facet.materialart.
    Unknown
    BAFF-R, a newly identified TNF receptor that specifically interacts with BAFF (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-18
    Description: B cell homeostasis has been shown to critically depend on BAFF, the B cell activation factor from the tumor necrosis factor (TNF) family. Although BAFF is already known to bind two receptors, BCMA and TACI, we have identified a third receptor for BAFF that we have termed BAFF-R. BAFF-R binding appears to be highly specific for BAFF, suggesting a unique role for this ligand-receptor interaction. Consistent with this, the BAFF-R locus is disrupted in A/WySnJ mice, which display a B cell phenotype qualitatively similar to that of the BAFF-deficient mice. Thus, BAFF-R appears to be the principal receptor for BAFF-mediated mature B cell survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, J S -- Bixler, S A -- Qian, F -- Vora, K -- Scott, M L -- Cachero, T G -- Hession, C -- Schneider, P -- Sizing, I D -- Mullen, C -- Strauch, K -- Zafari, M -- Benjamin, C D -- Tschopp, J -- Browning, J L -- Ambrose, C -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2108-11. Epub 2001 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen, 12 Cambridge Center, Cambridge, MA 02142, USA., The Institute of Biochemistry, University of Lausanne, CH-1066, Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11509692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Cell Maturation Antigen ; B-Lymphocytes/immunology/metabolism/*physiology ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 22 ; Cloning, Molecular ; Homeostasis ; Humans ; Ligands ; Lymphoid Tissue/metabolism ; Male ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Molecular Sequence Data ; RNA, Messenger/chemistry/genetics/metabolism ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Transmembrane Activator and CAML Interactor Protein ; Tumor Necrosis Factor-alpha/*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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 19
    facet.materialart.
    Unknown
    Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-04-09
    Description: The Drosophila melanogaster gene chico encodes an insulin receptor substrate that functions in an insulin/insulin-like growth factor (IGF) signaling pathway. In the nematode Caenorhabditis elegans, insulin/IGF signaling regulates adult longevity. We found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes. Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance. The dwarf phenotype of chico homozygotes was also unnecessary for extension of life-span. The role of insulin/IGF signaling in regulating animal aging is therefore evolutionarily conserved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clancy, D J -- Gems, D -- Harshman, L G -- Oldham, S -- Stocker, H -- Hafen, E -- Leevers, S J -- Partridge, L -- New York, N.Y. -- Science. 2001 Apr 6;292(5514):104-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University College London, Wolfson House, 4 Stephenson Way, London NW1 2HE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11292874" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Alleles ; Animals ; Body Constitution ; Carrier Proteins/genetics/metabolism ; Crosses, Genetic ; *Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Female ; Fertility ; Genes, Insect ; Heterozygote ; Hot Temperature ; Insect Proteins/*genetics/*metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins ; *Intracellular Signaling Peptides and Proteins ; Longevity/*physiology ; Male ; Mutation ; Oxidative Stress ; Protein-Tyrosine Kinases/genetics/metabolism ; *Receptor Protein-Tyrosine Kinases ; Receptor, Insulin/*metabolism ; Reproduction ; Signal Transduction ; Somatomedins/metabolism ; Starvation ; Superoxide Dismutase
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 20
    facet.materialart.
    Unknown
    Epigenetic instability in ES cells and cloned mice (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-07
    Description: Cloning by nuclear transfer (NT) is an inefficient process in which most clones die before birth and survivors often display growth abnormalities. In an effort to correlate gene expression with survival and fetal overgrowth, we have examined imprinted gene expression in both mice cloned by nuclear transfer and in the embryonic stem (ES) cell donor populations from which they were derived. The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome. These data imply that even apparently normal cloned animals may have subtle abnormalities in gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Humpherys, D -- Eggan, K -- Akutsu, H -- Hochedlinger, K -- Rideout , W M 3rd -- Biniszkiewicz, D -- Yanagimachi, R -- Jaenisch, R -- 5-R35-CA44339/CA/NCI NIH HHS/ -- R01-CA84198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 6;293(5527):95-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11441181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Birth Weight ; Cell Nucleus/*genetics ; Cesarean Section ; *Cloning, Organism/methods ; Congenital Abnormalities/genetics ; DNA Methylation ; Embryo Loss/genetics ; Embryo Transfer ; Embryo, Mammalian/*cytology/metabolism ; Female ; Fetal Death/genetics ; *Gene Expression Regulation, Developmental ; Gene Silencing ; Genomic Imprinting/*genetics ; Mice ; Oocytes/metabolism ; Placenta/metabolism ; Placentation ; Polyploidy ; Pregnancy ; RNA, Messenger/genetics/metabolism ; Respiration ; Stem Cells/*cytology/*metabolism ; Survival Rate
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...