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  • 1
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    Synaptic integration mediated by striatal cholinergic interneurons in basal ganglia function (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-01
    Description: The physiological role of striatal cholinergic interneurons was investigated with immunotoxin-mediated cell targeting (IMCT). Unilateral cholinergic cell ablation caused an acute abnormal turning behavior. These mice showed gradual recovery but displayed abnormal turning by both excess stimulation and inhibition of dopamine actions. In the acute phase, basal ganglia function was shifted to a hyperactive state by stimulation and suppression of striatonigral and striatopallidal neurons, respectively. D1 and D2 dopamine receptors were then down-regulated, relieving dopamine-predominant synaptic perturbation but leaving a defect in controlling dopamine responses. The acetylcholine-dopamine interaction is concertedly and adaptively regulated for basal ganglia synaptic integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaneko, S -- Hikida, T -- Watanabe, D -- Ichinose, H -- Nagatsu, T -- Kreitman, R J -- Pastan, I -- Nakanishi, S -- New York, N.Y. -- Science. 2000 Jul 28;289(5479):633-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10915629" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*metabolism ; Animals ; Apomorphine/pharmacology ; Basal Ganglia/cytology/*physiology ; Choline O-Acetyltransferase/metabolism ; Corpus Striatum/cytology/*physiology ; Dopamine/*metabolism ; Dopamine Agonists/pharmacology ; Down-Regulation ; Enkephalins/genetics/metabolism ; Immunotoxins ; Interneurons/*physiology ; Mice ; Mice, Transgenic ; Motor Activity ; Oxidopamine/pharmacology ; Posture ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism ; Receptors, Glutamate/genetics/metabolism ; Substance P/genetics/metabolism ; Synapses/metabolism/*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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  • 2
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    Independent photoreceptive circadian clocks throughout Drosophila (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Transgenic Drosophila that expressed either luciferase or green fluorescent protein driven from the promoter of the clock gene period were used to monitor the circadian clock in explanted head, thorax, and abdominal tissues. The tissues (including sensory bristles in the leg and wing) showed rhythmic bioluminescence, and the rhythms could be reset by light. The photoreceptive properties of the explanted tissues indicate that unidentified photoreceptors are likely to contribute to photic signal transduction to the clock. These results show that autonomous circadian oscillators are present throughout the body, and they suggest that individual cells in Drosophila are capable of supporting their own independent clocks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plautz, J D -- Kaneko, M -- Hall, J C -- Kay, S A -- MH-51573/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1632-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and National Science Foundation Center for Biological Timing, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Biological Clocks/*physiology ; Brain/physiology ; Chemoreceptor Cells/physiology ; Circadian Rhythm/*physiology ; Darkness ; Drosophila/genetics/*physiology ; Drosophila Proteins ; Gene Expression Regulation ; Genes, Insect ; Green Fluorescent Proteins ; Light ; Light Signal Transduction ; Luciferases/genetics ; Luminescence ; Luminescent Proteins/genetics ; Nuclear Proteins/genetics/*physiology ; Period Circadian Proteins ; Photoreceptor Cells, Invertebrate/*physiology ; Promoter Regions, Genetic ; Receptors, Cell Surface ; Recombinant Fusion Proteins
    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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    Requirement for Valpha14 NKT cells in IL-12-mediated rejection of tumors (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: A lymphocyte subpopulation, the Valpha14 natural killer T (NKT) cells, expresses both NK1.1 and a single invariant T cell receptor encoded by the Valpha14 and Jalpha281 gene segments. Mice with a deletion of the Jalpha281 gene segment were found to exclusively lack this subpopulation. The Valpha14 NKT cell-deficient mice could no longer mediate the interleukin-12 (IL-12)-induced rejection of tumors. Although the antitumor effect of IL-12 was thought to be mediated through natural killer cells and T cells, Valpha14 NKT cells were found to be an essential target of IL-12, and they mediated their cytotoxicity by an NK-like effector mechanism after activation with IL-12.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, J -- Shin, T -- Kawano, T -- Sato, H -- Kondo, E -- Toura, I -- Kaneko, Y -- Koseki, H -- Kanno, M -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1623-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Core Research for Evolutional Science and Technology (CREST) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo-ku, Chiba, Japan 260.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374462" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; *Cytotoxicity, Immunologic ; Gene Deletion ; Gene Targeting ; Genes, RAG-1 ; Genes, T-Cell Receptor alpha ; Interferon-gamma/immunology ; Interleukin-12/*immunology ; Killer Cells, Natural/*immunology ; *Macrolides ; Melanoma, Experimental/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasms, Experimental/*immunology ; Poly I-C/pharmacology ; Proton-Translocating ATPases/antagonists & inhibitors ; Receptors, Antigen, T-Cell, alpha-beta/genetics/*immunology ; T-Lymphocyte Subsets/*immunology
    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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    CD1d-restricted and TCR-mediated activation of valpha14 NKT cells by glycosylceramides (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: Natural killer T (NKT) lymphocytes express an invariant T cell antigen receptor (TCR) encoded by the Valpha14 and Jalpha281 gene segments. A glycosylceramide-containing alpha-anomeric sugar with a longer fatty acyl chain (C26) and sphingosine base (C18) was identified as a ligand for this TCR. Glycosylceramide-mediated proliferative responses of Valpha14 NKT cells were abrogated by treatment with chloroquine-concanamycin A or by monoclonal antibodies against CD1d/Vbeta8, CD40/CD40L, or B7/CTLA-4/CD28, but not by interference with the function of a transporter-associated protein. Thus, this lymphocyte shares distinct recognition systems with either T or NK cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawano, T -- Cui, J -- Koezuka, Y -- Toura, I -- Kaneko, Y -- Motoki, K -- Ueno, H -- Nakagawa, R -- Sato, H -- Kondo, E -- Koseki, H -- Taniguchi, M -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1626-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CREST (Core Research for Evolutional Science and Technology) Project, Japan Science and Technology Corporation (JST), 1-8-1 Inohana, Chuo, Chiba 260, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD1/*immunology ; Carbohydrate Conformation ; Cells, Cultured ; Ceramides/chemistry/metabolism/*pharmacology ; Cerebrosides/chemistry/metabolism/*pharmacology ; Coculture Techniques ; Galactosylceramides/chemistry/metabolism/pharmacology ; Glucosylceramides/chemistry/metabolism/pharmacology ; Killer Cells, Natural/*immunology ; Ligands ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/*immunology ; Structure-Activity Relationship ; T-Lymphocyte Subsets/*immunology
    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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    CCR3 is a target for age-related macular degeneration diagnosis and therapy (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-16
    Description: Age-related macular degeneration (AMD), a leading cause of blindness worldwide, is as prevalent as cancer in industrialized nations. Most blindness in AMD results from invasion of the retina by choroidal neovascularisation (CNV). Here we show that the eosinophil/mast cell chemokine receptor CCR3 is specifically expressed in choroidal neovascular endothelial cells in humans with AMD, and that despite the expression of its ligands eotaxin-1, -2 and -3, neither eosinophils nor mast cells are present in human CNV. Genetic or pharmacological targeting of CCR3 or eotaxins inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation because it occurred in mice lacking eosinophils or mast cells, and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor A (VEGF-A) neutralization, which is in clinical use at present, and, unlike VEGF-A blockade, is not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting might reduce vision loss due to AMD through early detection and therapeutic angioinhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712122/" 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/PMC2712122/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Atsunobu -- Baffi, Judit Z -- Kleinman, Mark E -- Cho, Won Gil -- Nozaki, Miho -- Yamada, Kiyoshi -- Kaneko, Hiroki -- Albuquerque, Romulo J C -- Dridi, Sami -- Saito, Kuniharu -- Raisler, Brian J -- Budd, Steven J -- Geisen, Pete -- Munitz, Ariel -- Ambati, Balamurali K -- Green, Martha G -- Ishibashi, Tatsuro -- Wright, John D -- Humbles, Alison A -- Gerard, Craig J -- Ogura, Yuichiro -- Pan, Yuzhen -- Smith, Justine R -- Grisanti, Salvatore -- Hartnett, M Elizabeth -- Rothenberg, Marc E -- Ambati, Jayakrishna -- AI039759/AI/NIAID NIH HHS/ -- AI45898/AI/NIAID NIH HHS/ -- DK076893/DK/NIDDK NIH HHS/ -- EY010572/EY/NEI NIH HHS/ -- EY015130/EY/NEI NIH HHS/ -- EY015422/EY/NEI NIH HHS/ -- EY017011/EY/NEI NIH HHS/ -- EY017182/EY/NEI NIH HHS/ -- EY017950/EY/NEI NIH HHS/ -- EY018350/EY/NEI NIH HHS/ -- EY018836/EY/NEI NIH HHS/ -- R01 DK076893/DK/NIDDK NIH HHS/ -- R01 EY015422/EY/NEI NIH HHS/ -- R01 EY015422-04/EY/NEI NIH HHS/ -- R01 EY018350/EY/NEI NIH HHS/ -- R01 EY018350-02/EY/NEI NIH HHS/ -- R01 EY018836/EY/NEI NIH HHS/ -- R01 EY018836-02/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jul 9;460(7252):225-30. doi: 10.1038/nature08151. Epub 2009 Jun 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology & Visual Science, University of Kentucky, Lexington, Kentucky 40506, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19525930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Chemokine CCL11/antagonists & inhibitors/metabolism ; Chemokine CCL24/antagonists & inhibitors/metabolism ; Chemokines, CC/antagonists & inhibitors/metabolism ; Choroid/blood supply/cytology/metabolism ; Choroidal Neovascularization/diagnosis/metabolism ; Disease Models, Animal ; Endothelial Cells/cytology/metabolism ; Humans ; Inflammation ; Leukocytes ; Ligands ; Macular Degeneration/*diagnosis/metabolism/*therapy ; Mice ; Mice, Inbred C57BL ; Quantum Dots ; Receptors, CCR3/analysis/*antagonists & ; inhibitors/genetics/immunology/*metabolism ; Retina/drug effects/pathology ; Vascular Endothelial Growth Factor A/antagonists & inhibitors/immunology
    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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  • 6
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    Regulation of pancreatic beta cell mass by neuronal signals from the liver (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-22
    Description: Metabolic regulation in mammals requires communication between multiple organs and tissues. The rise in the incidence of obesity and associated metabolic disorders, including type 2 diabetes, has renewed interest in interorgan communication. We used mouse models to explore the mechanism whereby obesity enhances pancreatic beta cell mass, pathophysiological compensation for insulin resistance. We found that hepatic activation of extracellular regulated kinase (ERK) signaling induced pancreatic beta cell proliferation through a neuronal-mediated relay of metabolic signals. This metabolic relay from the liver to the pancreas is involved in obesity-induced islet expansion. In mouse models of insulin-deficient diabetes, liver-selective activation of ERK signaling increased beta cell mass and normalized serum glucose levels. Thus, interorgan metabolic relay systems may serve as valuable targets in regenerative treatments for diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Imai, Junta -- Katagiri, Hideki -- Yamada, Tetsuya -- Ishigaki, Yasushi -- Suzuki, Toshinobu -- Kudo, Hirohito -- Uno, Kenji -- Hasegawa, Yutaka -- Gao, Junhong -- Kaneko, Keizo -- Ishihara, Hisamitsu -- Niijima, Akira -- Nakazato, Masamitsu -- Asano, Tomoichiro -- Minokoshi, Yasuhiko -- Oka, Yoshitomo -- New York, N.Y. -- Science. 2008 Nov 21;322(5905):1250-4. doi: 10.1126/science.1163971.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19023081" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Central Nervous System/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Hyperplasia ; Insulin/metabolism ; Insulin Resistance ; Insulin-Secreting Cells/*metabolism/pathology ; Liver/*metabolism ; MAP Kinase Kinase 1/*metabolism ; *MAP Kinase Signaling System ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/*metabolism ; Obesity/*metabolism ; Pancreas/innervation ; Recombinant Proteins/metabolism ; Vagus Nerve/cytology/metabolism ; Xenopus
    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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    Essential role of Fkbp6 in male fertility and homologous chromosome pairing in meiosis (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-24
    Description: Meiosis is a critical stage of gametogenesis in which alignment and synapsis of chromosomal pairs occur, allowing for the recombination of maternal and paternal genomes. Here we show that FK506 binding protein (Fkbp6) localizes to meiotic chromosome cores and regions of homologous chromosome synapsis. Targeted inactivation of Fkbp6 in mice results in aspermic males and the absence of normal pachytene spermatocytes. Moreover, we identified the deletion of Fkbp6 exon 8 as the causative mutation in spontaneously male sterile as/as mutant rats. Loss of Fkbp6 results in abnormal pairing and misalignments between homologous chromosomes, nonhomologous partner switches, and autosynapsis of X chromosome cores in meiotic spermatocytes. Fertility and meiosis are normal in Fkbp6 mutant females. Thus, Fkbp6 is a component of the synaptonemal complex essential for sex-specific fertility and for the fidelity of homologous chromosome pairing in meiosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882960/" 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/PMC2882960/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crackower, Michael A -- Kolas, Nadine K -- Noguchi, Junko -- Sarao, Renu -- Kikuchi, Kazuhiro -- Kaneko, Hiroyuki -- Kobayashi, Eiji -- Kawai, Yasuhiro -- Kozieradzki, Ivona -- Landers, Rushin -- Mo, Rong -- Hui, Chi-Chung -- Nieves, Edward -- Cohen, Paula E -- Osborne, Lucy R -- Wada, Teiji -- Kunieda, Tetsuo -- Moens, Peter B -- Penninger, Josef M -- 38103/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2003 May 23;300(5623):1291-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), c/o Dr. Bohrgasse 7, 1030, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12764197" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis ; Chromosome Pairing/*physiology ; Cloning, Molecular ; Exons ; Female ; Fertility/*physiology ; Gene Targeting ; Humans ; Infertility, Male/genetics/*physiopathology ; Male ; *Meiosis ; Mice ; Molecular Sequence Data ; Mutation ; Nuclear Proteins/genetics/metabolism ; Oogenesis ; Ovary/physiology ; Prophase ; Rats ; Sequence Deletion ; Spermatids/physiology ; Spermatocytes/physiology/ultrastructure ; Spermatogenesis ; Synaptonemal Complex/*physiology ; Tacrolimus Binding Proteins/chemistry/*genetics/*physiology ; Testis/physiology ; X Chromosome/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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  • 8
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    Stable SNPs in malaria antigen genes in isolated populations (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanabe, K -- Sakihama, N -- Kaneko, A -- New York, N.Y. -- Science. 2004 Jan 23;303(5657):493.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Osaka Institute of Technology, Osaka 535-8585, Japan. kztanabe@ge.oit.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14739451" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Antigens, Protozoan/chemistry/*genetics ; Antimalarials/pharmacology ; Chloroquine/pharmacology ; Drug Resistance ; Epitopes/genetics ; Genes, Protozoan ; Geography ; Haplotypes ; Humans ; Malaria, Falciparum/parasitology ; Membrane Proteins/chemistry/genetics ; Membrane Transport Proteins ; Merozoite Surface Protein 1/chemistry/genetics ; Molecular Sequence Data ; Plasmodium falciparum/drug effects/*genetics/*immunology ; *Polymorphism, Single Nucleotide ; Protozoan Proteins/chemistry/genetics ; Repetitive Sequences, Nucleic Acid ; Tandem Repeat Sequences ; Vanuatu
    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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  • 9
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    Faithful expression of imprinted genes in cloned mice (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inoue, Kimiko -- Kohda, Takashi -- Lee, Jiyoung -- Ogonuki, Narumi -- Mochida, Keiji -- Noguchi, Yoko -- Tanemura, Kentaro -- Kaneko-Ishino, Tomoko -- Ishino, Fumitoshi -- Ogura, Atsuo -- New York, N.Y. -- Science. 2002 Jan 11;295(5553):297.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary Science, National Institute of Infectious Diseases, 1-23-1, Toyama, Shinjuku, Tokyo 162-8640, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11786635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cloning, Organism ; Embryo Transfer ; Embryonic and Fetal Development ; Female ; Fetus/*metabolism ; Fibroblasts ; *Gene Expression ; Gene Expression Profiling ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Transfer Techniques ; Ovarian Follicle/cytology ; Placenta/*metabolism ; RNA, Messenger/genetics/metabolism ; Sertoli Cells
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    DICER1 deficit induces Alu RNA toxicity in age-related macular degeneration (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-02-08
    Description: Geographic atrophy (GA), an untreatable advanced form of age-related macular degeneration, results from retinal pigmented epithelium (RPE) cell degeneration. Here we show that the microRNA (miRNA)-processing enzyme DICER1 is reduced in the RPE of humans with GA, and that conditional ablation of Dicer1, but not seven other miRNA-processing enzymes, induces RPE degeneration in mice. DICER1 knockdown induces accumulation of Alu RNA in human RPE cells and Alu-like B1 and B2 RNAs in mouse RPE. Alu RNA is increased in the RPE of humans with GA, and this pathogenic RNA induces human RPE cytotoxicity and RPE degeneration in mice. Antisense oligonucleotides targeting Alu/B1/B2 RNAs prevent DICER1 depletion-induced RPE degeneration despite global miRNA downregulation. DICER1 degrades Alu RNA, and this digested Alu RNA cannot induce RPE degeneration in mice. These findings reveal a miRNA-independent cell survival function for DICER1 involving retrotransposon transcript degradation, show that Alu RNA can directly cause human pathology, and identify new targets for a major cause of blindness.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077055/" 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/PMC3077055/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaneko, Hiroki -- Dridi, Sami -- Tarallo, Valeria -- Gelfand, Bradley D -- Fowler, Benjamin J -- Cho, Won Gil -- Kleinman, Mark E -- Ponicsan, Steven L -- Hauswirth, William W -- Chiodo, Vince A -- Kariko, Katalin -- Yoo, Jae Wook -- Lee, Dong-ki -- Hadziahmetovic, Majda -- Song, Ying -- Misra, Smita -- Chaudhuri, Gautam -- Buaas, Frank W -- Braun, Robert E -- Hinton, David R -- Zhang, Qing -- Grossniklaus, Hans E -- Provis, Jan M -- Madigan, Michele C -- Milam, Ann H -- Justice, Nikki L -- Albuquerque, Romulo J C -- Blandford, Alexander D -- Bogdanovich, Sasha -- Hirano, Yoshio -- Witta, Jassir -- Fuchs, Elaine -- Littman, Dan R -- Ambati, Balamurali K -- Rudin, Charles M -- Chong, Mark M W -- Provost, Patrick -- Kugel, Jennifer F -- Goodrich, James A -- Dunaief, Joshua L -- Baffi, Judit Z -- Ambati, Jayakrishna -- NIHU10EY013729/EY/NEI NIH HHS/ -- P30 EY006360/EY/NEI NIH HHS/ -- P30 EY014800/EY/NEI NIH HHS/ -- P30 EY014800-07/EY/NEI NIH HHS/ -- P30 EY021721/EY/NEI NIH HHS/ -- P30EY003040/EY/NEI NIH HHS/ -- P30EY008571/EY/NEI NIH HHS/ -- P30EY06360/EY/NEI NIH HHS/ -- R01 EY018350/EY/NEI NIH HHS/ -- R01 EY018350-05/EY/NEI NIH HHS/ -- R01 EY018836/EY/NEI NIH HHS/ -- R01 EY018836-04/EY/NEI NIH HHS/ -- R01 EY020672/EY/NEI NIH HHS/ -- R01 EY020672-02/EY/NEI NIH HHS/ -- R01 GM068414/GM/NIGMS NIH HHS/ -- R01EY001545/EY/NEI NIH HHS/ -- R01EY011123/EY/NEI NIH HHS/ -- R01EY015240/EY/NEI NIH HHS/ -- R01EY015422/EY/NEI NIH HHS/ -- R01EY017182/EY/NEI NIH HHS/ -- R01EY017950/EY/NEI NIH HHS/ -- R01EY018350/EY/NEI NIH HHS/ -- R01EY018836/EY/NEI NIH HHS/ -- R01EY020672/EY/NEI NIH HHS/ -- R01GM068414/GM/NIGMS NIH HHS/ -- R01HD027215/HD/NICHD NIH HHS/ -- R21 EY019778/EY/NEI NIH HHS/ -- R21 EY019778-02/EY/NEI NIH HHS/ -- R21AI076757/AI/NIAID NIH HHS/ -- R21EY019778/EY/NEI NIH HHS/ -- RC1 EY020442/EY/NEI NIH HHS/ -- RC1 EY020442-02/EY/NEI NIH HHS/ -- RC1EY020442/EY/NEI NIH HHS/ -- T32HL091812/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 17;471(7338):325-30. doi: 10.1038/nature09830. Epub 2011 Feb 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology & Visual Sciences, University of Kentucky, Lexington, Kentucky 40506, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21297615" target="_blank"〉PubMed〈/a〉
    Keywords: Alu Elements/*genetics ; Animals ; Cell Death ; Cell Survival ; Cells, Cultured ; DEAD-box RNA Helicases/*deficiency/genetics/metabolism ; Gene Knockdown Techniques ; Humans ; Macular Degeneration/*genetics/*pathology ; Mice ; MicroRNAs/metabolism ; Molecular Sequence Data ; Oligonucleotides, Antisense ; Phenotype ; RNA/*genetics/*metabolism ; Retinal Pigment Epithelium/enzymology/metabolism/pathology ; Ribonuclease III/*deficiency/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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