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  • 1
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    Neuroscience. ORs rule the roost in the olfactory system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewcock, Joseph W -- Reed, Randall R -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2078-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684811" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Alleles ; Animals ; Cell Nucleus/metabolism ; Chromosomes, Artificial, Yeast ; Feedback, Physiological ; *Gene Expression Regulation ; Genes, Reporter ; Mice ; Mice, Transgenic ; Multigene Family ; Odors ; Olfactory Receptor Neurons/*metabolism ; Promoter Regions, Genetic ; Pseudogenes ; Receptors, Odorant/*genetics/*metabolism ; Signal Transduction ; Transgenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Transcription-coupled events associating with immunoglobulin switch region chromatin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: Class switch recombination (CSR) at the antibody immunoglobulin locus is regulated by germline transcription (GLT)-coupled modifications in the accessibility of the switch region, where CSR takes place. Here we show that histone acetylation of switch regions is linked to CSR but that histone acetylation cannot alone promote CSR or GLT. Activation-induced cytidine deaminase (AID) specifically associates with the CSR target chromatin in a GLT-coupled manner, which may occur potentially by means of physical interaction between AID and the transcription machinery. These data indicate an important role of GLT in the regulation of chromatin accessibility, strongly suggesting that the target of AID is chromatin DNA. Our results give insights on the role of AID and the regulatory mechanism of CSR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nambu, Yukiko -- Sugai, Manabu -- Gonda, Hiroyuki -- Lee, Chung-Gi -- Katakai, Tomoya -- Agata, Yasutoshi -- Yokota, Yoshifumi -- Shimizu, Akira -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2137-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Biology and Genetics, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684824" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; B-Lymphocytes/*immunology ; Cells, Cultured ; Chromatin/*metabolism ; Cytidine Deaminase/*metabolism ; DNA/metabolism ; Histone Deacetylase Inhibitors ; Histones/metabolism ; Hydroxamic Acids/pharmacology ; *Immunoglobulin Class Switching ; Immunoglobulin E/biosynthesis ; Immunoglobulin G/biosynthesis ; *Immunoglobulin Switch Region ; Interleukin-4/immunology ; Lipopolysaccharides/immunology ; Lymphocyte Activation ; Mice ; Precipitin Tests ; RNA/metabolism ; RNA Polymerase II/metabolism ; Recombination, Genetic ; *Transcription, Genetic ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta1
    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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    Generation of viable cholesterol-free mice (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wechsler, A -- Brafman, A -- Shafir, M -- Heverin, M -- Gottlieb, H -- Damari, G -- Gozlan-Kelner, S -- Spivak, I -- Moshkin, O -- Fridman, E -- Becker, Y -- Skaliter, R -- Einat, P -- Faerman, A -- Bjorkhem, I -- Feinstein, E -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Quark Biotech, Inc., 10265 Carnegie Avenue, Cleveland, OH 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684813" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Bile Acids and Salts/biosynthesis ; Cholesterol/blood/*deficiency/metabolism/*physiology ; Desmosterol/*metabolism ; Female ; Gene Targeting ; Growth ; Humans ; Infertility ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Nerve Tissue Proteins/*genetics/metabolism ; Oxidoreductases Acting on CH-CH Group Donors/*genetics/metabolism ; Phenotype ; Sex Characteristics ; Testis/pathology
    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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    Editing of CD1d-bound lipid antigens by endosomal lipid transfer proteins (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: It is now established that CD1 molecules present lipid antigens to T cells, although it is not clear how the exchange of lipids between membrane compartments and the CD1 binding groove is assisted. We report that mice deficient in prosaposin, the precursor to a family of endosomal lipid transfer proteins (LTP), exhibit specific defects in CD1d-mediated antigen presentation and lack Valpha14 NKT cells. In vitro, saposins extracted monomeric lipids from membranes and from CD1, thereby promoting the loading as well as the editing of lipids on CD1. Transient complexes between CD1, lipid, and LTP suggested a "tug-of-war" model in which lipid exchange between CD1 and LTP is on the basis of their respective affinities for lipids. LTPs constitute a previously unknown link between lipid metabolism and immunity and are likely to exert a profound influence on the repertoire of self, tumor, and microbial lipid antigens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918537/" 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/PMC2918537/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Dapeng -- Cantu, Carlos 3rd -- Sagiv, Yuval -- Schrantz, Nicolas -- Kulkarni, Ashok B -- Qi, Xiaoyang -- Mahuran, Don J -- Morales, Carlos R -- Grabowski, Gregory A -- Benlagha, Kamel -- Savage, Paul -- Bendelac, Albert -- Teyton, Luc -- 10435/Canadian Institutes of Health Research/Canada -- AI38339/AI/NIAID NIH HHS/ -- AI50867/AI/NIAID NIH HHS/ -- P01 AI53725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2004 Jan 23;303(5657):523-7. Epub 2003 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD1/*immunology/metabolism ; Antigens, CD1d ; Carrier Proteins/*metabolism ; Endosomes/*metabolism ; G(M2) Activator Protein ; Glycolipids/immunology ; Glycoproteins/deficiency/genetics/metabolism/*physiology ; Killer Cells, Natural/immunology ; Lipid Metabolism ; Lipids/*immunology ; Mice ; Proteins/metabolism ; Receptors, Antigen, T-Cell/immunology ; Saposins ; Sphingolipid Activator Proteins ; T-Lymphocytes/*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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    Cell biology. In sex reversal, protein deterred by nuclear barrier (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sreenivasan, Aparna -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2050.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684795" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Amino Acid Sequence ; Animals ; Calmodulin/metabolism ; Cell Nucleus/*metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Female ; Gonadal Dysgenesis, 46,XY/*etiology/genetics/metabolism ; Gonads/cytology/embryology/metabolism ; Humans ; Male ; Mice ; Mutation ; Nuclear Localization Signals ; Nuclear Pore/metabolism ; *Nuclear Proteins ; Protein Binding ; Sex-Determining Region Y Protein ; *Transcription Factors ; beta Karyopherins/metabolism
    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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    Comment on "Tumor response to radiotherapy regulated by endothelial cell apoptosis" (II) (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Martin -- Bristow, Robert -- Glazer, Peter -- Hill, Richard -- McBride, William -- McKenna, Gillies -- Muschel, Ruth -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1894; author reply 1894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671275" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Disease Models, Animal ; Endothelium, Vascular/*pathology/radiation effects ; Melanoma, Experimental/blood supply/immunology/pathology/*radiotherapy ; Mice ; Radiation Tolerance ; Sphingomyelin Phosphodiesterase/genetics/metabolism
    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 muscleblind knockout model for myotonic dystrophy (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: The neuromuscular disease myotonic dystrophy (DM) is caused by microsatellite repeat expansions at two different genomic loci. Mutant DM transcripts are retained in the nucleus together with the muscleblind (Mbnl) proteins, and these abnormal RNAs somehow interfere with pre-mRNA splicing regulation. Here, we show that disruption of the mouse Mbnl1 gene leads to muscle, eye, and RNA splicing abnormalities that are characteristic of DM disease. Our results support the hypothesis that manifestations of DM can result from sequestration of specific RNA binding proteins by a repetitive element expansion in a mutant RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanadia, Rahul N -- Johnstone, Karen A -- Mankodi, Ami -- Lungu, Codrin -- Thornton, Charles A -- Esson, Douglas -- Timmers, Adrian M -- Hauswirth, William W -- Swanson, Maurice S -- AR46799/AR/NIAMS NIH HHS/ -- AR46806/AR/NIAMS NIH HHS/ -- AR48143/AR/NIAMS NIH HHS/ -- R01 AR046799/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1978-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Powell Gene Therapy Center, Gainesville, FL 32610, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671308" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; CELF1 Protein ; Cataract/etiology/pathology ; Cell Nucleus/metabolism ; Chloride Channels/genetics/metabolism ; DNA-Binding Proteins ; Disease Models, Animal ; Electromyography ; Exons ; Gene Targeting ; Introns ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Fibers, Skeletal/pathology ; Muscle Relaxation ; Muscle, Skeletal/pathology/physiopathology ; Myocardium/metabolism ; Myotonic Dystrophy/*genetics/pathology/*physiopathology ; Protein Isoforms ; RNA Splicing ; RNA-Binding Proteins/*genetics/metabolism/*physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Trinucleotide Repeat Expansion ; Troponin T/genetics/metabolism
    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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    Mono- versus polyubiquitination: differential control of p53 fate by Mdm2 (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Although Mdm2-mediated ubiquitination is essential for both degradation and nuclear export of p53, the molecular basis for the differential effects of Mdm2 remains unknown. Here we show that low levels of Mdm2 activity induce monoubiquitination and nuclear export of p53, whereas high levels promote p53's polyubiquitination and nuclear degradation. A p53-ubiquitin fusion protein that mimics monoubiquitinated p53 was found to accumulate in the cytoplasm in an Mdm2-independent manner, indicating that monoubiquitination is critical for p53 trafficking. These results clarify the nature of ubiquitination-mediated p53 regulation and suggest that distinct mechanisms regulate p53 function in accordance with the levels of Mdm2 activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Muyang -- Brooks, Christopher L -- Wu-Baer, Foon -- Chen, Delin -- Baer, Richard -- Gu, Wei -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1972-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics and Department of Pathology, College of Physicians & Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671306" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/metabolism ; Humans ; Mice ; Mice, Knockout ; Mutation ; *Nuclear Proteins ; Protein Transport ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-mdm2 ; Recombinant Fusion Proteins/metabolism ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism ; Ubiquitin/genetics/*metabolism
    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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    Anterior-posterior guidance of commissural axons by Wnt-frizzled signaling (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Commissural neurons in the mammalian dorsal spinal cord send axons ventrally toward the floor plate, where they cross the midline and turn anteriorly toward the brain; a gradient of chemoattractant(s) inside the spinal cord controls this turning. In rodents, several Wnt proteins stimulate the extension of commissural axons after midline crossing (postcrossing). We found that Wnt4 messenger RNA is expressed in a decreasing anterior-to-posterior gradient in the floor plate, and that a directed source of Wnt4 protein attracted postcrossing commissural axons. Commissural axons in mice lacking the Wnt receptor Frizzled3 displayed anterior-posterior guidance defects after midline crossing. Thus, Wnt-Frizzled signaling guides commissural axons along the anterior-posterior axis of the spinal cord.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lyuksyutova, Anna I -- Lu, Chin-Chun -- Milanesio, Nancy -- King, Leslie A -- Guo, Nini -- Wang, Yanshu -- Nathans, Jeremy -- Tessier-Lavigne, Marc -- Zou, Yimin -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1984-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Brain/embryology/metabolism ; COS Cells ; Central Nervous System/cytology/*embryology/metabolism ; Cues ; Culture Techniques ; Diffusion ; Frizzled Receptors ; Gene Expression Profiling ; Growth Cones/physiology/ultrastructure ; In Situ Hybridization ; *Membrane Proteins ; Mice ; Mice, Knockout ; Neurons/*physiology ; Proteins/pharmacology ; Proto-Oncogene Proteins/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/genetics/*metabolism ; *Signal Transduction ; Spinal Cord/*cytology/embryology/metabolism ; Transfection ; Wnt Proteins ; Wnt4 Protein
    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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    Embryonic stem cells. Scientists make sperm in a dish (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1875.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Division ; Cell Separation ; Cells, Cultured ; Embryo, Mammalian/*cytology ; Fertilization ; Genomic Imprinting ; Male ; Mice ; Spermatozoa/*cytology/drug effects/physiology ; Stem Cells/drug effects/*physiology ; Tretinoin/pharmacology
    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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