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  • Articles  (36)
  • Base Sequence  (36)
  • Chemistry and Pharmacology  (36)
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  • Articles  (36)
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  • 1
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    Human hypertension caused by mutations in WNK kinases (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-11
    Description: Hypertension is a major public health problem of largely unknown cause. Here, we identify two genes causing pseudohypoaldosteronism type II, a Mendelian trait featuring hypertension, increased renal salt reabsorption, and impaired K+ and H+ excretion. Both genes encode members of the WNK family of serine-threonine kinases. Disease-causing mutations in WNK1 are large intronic deletions that increase WNK1 expression. The mutations in WNK4 are missense, which cluster in a short, highly conserved segment of the encoded protein. Both proteins localize to the distal nephron, a kidney segment involved in salt, K+, and pH homeostasis. WNK1 is cytoplasmic, whereas WNK4 localizes to tight junctions. The WNK kinases and their associated signaling pathway(s) may offer new targets for the development of antihypertensive drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, F H -- Disse-Nicodeme, S -- Choate, K A -- Ishikawa, K -- Nelson-Williams, C -- Desitter, I -- Gunel, M -- Milford, D V -- Lipkin, G W -- Achard, J M -- Feely, M P -- Dussol, B -- Berland, Y -- Unwin, R J -- Mayan, H -- Simon, D B -- Farfel, Z -- Jeunemaitre, X -- Lifton, R P -- New York, N.Y. -- Science. 2001 Aug 10;293(5532):1107-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute; Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06510 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11498583" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 12/genetics ; Chromosomes, Human, Pair 17/genetics ; Cytoplasm/enzymology ; Female ; Gene Expression Regulation, Enzymologic ; Genetic Linkage ; Humans ; Hypertension/enzymology/*genetics/physiopathology ; Intercellular Junctions/enzymology ; Intracellular Signaling Peptides and Proteins ; Introns ; Kidney Tubules, Collecting/enzymology/ultrastructure ; Kidney Tubules, Distal/enzymology/ultrastructure ; Male ; Membrane Proteins/metabolism ; Microscopy, Fluorescence ; Molecular Sequence Data ; *Mutation ; Mutation, Missense ; Pedigree ; Phosphoproteins/metabolism ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Pseudohypoaldosteronism/enzymology/*genetics/physiopathology ; Sequence Deletion ; Signal Transduction ; Zonula Occludens-1 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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  • 2
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    Cooperativity induced by a single mutation at the subunit interface of a dimeric enzyme: glutathione reductase (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-13
    Description: When glycine418 of Escherichia coli glutathione reductase, which is in a closely packed region of the dimer interface, is replaced with a bulky tryptophan residue, the enzyme becomes highly cooperative (Hill coefficient 1.76) for glutathione binding. The cooperativity is lost when the mutant subunit is hybridized with a wild-type subunit to create a heterodimer. The mutation appears to disrupt atomic packing at the dimer interface, which induces a change of kinetic mechanism. A single mutation in a region of the protein remote from the active site can thus act as a molecular switch to confer cooperativity on an enzyme.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scrutton, N S -- Deonarain, M P -- Berry, A -- Perham, R N -- New York, N.Y. -- Science. 1992 Nov 13;258(5085):1140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439821" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Binding Sites ; Escherichia coli/*enzymology/genetics ; Genes, Bacterial ; Glutathione/metabolism ; Glutathione Reductase/*chemistry/genetics/metabolism ; Glycine/chemistry ; Kinetics ; Macromolecular Substances ; Models, Molecular ; Molecular Sequence Data ; Molecular Structure ; *Mutagenesis, Site-Directed ; NADP/metabolism ; Plasmids ; Protein Multimerization ; Tryptophan/chemistry
    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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    Amplification of a gene related to mammalian mdr genes in drug-resistant Plasmodium falciparum (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-09
    Description: The malaria parasite Plasmodium falciparum contains at least two genes related to the mammalian multiple drug resistance genes, and at least one of the P. falciparum genes is expressed at a higher level and is present in higher copy number in a strain that is resistant to multiple drugs than in a strain that is sensitive to the drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, C M -- Serrano, A E -- Wasley, A -- Bogenschutz, M P -- Shankar, A H -- Wirth, D F -- 1F23 AI07801-01/AI/NIAID NIH HHS/ -- 1K11 AI00892-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1184-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tropical Public Health Harvard School of Public Health, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658061" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Amino Acid Sequence ; Animals ; Base Sequence ; Drug Resistance/genetics ; *Gene Amplification ; Invertebrate Hormones/*genetics ; Mice ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Plasmodium falciparum/*genetics ; *Protozoan Proteins ; Sequence Homology, Nucleic Acid
    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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    Nitrogen fixation at 92 degrees C by a hydrothermal vent archaeon (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-16
    Description: A methanogenic archaeon isolated from deep-sea hydrothermal vent fluid was found to reduce N(2) to NH(3) at up to 92 degrees C, which is 28 degrees C higher than the current upper temperature limit of biological nitrogen fixation. The 16S ribosomal RNA gene of the hyperthermophilic nitrogen fixer, designated FS406-22, was 99% similar to that of non-nitrogen fixing Methanocaldococcus jannaschii DSM 2661. At its optimal growth temperature of 90 degrees C, FS406-22 incorporated (15)N(2) and expressed nifH messenger RNA. This increase in the temperature limit of nitrogen fixation could reveal a broader range of conditions for life in the subseafloor biosphere and other nitrogen-limited ecosystems than previously estimated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mehta, Mausmi P -- Baross, John A -- New York, N.Y. -- Science. 2006 Dec 15;314(5806):1783-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Oceanography, University of Washington, Seattle, WA 98195, USA. mausmi@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17170307" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Archaea/classification/genetics/*isolation & purification/*metabolism ; Archaeal Proteins/chemistry/genetics/metabolism ; Base Sequence ; *Ecosystem ; Genes, Archaeal ; Genes, rRNA ; Geologic Sediments/microbiology ; *Hot Temperature ; Molecular Sequence Data ; Nitrogen/metabolism ; *Nitrogen Fixation/genetics ; Nitrogenase/chemistry/*genetics/metabolism ; Operon ; Oxidation-Reduction ; Oxidoreductases/chemistry/genetics/metabolism ; Pacific Ocean ; Phylogeny ; RNA, Ribosomal, 16S/genetics ; Seawater/*microbiology ; Volcanic Eruptions
    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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    Complete genome sequence of Treponema pallidum, the syphilis spirochete (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-17
    Description: The complete genome sequence of Treponema pallidum was determined and shown to be 1,138,006 base pairs containing 1041 predicted coding sequences (open reading frames). Systems for DNA replication, transcription, translation, and repair are intact, but catabolic and biosynthetic activities are minimized. The number of identifiable transporters is small, and no phosphoenolpyruvate:phosphotransferase carbohydrate transporters were found. Potential virulence factors include a family of 12 potential membrane proteins and several putative hemolysins. Comparison of the T. pallidum genome sequence with that of another pathogenic spirochete, Borrelia burgdorferi, the agent of Lyme disease, identified unique and common genes and substantiates the considerable diversity observed among pathogenic spirochetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fraser, C M -- Norris, S J -- Weinstock, G M -- White, O -- Sutton, G G -- Dodson, R -- Gwinn, M -- Hickey, E K -- Clayton, R -- Ketchum, K A -- Sodergren, E -- Hardham, J M -- McLeod, M P -- Salzberg, S -- Peterson, J -- Khalak, H -- Richardson, D -- Howell, J K -- Chidambaram, M -- Utterback, T -- McDonald, L -- Artiach, P -- Bowman, C -- Cotton, M D -- Fujii, C -- Garland, S -- Hatch, B -- Horst, K -- Roberts, K -- Sandusky, M -- Weidman, J -- Smith, H O -- Venter, J C -- AI31068/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):375-88.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, Rockville, MD 20850, USA. tpdb@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665876" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/genetics/metabolism ; Base Sequence ; Borrelia burgdorferi Group/genetics ; Carrier Proteins/genetics/metabolism ; DNA Repair/genetics ; DNA Replication/genetics ; DNA Restriction Enzymes/genetics ; Energy Metabolism/genetics ; Genes, Bacterial ; Genes, Regulator ; *Genome, Bacterial ; Heat-Shock Response/genetics ; Lipoproteins/genetics ; Membrane Proteins/genetics ; Molecular Sequence Data ; Movement ; Open Reading Frames ; Oxygen Consumption/genetics ; Protein Biosynthesis ; Recombination, Genetic ; Replication Origin ; *Sequence Analysis, DNA ; Transcription, Genetic ; Treponema pallidum/*genetics/metabolism/pathogenicity
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Differential microRNA regulation of HLA-C expression and its association with HIV control (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-19
    Description: The HLA-C locus is distinct relative to the other classical HLA class I loci in that it has relatively limited polymorphism, lower expression on the cell surface, and more extensive ligand-receptor interactions with killer-cell immunoglobulin-like receptors. A single nucleotide polymorphism (SNP) 35 kb upstream of HLA-C (rs9264942; termed -35) associates with control of HIV, and with levels of HLA-C messenger RNA transcripts and cell-surface expression, but the mechanism underlying its varied expression is unknown. We proposed that the -35 SNP is not the causal variant for differential HLA-C expression, but rather is marking another polymorphism that directly affects levels of HLA-C. Here we show that variation within the 3' untranslated region (UTR) of HLA-C regulates binding of the microRNA hsa-miR-148 to its target site, resulting in relatively low surface expression of alleles that bind this microRNA and high expression of HLA-C alleles that escape post-transcriptional regulation. The 3' UTR variant associates strongly with control of HIV, potentially adding to the effects of genetic variation encoding the peptide-binding region of the HLA class I loci. Variation in HLA-C expression adds another layer of diversity to this highly polymorphic locus that must be considered when deciphering the function of these molecules in health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084326/" 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/PMC3084326/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kulkarni, Smita -- Savan, Ram -- Qi, Ying -- Gao, Xiaojiang -- Yuki, Yuko -- Bass, Sara E -- Martin, Maureen P -- Hunt, Peter -- Deeks, Steven G -- Telenti, Amalio -- Pereyra, Florencia -- Goldstein, David -- Wolinsky, Steven -- Walker, Bruce -- Young, Howard A -- Carrington, Mary -- 5-M01-RR-00722/RR/NCRR NIH HHS/ -- HHSN261200800001E/CO/NCI NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- N02-CP-55504/CP/NCI NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01-DA04334/DA/NIDA NIH HHS/ -- R01-DA12568/DA/NIDA NIH HHS/ -- U01-AI-35039/AI/NIAID NIH HHS/ -- U01-AI-35040/AI/NIAID NIH HHS/ -- U01-AI-35041/AI/NIAID NIH HHS/ -- U01-AI-35042/AI/NIAID NIH HHS/ -- U01-AI-35043/AI/NIAID NIH HHS/ -- U01-AI-37613/AI/NIAID NIH HHS/ -- U01-AI-37984/AI/NIAID NIH HHS/ -- UL1 RR024131/RR/NCRR NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2011 Apr 28;472(7344):495-8. doi: 10.1038/nature09914. Epub 2011 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21499264" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Alleles ; Base Sequence ; Cell Line ; *Gene Expression Regulation/genetics/immunology ; Genes, Reporter/genetics ; HIV/*immunology ; HIV Infections/*genetics/*immunology/therapy ; HLA-C Antigens/*genetics ; Humans ; MicroRNAs/*genetics ; Polymorphism, Single Nucleotide/genetics ; Viral Load
    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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  • 7
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    Landscape and variation of RNA secondary structure across the human transcriptome (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-01-31
    Description: In parallel to the genetic code for protein synthesis, a second layer of information is embedded in all RNA transcripts in the form of RNA structure. RNA structure influences practically every step in the gene expression program. However, the nature of most RNA structures or effects of sequence variation on structure are not known. Here we report the initial landscape and variation of RNA secondary structures (RSSs) in a human family trio (mother, father and their child). This provides a comprehensive RSS map of human coding and non-coding RNAs. We identify unique RSS signatures that demarcate open reading frames and splicing junctions, and define authentic microRNA-binding sites. Comparison of native deproteinized RNA isolated from cells versus refolded purified RNA suggests that the majority of the RSS information is encoded within RNA sequence. Over 1,900 transcribed single nucleotide variants (approximately 15% of all transcribed single nucleotide variants) alter local RNA structure. We discover simple sequence and spacing rules that determine the ability of point mutations to impact RSSs. Selective depletion of 'riboSNitches' versus structurally synonymous variants at precise locations suggests selection for specific RNA shapes at thousands of sites, including 3' untranslated regions, binding sites of microRNAs and RNA-binding proteins genome-wide. These results highlight the potentially broad contribution of RNA structure and its variation to gene regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973747/" 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/PMC3973747/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wan, Yue -- Qu, Kun -- Zhang, Qiangfeng Cliff -- Flynn, Ryan A -- Manor, Ohad -- Ouyang, Zhengqing -- Zhang, Jiajing -- Spitale, Robert C -- Snyder, Michael P -- Segal, Eran -- Chang, Howard Y -- P30 CA034196/CA/NCI NIH HHS/ -- R01 HG004361/HG/NHGRI NIH HHS/ -- R01-HG004361/HG/NHGRI NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jan 30;505(7485):706-9. doi: 10.1038/nature12946.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA [2] Stem Cell and Development, Genome Institute of Singapore, 60 Biopolis Street, Singapore 138672 [3]. ; 1] Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA [2]. ; Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA. ; Department of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovet 76100, Israel. ; 1] Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California 94305, USA [2] The Jackson Laboratory for Genomic Medicine, 263 Farmington Avenue, ASB Call Box 901 Farmington, Connecticut 06030, USA. ; Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24476892" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/genetics ; Base Sequence ; Binding Sites ; Child ; Female ; Gene Expression Regulation/genetics ; Genome, Human/genetics ; Humans ; Male ; MicroRNAs/chemistry/genetics/metabolism ; *Nucleic Acid Conformation ; Open Reading Frames/genetics ; Point Mutation/genetics ; RNA/*chemistry/*genetics/metabolism ; RNA Splice Sites/genetics ; RNA-Binding Proteins/metabolism ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Interleukin-7: a cofactor for V(D)J rearrangement of the T cell receptor beta gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-07-02
    Description: The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muegge, K -- Vila, M P -- Durum, S K -- New York, N.Y. -- Science. 1993 Jul 2;261(5117):93-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7686307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Survival/drug effects ; Cells, Cultured ; *DNA-Binding Proteins ; Gene Expression ; *Gene Rearrangement, beta-Chain T-Cell Antigen Receptor ; Genes, RAG-1 ; Hematopoietic Cell Growth Factors/pharmacology ; Interleukin-7/*pharmacology ; Ionomycin/pharmacology ; Mice ; Molecular Sequence Data ; Organ Culture Techniques ; Proteins/genetics ; Stem Cell Factor ; T-Lymphocytes/cytology/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Thymus Gland/embryology/immunology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Inactivation of the mouse Huntington's disease gene homolog Hdh (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-07-21
    Description: Huntington's disease (HD) is a dominant neurodegenerative disorder caused by expansion of a CAG repeat in the gene encoding huntingtin, a protein of unknown function. To distinguish between "loss of function" and "gain of function" models of HD, the murine HD homolog Hdh was inactivated by gene targeting. Mice heterozygous for Hdh inactivation were phenotypically normal, whereas homozygosity resulted in embryonic death. Homozygotes displayed abnormal gastrulation at embryonic day 7.5 and were resorbing by day 8.5. Thus, huntingtin is critical early in embryonic development, before the emergence of the nervous system. That Hdh inactivation does not mimic adult HD neuropathology suggests that the human disease involves a gain of function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duyao, M P -- Auerbach, A B -- Ryan, A -- Persichetti, F -- Barnes, G T -- McNeil, S M -- Ge, P -- Vonsattel, J P -- Gusella, J F -- Joyner, A L -- NS16367/NS/NINDS NIH HHS/ -- NS32765/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jul 21;269(5222):407-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurogenetics Unit, Massachusetts General Hospital, Charlestown 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7618107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Ectoderm/cytology ; Embryonic and Fetal Development ; Female ; Gene Targeting ; Genotype ; Heterozygote ; Homozygote ; Humans ; Huntington Disease/*genetics ; Male ; Mesoderm/cytology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Nerve Tissue Proteins/*genetics/physiology ; Nuclear Proteins/*genetics/physiology ; Phenotype ; Stem Cells/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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  • 10
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    Gastric mucosa abnormalities and tumorigenesis in mice lacking the pS2 trefoil protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-10-11
    Description: To determine the function of the pS2 trefoil protein, which is normally expressed in the gastric mucosa, the mouse pS2 (mpS2) gene was inactivated. The antral and pyloric gastric mucosa of mpS2-null mice was dysfunctional and exhibited severe hyperplasia and dysplasia. All homozygous mutant mice developed antropyloric adenoma, and 30 percent developed multifocal intraepithelial or intramucosal carcinomas. The small intestine was characterized by enlarged villi and an abnormal infiltrate of lymphoid cells. These results indicate that mpS2 is essential for normal differentiation of the antral and pyloric gastric mucosa and may function as a gastric-specific tumor suppressor gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lefebvre, O -- Chenard, M P -- Masson, R -- Linares, J -- Dierich, A -- LeMeur, M -- Wendling, C -- Tomasetto, C -- Chambon, P -- Rio, M C -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):259-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/Universite Louis Pasteur/College de France, Communaute Urbaine de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824193" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/etiology/pathology ; Animals ; Base Sequence ; Cell Differentiation ; Cloning, Molecular ; Female ; Gastric Mucosa/cytology/*pathology ; Gene Targeting ; Genes, Tumor Suppressor ; Intestinal Mucosa/cytology/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Neoplasm Proteins/genetics/*physiology ; Phenotype ; *Proteins ; Pyloric Antrum ; Stomach Neoplasms/*etiology/pathology ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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