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  • Animals  (332)
  • American Association for the Advancement of Science (AAAS)  (332)
  • 1985-1989  (332)
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  • American Association for the Advancement of Science (AAAS)  (332)
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  • 1
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    Mesoderm induction in amphibians: the role of TGF-beta 2-like factors (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1988-02-12
    Beschreibung: Mesoderm induction in the amphibian embryo can be studied by exposing animal region explants (destined to become ectoderm) to appropriate stimuli and assaying the appearance of mesodermal products like alpha-actin messenger RNA. Transforming growth factor beta 2 (TGF-beta 2), but not TGF-beta 1, was active in alpha-actin induction, while addition of fibroblast growth factor had a small synergistic effect. Medium conditioned by Xenopus XTC cells (XTC-CM), known to have powerful mesoderm-inducing activity, was shown to contain TGF-beta-like activity as measured by a radioreceptor binding assay, colony formation in NRK cells, and growth inhibition in CCL64 cells. The activity of XTC-CM in mesoderm induction and in growth inhibition of CCL64 cells was inhibited partially by antibodies to TGF-beta 2 but not by antibodies to TGF-beta 1. Thus, a TGF-beta 2-like molecule may be involved in mesoderm induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosa, F -- Roberts, A B -- Danielpour, D -- Dart, L L -- Sporn, M B -- Dawid, I B -- New York, N.Y. -- Science. 1988 Feb 12;239(4841 Pt 1):783-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3422517" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Actins/genetics ; Amphibians/*embryology ; Animals ; Cell Division/drug effects ; Cell Line ; Embryo, Nonmammalian/physiology ; Growth Substances/*physiology ; Mesoderm/*physiology ; Peptides/pharmacology/*physiology ; RNA, Messenger/genetics ; Transforming Growth Factors ; Xenopus
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 2
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    Recombinant human tumor necrosis factor-alpha: effects on proliferation of normal and transformed cells in vitro (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1985-11-22
    Beschreibung: Modulation of the growth of human and murine cell lines in vitro by recombinant human tumor necrosis factor-alpha (rTNF-alpha) and recombinant human interferon-gamma (rIFN-gamma) was investigated. rTNF-alpha had cytostatic or cytolytic effects on only some tumor cell lines. When administered together with rIFN-gamma, rTNF-alpha showed enhanced antiproliferative effects on a subset of the cell lines tested. In contrast to its effects on sensitive tumor cells, rTNF-alpha augmented the growth of normal diploid fibroblasts. Variations in the proliferative response induced by rTNF-alpha were apparently not due to differences in either the number of binding sites per cell or their affinity for rTNF-alpha. These observations indicate that the effects of rTNF-alpha on cell growth are not limited to tumor cells, but rather that this protein may have a broad spectrum of activities in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugarman, B J -- Aggarwal, B B -- Hass, P E -- Figari, I S -- Palladino, M A Jr -- Shepard, H M -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):943-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3933111" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cell Division/*drug effects ; Cell Line ; Cell Survival/drug effects ; Cell Transformation, Neoplastic/pathology ; Drug Synergism ; Glycoproteins/*pharmacology ; Humans ; Interferon-gamma/pharmacology ; Mice ; Recombinant Proteins/*pharmacology ; Tumor Necrosis Factor-alpha
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 3
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    Peroxisomal defects in neonatal-onset and X-linked adrenoleukodystrophies (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1985-01-04
    Beschreibung: Accumulation of very long chain fatty acids in X-linked and neonatal forms of adrenoleukodystrophy (ALD) appears to be a consequence of deficient peroxisomal oxidation of very long chain fatty acids. Peroxisomes were readily identified in liver biopsies taken from a patient having the X-linked disorder. However, in liver biopsies from a patient having neonatal-onset ALD, hepatocellular peroxisomes were greatly reduced in size and number, and sedimentable catalase was markedly diminished. The presence of increased concentrations of serum pipecolic acid and the bile acid intermediate, trihydroxycoprostanic acid, in the neonatal ALD patient are associated with a generalized diminution of peroxisomal activities that was not observed in the patient with X-linked ALD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldfischer, S -- Collins, J -- Rapin, I -- Coltoff-Schiller, B -- Chang, C H -- Nigro, M -- Black, V H -- Javitt, N B -- Moser, H W -- Lazarow, P B -- AG-01468/AG/NIA NIH HHS/ -- AM-17702/AM/NIADDK NIH HHS/ -- N5-03356/PHS HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):67-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3964959" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adrenoleukodystrophy/genetics/metabolism/*pathology ; Adult ; Animals ; Bile Acids and Salts/metabolism ; Catalase/metabolism ; Child ; Child, Preschool ; Diffuse Cerebral Sclerosis of Schilder/*pathology ; Female ; Humans ; Liver/pathology ; Male ; Microbodies/*pathology ; Oxidation-Reduction ; Pipecolic Acids/blood ; Rats ; *X Chromosome
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 4
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    Atrial natriuretic peptide inhibits a cation channel in renal inner medullary collecting duct cells (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-01-20
    Beschreibung: The patch-clamp technique was used to examine the effects of atrial natriuretic peptide (ANP) and its second messenger guanosine 3',5'-monophosphate (cGMP) on an amiloride-sensitive cation channel in the apical membrane of renal inner medullary collecting duct cells. Both ANP (10(-11) M) and dibutyryl guanosine 3',5'-monophosphate (10(-4) M) inhibited the channel in cell-attached patches, and cGMP (10(-5) M) inhibited the channel in inside-out patches. The inner medullary collecting duct is the first tissue in which ANP, via its second messenger cGMP, has been shown to regulate single ion channels. The results suggest that the natriuretic action of ANP is related in part to cGMP-mediated inhibition of electrogenic Na+ absorption by the inner medullary collecting duct.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Light, D B -- Schwiebert, E M -- Karlson, K H -- Stanton, B A -- DK-34533/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 20;243(4889):383-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Dartmouth Medical School, Hanover, NH 03756.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2463673" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aminoquinolines/pharmacology ; Animals ; Atrial Natriuretic Factor/*pharmacology ; Cell Membrane/drug effects ; Cells, Cultured ; Cyclic GMP/pharmacology ; Ion Channels/*drug effects ; Kidney Medulla/drug effects ; Kidney Tubules/*drug effects ; Kidney Tubules, Collecting/*drug effects ; Natriuresis ; Rats ; Sodium/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 5
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    Metastatic hibernomas in transgenic mice expressing an alpha-amylase-SV40 T antigen hybrid gene (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-04-28
    Beschreibung: Mice transgenic for a hybrid gene containing the liver promoter of the mouse amylase gene (Amy-1a) fused to the SV40 tumor antigen coding region unexpected developed malignant brown adipose tissue tumors (malignant hibernomas). Expression of the alpha-amylase gene had previously been thought to be confined to the liver parotid, and pancreas; however, analysis of white and brown adipose tissue from nontransgenic mice revealed expression of the endogenous Amy-1a gene in these tissues. Gene constructs driven by the Amy-1a liver promoter thus provide a means of targeting gene expression to the adipocyte cell lineage in transgenic mice. Moreover the high frequency of metastases in the liver, lungs, spleen, heart, and adrenals of these mice provides an experimental system in which to study the development of disseminated malignancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, N -- Crooke, R -- Hwang, L H -- Schibler, U -- Knowles, B B -- Solter, D -- CA-10815/CA/NCI NIH HHS/ -- CA-18470/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 28;244(4903):460-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2785714" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipose Tissue/metabolism/pathology ; *Adipose Tissue, Brown/metabolism/pathology ; Animals ; Antigens, Polyomavirus Transforming/*genetics ; Cloning, Molecular ; Gene Expression Regulation ; Liver/metabolism ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Neoplasms, Experimental/*genetics/pathology ; Nucleic Acid Hybridization ; Promoter Regions, Genetic ; RNA, Messenger/metabolism ; Tissue Distribution ; Transcription, Genetic ; alpha-Amylases/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 6
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    A novel vasodilatory peptide from the salivary glands of the sand fly Lutzomyia longipalpis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-01-13
    Beschreibung: Salivary gland lysates of the sand fly Lutzomyia longipalpis contain a potent vasodilator that aids the fly to feed on the blood of its vertebrate hosts. Chromatographic analysis, antibody reactivity, and data obtained from bioassays of the salivary erythema-inducing factor indicate striking similarity with human calcitonin gene-related peptide. The erythema-inducing factor is, however, at least one order of magnitude more potent than calcitonin gene-related peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ribeiro, J M -- Vachereau, A -- Modi, G B -- Tesh, R B -- AI18694-0481/AI/NIAID NIH HHS/ -- AI21049/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):212-4.〈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/2783496" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Aorta/drug effects/physiology ; Calcitonin/pharmacology ; Calcitonin Gene-Related Peptide ; Chromatography, High Pressure Liquid ; Diptera ; Erythema ; Humans ; In Vitro Techniques ; Muscle, Smooth, Vascular/drug effects/*physiology ; Neuropeptides/pharmacology ; Rabbits ; Salivary Proteins and Peptides/*isolation & purification/pharmacology ; Vasodilation ; *Vasodilator Agents
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 7
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    Adipsin and complement factor D activity: an immune-related defect in obesity (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-06-23
    Beschreibung: Adipsin is a serine protease that is secreted by adipocytes into the bloodstream; it is deficient in several animal models of obesity, representing a striking example of defective gene expression in this disorder. Recombinant mouse adipsin was purified and its biochemical and enzymatic properties were studied in order to elucidate the function of this protein. Activated adipsin has little or no proteolytic activity toward most substrates but has the same activity as human complement factor D, cleaving complement factor B when it is complexed with activated complement component C3. Like authentic factor D, adipsin can activate the alternative pathway of complement, resulting in red blood cell lysis. Decreased (58 to 80 percent) complement factor D activity, relative to lean controls, was observed as a common feature of several experimental models of obesity, including the ob/ob, db/db, and monosodium glutamate (MSG)-injected mouse and the fa/fa rat. These results suggest that adipsin and the alternative pathway of complement may play an unexpected but important role in the regulation of systemic energy balance in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosen, B S -- Cook, K S -- Yaglom, J -- Groves, D L -- Volanakis, J E -- Damm, D -- White, T -- Spiegelman, B M -- DK31403/DK/NIDDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 23;244(4911):1483-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734615" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adipose Tissue/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Complement Activating Enzymes/*metabolism ; Complement Factor D/*metabolism ; Complement Pathway, Alternative ; Cricetinae ; DNA/genetics ; Gene Expression Regulation ; Humans ; Immunoblotting ; Mice ; Molecular Sequence Data ; Obesity/genetics/*immunology/metabolism ; RNA, Messenger/metabolism ; Recombinant Proteins ; Serine Endopeptidases/genetics/isolation & purification/*metabolism ; Substrate Specificity ; Transfection
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 8
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    Epithelial cell surfaces induce Salmonella proteins required for bacterial adherence and invasion (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-02-17
    Beschreibung: Salmonella bacteria are capable of entering (invading) and multiplying within eukaryotic cells. Stable adherence to and invasion of epithelial cells by S. choleraesuis and S. typhimurium were found to require de novo synthesis of several new bacterial proteins. This inducible event appears to be a coordinately regulated system dependent on trypsin- and neuraminidase-sensitive structures present on the epithelial cell surface. Mutants of S. choleraesuis and S. typhimurium were unable to synthesize these proteins and did not stably adhere to nor invade eukaryotic cells. Two such S. typhimurium mutants were avirulent in mice, an indication that these proteins are required for Salmonella virulence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finlay, B B -- Heffron, F -- Falkow, S -- AI26195/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 17;243(4893):940-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Microbiology, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2919285" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Bacterial Adhesion ; Bacterial Proteins/*biosynthesis ; Cell Line ; Epithelium/physiology ; Kinetics ; Methionine/metabolism ; Salmonella/pathogenicity/*physiology ; Sulfur Radioisotopes
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 9
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    A formalin-inactivated whole SIV vaccine confers protection in macaques (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-12-08
    Beschreibung: A vaccine against human immunodeficiency virus (HIV) would be highly effective in stopping the acquired immunodeficiency syndrome (AIDS) epidemic. A comprehensive evaluation of potential vaccine methodologies can be made by means of the simian model for AIDS, which takes advantage of the similarities in viral composition and disease potential between simian immunodeficiency virus (SIV) infection of rhesus macaques and HIV infection in humans. Immunization with a formalin-inactivated whole SIV vaccine potentiated with either alum and the Syntex adjuvant threonyl muramyl dipeptide (MDP) or MDP alone resulted in the protection of eight of nine rhesus monkeys challenged with ten animal-infectious doses of pathogenic virus. These results demonstrate that a whole virus vaccine is highly effective in inducing immune responses that can protect against lentivirus infection and AIDS-like disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphey-Corb, M -- Martin, L N -- Davison-Fairburn, B -- Montelaro, R C -- Miller, M -- West, M -- Ohkawa, S -- Baskin, G B -- Zhang, J Y -- Putney, S D -- New York, N.Y. -- Science. 1989 Dec 8;246(4935):1293-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Delta Regional Primate Research Center, Tulane University, Covington, LA 70434.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2555923" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylmuramyl-Alanyl-Isoglutamine/immunology ; Adjuvants, Immunologic/administration & dosage ; Alum Compounds/administration & dosage ; Animals ; Antibodies, Viral/biosynthesis ; Chromatography, High Pressure Liquid ; Disease Models, Animal ; Formaldehyde ; Immunization, Secondary ; Leukocyte Count ; Lymphocytes/immunology/microbiology ; Macaca mulatta ; Retroviridae Infections/*prevention & control ; Retroviridae Proteins/immunology ; Simian Immunodeficiency Virus/*immunology/isolation & purification ; Vaccines, Inactivated/administration & dosage/immunology ; Viral Vaccines/administration & dosage/*immunology ; Virion/immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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  • 10
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    Inhibition of DNA binding proteins by oligonucleotide-directed triple helix formation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1989-08-18
    Beschreibung: Oligonucleotides that bind to duplex DNA in a sequence-specific manner by triple helix formation offer an approach to the experimental manipulation of sequence-specific protein binding. Micromolar concentrations of pyrimidine oligodeoxyribonucleotides are shown to block recognition of double helical DNA by prokaryotic modifying enzymes and a eukaryotic transcription factor at a homopurine target site. Inhibition is sequence-specific. Oligonucleotides containing 5-methylcytosine provide substantially more efficient inhibition than oligonucleotides containing cytosine. The results have implications for gene-specific repression by oligonucleotides or their analogs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maher, L J 3rd -- Wold, B -- Dervan, P B -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):725-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549631" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 5-Methylcytosine ; Animals ; Base Sequence ; Cytosine/analogs & derivatives ; DNA/*metabolism ; DNA Restriction Enzymes ; DNA, Recombinant ; DNA-Binding Proteins/*antagonists & inhibitors/metabolism ; Deoxyribonucleases, Type II Site-Specific/metabolism ; Metallothionein/genetics ; Methylation ; Mice ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Oligodeoxyribonucleotides/*pharmacology ; Plasmids ; Promoter Regions, Genetic ; Structure-Activity Relationship ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
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