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  • *Cell Transformation, Viral  (2)
  • DNA-repair enzyme  (2)
  • Fires  (2)
  • American Association for the Advancement of Science (AAAS)  (4)
  • Elsevier  (2)
  • Amsterdam : Elsevier
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Schlagwörter
Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (4)
  • Elsevier  (2)
  • Amsterdam : Elsevier
Erscheinungszeitraum
  • 1
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    Mutation Research/DNA Repair 236 (1990), S. 269-275 
    ISSN: 0921-8777
    Schlagwort(e): Alkylating agents ; DNA-repair enzyme ; Mer phenotype ; Mex phenotype ; Mismatch binding proteins ; N-Methyl-N'-nitro-N-nitrosoguanidine N-Methyl-N-nitrosourea
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Medizin
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Amsterdam : Elsevier
    Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 233 (1990), S. 23-30 
    ISSN: 0027-5107
    Schlagwort(e): Burkitt's lymphoma cell line Raji ; DNA-repair enzyme ; Galactokinase ; O^6-Methylguanine-DNA methyltransferase ; Thymidine kinase
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Biologie , Medizin
    Materialart: Digitale Medien
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2009-01-24
    Beschreibung: Persistent changes in tree mortality rates can alter forest structure, composition, and ecosystem services such as carbon sequestration. Our analyses of longitudinal data from unmanaged old forests in the western United States showed that background (noncatastrophic) mortality rates have increased rapidly in recent decades, with doubling periods ranging from 17 to 29 years among regions. Increases were also pervasive across elevations, tree sizes, dominant genera, and past fire histories. Forest density and basal area declined slightly, which suggests that increasing mortality was not caused by endogenous increases in competition. Because mortality increased in small trees, the overall increase in mortality rates cannot be attributed solely to aging of large trees. Regional warming and consequent increases in water deficits are likely contributors to the increases in tree mortality rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Mantgem, Phillip J -- Stephenson, Nathan L -- Byrne, John C -- Daniels, Lori D -- Franklin, Jerry F -- Fule, Peter Z -- Harmon, Mark E -- Larson, Andrew J -- Smith, Jeremy M -- Taylor, Alan H -- Veblen, Thomas T -- New York, N.Y. -- Science. 2009 Jan 23;323(5913):521-4. doi: 10.1126/science.1165000.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Geological Survey, Western Ecological Research Center, Three Rivers, CA 93271, USA. pvanmantgem@usgs.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19164752" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Abies/anatomy & histology/growth & development ; *Climate ; *Coniferophyta/anatomy & histology/growth & development ; *Ecosystem ; Fires ; Models, Statistical ; Nonlinear Dynamics ; Northwestern United States ; Pinus/anatomy & histology/growth & development ; Temperature ; *Trees/growth & development ; Tsuga/anatomy & histology/growth & development ; United States
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2015-08-22
    Beschreibung: Although disturbances such as fire and native insects can contribute to natural dynamics of forest health, exceptional droughts, directly and in combination with other disturbance factors, are pushing some temperate forests beyond thresholds of sustainability. Interactions from increasing temperatures, drought, native insects and pathogens, and uncharacteristically severe wildfire are resulting in forest mortality beyond the levels of 20th-century experience. Additional anthropogenic stressors, such as atmospheric pollution and invasive species, further weaken trees in some regions. Although continuing climate change will likely drive many areas of temperate forest toward large-scale transformations, management actions can help ease transitions and minimize losses of socially valued ecosystem services.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, Constance I -- Stephenson, Nathan L -- New York, N.Y. -- Science. 2015 Aug 21;349(6250):823-6. doi: 10.1126/science.aaa9933.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Agriculture Forest Service, Pacific Southwest Research Station, Albany, CA 94710, USA. cmillar@fs.fed.us. ; U.S. Geological Survey, Western Ecological Research Center, Three Rivers, CA 93271, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26293954" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; *Climate Change ; *Disasters ; Droughts ; Environmental Restoration and Remediation ; Fires ; *Forests ; Insects ; *Trees
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 1982-05-21
    Beschreibung: Rat embryo fibroblasts transformed by Abelson murine leukemia virus (MuLV) produce and release a transforming growth factor (TGF). Production of this factor is correlated with a tyrosine-specific protein kinase that is functionally active and is associated with the major Abelson MuLV gene product, P120. Transformation-defective mutants of Abelson MuLV do not transform cells, do not have their virus coded transforming gene product phosphorylated in tyrosine, and do not induce TGF production. Abelson MuLV-induced TGF morphologically transforms cells in culture, competes with 125I-labeled epidermal growth factor (EGF) for binding to cell receptors, and induces phosphorylation of tyrosine acceptor sites in the 160,000-dalton EGF membrane receptor. After purification to homogeneity, Abelson virus-induced TGF migrates as a single polypeptide with an apparent size of 7400 daltons as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Twardzik, D R -- Todaro, G J -- Marquardt, H -- Reynolds, F H Jr -- Stephenson, J R -- New York, N.Y. -- Science. 1982 May 21;216(4548):894-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6177040" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Abelson murine leukemia virus ; Animals ; *Cell Transformation, Neoplastic ; *Cell Transformation, Viral ; Molecular Weight ; Peptides/*metabolism ; Phosphotyrosine ; Rats ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; Transforming Growth Factors ; Tyrosine/analogs & derivatives/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
    Publikationsdatum: 1982-06-04
    Beschreibung: To define the human homolog (or homologs) of transforming sequences (v-fes gene) common to Gardner (GA) and Snyder Theilen (ST) isolates of feline sarcoma virus (FeSV), a representative library of human lung carcinoma DNA in a cosmid vector system was constructed. Three cosmid clones were isolated containing GA/ST FeSV v-fes homologous cellular sequences, within 32- to 42-kilobase cellular inserts representing 56 kilobases of contiguous human cellular DNA. Sequences both homologous to, and colinear with, GA or ST FeSV v-fes are distributed discontinuously over a region of up to 9.5 kilobases and contain a minimum of three regions of nonhomology representing probable introns. A thymidine kinase selection system was used to show that, upon transfection to RAT-2 cells, the human c-fes sequence lacked detectable transforming activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Groffen, J -- Heisterkamp, N -- Grosveld, F -- Van de Ven, W -- Stephenson, J R -- N0I-CO-75380/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1982 Jun 4;216(4550):1136-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6281890" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Bacteriophage lambda/genetics ; *Cell Transformation, Viral ; Cloning, Molecular/methods ; DNA Restriction Enzymes ; DNA, Recombinant ; Escherichia coli/genetics ; *Genes, Viral ; Humans ; Retroviridae/*genetics
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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