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  • 1
    Publication Date: 2016-04-30
    Description: Noncoding variants play a central role in the genetics of complex traits, but we still lack a full understanding of the molecular pathways through which they act. We quantified the contribution of cis-acting genetic effects at all major stages of gene regulation from chromatin to proteins, in Yoruba lymphoblastoid cell lines (LCLs). About ~65% of expression quantitative trait loci (eQTLs) have primary effects on chromatin, whereas the remaining eQTLs are enriched in transcribed regions. Using a novel method, we also detected 2893 splicing QTLs, most of which have little or no effect on gene-level expression. These splicing QTLs are major contributors to complex traits, roughly on a par with variants that affect gene expression levels. Our study provides a comprehensive view of the mechanisms linking genetic variation to variation in human gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Yang I -- van de Geijn, Bryce -- Raj, Anil -- Knowles, David A -- Petti, Allegra A -- Golan, David -- Gilad, Yoav -- Pritchard, Jonathan K -- R01MH084703/MH/NIMH NIH HHS/ -- R01MH101825/MH/NIMH NIH HHS/ -- U01HG007036/HG/NHGRI NIH HHS/ -- U54CA149145/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):600-4. doi: 10.1126/science.aad9417. Epub 2016 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University, Stanford, CA, USA. ; Department of Human Genetics, University of Chicago, Chicago, IL, USA. ; Department of Computer Science, Stanford University, Stanford, CA, USA. Department of Radiology, Stanford University, Stanford, CA, USA. ; Genome Institute, Washington University in St. Louis, St. Louis, MO, USA. ; Department of Human Genetics, University of Chicago, Chicago, IL, USA. gilad@uchicago.edu pritch@stanford.edu. ; Department of Genetics, Stanford University, Stanford, CA, USA. Department of Biology, Stanford University, Stanford, CA, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA, USA. gilad@uchicago.edu pritch@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126046" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromatin/metabolism ; *Gene Expression Regulation ; *Genetic Variation ; Genome-Wide Association Study ; Humans ; Immune System Diseases/*genetics ; Lymphocytes/immunology ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; RNA Splicing/*genetics
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  • 2
    Publication Date: 2016-01-28
    Description: Hydroxymethylcytosine, well described in DNA, occurs also in RNA. Here, we show that hydroxymethylcytosine preferentially marks polyadenylated RNAs and is deposited by Tet in Drosophila. We map the transcriptome-wide hydroxymethylation landscape, revealing hydroxymethylcytosine in the transcripts of many genes, notably in coding sequences, and identify consensus sites for hydroxymethylation. We found that RNA hydroxymethylation can favor mRNA translation. Tet and hydroxymethylated RNA are found to be most abundant in the Drosophila brain, and Tet-deficient fruitflies suffer impaired brain development, accompanied by decreased RNA hydroxymethylation. This study highlights the distribution, localization, and function of cytosine hydroxymethylation and identifies central roles for this modification in Drosophila.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delatte, Benjamin -- Wang, Fei -- Ngoc, Long Vo -- Collignon, Evelyne -- Bonvin, Elise -- Deplus, Rachel -- Calonne, Emilie -- Hassabi, Bouchra -- Putmans, Pascale -- Awe, Stephan -- Wetzel, Collin -- Kreher, Judith -- Soin, Romuald -- Creppe, Catherine -- Limbach, Patrick A -- Gueydan, Cyril -- Kruys, Veronique -- Brehm, Alexander -- Minakhina, Svetlana -- Defrance, Matthieu -- Steward, Ruth -- Fuks, Francois -- R01 GM089992/GM/NIGMS NIH HHS/ -- T32 CA117846/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):282-5. doi: 10.1126/science.aac5253.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ; Waksman Institute, Department of Molecular Biology and Biochemistry, Cancer Institute of New Jersey, Rutgers University, Piscataway, NJ, USA. ; Laboratory of Molecular Biology of the Gene, Faculty of Sciences, Universite Libre de Bruxelles, Gosselies, Belgium. ; Institut fur Molekularbiologie und Tumorforschung, Philipps-Universitat Marburg, Marburg, Germany. ; Department of Chemistry, University of Cincinnati, Cincinnati, OH, USA. ; Laboratory of Cancer Epigenetics, Faculty of Medicine, ULB Cancer Research Center (U-CRC), Universite Libre de Bruxelles (ULB), Brussels, Belgium. ffuks@ulb.ac.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816380" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*abnormalities/metabolism ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; Dioxygenases/genetics/metabolism ; Drosophila melanogaster/genetics/*growth & development/metabolism ; Methylation ; RNA, Messenger/genetics/*metabolism ; Transcriptome
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  • 3
    Publication Date: 2016-01-28
    Description: Genes encoding human beta-type globin undergo a developmental switch from embryonic to fetal to adult-type expression. Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle cell disease and thalassemia. Some experimental results have suggested that these diseases could be treated by induction of fetal-type hemoglobin (HbF). However, the mechanisms that repress HbF in adults remain unclear. We found that the LRF/ZBTB7A transcription factor occupies fetal gamma-globin genes and maintains the nucleosome density necessary for gamma-globin gene silencing in adults, and that LRF confers its repressive activity through a NuRD repressor complex independent of the fetal globin repressor BCL11A. Our study may provide additional opportunities for therapeutic targeting in the treatment of hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" 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/PMC4778394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masuda, Takeshi -- Wang, Xin -- Maeda, Manami -- Canver, Matthew C -- Sher, Falak -- Funnell, Alister P W -- Fisher, Chris -- Suciu, Maria -- Martyn, Gabriella E -- Norton, Laura J -- Zhu, Catherine -- Kurita, Ryo -- Nakamura, Yukio -- Xu, Jian -- Higgs, Douglas R -- Crossley, Merlin -- Bauer, Daniel E -- Orkin, Stuart H -- Kharchenko, Peter V -- Maeda, Takahiro -- R01 AI084905/AI/NIAID NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R56 DK105001/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):285-9. doi: 10.1126/science.aad3312.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia. ; Medical Research Council, Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, UK. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Children's Research Institute, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org. ; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816381" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Erythroblasts/cytology ; Erythropoiesis/genetics ; Fetal Hemoglobin/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Sequence Deletion ; Thalassemia/genetics ; Transcription Factors/genetics/*metabolism ; gamma-Globins/*genetics
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  • 4
    Publication Date: 2016-04-16
    Description: Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, Christopher D -- Siregar, Josephine E -- Mollard, Vanessa -- Vega-Rodriguez, Joel -- Syafruddin, Din -- Matsuoka, Hiroyuki -- Matsuzaki, Motomichi -- Toyama, Tomoko -- Sturm, Angelika -- Cozijnsen, Anton -- Jacobs-Lorena, Marcelo -- Kita, Kiyoshi -- Marzuki, Sangkot -- McFadden, Geoffrey I -- AI031478/AI/NIAID NIH HHS/ -- RR00052/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):349-53. doi: 10.1126/science.aad9279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. gim@unimelb.edu.au deang@unimelb.edu.au. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. ; Johns Hopkins University Bloomberg School of Public Health, Department of Molecular Microbiology and Immunology, Malaria Research Institute, Baltimore, MD 21205, USA. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Parasitology, Faculty of Medicine, Hasanuddin University, Jalan Perintis Kemerdekaan Km10, Makassar 90245, Indonesia. ; Division of Medical Zoology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. School of Tropical Medicine and Global Health, Nagasaki University, Sakamoto, Nagasaki 852-8523, Japan. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*parasitology ; Antimalarials/*pharmacology/therapeutic use ; Atovaquone/*pharmacology/therapeutic use ; Cell Line ; Cytochromes b/*genetics ; Drug Resistance/*genetics ; Genes, Mitochondrial/genetics ; Humans ; Life Cycle Stages/drug effects/genetics ; Malaria/drug therapy/*parasitology/transmission ; Male ; Mice ; Mitochondria/*genetics ; Mutation ; Plasmodium berghei/*drug effects/genetics/growth & development ; Selection, Genetic
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  • 5
    Publication Date: 2015-01-24
    Description: Resolving the molecular details of proteome variation in the different tissues and organs of the human body will greatly increase our knowledge of human biology and disease. Here, we present a map of the human tissue proteome based on an integrated omics approach that involves quantitative transcriptomics at the tissue and organ level, combined with tissue microarray-based immunohistochemistry, to achieve spatial localization of proteins down to the single-cell level. Our tissue-based analysis detected more than 90% of the putative protein-coding genes. We used this approach to explore the human secretome, the membrane proteome, the druggable proteome, the cancer proteome, and the metabolic functions in 32 different tissues and organs. All the data are integrated in an interactive Web-based database that allows exploration of individual proteins, as well as navigation of global expression patterns, in all major tissues and organs in the human body.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uhlen, Mathias -- Fagerberg, Linn -- Hallstrom, Bjorn M -- Lindskog, Cecilia -- Oksvold, Per -- Mardinoglu, Adil -- Sivertsson, Asa -- Kampf, Caroline -- Sjostedt, Evelina -- Asplund, Anna -- Olsson, IngMarie -- Edlund, Karolina -- Lundberg, Emma -- Navani, Sanjay -- Szigyarto, Cristina Al-Khalili -- Odeberg, Jacob -- Djureinovic, Dijana -- Takanen, Jenny Ottosson -- Hober, Sophia -- Alm, Tove -- Edqvist, Per-Henrik -- Berling, Holger -- Tegel, Hanna -- Mulder, Jan -- Rockberg, Johan -- Nilsson, Peter -- Schwenk, Jochen M -- Hamsten, Marica -- von Feilitzen, Kalle -- Forsberg, Mattias -- Persson, Lukas -- Johansson, Fredric -- Zwahlen, Martin -- von Heijne, Gunnar -- Nielsen, Jens -- Ponten, Fredrik -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):1260419. doi: 10.1126/science.1260419.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science for Life Laboratory, KTH-Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Department of Proteomics, KTH-Royal Institute of Technology, SE-106 91 Stockholm, Sweden. Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark, DK-2970 Horsholm, Denmark. mathias.uhlen@scilifelab.se. ; Science for Life Laboratory, KTH-Royal Institute of Technology, SE-171 21 Stockholm, Sweden. ; Science for Life Laboratory, KTH-Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Department of Proteomics, KTH-Royal Institute of Technology, SE-106 91 Stockholm, Sweden. ; Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden. ; Department of Chemical and Biological Engineering, Chalmers University of Technology, SE-412 96 Gothenburg, Sweden. ; Science for Life Laboratory, KTH-Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden. ; Leibniz Research Centre for Working Environment and Human Factors (IfADo) at Dortmund TU, D-44139 Dortmund, Germany. ; Lab Surgpath, Mumbai, India. ; Department of Proteomics, KTH-Royal Institute of Technology, SE-106 91 Stockholm, Sweden. ; Science for Life Laboratory, Department of Neuroscience, Karolinska Institute, SE-171 77 Stockholm, Sweden. ; Center for Biomembrane Research, Department of Biochemistry and Biophysics, Stockholm University, Stockholm, Sweden. ; Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark, DK-2970 Horsholm, Denmark. Department of Chemical and Biological Engineering, Chalmers University of Technology, SE-412 96 Gothenburg, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25613900" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Cell Line ; *Databases, Protein ; Female ; Genes ; Genetic Code ; Humans ; Internet ; Male ; Membrane Proteins/genetics/metabolism ; Mitochondrial Proteins/genetics/metabolism ; Neoplasms/genetics/metabolism ; Protein Array Analysis ; Protein Isoforms/genetics/metabolism ; Proteome/genetics/*metabolism ; Tissue Distribution ; Transcription, Genetic
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  • 6
    Publication Date: 2015-08-01
    Description: The actin cross-linking domain (ACD) is an actin-specific toxin produced by several pathogens, including life-threatening spp. of Vibrio cholerae, Vibrio vulnificus, and Aeromonas hydrophila. Actin cross-linking by ACD is thought to lead to slow cytoskeleton failure owing to a gradual sequestration of actin in the form of nonfunctional oligomers. Here, we found that ACD converted cytoplasmic actin into highly toxic oligomers that potently "poisoned" the ability of major actin assembly proteins, formins, to sustain actin polymerization. Thus, ACD can target the most abundant cellular protein by using actin oligomers as secondary toxins to efficiently subvert cellular functions of actin while functioning at very low doses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648357/" 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/PMC4648357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heisler, David B -- Kudryashova, Elena -- Grinevich, Dmitry O -- Suarez, Cristian -- Winkelman, Jonathan D -- Birukov, Konstantin G -- Kotha, Sainath R -- Parinandi, Narasimham L -- Vavylonis, Dimitrios -- Kovar, David R -- Kudryashov, Dmitri S -- R01 GM079265/GM/NIGMS NIH HHS/ -- R01 GM098430/GM/NIGMS NIH HHS/ -- R01 GM114666/GM/NIGMS NIH HHS/ -- R01 HL076259/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 31;349(6247):535-9. doi: 10.1126/science.aab4090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. The Ohio State Biochemistry Program, The Ohio State University, Columbus, OH 43210, USA. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. kudryashov.1@osu.edu kudryashova.1@osu.edu. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. ; Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA. ; Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA. ; Lipid Signaling and Lipidomics Laboratory, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH 43210, USA. ; Department of Physics, Lehigh University, Bethlehem, PA 18015, USA. ; Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA. Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL 60637, USA. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. The Ohio State Biochemistry Program, The Ohio State University, Columbus, OH 43210, USA. kudryashov.1@osu.edu kudryashova.1@osu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26228148" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Animals ; Antigens, Bacterial/*chemistry/genetics/*toxicity ; Bacterial Toxins/*chemistry/genetics/*toxicity ; Cell Line ; Fetal Proteins/*antagonists & inhibitors ; Intestinal Mucosa/drug effects/metabolism ; Microfilament Proteins/*antagonists & inhibitors ; Nuclear Proteins/*antagonists & inhibitors ; Polymerization/drug effects ; Protein Structure, Tertiary ; Rats
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  • 7
    Publication Date: 2015-09-01
    Description: Super-resolution fluorescence microscopy is distinct among nanoscale imaging tools in its ability to image protein dynamics in living cells. Structured illumination microscopy (SIM) stands out in this regard because of its high speed and low illumination intensities, but typically offers only a twofold resolution gain. We extended the resolution of live-cell SIM through two approaches: ultrahigh numerical aperture SIM at 84-nanometer lateral resolution for more than 100 multicolor frames, and nonlinear SIM with patterned activation at 45- to 62-nanometer resolution for approximately 20 to 40 frames. We applied these approaches to image dynamics near the plasma membrane of spatially resolved assemblies of clathrin and caveolin, Rab5a in early endosomes, and alpha-actinin, often in relationship to cortical actin. In addition, we examined mitochondria, actin, and the Golgi apparatus dynamics in three dimensions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659358/" 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/PMC4659358/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Dong -- Shao, Lin -- Chen, Bi-Chang -- Zhang, Xi -- Zhang, Mingshu -- Moses, Brian -- Milkie, Daniel E -- Beach, Jordan R -- Hammer, John A 3rd -- Pasham, Mithun -- Kirchhausen, Tomas -- Baird, Michelle A -- Davidson, Michael W -- Xu, Pingyong -- Betzig, Eric -- GM-075252/GM/NIGMS NIH HHS/ -- R01 GM075252/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):aab3500. doi: 10.1126/science.aab3500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. ; Key Laboratory of RNA Biology and Beijing Key Laboratory of Noncoding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. College of Life Sciences, Central China Normal University, Wuhan 430079, Hubei, China. ; Key Laboratory of RNA Biology and Beijing Key Laboratory of Noncoding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. ; Coleman Technologies, 5131 West Chester Pike, Newtown Square, PA 19073, USA. ; Cell Biology and Physiology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Cell Biology and Pediatrics, Harvard Medical School and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA. ; Cell Biology and Physiology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. National High Magnetic Field Laboratory and Department of Biological Science, Florida State University, Tallahassee, FL 32310, USA. ; National High Magnetic Field Laboratory and Department of Biological Science, Florida State University, Tallahassee, FL 32310, USA. ; Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. betzige@janelia.hhmi.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26315442" target="_blank"〉PubMed〈/a〉
    Keywords: Actinin/analysis ; Actins/analysis ; Animals ; Cell Line ; Clathrin/analysis ; Clathrin-Coated Vesicles/chemistry/ultrastructure ; Coated Pits, Cell-Membrane/chemistry/ultrastructure ; Cytoskeleton/chemistry/metabolism/*ultrastructure ; *Endocytosis ; Endosomes/chemistry/ultrastructure ; Golgi Apparatus/ultrastructure ; Image Processing, Computer-Assisted ; Imaging, Three-Dimensional/instrumentation/*methods ; Microscopy, Fluorescence/instrumentation/*methods ; Mitochondria/chemistry/ultrastructure ; Organelles/chemistry/metabolism/*ultrastructure ; rab5 GTP-Binding Proteins/analysis
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  • 8
    Publication Date: 2015-02-01
    Description: During virus infection, the adaptor proteins MAVS and STING transduce signals from the cytosolic nucleic acid sensors RIG-I and cGAS, respectively, to induce type I interferons (IFNs) and other antiviral molecules. Here we show that MAVS and STING harbor two conserved serine and threonine clusters that are phosphorylated by the kinases IKK and/or TBK1 in response to stimulation. Phosphorylated MAVS and STING then bind to a positively charged surface of interferon regulatory factor 3 (IRF3) and thereby recruit IRF3 for its phosphorylation and activation by TBK1. We further show that TRIF, an adaptor protein in Toll-like receptor signaling, activates IRF3 through a similar phosphorylation-dependent mechanism. These results reveal that phosphorylation of innate adaptor proteins is an essential and conserved mechanism that selectively recruits IRF3 to activate the type I IFN pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Siqi -- Cai, Xin -- Wu, Jiaxi -- Cong, Qian -- Chen, Xiang -- Li, Tuo -- Du, Fenghe -- Ren, Junyao -- Wu, You-Tong -- Grishin, Nick V -- Chen, Zhijian J -- AI-93967/AI/NIAID NIH HHS/ -- GM-094575/GM/NIGMS NIH HHS/ -- GM-63692/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):aaa2630. doi: 10.1126/science.aaa2630. Epub 2015 Jan 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. ; Departments of Biophysics and Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. Howard Hughes Medical Institute (HHMI), University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. ; Departments of Biophysics and Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. Howard Hughes Medical Institute (HHMI), University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. Howard Hughes Medical Institute (HHMI), University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. zhijian.chen@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25636800" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/chemistry/*metabolism ; Adaptor Proteins, Vesicular Transport/chemistry/*metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Humans ; I-kappa B Kinase/metabolism ; Interferon Regulatory Factor-3/chemistry/*metabolism ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Membrane Proteins/chemistry/*metabolism ; Mice ; Molecular Sequence Data ; Phosphorylation ; Protein Binding ; Protein Multimerization ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Proteins/metabolism ; Sendai virus/physiology ; Serine/metabolism ; Signal Transduction ; Ubiquitination ; Vesiculovirus/physiology
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  • 9
    Publication Date: 2015-10-31
    Description: Transcription factors (TFs) bind specific sequences in promoter-proximal and -distal DNA elements to regulate gene transcription. RNA is transcribed from both of these DNA elements, and some DNA binding TFs bind RNA. Hence, RNA transcribed from regulatory elements may contribute to stable TF occupancy at these sites. We show that the ubiquitously expressed TF Yin-Yang 1 (YY1) binds to both gene regulatory elements and their associated RNA species across the entire genome. Reduced transcription of regulatory elements diminishes YY1 occupancy, whereas artificial tethering of RNA enhances YY1 occupancy at these elements. We propose that RNA makes a modest but important contribution to the maintenance of certain TFs at gene regulatory elements and suggest that transcription of regulatory elements produces a positive-feedback loop that contributes to the stability of gene expression programs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720525/" 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/PMC4720525/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sigova, Alla A -- Abraham, Brian J -- Ji, Xiong -- Molinie, Benoit -- Hannett, Nancy M -- Guo, Yang Eric -- Jangi, Mohini -- Giallourakis, Cosmas C -- Sharp, Phillip A -- Young, Richard A -- HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 20;350(6263):978-81. doi: 10.1126/science.aad3346. Epub 2015 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. ; Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. David H. Koch Institute for Integrative Cancer Research, Cambridge, MA 02140, USA. ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. young@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26516199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Cell Line ; Consensus Sequence ; DNA/metabolism ; Embryonic Stem Cells/metabolism ; *Enhancer Elements, Genetic ; *Gene Expression Regulation ; Mice ; *Promoter Regions, Genetic ; RNA, Messenger/*metabolism ; *Transcription, Genetic ; YY1 Transcription Factor/*metabolism
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  • 10
    Publication Date: 2015-01-09
    Description: Naive and primed pluripotent states retain distinct molecular properties, yet limited knowledge exists on how their state transitions are regulated. Here, we identify Mettl3, an N(6)-methyladenosine (m(6)A) transferase, as a regulator for terminating murine naive pluripotency. Mettl3 knockout preimplantation epiblasts and naive embryonic stem cells are depleted for m(6)A in mRNAs, yet are viable. However, they fail to adequately terminate their naive state and, subsequently, undergo aberrant and restricted lineage priming at the postimplantation stage, which leads to early embryonic lethality. m(6)A predominantly and directly reduces mRNA stability, including that of key naive pluripotency-promoting transcripts. This study highlights a critical role for an mRNA epigenetic modification in vivo and identifies regulatory modules that functionally influence naive and primed pluripotency in an opposing manner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geula, Shay -- Moshitch-Moshkovitz, Sharon -- Dominissini, Dan -- Mansour, Abed AlFatah -- Kol, Nitzan -- Salmon-Divon, Mali -- Hershkovitz, Vera -- Peer, Eyal -- Mor, Nofar -- Manor, Yair S -- Ben-Haim, Moshe Shay -- Eyal, Eran -- Yunger, Sharon -- Pinto, Yishay -- Jaitin, Diego Adhemar -- Viukov, Sergey -- Rais, Yoach -- Krupalnik, Vladislav -- Chomsky, Elad -- Zerbib, Mirie -- Maza, Itay -- Rechavi, Yoav -- Massarwa, Rada -- Hanna, Suhair -- Amit, Ido -- Levanon, Erez Y -- Amariglio, Ninette -- Stern-Ginossar, Noam -- Novershtern, Noa -- Rechavi, Gideon -- Hanna, Jacob H -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):1002-6. doi: 10.1126/science.1261417. Epub 2015 Jan 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. ; Cancer Research Center, Chaim Sheba Medical Center, Tel Hashomer, Israel, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. ; Department of Chemistry and Institute for Biophysical Dynamics, The University of Chicago, Chicago, IL 60637, USA. ; Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, Israel. ; The Department of Immunology, Weizmann Institute of Science, Rehovot, Israel. ; The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. The Department of Pediatrics and the Pediatric Immunology Unit, Rambam Medical Center, and the B. Rappaport Faculty of Medicine, Technion, Haifa, Israel. ; Cancer Research Center, Chaim Sheba Medical Center, Tel Hashomer, Israel, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, Israel. ; The Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel. jacob.hanna@weizmann.ac.il noa.novershtern@weizmann.ac.il gidi.rechavi@sheba.health.gov.il. ; Cancer Research Center, Chaim Sheba Medical Center, Tel Hashomer, Israel, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. jacob.hanna@weizmann.ac.il noa.novershtern@weizmann.ac.il gidi.rechavi@sheba.health.gov.il.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25569111" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*analogs & derivatives/metabolism ; Animals ; Blastocyst/enzymology ; Cell Differentiation/genetics/*physiology ; Cell Line ; Embryo Loss/genetics ; Epigenesis, Genetic ; Female ; Gene Knockout Techniques ; Male ; Methylation ; Methyltransferases/genetics/*physiology ; Mice ; Mice, Knockout ; Pluripotent Stem Cells/*cytology/enzymology ; RNA, Messenger/*metabolism
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  • 11
    Publication Date: 2015-02-24
    Description: Notch receptors guide mammalian cell fate decisions by engaging the proteins Jagged and Delta-like (DLL). The 2.3 angstrom resolution crystal structure of the interacting regions of the Notch1-DLL4 complex reveals a two-site, antiparallel binding orientation assisted by Notch1 O-linked glycosylation. Notch1 epidermal growth factor-like repeats 11 and 12 interact with the DLL4 Delta/Serrate/Lag-2 (DSL) domain and module at the N-terminus of Notch ligands (MNNL) domains, respectively. Threonine and serine residues on Notch1 are functionalized with O-fucose and O-glucose, which act as surrogate amino acids by making specific, and essential, contacts to residues on DLL4. The elucidation of a direct chemical role for O-glycans in Notch1 ligand engagement demonstrates how, by relying on posttranslational modifications of their ligand binding sites, Notch proteins have linked their functional capacity to developmentally regulated biosynthetic pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445638/" 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/PMC4445638/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luca, Vincent C -- Jude, Kevin M -- Pierce, Nathan W -- Nachury, Maxence V -- Fischer, Suzanne -- Garcia, K Christopher -- 1R01-GM097015/GM/NIGMS NIH HHS/ -- R01 GM097015/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):847-53. doi: 10.1126/science.1261093.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. kcgarcia@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700513" target="_blank"〉PubMed〈/a〉
    Keywords: Alagille Syndrome/genetics ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cell Line ; Conserved Sequence ; Crystallography, X-Ray ; Fucose/chemistry ; Glucose/chemistry ; Glycosylation ; Intracellular Signaling Peptides and Proteins/*chemistry/genetics ; Ligands ; Membrane Proteins/*chemistry/genetics/ultrastructure ; Molecular Sequence Data ; Molecular Targeted Therapy ; Polysaccharides/chemistry ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/genetics ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptor, Notch1/*chemistry/genetics/ultrastructure ; Serine/chemistry/genetics ; Threonine/chemistry/genetics
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  • 12
    Publication Date: 2015-06-20
    Description: During clathrin-mediated endocytosis (CME), plasma membrane regions are internalized to retrieve extracellular molecules and cell surface components. Whether endocytosis occurs by direct clathrin assembly into curved lattices on the budding vesicle or by initial recruitment to flat membranes and subsequent reshaping has been controversial. To distinguish between these models, we combined fluorescence microscopy and electron tomography to locate endocytic sites and to determine their coat and membrane shapes during invagination. The curvature of the clathrin coat increased, whereas the coated surface area remained nearly constant. Furthermore, clathrin rapidly exchanged at all stages of CME. Thus, coated vesicle budding appears to involve bending of a dynamic preassembled clathrin coat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Avinoam, Ori -- Schorb, Martin -- Beese, Carsten J -- Briggs, John A G -- Kaksonen, Marko -- New York, N.Y. -- Science. 2015 Jun 19;348(6241):1369-72. doi: 10.1126/science.aaa9555.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Biophysics Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. Structural and Computational Biology Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. ; Structural and Computational Biology Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. Electron Microscopy Core Facility, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. ; Cell Biology and Biophysics Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. ; Structural and Computational Biology Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. Cell Biology and Biophysics Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. marko.kaksonen@unige.ch john.briggs@embl.de. ; Cell Biology and Biophysics Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. Structural and Computational Biology Unit, The European Molecular Biology Laboratory, Heidelberg 69117, Germany. marko.kaksonen@unige.ch john.briggs@embl.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26089517" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clathrin/*chemistry ; Coated Pits, Cell-Membrane/*chemistry ; Electron Microscope Tomography ; *Endocytosis ; Fluorescence Recovery After Photobleaching ; Humans ; Microscopy, Fluorescence
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  • 13
    Publication Date: 2015-04-04
    Description: By dividing asymmetrically, stem cells can generate two daughter cells with distinct fates. However, evidence is limited in mammalian systems for the selective apportioning of subcellular contents between daughters. We followed the fates of old and young organelles during the division of human mammary stemlike cells and found that such cells apportion aged mitochondria asymmetrically between daughter cells. Daughter cells that received fewer old mitochondria maintained stem cell traits. Inhibition of mitochondrial fission disrupted both the age-dependent subcellular localization and segregation of mitochondria and caused loss of stem cell properties in the progeny cells. Hence, mechanisms exist for mammalian stemlike cells to asymmetrically sort aged and young mitochondria, and these are important for maintaining stemness properties.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405120/" 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/PMC4405120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katajisto, Pekka -- Dohla, Julia -- Chaffer, Christine L -- Pentinmikko, Nalle -- Marjanovic, Nemanja -- Iqbal, Sharif -- Zoncu, Roberto -- Chen, Walter -- Weinberg, Robert A -- Sabatini, David M -- P30 CA014051/CA/NCI NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R37 AI047389/AI/NIAID NIH HHS/ -- T32 GM007287/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Apr 17;348(6232):340-3. doi: 10.1126/science.1260384. Epub 2015 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. Institute of Biotechnology, University of Helsinki, P.O. Box 00014, Helsinki, Finland. pekka.katajisto@helsinki.fi sabatini@wi.mit.edu. ; Institute of Biotechnology, University of Helsinki, P.O. Box 00014, Helsinki, Finland. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. ; Whitehead Institute for Biomedical Research, Boston, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA. Broad Institute, Cambridge, MA 02142, USA. The David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, MA 02139, USA. pekka.katajisto@helsinki.fi sabatini@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25837514" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Aging/genetics/*physiology ; Cell Division/genetics/*physiology ; Cell Line ; Humans ; Mitochondria/*physiology/ultrastructure ; Stem Cells/*physiology/*ultrastructure
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  • 14
    Publication Date: 2015-10-13
    Description: The shortage of organs for transplantation is a major barrier to the treatment of organ failure. Although porcine organs are considered promising, their use has been checked by concerns about the transmission of porcine endogenous retroviruses (PERVs) to humans. Here we describe the eradication of all PERVs in a porcine kidney epithelial cell line (PK15). We first determined the PK15 PERV copy number to be 62. Using CRISPR-Cas9, we disrupted all copies of the PERV pol gene and demonstrated a 〉1000-fold reduction in PERV transmission to human cells, using our engineered cells. Our study shows that CRISPR-Cas9 multiplexability can be as high as 62 and demonstrates the possibility that PERVs can be inactivated for clinical application of porcine-to-human xenotransplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Luhan -- Guell, Marc -- Niu, Dong -- George, Haydy -- Lesha, Emal -- Grishin, Dennis -- Aach, John -- Shrock, Ellen -- Xu, Weihong -- Poci, Jurgen -- Cortazio, Rebeca -- Wilkinson, Robert A -- Fishman, Jay A -- Church, George -- P50 HG005550/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 Nov 27;350(6264):1101-4. doi: 10.1126/science.aad1191. Epub 2015 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA, USA. Wyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA. eGenesis Biosciences, Boston, MA 02115, USA. gchurch@genetics.med.harvard.edu luhan.yang@egenesisbio.com. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. Wyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA. eGenesis Biosciences, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. College of Animal Sciences, Zhejiang University, Hangzhou 310058, China. ; Department of Genetics, Harvard Medical School, Boston, MA, USA. ; Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. ; Transplant Infectious Disease and Compromised Host Program, Massachusetts General Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26456528" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; CRISPR-Cas Systems ; Cell Line ; Endogenous Retroviruses/*genetics ; Epithelial Cells/virology ; Gene Dosage ; Gene Targeting/*methods ; Genes, pol ; HEK293 Cells ; Humans ; Kidney/virology ; Molecular Sequence Data ; Retroviridae Infections/*prevention & control/transmission/virology ; Swine/*virology ; Transplantation, Heterologous/*methods ; *Virus Inactivation
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  • 15
    Publication Date: 2015-02-07
    Description: The phenotypic consequences of expression quantitative trait loci (eQTLs) are presumably due to their effects on protein expression levels. Yet the impact of genetic variation, including eQTLs, on protein levels remains poorly understood. To address this, we mapped genetic variants that are associated with eQTLs, ribosome occupancy (rQTLs), or protein abundance (pQTLs). We found that most QTLs are associated with transcript expression levels, with consequent effects on ribosome and protein levels. However, eQTLs tend to have significantly reduced effect sizes on protein levels, which suggests that their potential impact on downstream phenotypes is often attenuated or buffered. Additionally, we identified a class of cis QTLs that affect protein abundance with little or no effect on messenger RNA or ribosome levels, which suggests that they may arise from differences in posttranslational regulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4507520/" 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/PMC4507520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Battle, Alexis -- Khan, Zia -- Wang, Sidney H -- Mitrano, Amy -- Ford, Michael J -- Pritchard, Jonathan K -- Gilad, Yoav -- F32 HG006972/HG/NHGRI NIH HHS/ -- F32HG006972/HG/NHGRI NIH HHS/ -- GM077959/GM/NIGMS NIH HHS/ -- HG007036/HG/NHGRI NIH HHS/ -- MH084703/MH/NIMH NIH HHS/ -- R01 GM077959/GM/NIGMS NIH HHS/ -- R01 MH084703/MH/NIMH NIH HHS/ -- U01 HG007036/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 6;347(6222):664-7. doi: 10.1126/science.1260793. Epub 2014 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Stanford University, Stanford, CA 94305, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. ; MS Bioworks, LLC, 3950 Varsity Drive, Ann Arbor, MI 48108, USA. ; Department of Genetics, Stanford University, Stanford, CA 94305, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA. Department of Biology, Stanford University, Stanford, CA 94305, USA. pritch@stanford.edu gilad@uchicago.edu. ; Department of Human Genetics, University of Chicago, Chicago, IL 60637, USA. pritch@stanford.edu gilad@uchicago.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25657249" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Flanking Region ; 5' Flanking Region ; Cell Line ; Exons ; *Gene Expression Regulation ; *Genetic Variation ; Humans ; Phenotype ; Protein Biosynthesis/*genetics ; *Quantitative Trait Loci ; RNA, Messenger/*genetics ; Ribosomes/metabolism ; *Transcription, Genetic
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  • 16
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-08-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1984 Aug 17;225(4663):670-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6087452" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinoma, Hepatocellular/genetics ; Cell Line ; DNA, Bacterial ; *DNA, Neoplasm ; DNA, Viral ; Hepatitis B virus/genetics ; Humans ; Liver Neoplasms/genetics ; Oncogenes
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  • 17
    facet.materialart.
    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-04-27
    Description: Recent advances in biotechnology have created many public policy and legal issues, one of the most significant of which is the treatment of biotechnological industrial products, particularly under the patent system. Patents represent one of several types of intellectual property; their ownership confers the right to exclude others from benefitting from the tangible products of a proprietary subject matter. Intellectual property law and its protections will play a major role in the rate at which biotechnology develops in the United States. In this article biotechnological intellectual property issues are reviewed in the context of their underlying legal requirements. The implications of other factors, such as international competition, research funding, and gene ownership, are also considered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adler, R G -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):357-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6584975" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; Cell Line ; Copyright ; DNA, Recombinant ; Economic Competition ; Federal Government ; *Genetic Engineering ; *Genetics, Microbial ; Government Regulation ; Legislation as Topic ; Ownership ; *Patents as Topic ; Research ; *Technology ; United States ; as a question of intellectual property rights. Attention is focused on the major ; role played by the U.S. patent system in establishing such rights, as illustrated ; by the case of products of recombinant DNA research. Trade secret, copyright, and ; trademark protections are also considered, as are policy issues such as ; international competition in the development of biomedical technologies and ; financing arrangements.
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-05-04
    Description: Stress stimulates several adaptive hormonal responses. Prominent among these responses are the secretion of catecholamines from the adrenal medulla, corticosteroids from the adrenal cortex, and adrenocorticotropin from the anterior pituitary. A number of complex interactions are involved in the regulation of these hormones. Glucocorticoids regulate catecholamine biosynthesis in the adrenal medulla and catecholamines stimulate adrenocorticotropin release from the anterior pituitary. In addition, other hormones, including corticotropin-releasing factor, vasoactive intestinal peptide, and arginine vasopressin stimulate while the corticosteroids and somatostatin inhibit adrenocorticotropin secretion. Together these agents appear to determine the complex physiologic responses to a variety of stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Axelrod, J -- Reisine, T D -- New York, N.Y. -- Science. 1984 May 4;224(4648):452-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6143403" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Adrenal Cortex/metabolism ; Adrenal Medulla/metabolism ; Adrenocorticotropic Hormone/*metabolism ; Animals ; Brain/metabolism ; Catecholamines/*metabolism ; Cell Line ; Corticotropin-Releasing Hormone/metabolism ; Cyclic AMP/metabolism ; Glucocorticoids/*metabolism ; Humans ; Phospholipases A/metabolism ; Pituitary Gland, Anterior/metabolism ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Adrenergic, beta/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Somatostatin ; Somatostatin/pharmacology ; Stress, Physiological/*metabolism ; Stress, Psychological/metabolism ; Sympathetic Nervous System/metabolism ; Vasoactive Intestinal Peptide/pharmacology ; Vasopressins/pharmacology
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-10-12
    Description: A novel eukaryotic hybrid gene has been constructed from the 5' sequence of a rat gene and the bacterial neomycin-resistance gene. After transfection into hamster fibroblasts, the neo transcripts can be induced to high levels by the absence of glucose. Furthermore, this hybrid gene can be regulated by temperature when it is introduced into a temperature-sensitive mutant cell line.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Attenello, J W -- Lee, A S -- CA-27607/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 12;226(4671):187-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6484570" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; DNA, Recombinant ; Drug Resistance, Microbial ; Fibroblasts ; *Gene Expression Regulation ; Genes, Bacterial ; *Genes, Regulator ; Glucose/*pharmacology ; *HSP70 Heat-Shock Proteins ; Membrane Proteins/biosynthesis/*genetics ; Mutation ; Neomycin/pharmacology ; Rats ; Temperature ; Transcription, Genetic ; Transfection
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  • 20
    Publication Date: 1984-03-09
    Description: Activated mature T cells require T-cell growth factor (TCGF) for continuous proliferation. However, many mature T cells infected with human T-cell leukemia-lymphoma virus grow independently of exogenously added TCGF. It is now reported that cells infected with this virus also lack detectable TCGF messenger RNA (less than one copy per cell) and thus do not produce their own growth factor. The results apparently rule out an autostimulation mechanism of growth control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arya, S K -- Wong-Staal, F -- Gallo, R C -- New York, N.Y. -- Science. 1984 Mar 9;223(4640):1086-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320374" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Deltaretrovirus/*physiology ; *Gene Expression Regulation/drug effects ; Humans ; Interferon-gamma/genetics ; Interleukin-2/*genetics ; Phytohemagglutinins/pharmacology ; RNA, Messenger/*genetics ; T-Lymphocytes/metabolism/*microbiology ; Tetradecanoylphorbol Acetate/pharmacology
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  • 21
    Publication Date: 1984-08-31
    Description: Bromodeoxyuridine (BrdUrd) treatment of the prolactin nonproducing subclone of GH cells (rat pituitary tumor cells) induces amplification of a 20-kilobase DNA fragment including all of the prolactin gene coding sequences. This amplified DNA segment, which is flanked by two unamplified regions, thus designates a unit of BrdUrd-induced amplified sequence. Cloned DNA segments, 10.3 kilobases long, from the 5' end of the rat prolactin gene of BrdUrd-responsive and -nonresponsive cells, were ligated to the thymidine kinase gene of herpes simplex virus type 1 (HSV1TK), and the hybrid DNA was transferred to thymidine kinase-deficient mouse fibroblast cells by transfection. The HSV1TK gene and the rat prolactin gene were amplified together in drug-treated transfectants carrying the hybrid DNA HSV1TK gene and rat prolactin gene of BrdUrd-responsive GH cells. These results suggest that the 10.3-kilobase DNA segment at the 5' end of the rat prolactin gene of BrdUrd-responsive GH cells carries the information for drug-induced gene amplification (amplicon) and that another gene, such as the HSV1TK gene, is also amplified when the latter is placed adjacent to this segment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biswas, D K -- Hartigan, J A -- Pichler, M H -- CA28218/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 31;225(4665):941-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bromodeoxyuridine/*pharmacology ; Cell Line ; Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant ; *Gene Amplification ; Genes, Viral ; Mice ; Prolactin/genetics ; Rats ; Simplexvirus/genetics ; Thymidine Kinase/genetics ; Transfection
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  • 22
    Publication Date: 1984-07-06
    Description: Expression of the cellular abl (c- abl ) oncogene was studied in K-562 and other chronic myelogenous leukemia (CML) cells and cell lines by means of Northern blot hybridization. In contrast to non-CML cells, which contained 7.4- and 6.8-kilobase abl -related transcripts, the CML cells contained a predominant and novel 8.2-kilobase abl -related RNA. In addition, the levels of abl -related message were up to eight times higher in CML cell lines from patients at the blast crisis stage of the disease compared with CML cells obtained during the chronic phase and with non-CML cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, S J -- Kubonishi, I -- Miyoshi, I -- Groudine, M T -- New York, N.Y. -- Science. 1984 Jul 6;225(4657):72-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6587568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; DNA, Neoplasm/genetics ; Humans ; Leukemia, Myeloid/*genetics ; Mice ; Nucleic Acid Hybridization ; *Oncogenes ; RNA, Messenger/genetics ; *Transcription, Genetic
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  • 23
    Publication Date: 1984-06-15
    Description: Several lines of mouse mammary tissue that had been serially transplanted until mitotic senescence was reached were exposed in vivo to plastic implants that slowly released cholera toxin. Gland tissue surrounding the implants displayed new end buds, indicating reinitiation of growth and morphogenesis. The ability of cholera toxin, which elevates intracellular adenosine 3',5'-monophosphate, to temporarily reverse the senescent phenotype suggests that this mitotic dysfunction results not from generalized cellular deterioration but from specific changes in cell regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, C W -- Silberstein, G B -- Strickland, P -- 1050/PHS HHS/ -- New York, N.Y. -- Science. 1984 Jun 15;224(4654):1245-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6328652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/*drug effects ; Cell Line ; Cholera Toxin/*pharmacology ; Cyclic AMP/physiology ; DNA/biosynthesis ; Epithelium/drug effects ; Female ; Fibroblasts/drug effects ; Humans ; Mammary Glands, Animal/*drug effects ; Mice ; Mice, Inbred BALB C ; Mitosis/drug effects
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  • 24
    Publication Date: 1984-02-10
    Description: Macaque monkeys with the recently described acquired immunodeficiency syndrome show a marked defect in T-lymphocyte function and die with opportunistic infections and lymphoproliferative abnormalities. In the study described here a new type D retrovirus was isolated from two Macaca cyclopis with this syndrome. This virus is related to, but distinct from, Mason-Pfizer monkey virus, a type D retrovirus previously isolated from a mammary tumor of a rhesus monkey (Macaca mulatta).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daniel, M D -- King, N W -- Letvin, N L -- Hunt, R D -- Sehgal, P K -- Desrosiers, R C -- R01-A1 20729/PHS HHS/ -- RR00168/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):602-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695172" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Burkitt Lymphoma ; Cell Line ; Humans ; Immunologic Deficiency Syndromes/*microbiology ; Macaca ; Nucleic Acid Hybridization ; Retroviridae/genetics/immunology/*isolation & purification
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  • 25
    Publication Date: 1984-08-03
    Description: The nucleotide sequence of a human Blym-1 transforming gene activated in a Burkitt's lymphoma cell line was determined. This sequence predicts a small protein of 58 amino acids that is 33 percent identical to the predicted product of chicken Blym-1, the activated transforming gene of chicken B cell lymphomas. Both the human and chicken Blym-1 genes exhibit significant identity to an amino-terminal region of transferrins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, A -- Devine, J M -- Cooper, G M -- CA 07250/CA/NCI NIH HHS/ -- CA 28946/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 3;225(4661):516-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6330897" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Burkitt Lymphoma/*genetics ; Cell Line ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Humans ; *Oncogenes ; Structure-Activity Relationship ; Transcription, Genetic ; Transferrin/genetics
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  • 26
    Publication Date: 1984-12-14
    Description: Neutrophil migration inhibition factor from T lymphocytes (NIF-T) is a lymphokine that acts to localize granulocytes. Medium conditioned by the Mo human T-lymphoblast cell line was used to purify NIF-T, a glycoprotein with a molecular weight of 22,000. The NIF-T was found to potently stimulate the growth of granulocyte and macrophage colonies from human bone marrow and colony formation by the KG-1 myeloid leukemia cell line. Thus a human lymphokine (NIF-T) that modulates the activities of mature neutrophilic granulocytes is also a colony-stimulating factor acting on precursors to induce growth and differentiation of new effector cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gasson, J C -- Weisbart, R H -- Kaufman, S E -- Clark, S C -- Hewick, R M -- Wong, G G -- Golde, D W -- CA 30280/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1339-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6390681" target="_blank"〉PubMed〈/a〉
    Keywords: Bone Marrow Cells ; Cell Division ; Cell Line ; Chromatography, High Pressure Liquid ; Colony-Stimulating Factors/*isolation & purification ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/*cytology ; Humans ; Leukocyte Migration-Inhibitory Factors/*pharmacology ; Lymphokines/*pharmacology ; Macrophages/*cytology ; Molecular Weight
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  • 27
    Publication Date: 1984-04-13
    Description: To study the mode of action of human cytomegalovirus, an important teratogenic agent in human populations, the susceptibility of a pluripotent human embryonal carcinoma cell line to the virus was investigated. Viral antigens were not expressed nor was infectious virus produced by human embryonal carcinoma cells after infection, although the virus was able to penetrate these cells. In contrast, retinoic acid-induced differentiated derivatives of embryonal carcinoma cells were permissive for antigen expression and infectious virus production. Replication of human cytomegalovirus in human teratocarcinoma cells may therefore depend on cellular functions associated with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonczol, E -- Andrews, P W -- Plotkin, S A -- AI-14927/AI/NIAID NIH HHS/ -- CA-29894/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 13;224(4645):159-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322309" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Transformation, Neoplastic/drug effects/metabolism ; Cell Transformation, Viral/drug effects ; Cytomegalovirus/*physiology ; Embryonal Carcinoma Stem Cells ; Humans ; Neoplastic Stem Cells/*microbiology ; Stem Cells/*microbiology ; Teratoma/*microbiology ; Tretinoin/pharmacology ; *Virus Replication
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  • 28
    Publication Date: 1984-11-23
    Description: Platelet-derived growth factor (PDGF) has been previously shown to be homologous to the transforming gene of simian sarcoma virus (v-sis), and inappropriate expression of the cellular counterpart of the v-sis gene (c-sis) has been implicated in the generation of mesenchymal tumors. The U-2 OS human osteosarcoma line was shown to contain multiple c-sis transcripts. Immunoprecipitation experiments with antiserum to PDGF identified a variety of polypeptides ranging in size from 18,000 to 165,000 daltons that were immunoprecipitated specifically from U-2 OS cell extracts. The osteosarcoma also was shown to secrete a 29,000-dalton protein having the serological and structural characteristics of PDGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, D T -- Owen, A J -- Barth, R K -- Tempst, P -- Winoto, A -- Fors, L -- Hood, L E -- Antoniades, H N -- CA30101/CA/NCI NIH HHS/ -- HL27607/HL/NHLBI NIH HHS/ -- HL29583/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):972-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6209798" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA Replication ; Humans ; Molecular Weight ; Neoplasm Proteins/*genetics ; *Oncogenes ; Osteosarcoma/*genetics ; *Platelet-Derived Growth Factor ; Poly A/genetics/isolation & purification ; RNA/genetics/isolation & purification ; RNA, Messenger ; *Transcription, Genetic
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-12-14
    Description: In neuroblastoma lines in which the N-myc gene is present as a single copy, the expression of N-myc as messenger RNA is increased relative to that in nonneuroblastoma cell lines and tumors. The increase of expression in neuroblastomas with amplified N-myc genes is the result of (i) an increase in the absolute amount of expression of each N-myc gene and (ii) an increase in the copy number of the N-myc gene. A second gene--which is amplified in many of the same lines as N-myc--is expressed to about the same degree in most human cell lines and primary tumors regardless of origin (when normalized to gene copy number). Thus, a change in the regulation of N-myc expression in neuroblastomas and certain other tumors results in greatly increased expression of each N-myc gene copy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kohl, N E -- Gee, C E -- Alt, F W -- 2-P01 CA 23767-06/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Dec 14;226(4680):1335-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505694" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Gene Amplification ; Gene Expression Regulation ; Humans ; Neuroblastoma/*genetics ; *Oncogenes ; RNA, Messenger/metabolism
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  • 30
    Publication Date: 1984-10-05
    Description: Antibodies in sera from patients with adult T-cell leukemia-lymphoma or from healthy carriers of type I human T-cell leukemia virus (HTLV) recognize an antigen of approximately 42 kilodaltons (p42) in cell lines infected with HTLV-I. Radiolabel sequence analysis of cyanogen bromide fragments of p42 led to the conclusion that this antigen is encoded in part by LOR, a conserved portion of the "X" region that is flanked by the envelope gene and the 3' long terminal repeat of HTLV-I. It is possible that this novel product mediates the unique transformation properties of the HTLV family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, T H -- Coligan, J E -- Sodroski, J G -- Haseltine, W A -- Salahuddin, S Z -- Wong-Staal, F -- Gallo, R C -- Essex, M -- 2-T32-CA0903/CA/NCI NIH HHS/ -- CA07094/CA/NCI NIH HHS/ -- CA13885/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):57-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089350" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens, Viral/*genetics ; Base Sequence ; Cell Line ; Cyanogen Bromide ; Deltaretrovirus/*genetics/immunology ; *Genes, Viral ; Humans ; Peptide Fragments ; Trans-Activators ; Viral Proteins/*genetics
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  • 31
    Publication Date: 1984-08-24
    Description: Infectious retroviruses have been detected in 22 of 45 randomly selected patients with acquired immune deficiency syndrome (AIDS) and in other individuals from San Francisco. The AIDS-associated retroviruses (ARV) studied in detail had a type D morphology, Mg2+-dependent reverse transcriptase, and cytopathic effects on lymphocytes. The viruses can be propagated in an established adult human T cell line, HUT-78. They cross-react with antiserum to the lymphadenopathy-associated retrovirus isolated from AIDS patients in France. Antibodies to ARV were found in all 86 AIDS patients and in a high percentage of 88 other homosexual men in San Francisco. This observation indicates the widespread presence of these lymphocytopathic retroviruses and their close association with AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, J A -- Hoffman, A D -- Kramer, S M -- Landis, J A -- Shimabukuro, J M -- Oshiro, L S -- CA-34980/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 24;225(4664):840-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206563" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology/*microbiology ; Antibodies, Viral/analysis ; Bone Marrow/microbiology ; California ; Cell Line ; Cells, Cultured ; Cross Reactions ; Cytopathogenic Effect, Viral ; Deltaretrovirus/immunology/*isolation & purification/physiology/ultrastructure ; *Homosexuality ; Humans ; Leukocytes/microbiology ; Lymphatic Diseases/immunology ; Male ; RNA-Directed DNA Polymerase/metabolism ; Syndrome ; T-Lymphocytes ; Virus Cultivation
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  • 32
    Publication Date: 1984-05-25
    Description: In order to further define the mechanisms by which polypeptide growth factors regulate gene transcription and cellular growth, expression cloning techniques were used to select human epidermal growth factor (EGF) receptor complementary DNA clones. The EGF 3' coding domain shows striking homology to the transforming gene product of avian erythroblastosis virus (v-erbB). Over-expression of EGF receptors in A431 cell lines correlates with increased EGF receptor mRNA levels and amplification (up to 110 times) of the apparently singular EGF receptor gene. There appear to be three cytoplasmic polyadenylated RNA products of EGF receptor gene expression in A431 cells, one of which contains only 5' (EGF binding domain) sequences and is postulated to encode the secreted EGF receptor-related protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, C R -- Chen, W S -- Kruiger, W -- Stolarsky, L S -- Weber, W -- Evans, R M -- Verma, I M -- Gill, G N -- Rosenfeld, M G -- New York, N.Y. -- Science. 1984 May 25;224(4651):843-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6326261" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cloning, Molecular ; DNA/*genetics ; Gene Amplification ; Gene Expression Regulation ; Polymorphism, Genetic ; RNA, Messenger/genetics ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/*genetics
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-11-16
    Description: DNA polymerase-alpha is the major replicative DNA polymerase in animal cells. The gene coding for a mutant DNA polymerase-alpha was transferred from one cell to another by transfection of DNA from mutant cells. The DNA was isolated from a mutant hamster cell line resistant to aphidicolin, a specific inhibitor of DNA polymerase-alpha, and transferred into an aphidicolin-sensitive cell line. The resulting transfectants exhibited increased survival in the presence of aphidicolin and contained an aphidicolin-resistant DNA polymerase-alpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, P K -- Loeb, L A -- CA07418/CA/NCI NIH HHS/ -- CA24845/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):833-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6436977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphidicolin ; Cell Line ; Clone Cells ; Cricetinae ; Cricetulus/genetics ; DNA Polymerase II/*genetics ; Diterpenes/pharmacology ; Escherichia coli/genetics ; Humans ; Mice ; Mutation ; Salmon/genetics ; *Transfection
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  • 34
    Publication Date: 1984-06-29
    Description: Human T lymphocytes transformed by human T cell leukemia-lymphoma viruses or activated by lectins were found to produce stimulating factors that promoted both proliferation and maturation of oligodendroglial and astroglial cells in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merrill, J E -- Kutsunai, S -- Mohlstrom, C -- Hofman, F -- Groopman, J -- Golde, D W -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1428-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6610212" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Astrocytes/*drug effects ; Cell Division/*drug effects ; Cell Line ; Growth Substances/*pharmacology ; Humans ; Lymphocyte Activation ; Lymphokines/pharmacology ; Neuroglia/*drug effects ; Oligodendroglia/*drug effects ; Rats ; Receptors, Fc/metabolism ; T-Lymphocytes/*physiology
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  • 35
    Publication Date: 1984-04-27
    Description: The sequence of the human epidermal growth factor (EGF) receptor shows great homology with the avian erythroblastosis virus v-erb B oncogene, raising the possibility that the receptor gene is identical to the c-erb B protooncogene. Human A431 epidermoid carcinoma cells, which have an unusually high number of EGF receptors, were examined to determine whether elevated EGF receptor levels correlate with gene amplification. Southern blots of genomic DNA's from A431 and other human cell lines were probed with either a v-erb B gene fragment or a human EGF receptor complementary DNA clone (pE7), previously isolated from an A431 complementary DNA library. When either probe was used to analyze Eco RI- or Hind III-generated DNA fragments, EGF receptor DNA sequences were amplified about 30-fold in A431. Differences in the banding pattern of A431 DNA fragments relative to normal fibroblast DNA indicate the occurrence of a rearrangement in the region of the receptor gene. Furthermore, A431 cells contain a characteristic, prominent 2.9-kilobase RNA. These results are consistent with the hypothesis that, in A431 cells, gene amplification, possibly associated with a translocation event, may result in the overproduction of EGF receptor protein or the appearance of the transformed phenotype (or both).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merlino, G T -- Xu, Y H -- Ishii, S -- Clark, A J -- Semba, K -- Toyoshima, K -- Yamamoto, T -- Pastan, I -- New York, N.Y. -- Science. 1984 Apr 27;224(4647):417-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200934" target="_blank"〉PubMed〈/a〉
    Keywords: Alpharetrovirus/genetics ; Base Sequence ; Carcinoma, Squamous Cell ; Cell Line ; Dna ; DNA Restriction Enzymes ; Epidermal Growth Factor/metabolism ; *Gene Amplification ; Genes, Viral ; Humans ; Nucleic Acid Hybridization ; Oncogenes ; Poly A/genetics ; RNA/genetics ; RNA, Messenger ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/biosynthesis/*genetics ; Translocation, Genetic
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  • 36
    Publication Date: 1984-02-10
    Description: 3-Aminobenzamide and benzamide, purported to be specific inhibitors of the synthesis of poly(adenosine diphosphate-ribose), were used to elucidate possible functions of this biopolymer. These compounds, at frequently used experimental concentrations, not only inhibited the action of poly(adenosine diphosphate-ribose) synthetase but also affected cell viability, glucose metabolism, and DNA synthesis. Thus, the usefulness of 3-aminobenzamide and benzamide may be severely restricted by the difficulty of finding a dose small enough to inhibit the synthetase without producing additional metabolic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milam, K M -- Cleaver, J E -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):589-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6420886" target="_blank"〉PubMed〈/a〉
    Keywords: Benzamides/*toxicity ; Cell Line ; DNA Replication/drug effects ; Humans ; Kinetics ; Lymphocytes ; Nucleoside Diphosphate Sugars/*biosynthesis ; Poly Adenosine Diphosphate Ribose/*biosynthesis ; Poly(ADP-ribose) Polymerases/metabolism ; Structure-Activity Relationship
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  • 37
    Publication Date: 1984-09-07
    Description: A growth hormone minigene carrying its natural promoter (237 nucleotides of chromosomal DNA) was stably propagated in a murine retrovirus containing hypoxanthine-guanine phosphoribosyltransferase as a selectable marker. Glucocorticoid and thyroid hormone inducibility was transferred with the growth hormone gene. Recombinant virus with titers of 10(6) per milliliter was recovered. This demonstration that retroviruses can be used to transfer a nonselectable gene under its own regulatory control enlarges the scope of retroviral vectors as potent tools for gene transfer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, A D -- Ong, E S -- Rosenfeld, M G -- Verma, I M -- Evans, R M -- New York, N.Y. -- Science. 1984 Sep 7;225(4666):993-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089340" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; DNA, Recombinant ; DNA, Viral/analysis ; Dexamethasone/pharmacology ; Gene Expression Regulation ; *Genes ; Genes, Viral ; Genetic Markers ; *Genetic Vectors ; Growth Hormone/biosynthesis/*genetics ; Hypoxanthine Phosphoribosyltransferase/genetics ; Mice ; Operon ; Phenotype ; RNA, Viral/genetics ; Rats ; Retroviridae/*genetics ; Transcription, Genetic ; Transfection ; Triiodothyronine/pharmacology
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  • 38
    Publication Date: 1984-07-06
    Description: A strain of lymphadenopathy associated retrovirus ( LAV ) passaged in vitro was used to infect a lymphoblastoid cell line obtained by transformation with Epstein-Barr virus of B lymphocytes from a healthy donor. The virus produced from this line (B- LAV ) was also able to grow at a high rate in some other lymphoblastoid lines and in a Burkitt lymphoma line. This adapted strain retained the biochemical, ultrastructural, and antigenic characteristics of the original strain, as well as its tropism for normal T4+ lymphocytes. It is thus possible to grow LAV in large quantities that can be used for the preparation of diagnostic reagents. The interaction between such a human retrovirus and Epstein-Barr virus, a DNA virus, may have some implication for the pathology of the acquired immunodeficiency syndrome and related diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montagnier, L -- Gruest, J -- Chamaret, S -- Dauguet, C -- Axler, C -- Guetard, D -- Nugeyre, M T -- Barre-Sinoussi, F -- Chermann, J C -- Brunet, J B -- New York, N.Y. -- Science. 1984 Jul 6;225(4657):63-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6328661" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Antibodies, Monoclonal/immunology ; B-Lymphocytes/*microbiology ; Cell Line ; Cell Transformation, Viral ; Deltaretrovirus/metabolism ; Herpesvirus 4, Human/*metabolism ; Humans ; Retroviridae/*growth & development ; T-Lymphocytes/microbiology ; *Virus Replication
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-06-08
    Description: Binding of tumor cells to cryostat sections of host organs was studied. B16-F10 melanoma cells and reticulum cell sarcoma cells demonstrated an organ specificity in their binding in vitro that reflected the organ specificity of their metastatic distribution 25 days after intravenous injection. These results provide evidence for specific binding of tumor cells to the tissues that they selectively colonize in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Netland, P A -- Zetter, B R -- 5 T32 GM 07258/GM/NIGMS NIH HHS/ -- R01 CA 28540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1113-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6372098" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesiveness ; Animals ; Cell Line ; Humans ; Liver/physiopathology ; Lung/physiopathology ; Lymphoma, Large B-Cell, Diffuse/physiopathology ; Melanoma/physiopathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Metastasis/physiopathology ; Neoplasms/*physiopathology ; Neoplasms, Experimental/physiopathology ; *Organ Specificity
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  • 40
    Publication Date: 1984-02-17
    Description: Cell-free conditioned media from human T cells transformed by human T-cell leukemia-lymphoma virus (HTLV-I) were tested for the production of soluble biologically active factors, including several known lymphokines. The cell lines used were established from patients with T-cell leukemia-lymphoma and from human umbilical cord blood and bone marrow leukocytes transformed by HTLV-I in vitro. All of the cell lines liberated constitutively one or more of the 12 biological activities assayed. These included macrophage migration inhibitory factor (MIF), leukocyte migration inhibitory factor (LIF), leukocyte migration enhancing factor (MEF), macrophage activating factor (MAF), differentiation inducing factor (DIF), colony stimulating factor (CSF), eosinophil growth and maturation activity (eos. GMA), fibroblast activating factor (FAF), gamma-interferon and, in rare instances, T-cell growth factor (TCGF). Some cell lines produced interleukin 3 (IL-3), platelet-derived growth factor (PDGF), or B-cell growth factors (BCGF). Such cells should prove useful for the production of lymphokines and as sources of specific messenger RNA's for their genetic cloning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Markham, P D -- Lindner, S G -- Gootenberg, J -- Popovic, M -- Hemmi, H -- Sarin, P S -- Gallo, R C -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):703-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320367" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Antigens, Neoplasm/analysis ; Bone Marrow ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Deltaretrovirus/*genetics ; Female ; Humans ; Leukemia/*microbiology ; Lymphokines/*biosynthesis ; Lymphoma/*microbiology ; Phenotype ; Pregnancy ; T-Lymphocytes/*immunology
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  • 41
    Publication Date: 1984-12-07
    Description: The human T-cell leukemia (lymphotropic) virus type III (HTLV-III) appears to be central to the causation of the acquired immune deficiency syndrome (AIDS). Two full-length integrated proviral DNA forms of HTLV-III have now been cloned and analyzed, and DNA sequences of the virus in cell lines and fresh tissues from patients with AIDS or AIDS-related complex (ARC) have been characterized. The results revealed that (i) HTLV-III is an exogenous human retrovirus, approximately 10 kilobases in length, that lacks nucleic acid sequences derived from normal human DNA; (ii) HTLV-III, unlike HTLV types I and II, shows substantial diversity in its genomic restriction enzyme cleavage pattern; (iii) HTLV-III persists in substantial amounts in cells as unintegrated linear DNA, an uncommon property that has been linked to the cytopathic effects of certain animal retroviruses; and (iv) HTLV-III viral DNA can be detected in low levels in fresh (primary) lymphoid tissue of a minority of patients with AIDS or ARC but appears not to be present in Kaposi's sarcoma tissue. These findings have important implications concerning the biological properties of HTLV-III and the pathophysiology of AIDS and Kaposi's sarcoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaw, G M -- Hahn, B H -- Arya, S K -- Groopman, J E -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1984 Dec 7;226(4679):1165-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6095449" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Base Sequence ; Cell Line ; Child ; Cloning, Molecular ; Cytopathogenic Effect, Viral ; DNA Restriction Enzymes/metabolism ; DNA, Viral/*analysis ; Deltaretrovirus/*genetics ; Humans ; Male ; Nucleic Acid Hybridization
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  • 42
    Publication Date: 1984-06-08
    Description: A domain of DNA designated N-myc is amplified 20- to 140-fold in human neuroblastoma cell lines but not in cell lines from other tumor types. N-myc has now been found to be amplified in neuroblastoma tissue from 24 of 63 untreated patients (38 percent). The extent of amplification appears to be bimodal, with amplification of 100- to 300-fold in 12 cases and 3- to 10-fold in 10 others. Amplification was found in 0 of 15 patients with stage 1 or 2 disease, whereas 24 of 48 cases (50 percent) with stage 3 or 4 had evidence of N-myc amplification. These data indicate that N-myc amplification is a common event in untreated human neuroblastomas. Furthermore, N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodeur, G M -- Seeger, R C -- Schwab, M -- Varmus, H E -- Bishop, J M -- CA02971/CA/NCI NIH HHS/ -- CA13539/CA/NCI NIH HHS/ -- CA17829/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1121-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719137" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Cell Line ; Child ; Child, Preschool ; DNA, Neoplasm/genetics ; Eye Neoplasms/genetics ; *Gene Amplification ; Humans ; Infant ; Lymphatic Metastasis ; Middle Aged ; Neuroblastoma/*genetics/physiopathology ; Nucleic Acid Hybridization ; *Oncogenes ; Prognosis ; Retinoblastoma/genetics
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  • 43
    Publication Date: 1984-08-24
    Description: Monoclonal antibody Mab D1.1 recognizes on human melanoma cells a ganglioside antigen characterized by an alkali-labile O-acetylated sialic acid residue. Immunochemical analysis showed that this molecule is an O-acetylated product of the neuroectoderm-associated disialoganglioside GD3. Controlled chemical O-acetylation of purified GD3 resulted in the generation of this same epitope. Lysates of human melanoma cells were found to contain O-acetyltransferase activity capable of generating the antigenic epitope recognized by Mab D1.1. Thus, the addition of a single O-acetyl group to a common cell surface-associated ganglioside can create a potentially tumor-specific antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheresh, D A -- Reisfeld, R A -- Varki, A P -- CA 07544/CA/NCI NIH HHS/ -- CA 28420/CA/NCI NIH HHS/ -- GM32373/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Aug 24;225(4664):844-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206564" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Antibodies, Monoclonal ; Antigens, Neoplasm/*immunology ; Cell Line ; Epitopes/immunology ; Gangliosides/analysis/*immunology/metabolism ; Humans ; Melanoma/enzymology/*immunology
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  • 44
    Publication Date: 1984-06-22
    Description: Treatment of exponentially growing Chinese hamster ovary cells with bleomycin causes a dose-dependent decrease in cell survival due to DNA damage. This lethal effect can be potentiated by the addition of a nonlethal dose of the anticalmodulin drug N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide ( W13 ) but not its inactive analog N-(4-aminobutyl)-2-naphthalenesulfonamide ( W12 ). By preventing the repair of damaged DNA, W13 also inhibits recovery from potentially lethal damage induced by bleomycin. These data suggest a role for calmodulin in the DNA repair pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chafouleas, J G -- Bolton, W E -- Means, A R -- RR-05425/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 22;224(4655):1346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6203171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bleomycin/*pharmacology ; Calmodulin/*antagonists & inhibitors/*physiology ; Cell Division/drug effects ; Cell Line ; Cell Survival/drug effects ; Cricetinae ; Cricetulus ; DNA Repair/*drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Sulfonamides/pharmacology
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  • 45
    Publication Date: 1984-03-30
    Description: A 60-kilodalton protein was identified in chromatin digested by micrococcal nuclease during retinoic acid-induced differentiation of human leukemia (HL-60) cells to mature-like granulocytes. The protein was not detected in a retinoic acid-resistant variant of the HL-60 cell line treated with retinoic acid, in HL-60 cells induced with dimethyl sulfoxide, or in normal human granulocytes. This protein may have an important role in the regulation of retinoic acid-induced leukemic cell differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chou, R H -- Chervenick, P A -- Barch, D R -- CA14278-08/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 30;223(4643):1420-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6583846" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Transformation, Neoplastic/drug effects ; Centrifugation, Density Gradient ; Dimethyl Sulfoxide/pharmacology ; Electrophoresis, Polyacrylamide Gel ; Granulocytes/metabolism ; Humans ; Leukemia, Myeloid, Acute/*metabolism ; Neoplasm Proteins/*isolation & purification ; Nucleosomes/*metabolism ; Tretinoin/pharmacology
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-10-26
    Description: A protein (27,000 molecular weight) was previously found in rat Leydig cells after treatment with estradiol (E2) and human chorionic gonadotropin (hCG) in vitro. The effect of hCG occurred through increased E2 production. This hormone-regulated rat testicular protein was compared to an estrogen-regulated protein of similar physical characteristics isolated from a human mammary cancer cell line (MCF-7) and present in normal human estrogen target organs. The Leydig cells from rat and human tissue showed specific immunofluorescence and immunoperoxidase staining in the cytoplasm upon incubation with a monoclonal antibody (C11) to the estrogen-regulated protein from MCF-7 cells. Leydig cells after exposure to E2 or hCG showed the highest fluorescence intensity; this intensity was reduced by treatment with Tamoxifen. No reaction was associated with other testicular cells. The estrogen-regulated protein from human cell lines is therefore immunologically similar to that from the rat Leydig cell. The monoclonal antibody should be useful for further characterization of the Leydig cell protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciocca, D R -- Dufau, M L -- CA 11378/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 26;226(4673):445-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6387908" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; *Antibodies, Monoclonal ; Breast Neoplasms/metabolism ; Cell Line ; Chorionic Gonadotropin/pharmacology ; Cross Reactions ; Estradiol/pharmacology ; Fluorescent Antibody Technique ; Humans ; Immunoenzyme Techniques ; Leydig Cells/*analysis ; Male ; Middle Aged ; Proteins/*analysis ; Rats
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-11-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culliton, B J -- New York, N.Y. -- Science. 1984 Nov 16;226(4676):813-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494909" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomedical Research ; California ; Cell Line ; *Human Body ; Humans ; *Jurisprudence ; Patents as Topic/legislation & jurisprudence ; *Patient Rights ; Spleen/cytology ; *Tissue and Organ Procurement ; Regents of the University of California on the grounds that two researchers at ; the Los Angeles campus took unfair advantage of him by misappropriating cells ; derived from his spleen in the course of leukemia therapy--cells that were then ; used in research that led to a patent. A federal court procedural hearing on 29 ; October 1984 yielded a ruling that the case will be heard in California state ; court, though it will probably be at least three years before a trial date can be ; scheduled. University officials and scientists see the case as an "outrageous" ; and legally unjustified attempt to assert a claim to the patent. Nevertheless, ; policy makers and university institutional review boards now face the question of ; whether, and how, consent forms should be rewritten to clarify the issue.
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  • 48
    Publication Date: 1984-12-21
    Description: Cyclosporin A blocked production of the lymphokine interleukin 2 by activated T lymphocytes. In a human and a murine cell line this inhibition reflected an absence of interleukin 2 messenger RNA. Under conditions in which these cells are normally stimulated to secrete high levels of interleukin 2, they failed to do so in the presence of cyclosporin A. In both cell lines this failure was accompanied by an absence of interleukin 2 messenger accumulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elliott, J F -- Lin, Y -- Mizel, S B -- Bleackley, R C -- Harnish, D G -- Paetkau, V -- New York, N.Y. -- Science. 1984 Dec 21;226(4681):1439-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6334364" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cyclosporins/*pharmacology ; Humans ; Interleukin-2/biosynthesis/*genetics ; Mice ; Protein Biosynthesis/drug effects ; RNA, Messenger/*metabolism ; T-Lymphocytes/metabolism
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-02-17
    Description: A tumor isolate from a patient with serous cystadenocarcinoma of the ovary contained an activated rasK gene detected hy transfection of NIH/3T3 cells. In contrast, DNA from normal cells of the same patient lacked transforming activity, indicating that activation of this transforming gene was the consequence of somatic mutation in the neoplastic cells. The transforming gene product displayed an electrophoretic mobility in sodium dodecyl sulfate-polyacrylamide gels that differed from the mobilities of rasK transforming proteins in other tumors, indicating that a previously undescribed mutation was responsible for activation of rasK in this ovarian carcinoma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feig, L A -- Bast, R C Jr -- Knapp, R C -- Cooper, G M -- CA07101/CA/NCI NIH HHS/ -- CA18689/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):698-701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Neoplastic ; Cystadenocarcinoma/*genetics ; DNA, Neoplasm/genetics/isolation & purification ; Female ; Humans ; Lung Neoplasms/genetics ; Mice ; *Oncogenes ; Ovarian Neoplasms/*genetics ; Transfection
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  • 50
    Publication Date: 1984-02-10
    Description: Cells of the 10T 1/2 mouse fibroblast line transformed in vitro by ultraviolet radiation are antigenically similar to those from skin cancers produced in mice by repeated exposure to ultraviolet radiation. Both types of tumor cells grew preferentially in ultraviolet-irradiated syngeneic mice relative to untreated animals, and both were recognized by ultraviolet radiation-induced tumor-specific suppressor lymphocytes. These properties were not shared by 10T 1/2 cells transformed in vitro by x-rays or 3-methylcholanthrene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, M S -- Kripke, M L -- Chan, G L -- CA-09078/CA/NCI NIH HHS/ -- CA-11751/CA/NCI NIH HHS/ -- N01-CO-23909/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Feb 10;223(4636):593-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*analysis ; Carcinogens ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Mice ; Mice, Inbred C3H ; Neoplasm Transplantation ; Transplantation, Isogeneic ; *Ultraviolet Rays
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-08-17
    Description: A stable cell line expressing a complementary DNA clone encoding the vesicular stomatitis virus glycoprotein fused and formed polykaryons at pH 5.5. The formation of polykaryons was dependent on the presence of glycoprotein anchored at the cell surface and could be prevented by incubation of cells with a monoclonal antibody to the glycoprotein. Fusion occurred at a pH 0.5 unit lower than that observed for cells infected with vesicular stomatitis virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Florkiewicz, R Z -- Rose, J K -- 1 F32 AI06911-01/AI/NIAID NIH HHS/ -- AI15481/AI/NIAID NIH HHS/ -- CA 14195/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Aug 17;225(4663):721-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6087454" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/metabolism ; *Cell Fusion ; Cell Line ; Cell Membrane/*metabolism ; Glycoproteins/*metabolism ; Hydrogen-Ion Concentration ; *Membrane Glycoproteins ; Mice ; Vesicular stomatitis Indiana virus/*metabolism ; *Viral Envelope Proteins ; Viral Proteins/*metabolism
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  • 52
    Publication Date: 1984-09-07
    Description: Treatment of mice with the carcinogen N-methylnitrosourea results in the development of thymic lymphomas with frequent involvement of the N-ras oncogene. The activated mouse N-ras gene was isolated from one of these lymphomas and, by transformation in concert with restriction digestion, a map of the gene was prepared and its approximate boundaries were determined. By means of somatic cell hybrids the normal N-ras gene was found to be unlinked to other members of the ras gene family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guerrero, I -- Villasante, A -- D'Eustachio, P -- Pellicer, A -- CA-16239/CA/NCI NIH HHS/ -- GM-32105/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1984 Sep 7;225(4666):1041-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic ; Chromosome Mapping ; Cloning, Molecular ; Cricetinae ; DNA Restriction Enzymes ; Deoxyribonuclease EcoRI ; Genetic Linkage ; Hybrid Cells ; Lymphoma/chemically induced/*genetics ; Methylnitrosourea ; Mice ; Mice, Inbred Strains ; *Oncogenes ; Thymus Neoplasms/chemically induced/*genetics
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  • 53
    Publication Date: 1984-03-16
    Description: Antibodies reactive with proteins of human T-cell leukemia virus (HTLV) can be found in Old World monkeys. A T-lymphocyte cell line established from a seropositive baboon (Papio cynocephalus) was analyzed for the presence of viral DNA sequences. The provirus found in these cells was related to but distinct from HTLV subgroup I. These results add to recent evidence from human studies that HTLV represents a spectrum of infectious T-lymphotropic retroviruses that includes closely and distantly related members.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, H G -- Wong-Stall, F -- Gallo, R C -- New York, N.Y. -- Science. 1984 Mar 16;223(4641):1195-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322297" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/analysis ; Antigens, Viral/immunology ; Base Sequence ; Cell Line ; DNA Restriction Enzymes ; DNA, Viral/*analysis ; Deltaretrovirus/*genetics/immunology ; *Genes, Viral ; Humans ; Nucleic Acid Hybridization ; Papio/immunology/*microbiology ; Repetitive Sequences, Nucleic Acid ; T-Lymphocytes/*analysis/microbiology
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  • 54
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-12-21
    Description: Chromosome 14 breakpoints in malignant human lymphocytes cluster on the long (q) arm near bands q11 and q32. An inversion of chromosome 14 due to breaks in q11.2 and q32.3 has now been found in a newly established childhood T-cell lymphoma cell line and confirmed in T-cell chronic lymphocytic leukemia. A translocation was also found between chromosomes 10 and 14 with a breakpoint at 14q11.2 in another T-cell lymphoma cell line. It is proposed that a proximal region on chromosome 14 in or near sub-band q11.2 is related to T-cell function. Rearrangements in this region may affect the growth of T lymphocytes and be involved in the development of T-cell malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hecht, F -- Morgan, R -- Hecht, B K -- Smith, S D -- 25055/PHS HHS/ -- New York, N.Y. -- Science. 1984 Dec 21;226(4681):1445-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6438800" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosome Aberrations ; Humans ; Immunoglobulin Heavy Chains/genetics ; Leukemia, Lymphoid/*genetics ; Lymphoma/*genetics ; Male ; Middle Aged ; T-Lymphocytes ; Translocation, Genetic
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  • 55
    Publication Date: 1984-06-01
    Description: The ability of clonally derived lines of B16F1 and B16F10 melanoma cells to form experimental metastases in C57BL mice after intravenous injection was examined. Luria- Delbruck fluctuation analysis was applied to the results obtained with parallel subclones grown to small population sizes before testing for metastatic ability. The analysis demonstrated that variant cells capable of forming experimental metastases were generated in B16F1 cell populations at an effective rate of about 1.3 X 10(-5) per cell per generation while in B16F10 cell populations the effective rate of production was about 5 X 10(-5) per cell per generation. These results are consistent with a dynamic heterogeneity model of tumor progression. They suggest that the majority of cells in both lines are effectively nonmetastatic and that the higher metastatic ability of the B16F10 population may be due in part to a higher rate of generation of metastatic variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hill, R P -- Chambers, A F -- Ling, V -- Harris, J F -- New York, N.Y. -- Science. 1984 Jun 1;224(4652):998-1001.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Clone Cells ; Humans ; Melanoma/genetics/*physiopathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/physiopathology ; Neoplasms, Experimental/genetics/physiopathology ; Phenotype
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  • 56
    Publication Date: 1984-11-02
    Description: The tumor promoters 12-O-tetradecanoyl-phorbol-13-acetate and teleocidin markedly enhanced the transformation of C3H 10T1/2 mouse fibroblasts when these cells were transfected with the cloned human bladder cancer c-rasH oncogene. Transfection studies with the drug resistance marker gpt and time course studies indicate that this enhancement is not simply an effect on the process of DNA transfection. These findings, together with parallel studies with NIH 3T3 fibroblasts, also indicate that the competence of animal cells for DNA transfection is a function of the recipient cell line, the transfected marker, and the growth conditions. Our findings suggest that during multistage carcinogenesis tumor promoters may complement the function of activated cellular oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsiao, W L -- Gattoni-Celli, S -- Weinstein, I B -- CA 26056/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 2;226(4674):552-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6436974" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/*pharmacology ; Cell Line ; Cell Transformation, Neoplastic/*chemically induced ; DNA, Neoplasm/metabolism ; Humans ; Lyngbya Toxins/pharmacology ; Mice ; Mice, Inbred C3H ; Oncogenes/*drug effects ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection/drug effects
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  • 57
    Publication Date: 1984-03-09
    Description: The complete amino acid sequence of rat transforming growth factor type 1 has been determined. This growth factor, obtained from retrovirus-transformed fibroblasts, is structurally and functionally related to mouse epidermal growth factor and human urogastrone. Production of this polypeptide by various neoplastic cells might contribute to the continued expression of the transformed phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marquardt, H -- Hunkapiller, M W -- Hood, L E -- Todaro, G J -- New York, N.Y. -- Science. 1984 Mar 9;223(4640):1079-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6320373" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; *Cell Transformation, Neoplastic ; DNA/biosynthesis ; Epidermal Growth Factor/*metabolism/pharmacology ; Humans ; Idoxuridine/metabolism ; Mice ; Peptide Biosynthesis ; Peptides/*metabolism/pharmacology ; Rats ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; Structure-Activity Relationship ; Transforming Growth Factors
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):40-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6691135" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic ; Chromosome Aberrations ; *Gene Amplification ; Humans ; Leukemia/genetics ; Lung Neoplasms/genetics ; Neoplasms/*genetics/metabolism ; Neuroblastoma/genetics ; *Oncogenes ; RNA, Messenger/biosynthesis ; RNA, Neoplasm/biosynthesis ; Translocation, Genetic
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  • 59
    Publication Date: 1984-09-28
    Description: Tetanus-toxoid specific helper-inducer T-cell clones, which had been infected and transformed by human T-cell leukemia-lymphoma virus (HTLV-I), were obtained from an antigen-specific human T cell line by using a limiting dilution technique in the presence of the virus. These HTLV-I-infected T-cell clones proliferated specifically in response to soluble tetanus toxoid but, unlike normal T cells, they could do so in the absence of accessory cells. The HTLV-I-infected T-cell clones did not present the antigen to autologous antigen-specific T cells that were not infected with HTLV-I. The capacity of helper-inducer T cells to retain antigen-specific reactivity after infection by HTLV-I, while losing the normal T-cell requirement for accessory cells, has clinical and theoretical implications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitsuya, H -- Guo, H G -- Cossman, J -- Megson, M -- Reitz, M S Jr -- Broder, S -- New York, N.Y. -- Science. 1984 Sep 28;225(4669):1484-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6206569" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Surface/analysis ; Binding Sites ; Cell Line ; Cell Transformation, Viral ; Deltaretrovirus/genetics/*physiology ; Epitopes/metabolism ; Genes, Viral ; Humans ; *Lymphocyte Activation ; Phenotype ; T-Lymphocytes/*immunology/microbiology ; Tetanus Toxoid/immunology ; Viral Proteins/biosynthesis
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  • 60
    Publication Date: 1984-10-12
    Description: A recently discovered member of the human T-cell leukemia virus (HTLV) family of retroviruses has been etiologically linked to the acquired immune deficiency syndrome (AIDS). This virus, which has been designated HTLV-III, is tropic for OKT4-bearing (helper-inducer) T cells. Moreover, the virus is cytopathic for these cells. Suramin is a drug used in the therapy of Rhodesian trypanosomiasis and onchocerciasis, and it is known to inhibit the reverse transcriptase of a number of retroviruses. Suramin has now been found to block in vitro the infectivity and cytopathic effect of HTLV-III at doses that are clinically attainable in human beings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitsuya, H -- Popovic, M -- Yarchoan, R -- Matsushita, S -- Gallo, R C -- Broder, S -- New York, N.Y. -- Science. 1984 Oct 12;226(4671):172-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6091268" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Cell Survival/drug effects ; Clone Cells ; Cytopathogenic Effect, Viral/drug effects ; Deltaretrovirus/*drug effects/physiology ; Humans ; Suramin/*pharmacology ; T-Lymphocytes/*microbiology/physiology ; T-Lymphocytes, Helper-Inducer/*microbiology/physiology ; Virus Replication/drug effects
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  • 61
    Publication Date: 1984-12-21
    Description: High-resolution proton nuclear magnetic resonance (NMR) studies of intact cancer cells revealed differences between cells with the capacity to metastasize and those that produce locally invasive tumors. The NMR resonances that characterize the metastatic cells were associated with an increased ratio of cholesterol to phospholipid and an increased amount of plasma membrane-bound cholesterol ester. High-resolution NMR spectroscopy could therefore be used to assess the metastatic potential of primary tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountford, C E -- Wright, L C -- Holmes, K T -- Mackinnon, W B -- Gregory, P -- Fox, R M -- New York, N.Y. -- Science. 1984 Dec 21;226(4681):1415-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505699" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/analysis ; Cholesterol Esters/analysis ; *Magnetic Resonance Spectroscopy ; Membrane Lipids/analysis ; Neoplasm Metastasis/*etiology ; Neoplasms, Experimental/*analysis/pathology ; Rats ; Rats, Inbred Strains ; Triglycerides/analysis
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  • 62
    Publication Date: 1984-11-09
    Description: Antisera to synthetic peptides representing sequences of both chains of platelet-derived growth factor (PDGF) were used to structurally analyze PDGF isolated from outdated human platelets and PDGF-like proteins in normal and transformed cells. Most PDGF isolated from platelets did not contain the carboxyl portion of PDGF-2 in contrast to p20sis, the major form of p28sis detected in simian sarcoma virus-transformed cells. In addition, higher molecular weight forms of molecules containing PDGF-1 and PDGF-2 sequences were detected in all cell lines tested. These lines were heterogeneous with respect to species, cell type, and transforming agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Niman, H L -- Houghten, R A -- Bowen-Pope, D F -- CA 25803/CA/NCI NIH HHS/ -- HL 18645/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 9;226(4675):701-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494905" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Electrophoresis, Polyacrylamide Gel ; Humans ; Immune Sera/immunology ; Molecular Weight ; Platelet-Derived Growth Factor/*immunology/isolation & purification ; Rats
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  • 63
    Publication Date: 1984-06-08
    Description: Amplification is one of the mechanisms by which cellular oncogenes may be altered in their function, possibly leading to neoplastic transformation. The oncogenes c-myc, c- abl , and c-Ki-ras are amplified in several different human neoplasias. The oncogene c-myb, which is specifically expressed and regulated in hematopoietic cells, was found to be amplified in cell lines ML-1, ML-2, and ML-3, which were separately cultured from cells of a patient with acute myelogenous leukemia (AML). A five- to tenfold amplification was correlated with high levels of expression of normal size c-myb messenger RNA and with chromosomal abnormalities in the region 6q22 -24, where the c-myb locus is normally located. Amplification and cytogenetic abnormalities were detected in DNA's from primary and secondary cultures of ML cells, suggesting that they may have contributed to leukemogenesis. The similar AML cell lines HL-60 and ML's contain different amplified oncogenes: c-myc and c-myb, respectively. Alternative activation of structurally and possibly functionally similar oncogenes may distinguish--at the pathogenetic level--phenotypically similar tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelicci, P G -- Lanfrancone, L -- Brathwaite, M D -- Wolman, S R -- Dalla-Favera, R -- P30 CA-16087/CA/NCI NIH HHS/ -- RR 05399/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1117-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6585957" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; DNA, Neoplasm/genetics ; *Gene Amplification ; Humans ; Karyotyping ; Leukemia, Myeloid, Acute/*genetics ; Nucleic Acid Hybridization ; *Oncogenes
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  • 64
    Publication Date: 1984-05-04
    Description: A cell system was developed for the reproducible detection of human T-lymphotropic retroviruses (HTLV family) from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS). The cells are specific clones from a permissive human neoplastic T-cell line. Some of the clones permanently grow and continuously produce large amounts of virus after infection with cytopathic (HTLV-III) variants of these viruses. One cytopathic effect of HTLV-III in this system is the arrangement of multiple nuclei in a characteristic ring formation in giant cells of the infected T-cell population. These structures can be used as an indicator to detect HTLV-III in clinical specimens. This system opens the way to the routine detection of HTLV-III and related cytopathic variants of HTLV in patients with AIDS or pre-AIDS and in healthy carriers, and it provides large amounts of virus for detailed molecular and immunological analyses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Popovic, M -- Sarngadharan, M G -- Read, E -- Gallo, R C -- New York, N.Y. -- Science. 1984 May 4;224(4648):497-500.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6200935" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology ; Cell Division ; Cell Line ; Cell Nucleus/ultrastructure ; Cell Survival ; Clone Cells/microbiology ; Cytopathogenic Effect, Viral ; Deltaretrovirus/growth & development/*isolation & purification ; Genetic Variation ; Humans ; RNA-Directed DNA Polymerase/metabolism ; T-Lymphocytes/microbiology ; Virus Cultivation
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  • 65
    Publication Date: 1984-09-07
    Description: Four surface antigens previously recognized only in macrophages are present on human small cell lung carcinoma cells and tumors. Cancerous cells may arise from macrophage precursors in bone marrow, and these precursors migrate to lung to participate in the repair of damaged tissue produced by continuous heavy smoking. The characteristic presence of neuropeptides such as bombesin in small cell carcinoma, when considered along with these findings, presents new possibilities for the role of such peptides in nervous, endocrine, and immune system function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruff, M R -- Pert, C B -- New York, N.Y. -- Science. 1984 Sep 7;225(4666):1034-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089338" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Neoplasm/*analysis ; Antigens, Surface/*analysis ; Carcinoma, Small Cell/etiology/*immunology/pathology ; Cell Line ; Cell Transformation, Neoplastic ; *Hematopoietic Stem Cells ; Humans ; Lung Neoplasms/etiology/*immunology/pathology ; Macrophages/*immunology ; Monocytes/pathology ; Smoking
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  • 66
    Publication Date: 1984-10-05
    Description: The human T-cell leukemia viruses HTLV-I and HTLV-II are unique among the transforming retroviruses of vertebrates in their ability to transform human T cells in vitro and in their close association with human malignancies (T-cell lymphomas and leukemia). Their genomes are relatively simple, containing the genes gag, pol, env, and a 3' region termed "X." This 3' region may be responsible for the transforming potential of the viruses. The existence of proteins encoded by the 3' region has been postulated on the basis of multiple open reading frames. In the present study this region is shown to contain a gene encoding a protein of 40 kilodaltons in HTLV-I and 37 kilodaltons in HTLV-II. It is proposed that these proteins be called, respectively, p40xI and p37xII.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Shimotohno, K -- Cline, M J -- Golde, D W -- Chen, I S -- CA 16042/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- RR 00865/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 5;226(4670):61-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6089351" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; B-Lymphocytes/microbiology ; Cell Line ; *Cell Transformation, Viral ; Deltaretrovirus/analysis/*genetics/physiology ; *Genes, Viral ; Humans ; Immune Sera ; Molecular Weight ; T-Lymphocytes/*microbiology ; Trans-Activators ; Viral Proteins/genetics/immunology/*physiology
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  • 67
    Publication Date: 1984-11-30
    Description: A gene coding for the major histocompatibility antigen HLA-A2 was transferred into human HLA-A2 negative M1 cells and murine L cells. Following transfection, these cells expressed molecules at the cell surface that are biochemically indistinguishable from HLA-A2 antigens on the human cell line JY from which the HLA-A2 gene was isolated. The M1A2 cells were recognized and lysed by a cytolytic T-cell clone specific for HLA-A2. The transfected L cells which express HLA-A2 in association with human beta 2-microglobulin were not lysed by this T-cell clone. The specific cytolysis of M1A2 cells could be inhibited by monoclonal antibodies to HLA-A2, and monoclonal antibodies to T3, T8, and LFA-1 on cytotoxic T lymphocytes. These results suggest that killing by allospecific T cells requires HLA-A2 antigens as well as other species-specific structures on the target cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van de Rijn, M -- Bernabeu, C -- Royer-Pokora, B -- Weiss, J -- Seidman, J G -- de Vries, J -- Spits, H -- Terhorst, C -- AI 19148/AI/NIAID NIH HHS/ -- AI-15066/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1083-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6333726" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cytotoxicity, Immunologic ; *Genes ; HLA Antigens/*genetics ; HLA-A2 Antigen ; Humans ; L Cells (Cell Line)/immunology ; *Major Histocompatibility Complex ; Mice ; T-Lymphocytes, Cytotoxic/*immunology ; *Transfection
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-04-20
    Description: Human epidermoid carcinoma A431 cells in culture produce a soluble 105-kilodalton protein which, by the criteria of epidermal growth factor (EGF) binding, recognition by monoclonal and polyclonal antibodies to the EGF receptor, amino-terminal sequence analysis and carbohydrate content, is related to the cell surface domain of the EGF receptor. The high rate of production and the finding that with biosynthetic labeling the specific activity of this 105-kilodalton protein exceeds that of the intact receptor indicate that it is not derived from membrane-bound mature receptor but is separately produced by the cell. These cells thus separately synthesize an EGF receptor that is inserted into the membrane and an EGF receptor-related protein that is secreted.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, W -- Gill, G N -- Spiess, J -- AM13149/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Apr 20;224(4646):294-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6324343" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antibodies, Monoclonal/immunology ; Carbohydrates/analysis ; Carcinoma, Squamous Cell/*metabolism ; Cell Line ; Epidermal Growth Factor/metabolism ; Glycoproteins/analysis/*biosynthesis ; Humans ; Kinetics ; Molecular Weight ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/analysis/immunology/metabolism
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  • 69
    Publication Date: 1984-06-29
    Description: The gene encoding human interleukin-2 (IL-2) has been cloned from human spleen cells, peripheral blood lymphocytes, and the Jurkat cell line. Nucleotide sequence analysis of the gene revealed that the encoded IL-2 protein has three cysteines located at amino acid residues 58, 105, and 125 of the mature protein. Site-specific mutagenesis procedures were used to modify the IL-2 gene by changing each of the cysteine codons individually to serine codons. Substitution of serine for cysteine residues at either position 58 or 105 of the IL-2 protein substantially reduced biological activity, indicating that the cysteines at these positions are necessary for maintenance of the biologically active conformation and may therefore be linked by a disulfide bridge. The modified IL-2 protein containing a substitution at position 125 retained full biological activity, suggesting that the cysteine at this position is not involved in a disulfide bond and that a free sulfhydryl group at that position is not necessary for receptor binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, A -- Lu, S D -- Mark, D F -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1431-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6427925" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cell Line ; Cysteine/metabolism ; DNA, Recombinant/metabolism ; Escherichia coli/genetics ; Genes ; Humans ; Interleukin-2/*genetics ; *Mutation ; Receptors, Immunologic/metabolism ; Receptors, Interleukin-2 ; Serine/metabolism ; Structure-Activity Relationship
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  • 70
    Publication Date: 1984-01-20
    Description: The retroviral long terminal repeat (LTR) contains transcriptional control elements that affect viral gene expression. By deletion mutagenesis of the genome of the cloned Abelson murine leukemia virus, regulatory signals could be mapped to at least three domains within the LTR. A defective 5' LTR that did not sustain transforming gene function was complemented by an intact LTR positioned at the 3' end of the genome. This versatility of the retroviral genome with respect to its transcriptional control elements appears to provide a strong selective advantage for viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srinivasan, A -- Reddy, E P -- Dunn, C Y -- Aaronson, S A -- New York, N.Y. -- Science. 1984 Jan 20;223(4633):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322296" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/*genetics ; Animals ; Cell Line ; Cell Transformation, Viral ; Cloning, Molecular ; *Gene Expression Regulation ; *Genes, Viral ; Leukemia Virus, Murine/*genetics ; Mice ; Mutation ; *Repetitive Sequences, Nucleic Acid ; *Transcription, Genetic ; Transfection
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  • 71
    Publication Date: 1984-03-16
    Description: Fetal guinea pig cells were transformed by treatment with four different chemical carcinogens including nitroso compounds and polycyclic hydrocarbons. As a consequence of this treatment, oncogenes capable of transforming NIH/3T3 cells became activated in each of five independently established clonal guinea pig cell lines. Molecular characterization of representative NIH/3T3 transformants revealed that the same oncogene was present in each of the cell lines tested. Moreover, detection of this transforming gene paralleled the acquisition of tumorigenic properties by these neoplastic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sukumar, S -- Pulciani, S -- Doniger, J -- DiPaolo, J A -- Evans, C H -- Zbar, B -- Barbacid, M -- New York, N.Y. -- Science. 1984 Mar 16;223(4641):1197-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Benzo(a)pyrene ; Benzopyrenes ; *Carcinogens ; Cell Division ; Cell Line ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Diethylnitrosamine ; *Gene Expression Regulation ; Genes, Viral ; Guinea Pigs ; Methylcholanthrene ; Methylnitronitrosoguanidine ; Mice ; *Oncogenes ; Retroviridae/genetics
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  • 72
    Publication Date: 1984-11-23
    Description: Metastatic mouse melanoma cells have a high affinity for the basement membrane and the ability to degrade it; these properties may allow tumor cells to invade the membrane and disseminate. In this study it was found that the metastatic potential of mouse melanoma cells varied when the cells were exposed in culture to fibronectin or laminin. After removal of fibronectin or exposure to laminin, the cells had an increased affinity for basement membrane collagen, were more invasive of basement membranes in vitro, and produced more lung colonies in vivo. These changes are correlated with and may be due to an increase in the laminin-binding capacity of the tumor cell surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terranova, V P -- Williams, J E -- Liotta, L A -- Martin, G R -- New York, N.Y. -- Science. 1984 Nov 23;226(4677):982-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6505678" target="_blank"〉PubMed〈/a〉
    Keywords: Amnion/physiology ; Animals ; Cell Division/drug effects ; Cell Line ; Female ; Fibronectins/*pharmacology ; Humans ; Immune Sera ; Kinetics ; Laminin/*pharmacology ; Melanoma/*pathology ; Mice ; Neoplasm Metastasis/*pathology ; Pregnancy
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  • 73
    Publication Date: 1984-08-10
    Description: Early passages of the human teratocarcinoma cell line PA1 are not tumorigenic in nude mice, while late passages are. A transforming gene present in late passages of PA1 cells was isolated as a biologically active molecular clone and is a new isolate of the human rasN locus. Its transforming activity is due to a single G---A (G, guanine; A, adenine) point mutation at the codon for amino acid 12 which changes the codon for glycine so that an aspartic acid residue is expressed. In contrast to late passage PA1 cells (passages 106, 330, and 338), DNA from the PA1 cell line at early passages (passage 36) does not yield rasN foci in DNA transfection assays. Thus, the presence of an activated rasN in PA1 cells correlates with enhanced tumorigenicity of the cell line and, more importantly, may have arisen during cell culture in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tainsky, M A -- Cooper, C S -- Giovanella, B C -- Vande Woude, G F -- New York, N.Y. -- Science. 1984 Aug 10;225(4662):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6740333" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; DNA, Neoplasm/genetics ; Humans ; Mice ; Mice, Nude ; *Oncogenes ; Teratoma/*genetics ; Time Factors
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  • 74
    Publication Date: 1984-10-12
    Description: Human T-cell leukemia viruses (HTLV) are closely associated with some human T-cell leukemias and lymphomas. A unique 3' region of the HTLV genome is believed to be involved in HTLV-induced cellular transformation, although the function of this region has yet to be determined. A subgenomic messenger RNA transcribed from this region of HTLV has now been characterized. These results provide direct evidence for the expression of a novel gene in HTLV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Shimotohno, K -- Clark, S C -- Golde, D W -- Chen, I S -- CA 09297/CA/NCI NIH HHS/ -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Oct 12;226(4671):177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6091270" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cell Transformation, Viral ; Deltaretrovirus/*genetics/physiology ; *Genes, Viral ; Humans ; Nucleic Acid Hybridization ; RNA Splicing ; RNA, Messenger/genetics ; RNA, Viral/*genetics ; T-Lymphocytes ; Transcription, Genetic ; Viral Proteins/*genetics
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  • 75
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-05-25
    Description: A fluorescently labeled estradiol, N'-fluoresceino-N'-(17 beta-estradiol hemisuccinamide) thiourea (FE) was used for measuring estrogen receptor content per cell in tumor cells. The cellular content of FE was measured quantitatively by flow cytometry. Binding of FE occurs in the nanomolar concentration range, an indication of the high affinity of the labeled estradiol. Competition of FE for binding sites is observed with estrogens, but not with progestins, androgens, or glucocorticosteroids, indicating the specificity of FE binding. In contrast to other estrogen receptor assays, this new technique requires a small sample size (about 5000 cells) and permits the assessment of heterogeneity in estrogen receptor expression among tumor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van, N T -- Raber, M -- Barrows, G H -- Barlogie, B -- CA 16672/CA/NCI NIH HHS/ -- CA 28771/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 May 25;224(4651):876-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719116" target="_blank"〉PubMed〈/a〉
    Keywords: Binding, Competitive ; Breast Neoplasms/*analysis ; Cell Line ; Evaluation Studies as Topic ; Female ; *Flow Cytometry ; Humans ; Receptors, Estrogen/*analysis ; Temperature ; Time Factors
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  • 76
    Publication Date: 1984-06-29
    Description: The chromosomal breakpoint of chronic lymphocytic leukemia (CLL) cells of the B-cell type carrying the translocated long arms of chromosomes 11 and 14 [t(11;14) (q13;q32)] was cloned. The breakpoint was found to be within the joining segment of the human heavy chain locus on the translocated long arm of chromosome 14. A probe that is specific for chromosome 11 and that maps immediately 5' to the breakpoint on the 14q+ chromosome was isolated. The probe detected a rearrangement of the homologous genomic DNA segment in the parental CLL cells and also in DNA from a diffuse large cell lymphoma with the t(11;14) translocation. This rearranged DNA segment was not present in Burkitt lymphoma cells with the t(8;14) translocation or in nonneoplastic human lymphoblastoid cells. The probe can thus be used to identify and characterize a gene located on band q13 of chromosome 11 that appears to be involved in the malignant transformation of human B cells carrying the t(11;14) translocation. This gene, named bcl -1, appears to be unrelated to any of the known retrovirus oncogenes described to date.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsujimoto, Y -- Yunis, J -- Onorato-Showe, L -- Erikson, J -- Nowell, P C -- Croce, C M -- CA15882/CA/NCI NIH HHS/ -- CA16685/CA/NCI NIH HHS/ -- CA20034/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1403-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6610211" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Animals ; B-Lymphocytes ; Burkitt Lymphoma/genetics ; Cell Line ; *Chromosomes, Human, 13-15 ; *Cloning, Molecular ; DNA, Neoplasm/genetics ; DNA, Recombinant/metabolism ; Humans ; Hybrid Cells/metabolism ; Leukemia/*genetics ; Leukemia, Lymphoid/genetics ; Lymphoma/*genetics ; Male ; Mice ; Nucleic Acid Hybridization ; *Translocation, Genetic
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  • 77
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1984-06-29
    Description: The hormonal form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], at picomolar concentrations, inhibited the growth-promoting lymphokine interleukin-2, which is produced by human T lymphocytes activated in vitro by the mitogen phytohemagglutinin. Other metabolites of vitamin D3 were less effective than 1,25(OH)2D3 in suppressing interleukin-2; their order of potency corresponded to their respective affinity for the 1,25(OH)2D3 receptor, suggesting that the effect on interleukin-2 was mediated by this specific receptor. The proliferation of mitogen-activated lymphocytes was also inhibited by 1,25(OH)2D3. This effect of the hormone became more pronounced at later stages of the culture. These findings demonstrate that 1,25(OH)2D3 is an immunoregulatory hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsoukas, C D -- Provvedini, D M -- Manolagas, S C -- AM29779/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Jun 29;224(4656):1438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6427926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcitriol/*pharmacology ; Cell Division/drug effects ; Cell Line ; Humans ; Immunity, Cellular/*drug effects ; Interleukin-2/antagonists & inhibitors ; Lymphocyte Activation/drug effects ; Lymphocytes/drug effects ; Mice ; Monocytes/drug effects ; Receptors, Immunologic/drug effects ; Receptors, Interleukin-2
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  • 78
    Publication Date: 1984-03-30
    Description: The gene for interleukin-2 was isolated from the Jurkat cell line and from normal peripheral blood lymphocytes and, when inserted in Escherichia coli, was expressed at high concentrations. This interleukin-2 was purified to apparent homogeneity and tested for biological activity in a variety of assays in vitro and in vivo. The recombinant lymphokine supports the growth of murine and human interleukin-2 dependent cell lines, enhances the generation of murine and human cytolytic cells in vitro, and generates lymphokine activated killer cells from murine and human lymphocytes. It has a serum half-life of 2 to 3 minutes in the mouse and significantly enhances the generation of cytolytic cells in vivo after alloimmunization. No functional differences between native and the recombinant interleukin-2 molecules have been detected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, S A -- Grimm, E A -- McGrogan, M -- Doyle, M -- Kawasaki, E -- Koths, K -- Mark, D F -- New York, N.Y. -- Science. 1984 Mar 30;223(4643):1412-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6367046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA, Recombinant/metabolism ; Escherichia coli/*metabolism ; Humans ; Interleukin-2/biosynthesis/*genetics/physiology ; Killer Cells, Natural/physiology ; Lymphocytes/physiology ; Mice ; Mice, Inbred C57BL ; *Recombination, Genetic
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  • 79
    Publication Date: 1984-03-23
    Description: A tumor-derived growth factor that stimulates the proliferation of capillary endothelial cells has a very strong affinity for heparin. This heparin affinity makes it possible to purify the growth factor to a single-band preparation in a rapid two-step procedure. The purified growth factor is a cationic polypeptide, has a molecular weight of about 18,000, and stimulates capillary endothelial cell proliferation at a concentration of about 1 nanogram per milliliter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shing, Y -- Folkman, J -- Sullivan, R -- Butterfield, C -- Murray, J -- Klagsbrun, M -- CA 14019/CA/NCI NIH HHS/ -- CA 21763/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 23;223(4642):1296-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6199844" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification ; Animals ; Capillaries/*cytology ; Cell Division/drug effects ; Cell Line ; Chick Embryo ; Chondrosarcoma/*analysis ; Chromatography, Affinity ; DNA/biosynthesis ; Endothelium/cytology ; Growth Substances/*isolation & purification/metabolism/pharmacology ; Heparin/*metabolism ; Mice ; Neovascularization, Pathologic
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  • 80
    Publication Date: 1984-01-06
    Description: Immunotoxins containing pokeweed antiviral protein and monoclonal antibodies against human T cells or human transferrin receptor efficiently killed acute lymphoblastic leukemia cells. Chloroquine specifically enhanced the rate of protein synthesis inhibition by immunotoxin. Depending on its concentration, chloroquine (10 to 100 micromolar) reduced by up to 65-fold the amount of immunotoxin required to inhibit protein synthesis in the target cells 50 percent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramakrishnan, S -- Houston, L L -- CA 29889/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):58-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318313" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibodies, Monoclonal ; Cell Line ; Chloroquine/*pharmacology/therapeutic use ; Combined Modality Therapy ; Dose-Response Relationship, Drug ; Drug Synergism ; Humans ; Leukemia, Lymphoid/*metabolism/therapy ; *N-Glycosyl Hydrolases ; Neoplasm Proteins/*biosynthesis ; Plant Proteins/*pharmacology ; Receptors, Cell Surface/immunology ; Receptors, Transferrin ; Ribosome Inactivating Proteins, Type 1 ; T-Lymphocytes/immunology
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  • 81
    Publication Date: 1984-06-01
    Description: The effectiveness of adriamycin in the treatment of ovarian cancer and other human tumors has been limited by the development of drug resistance. Verapamil, a calcium channel blocking agent, completely reversed adriamycin resistance in human ovarian cancer cells with moderate (three- to sixfold) degrees of resistance and partially reversed resistance in highly (150-fold) resistant cells. The potentiating effect of verapamil was due to inhibition of adriamycin efflux in the resistant cells. These results have led to a clinical trial of adriamycin and verapamil in refractory ovarian cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogan, A M -- Hamilton, T C -- Young, R C -- Klecker, R W Jr -- Ozols, R F -- New York, N.Y. -- Science. 1984 Jun 1;224(4652):994-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6372095" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Doxorubicin/*therapeutic use ; Drug Resistance ; Female ; Humans ; Ovarian Neoplasms/*drug therapy ; Verapamil/*therapeutic use
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  • 82
    Publication Date: 1984-03-16
    Description: 5-Amino-4-imidazolecarboxamide riboside triphosphate (ZTP) is thought to play a regulatory role in cellular metabolism. Unlike other nucleoside triphosphates, ZTP is synthesized in a one-step reaction in which the pyrophosphate group of 5-phosphoribosyl-l-pyrophosphate is transferred to the riboside monophosphate (ZMP) in a reaction catalyzed by 5-phosphoribosyl-l-pyrophosphate synthetase; reversal of this reaction leads to dephosphorylation of ZTP to ZMP. This unusual route of synthesis (and catabolism) of ZTP may be important in defining its metabolic effects in the cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabina, R L -- Holmes, E W -- Becker, M A -- AM12413/AM/NIADDK NIH HHS/ -- AM28554/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1984 Mar 16;223(4641):1193-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6199843" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives/*biosynthesis/pharmacology ; Animals ; Cell Line ; Cricetinae ; Imidazoles/*biosynthesis ; Kinetics ; Phosphoribosyl Pyrophosphate/metabolism ; Phosphorylation ; Ribonucleosides/pharmacology ; Ribonucleotides/*biosynthesis ; Ribose-Phosphate Pyrophosphokinase/metabolism ; Substrate Specificity
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  • 83
    Publication Date: 1984-06-08
    Description: The CM-S cell line was established from the bone marrow of a child with congenital hypoplastic anemia and resembles its monocyte-macrophage lineage. Lethally x-irradiated CM-S cells from various passages and clones, representing different stages in the progression of the transformed growth phenotype, were tested for their ability to affect the survival and proliferation of normal human cord or adult blood leukocytes in co-culture. One clone, CM-SM, which is tumorigenic in athymic mice, consistently immortalized umbilical cord mononuclear cells but did not immortalize adult peripheral blood leukocytes. Six autonomous monocyte-like diploid cell lines were obtained and all were found to be of cord origin. Three lines were tumorigenic in athymic mice. Attempts to immortalize human leukocytes with cell-free supernatants from CM-S cells were unsuccessful.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Revoltella, R P -- Vigneti, E -- Ragona, G -- Rocchi, G -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1124-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719138" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; Cell Line ; Culture Media ; Female ; Fetal Blood/cytology ; Growth Substances/metabolism ; Humans ; Infant, Newborn ; Leukocytes/*metabolism ; Male ; Monocytes/*metabolism
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  • 84
    Publication Date: 1984-08-17
    Description: When isolated apical membrane vesicles prepared from cultured A6 epithelia were incubated in vitro with the methyl donor S-adenosylmethionine, the control rate of amiloride-inhibitable sodium transport was doubled. The methylation inhibitors 3-deazaadenosine and S-adenosyl homocysteine returned the S-adenosyl-methionine-stimulated sodium transport to control levels. Neither these agents nor adenosine affected sodium transport into control vesicles. In vesicles incubated with S-adenosyl-[3H-methyl]methionine, both membrane phospholipids and proteins were labeled, and this labeling was inhibited by deazaadenosine. In vesicles prepared from A6 cells treated with aldosterone, sodium transport was twice the control value and S-adenosylmethionine did not cause any further stimulation of transport. In those vesicles, both lipid and protein methylation were increased. These results suggest that methylation, which increases the rate of amiloride-sensitive sodium transport is involved in the action of aldosterone at the apical membrane level in epithelia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sariban-Sohraby, S -- Burg, M -- Wiesmann, W P -- Chiang, P K -- Johnson, J P -- New York, N.Y. -- Science. 1984 Aug 17;225(4663):745-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6463652" target="_blank"〉PubMed〈/a〉
    Keywords: Aldosterone/*physiology ; Amiloride/pharmacology ; Amphibians ; Animals ; Biological Transport, Active/drug effects ; Cell Line ; Cell Membrane/drug effects/*metabolism ; Kidney/metabolism ; Methylation ; S-Adenosylhomocysteine/pharmacology ; S-Adenosylmethionine/pharmacology ; Sodium/*metabolism ; Tubercidin/pharmacology
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-08-05
    Description: Tissue culture cells from several mammalian species, including three primate lines, were transfected with recombinant vectors carrying Escherichia coli xanthine-guanine phosphoribosyltransferase or Tn5 aminoglycoside phosphotransferase dominant selectable markers. Human HeLa and SV40-transformed xeroderma pigmentosum cells exhibited stable transformation frequencies of at least 10(-3) (0.1 percent). CV-1, an African green monkey kidney cell line, could be stably transformed with the exceptionally high frequency of 6 X 10(-2) (6 percent).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gorman, C -- Padmanabhan, R -- Howard, B H -- New York, N.Y. -- Science. 1983 Aug 5;221(4610):551-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6306768" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses/genetics ; Cell Line ; Cercopithecus aethiops ; Cricetinae ; Cricetulus ; DNA, Recombinant/*metabolism ; Genetic Vectors ; HeLa Cells/metabolism ; Humans ; Mice ; Plasmids ; *Transfection
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  • 86
    Publication Date: 1983-12-09
    Description: Three cell lines were derived from a homosexual patient with probable acquired immunodeficiency syndrome and Burkitt's lymphoma. The cell lines produce an unusual strain of Epstein-Barr virus which will both transform cord blood lymphocytes and induce early antigens in Raji cells. Translocations between chromosomes 8 and 22 have occurred in all three lines, but the cells synthesize immunoglobulin M with light chains of the kappa type, in contrast to the usual concordance between a translocation involving chromosome 22 and lambda chain synthesis. Both kappa genes and one lambda gene are rearranged. These findings indicate either that translocation may occur as a separate event from immunoglobulin gene rearrangement or that the proposed hierarchical sequence of immunoglobulin gene rearrangements is not always adhered to. The data also imply that in cells containing a translocation between the long arm of chromosome 8 and a chromosome bearing an immunoglobulin gene, alteration of cellular myc expression may occur regardless of the immunoglobulin gene that is expressed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magrath, I -- Erikson, J -- Whang-Peng, J -- Sieverts, H -- Armstrong, G -- Benjamin, D -- Triche, T -- Alabaster, O -- Croce, C M -- New York, N.Y. -- Science. 1983 Dec 9;222(4628):1094-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316501" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications ; Antigens, Viral/analysis ; Burkitt Lymphoma/complications/*genetics ; Cell Line ; Chromosomes, Human, 21-22 and Y ; Chromosomes, Human, 6-12 and X ; Epstein-Barr Virus Nuclear Antigens ; Herpesvirus 4, Human/analysis ; Homosexuality ; Humans ; Immunoglobulin Light Chains/*biosynthesis ; Immunoglobulin kappa-Chains/*biosynthesis ; Male ; Oncogenes
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-06-03
    Description: When normal diploid fibroblasts from mice, hamsters, and humans were grown in culture, the 5-methylcytosine content of their DNA's markedly decreased. The greatest rate of loss of 5-methylcytosine residues was observed in mouse cells, which survived the least number of division. Immortal mouse cell lines had more stable rates of methylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, V L -- Jones, P A -- 1-T32-CA09320/CA/NCI NIH HHS/ -- R01-GM30892/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1055-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6844925" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine ; *Aging ; Animals ; Cell Division ; Cell Line ; Cricetinae ; Cytosine/analogs & derivatives/metabolism ; DNA/metabolism/*physiology ; Fibroblasts/metabolism ; Humans ; Mesocricetus ; Methylation ; Mice ; Time Factors
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-01-21
    Description: Highly purified preparations of insulin receptor catalyzed the phosphorylation of the 95,000-dalton subunit of the insulin receptor. This subunit of the insulin receptor was also labeled with [alpha-32P]8-azidoadenosine 5'-triphosphate, a photoaffinity label for adenosine triphosphate binding sites. The identity of the 95,000-dalton band was confirmed in both cases by precipitation with a monoclonal antibody to the insulin receptor. These results suggest that the insulin receptor is itself a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roth, R A -- Cassell, D J -- New York, N.Y. -- Science. 1983 Jan 21;219(4582):299-301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849137" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Cell Line ; Cells, Cultured ; Lymphocytes ; Molecular Weight ; Phosphoproteins/physiology ; Protein Kinases/*physiology ; Receptor, Insulin/*physiology
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  • 89
    Publication Date: 1983-07-08
    Description: Normal bone marrow cells from a donor positive for herpes simplex virus were transformed with Epstein-Barr virus. The resulting lymphoblastoid cell line has secreted immunoglobulin G1 of the kappa type continuously for 2 years. This immunoglobulin, detected both on the cell surface and in the cytoplasm, reacts with cells infected with herpes simplex virus. It defines an antigen that comigrates with the 55-kilodalton glycoprotein D of herpes simplex virus type 1 and neutralizes the infectivity of herpes simplex viruses 1 and 2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seigneurin, J M -- Desgranges, C -- Seigneurin, D -- Paire, J -- Renversez, J C -- Jacquemont, B -- Micouin, C -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):173-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6304881" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Antibodies, Monoclonal/*immunology ; B-Lymphocytes/immunology ; Bone Marrow/*immunology ; Bone Marrow Cells ; Cell Line ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunoglobulin G/immunology ; Simplexvirus/*immunology ; Viral Envelope Proteins ; Viral Proteins/*immunology
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  • 90
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-04-29
    Description: The interspecific fusion of normal bovine lymphocytes with a nonsecreting mouse hybridoma produced stable cell lines secreting bovine immunoglobulins. One of these lines has continued to secrete immunoglobulin G1 (5 to 10 micrograms per milliliter) for over 16 months. The bovine x mouse hybrid cells can be expected to provide bovine monoclonal immunoglobulins for sequencing studies and for use as serological standards as well as to provide messenger RNA for cloning bovine immunoglobulin genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srikumaran, S -- Guidry, A J -- Goldsby, R A -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):522-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6403985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/biosynthesis ; Cattle ; Cell Line ; Hybridomas/*immunology ; Immunoglobulin G/*biosynthesis/immunology/isolation & purification ; Immunoglobulin Heavy Chains/immunology ; Immunoglobulin Light Chains/immunology ; Immunoglobulin M/immunology ; Mice ; Radioimmunoassay
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  • 91
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-06-10
    Description: Interleukin 2, a lymphokine that acts as a second signal of cellular immune response by way of its action as a T-cell growth factor, was morphologically identified by immunoperoxidase staining. With the use of a monoclonal antibody to interleukin 2 and several complex-forming antisera, the lymphokine was readily distinguished in cytocentrifuge preparations of peripheral blood leukocytes stimulated with a T-cell mitogen. When preparations of cloned interleukin 2 producer and responder cells were stained by the same procedures, discrete patterns of both responder and producer cell phenotypes were revealed. Interleukin 2 producer T cells exhibited a characteristic intense, ringlike cytoplasmic staining, whereas the responder cells (as exemplified by interleukin 2-dependent cell lines) exhibited a less intensive, spotlike membrane staining. In addition, intense membrane localization of interleukin 2, reminiscent of potential capping phenomena, could be observed in stained preparations of cloned responder cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinmann, G -- Conlon, P -- Hefeneider, S -- Gillis, S -- New York, N.Y. -- Science. 1983 Jun 10;220(4602):1188-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6344215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Cell Line ; Humans ; Immunoenzyme Techniques ; Interleukin-2/*physiology ; Leukocytes/physiology ; Mice ; T-Lymphocytes/physiology
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  • 92
    Publication Date: 1983-12-16
    Description: Aplysiatoxin and debromoaplysiatoxin, which are isolated from the seaweed, Lyngbya gracilis, differ in their chemical structure only by the presence or absence of a bromine residue in the hydrophilic region. The function and the structure-activity relation of the hydrophilic region are not known. Aplysiatoxin increased malignant transformation, stimulated DNA synthesis, and inhibited the binding of phorbol-12,13-dibutyrate and epidermal growth factor to cell receptors. Debromoaplysiatoxin inhibited the binding of these two substances as strongly as aplysiatoxin but did not increase malignant transformation or stimulate DNA synthesis. These results indicate that a slight change in the chemical structure of the hydrophilic region of aplysiatoxin affects its abilities to increase cell transformation and stimulate DNA synthesis and that the abilities of the tumor promoters to inhibit the binding of phorbol-12,13-dibutyrate and epidermal growth factor are dissociable from their abilities to increase cell transformation and stimulate DNA synthesis under some circumstances.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimomura, K -- Mullinix, M G -- Kakunaga, T -- Fujiki, H -- Sugimura, T -- New York, N.Y. -- Science. 1983 Dec 16;222(4629):1242-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316505" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Caenorhabditis elegans Proteins ; Carcinogens/*pharmacology ; Carrier Proteins ; Cell Line ; Cell Transformation, Neoplastic/*drug effects ; Chemical Phenomena ; Chemistry ; DNA/biosynthesis ; Epidermal Growth Factor/metabolism ; Lactones/analysis/*pharmacology ; *Lyngbya Toxins ; Mice ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/metabolism ; *Protein Kinase C ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/metabolism ; *Receptors, Drug ; Structure-Activity Relationship
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  • 93
    Publication Date: 1983-04-08
    Description: The involvement of plasma fibronectin in phagocytosis of bacteria was investigated by testing the binding of fibronectin to several species of bacteria and by evaluating the ability of fibronectin to promote binding and endocytosis of two species of these bacteria by phagocytic cells. Fibronectin binds non-covalently to Gram-positive and Gram-negative bacteria and to yeast but did not appear to be necessary or sufficient for uptake of Staphylococcus aureus and Salmonella typhimurium by several different phagocytic cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van de Water, L -- Destree, A T -- Hynes, R O -- R01CA17007/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):201-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6338594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*metabolism ; Cell Line ; Cricetinae ; Endocytosis ; Fibronectins/*metabolism ; Humans ; Macrophages/physiology ; Mice ; Opsonin Proteins/physiology ; *Phagocytosis ; Rabbits ; Salmonella typhimurium/metabolism ; Sepsis/immunology ; Staphylococcus aureus/metabolism
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  • 94
    Publication Date: 1983-06-10
    Description: Inhibiting protein synthesis by incubating C6-2B rat astrocytoma cells with cycloheximide or emetine for periods up to 24 hours caused a progressive decrease in the accumulation of adenosine 3',5'-monophosphate (cyclic AMP) when the cells were challenged for 30 minutes with 100 microM forskolin. In contrast, cholera toxin-stimulated (6 nM, 3 hours) cyclic AMP accumulation was not diminished in cycloheximide-treated cells, and cyclic AMP was only minimally diminished in response to a 30-minute challenge with 10 microM (-)-isoproterenol. These experiments suggest the presence of a previously unrecognized cyclase component, which is essential for forskolin-stimulated cyclic AMP accumulation and has a shorter half-life than the beta-adrenergic receptor, the guanine nucleotide regulatory proteins, or the cyclase catalytic component.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brooker, G -- Pedone, C -- Barovsky, K -- HL 06330/HL/NHLBI NIH HHS/ -- HL 28940/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 10;220(4602):1169-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6190226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytoma/metabolism ; Cell Line ; Cholera Toxin/pharmacology ; Colforsin ; Cyclic AMP/*biosynthesis/physiology ; Cycloheximide/pharmacology ; Dichlororibofuranosylbenzimidazole/pharmacology ; Diterpenes/*pharmacology ; Emetine/pharmacology ; Isoproterenol/pharmacology ; *Protein Biosynthesis ; RNA/biosynthesis ; Rats
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  • 95
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-12-16
    Description: The mouse neuroblastoma-rat glioma hybrid cell line NG108-15 was used to study the acute and chronic interaction of ethanol with intact neural cells. In the short term, ethanol inhibited opiate receptor binding, but after long-term exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High concentrations of ethanol (200 mM) increased opiate binding after 18 to 24 hours, whereas lower concentrations (25 to 50 mM) produced similar changes after 2 weeks. This model system has potential for exploring the cellular and molecular mechanisms underlying ethanol intoxication, tolerance, and withdrawal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Charness, M E -- Gordon, A S -- Diamond, I -- New York, N.Y. -- Science. 1983 Dec 16;222(4629):1246-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316506" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Dose-Response Relationship, Drug ; Enkephalin, Methionine/analogs & derivatives/metabolism ; Ethanol/*pharmacology ; Glioma ; Hybrid Cells ; Mice ; Neuroblastoma ; Neurons/*drug effects/metabolism ; Rats ; Receptors, Opioid/*drug effects/metabolism ; Time Factors
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-05-27
    Description: The DNA's from two of four methylcholanthrene-induced mouse fibrosarcomas contained transforming genes that were identical in their pattern of restriction endonuclease resistance to inactivation of biologic activity. This transforming gene was identified as the activated homolog of the Kirsten murine sarcoma virus onc gene, v-kis. The finding that a defined carcinogen reproducibly leads to activation of kis as a transforming gene should be of value in elucidating the role of oncogenes in the neoplastic process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eva, A -- Aaronson, S A -- New York, N.Y. -- Science. 1983 May 27;220(4600):955-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Transformation, Neoplastic/*drug effects ; DNA Restriction Enzymes ; DNA, Neoplasm/genetics ; Fibrosarcoma/chemically induced/*genetics ; Humans ; Methylcholanthrene/*pharmacology ; Mice ; Oncogenes/*drug effects ; Retroviridae/genetics ; Transfection
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-09-16
    Description: Shark cartilage contains a substance that strongly inhibits the growth of new blood vessels toward solid tumors, thereby restricting tumor growth. The abundance of this factor in shark cartilage, in contrast to cartilage from mammalian sources, may make sharks an ideal source of the inhibitor and may help to explain the rarity of neoplasms in these animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, A -- Langer, R -- EY04002/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 16;221(4616):1185-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6193581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cartilage/*physiology ; Cell Line ; Cornea ; Neoplasms/*blood supply ; *Neovascularization, Pathologic ; Rabbits ; Sharks
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  • 98
    Publication Date: 1983-09-23
    Description: The plasma membranes of hamster, mouse, and human tumor cell lines that display multiple resistance to drugs were examined by gel electrophoresis and immunoblotting. In every case, increased expression of a 170,000-dalton surface antigen was found to be correlated with multidrug resistance. This membrane component is of identical molecular size and shares some immunogenic homology with the previously characterized P-glycoprotein of colchicine-resistant Chinese hamster ovary cells. This finding may have application to cancer therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kartner, N -- Riordan, J R -- Ling, V -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1285-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6137059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane Permeability ; *Drug Resistance ; Glycoproteins/immunology/*physiology ; Membrane Proteins/*physiology ; Molecular Weight ; P-Glycoprotein
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  • 99
    Publication Date: 1983-11-04
    Description: The gene for glycoprotein D of herpes simplex virus type 1 (HSV-1) was expressed in stable mammalian cell lines. Glycoprotein D produced in these cells has a number of antigenic determinants in common with the native glycoprotein. Cell lines expressing glycoprotein D were used in an enzyme-linked immunosorbent assay to detect human antibodies to glycoprotein D. This strategy should prove useful in determining the extent to which the immune response to HSV-1 is directed toward glycoprotein D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berman, P W -- Dowbenko, D -- Lasky, L A -- Simonsen, C C -- New York, N.Y. -- Science. 1983 Nov 4;222(4623):524-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6312563" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/*analysis ; Base Sequence ; Cell Line ; Clone Cells ; DNA Restriction Enzymes ; DNA, Viral/genetics ; Enzyme-Linked Immunosorbent Assay ; *Genes ; *Genes, Viral ; Humans ; Plasmids ; Simplexvirus/genetics/*immunology ; Tetrahydrofolate Dehydrogenase/genetics ; *Viral Envelope Proteins ; Viral Proteins/*genetics/immunology
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  • 100
    Publication Date: 1983-10-14
    Description: Carcinoma cells and normal epithelial cells differ in the mitochondrial retention of a permeant cationic compound, rhodamine 123. The possibility of utilizing this difference in carcinoma chemotherapy was investigated. Rhodamine 123 exhibited anticarcinoma activity in mice, and this activity was potentiated by 2-deoxyglucose.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernal, S D -- Lampidis, T J -- McIsaac, R M -- Chen, L B -- CA22427/CA/NCI NIH HHS/ -- CA29793/CA/NCI NIH HHS/ -- CA33847/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Oct 14;222(4620):169-72.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6623064" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma/*drug therapy ; Carcinoma, Ehrlich Tumor/*drug therapy ; Cell Line ; Deoxyglucose/therapeutic use ; Drug Synergism ; Drug Therapy, Combination ; Energy Metabolism/drug effects ; Mice ; Mitochondria/drug effects ; Rhodamine 123 ; Rhodamines/*therapeutic use ; Urinary Bladder Neoplasms/*drug therapy ; Xanthenes/*therapeutic use
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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