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  • Articles  (115)
  • Rats  (67)
  • Phosphorylation  (55)
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  • American Association for the Advancement of Science (AAAS)  (115)
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  • 2020-2023
  • 1995-1999  (115)
  • 1996  (115)
  • Chemistry and Pharmacology  (115)
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  • Articles  (115)
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  • American Association for the Advancement of Science (AAAS)  (115)
  • UNESCO
  • Wiley-Blackwell  (3)
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  • 2020-2023
  • 1995-1999  (115)
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  • 1
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    Association of Src tyrosine kinase with a human potassium channel mediated by SH3 domain (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: The human Kv1.5 potassium channel (hKv1.5) contains proline-rich sequences identical to those that bind to Src homology 3 (SH3) domains. Direct association of the Src tyrosine kinase with cloned hKv1.5 and native hKv1.5 in human myocardium was observed. This interaction was mediated by the proline-rich motif of hKv1.5 and the SH3 domain of Src. Furthermore, hKv1.5 was tyrosine phosphorylated, and the channel current was suppressed, in cells coexpressing v-Src. These results provide direct biochemical evidence for a signaling complex composed of a potassium channel and a protein tyrosine kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, T C -- Fadool, D A -- Ren, R -- Levitan, I B -- F32 NS009952/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Volen Center for Complex Systems, Brandeis University, Waltham, MA 02254, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953041" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Cloning, Molecular ; Humans ; Kv1.5 Potassium Channel ; Molecular Sequence Data ; Myocardium/chemistry ; Oncogene Protein pp60(v-src)/metabolism ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Potassium Channels/chemistry/*metabolism ; *Potassium Channels, Voltage-Gated ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; src Homology Domains/*physiology ; src-Family Kinases/chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Control of EGF receptor signaling by clathrin-mediated endocytosis (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Epidermal growth factor receptor (EGFR) signaling was analyzed in mammalian cells conditionally defective for receptor-mediated endocytosis. EGF-dependent cell proliferation was enhanced in endocytosis-defective cells. However, early EGF-dependent signaling events were not uniformly up-regulated. A subset of signal transducers required the normal endocytic trafficking of EGFR for full activation. Thus, endocytic trafficking of activated EGFR plays a critical role not only in attenuating EGFR signaling but also in establishing and controlling specific signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vieira, A V -- Lamaze, C -- Schmid, S L -- CA58689/CA/NCI NIH HHS/ -- CA69099/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. slschmid@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953040" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; *Adaptor Proteins, Vesicular Transport ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Division/drug effects ; Cell Membrane/metabolism ; Clathrin/*physiology ; Coated Pits, Cell-Membrane/physiology ; Dynamins ; *Endocytosis ; Enzyme Activation ; Epidermal Growth Factor/metabolism/pharmacology ; GTP Phosphohydrolases/physiology ; HeLa Cells ; Humans ; Isoenzymes/metabolism ; Phosphatidylinositol 3-Kinases ; Phospholipase C gamma ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Phosphotyrosine/metabolism ; Proteins/metabolism ; Receptor, Epidermal Growth Factor/*metabolism ; Shc Signaling Adaptor Proteins ; *Signal Transduction ; Type C Phospholipases/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Immunologic NO synthase: elevation in severe AIDS dementia and induction by HIV-1 gp41 (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: Indirect mechanisms are implicated in the pathogenesis of the dementia associated with human immunodeficiency virus-type 1 (HIV-1) infection. Proinflammatory molecules such as tumor necrosis factor alpha and eicosanoids are elevated in the central nervous system of patients with HIV-1-related dementia. Nitric oxide (NO) is a potential mediator of neuronal injury, because cytokines may activate the immunologic (type II) isoform of NO synthase (iNOS). The levels of iNOS in severe HIV-1-associated dementia coincided with increased expression of the HIV-1 coat protein gp41. Furthermore, gp41 induced iNOS in primary cultures of mixed rat neuronal and glial cells and killed neurons through a NO-dependent mechanism. Thus, gp41-induced NO formation may contribute to the severe cognitive dysfunction associated with HIV-1 infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adamson, D C -- Wildemann, B -- Sasaki, M -- Glass, J D -- McArthur, J C -- Christov, V I -- Dawson, T M -- Dawson, V L -- AI35042/AI/NIAID NIH HHS/ -- NS07392/NS/NINDS NIH HHS/ -- NS22643/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1917-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Pathology 2-210, Baltimore, MD 21287, USA. valina.dawson@qmail.bs.jhu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943206" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Dementia Complex/*enzymology/metabolism ; Animals ; Brain/*enzymology/metabolism ; Cell Death ; Cells, Cultured ; Cerebral Cortex/enzymology/metabolism ; Enzyme Induction ; HIV Envelope Protein gp120/metabolism/pharmacology ; HIV Envelope Protein gp41/*metabolism/pharmacology ; *Hiv-1 ; Humans ; Neuroglia/cytology ; Neurons/cytology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/*biosynthesis/genetics ; Polymerase Chain Reaction ; Rats
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Reduction of voltage-dependent Mg2+ blockade of NMDA current in mechanically injured neurons (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-13
    Description: Activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors is implicated in the pathophysiology of traumatic brain injury. Here, the effects of mechanical injury on the voltage-dependent magnesium (Mg2+) block of NMDA currents in cultured rat cortical neurons were examined. Stretch-induced injury was found to reduce the Mg2+ blockade, resulting in significantly larger ionic currents and increases in intracellular free calcium (Ca2+) concentration after NMDA stimulation of injured neurons. The Mg2+ blockade was partially restored by increased extracellular Mg2+ concentration or by pretreatment with the protein kinase C inhibitor calphostin C. These findings could account for the secondary pathological changes associated with traumatic brain injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, L -- Rzigalinski, B A -- Ellis, E F -- Satin, L S -- HL07537-14/HL/NHLBI NIH HHS/ -- NS 27214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 13;274(5294):1921-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Post Office Box 980524, Richmond, VA 23298-0524, USA. lsatin@gems.vcu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8943207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cerebral Cortex/cytology/*metabolism ; Dizocilpine Maleate/pharmacology ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Magnesium/*pharmacology ; Membrane Potentials ; N-Methylaspartate/*pharmacology ; Naphthalenes/pharmacology ; Neurons/cytology/*metabolism ; Patch-Clamp Techniques ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/drug effects/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Survival of cholinergic forebrain neurons in developing p75NGFR-deficient mice (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: The functions of the low-affinity p75 nerve growth factor receptor (p75(NGFR)) in the central nervous system were explored in vivo. In normal mice, approximately 25 percent of the cholinergic basal forebrain neurons did not express TrkA and died between postnatal day 6 and 15. This loss did not occur in p75(NGFR)-deficient mice or in normal mice systemically injected with a p75(NGFR)-inhibiting peptide. Control, but not p75(NGFR)-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75(NGFR) mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75(NGFR) can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van der Zee, C E -- Ross, G M -- Riopelle, R J -- Hagg, T -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1729-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Tupper Building, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. thagg@is.dal.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Choline O-Acetyltransferase/metabolism ; DNA Fragmentation ; Interneurons/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neostriatum/cytology ; Neurons/*cytology/enzymology ; Oligopeptides/pharmacology ; Parasympathetic Nervous System/*cytology ; Phosphorylation ; Prosencephalon/*cytology ; Proto-Oncogene Proteins/metabolism ; Purkinje Cells/cytology ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkA ; Receptors, Nerve Growth Factor/deficiency/metabolism/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-06
    Description: Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. Transfection of antisense PS2 conferred protection against apoptosis induced by trophic withdrawal in nerve growth factor-differentiated or amyloid precursor protein-expressing PC12 cells. The apoptotic cell death induced by PS2 protein was sensitive to pertussis toxin, suggesting that heterotrimeric GTP-binding proteins are involved. A PS2 mutation associated with familial Alzheimer's disease was found to generate a molecule with enhanced basal apoptotic activity. This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolozin, B -- Iwasaki, K -- Vito, P -- Ganjei, J K -- Lacana, E -- Sunderland, T -- Zhao, B -- Kusiak, J W -- Wasco, W -- D'Adamio, L -- New York, N.Y. -- Science. 1996 Dec 6;274(5293):1710-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unit on Alzheimer Biology, Laboratory of Clinical Science, National Institute of Mental Health, Building 10, Room 3D41, 9000 Rockville Pike, Bethesda, MD 20892, USA. ldadamio@atlas.niaid.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8939861" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid beta-Peptides/pharmacology ; Amyloid beta-Protein Precursor/metabolism/pharmacology ; Animals ; *Apoptosis ; DNA, Antisense/genetics ; GTP-Binding Protein alpha Subunits, Gi-Go/physiology ; GTP-Binding Protein alpha Subunits, Gs/physiology ; Humans ; Membrane Proteins/*genetics/*physiology ; Mutation ; Nerve Growth Factors/pharmacology ; Neurons/*cytology ; PC12 Cells ; Peptide Fragments/pharmacology ; Pertussis Toxin ; Presenilin-2 ; Rats ; Transfection ; Virulence Factors, Bordetella/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    New view of spinal cord injury (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1996 Nov 29;274(5292):1466.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/drug effects ; Cycloheximide/pharmacology ; Humans ; Nerve Growth Factors/physiology ; Oligodendroglia/*pathology ; Rats ; Spinal Cord/*pathology ; Spinal Cord Injuries/drug therapy/*pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    RAC regulation of actin polymerization and proliferation by a pathway distinct from Jun kinase (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: The RAC guanine nucleotide binding proteins regulate multiple biological activities, including actin polymerization, activation of the Jun kinase (JNK) cascade, and cell proliferation. RAC effector loop mutants were identified that separate the ability of RAC to interact with different downstream effectors. One mutant of activated human RAC protein, RACV12H40 (with valine and histidine substituted at position 12 and 40, respectively), was defective in binding to PAK3, a Ste20-related p21-activated kinase (PAK), but bound to POR1, a RAC-binding protein. This mutant failed to stimulate PAK and JNK activity but still induced membrane ruffling and mediated transformation. A second mutant, RACV12L37 (with leucine substituted at position 37), which bound PAK but not POR1, induced JNK activation but was defective in inducing membrane ruffling and transformation. These results indicate that the effects of RAC on the JNK cascade and on actin polymerization and cell proliferation are mediated by distinct effector pathways that diverge at the level of RAC itself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joneson, T -- McDonough, M -- Bar-Sagi, D -- Van Aelst, L -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1374-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910277" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Actins/*metabolism ; *Adaptor Proteins, Signal Transducing ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Carrier Proteins/metabolism ; *Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP-Binding Proteins/genetics/metabolism/*physiology ; Humans ; JNK Mitogen-Activated Protein Kinases ; Mice ; *Mitogen-Activated Protein Kinases ; Mutagenesis ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Transfection ; p21-Activated Kinases ; rac GTP-Binding Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Activation of estrogen receptors (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joffe, M -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1285-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966591" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Synergism ; Estradiol/metabolism ; Estrogens, Non-Steroidal/metabolism/*pharmacology ; Humans ; Insecticides/metabolism/*pharmacology ; Polychlorinated Biphenyls/metabolism/*pharmacology ; Rats ; Receptors, Estrogen/drug effects/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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