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  • 1995-1999  (3,150)
  • 1996  (3,150)
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  • Articles  (3,150)
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  • 1995-1999  (3,150)
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  • 1
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    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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  • 6
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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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  • 7
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Neuroprotection by aspirin and sodium salicylate through blockade of NF-kappaB activation (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-22
    Description: Aspirin (acetylsalicylic acid) is a commonly prescribed drug with a wide pharmacological spectrum. At concentrations compatible with amounts in plasma during chronic anti-inflammatory therapy, acetylsalicylic acid and its metabolite sodium salicylate were found to be protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. The site of action of the drugs appeared to be downstream of glutamate receptors and to involve specific inhibition of glutamate-mediated induction of nuclear factor kappa B. These results may contribute to the emerging theme of anti-inflammatory drugs and neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grilli, M -- Pizzi, M -- Memo, M -- Spano, P -- New York, N.Y. -- Science. 1996 Nov 22;274(5291):1383-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pharmacology, Department of Biomedical Sciences and Biotechnologies, University of Brescia Medical School, Brescia, I-25123 Italy. mpharm@master.cci.unibs.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8910280" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspirin/*pharmacology ; Calcium/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology/drug effects/metabolism ; Dentate Gyrus/cytology/drug effects/metabolism ; Glutamic Acid/*pharmacology ; Hippocampus/cytology/*drug effects/metabolism ; In Vitro Techniques ; N-Methylaspartate/pharmacology ; NF-kappa B/*metabolism ; Neurons/cytology/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Pyramidal Cells/cytology/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium Salicylate/*pharmacology ; Transcription Factor AP-1/metabolism ; Up-Regulation
    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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    "Replay" of hippocampal "memories" (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, G P -- Rosenberg, J R -- Hary, D -- Breeze, P -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1216-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8966590" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bias (Epidemiology) ; Hippocampus/*physiology ; Memory/*physiology ; Motor Activity ; Rats ; Sleep/*physiology ; Time Factors
    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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    Neuronal gene expression in the waking state: a role for the locus coeruleus (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-11-15
    Description: Several transcription factors are expressed at higher levels in the waking than in the sleeping brain. In experiments with rats, the locus coeruleus, a noradrenergic nucleus with diffuse projections, was found to regulate such expression. In brain regions depleted of noradrenergic innervation, amounts of c-Fos and nerve growth factor-induced A after waking were as low as after sleep. Phosphorylation of cyclic adenosine monophosphate response element-binding protein was also reduced. In contrast, electroencephalographic activity was unchanged. The reduced activity of locus coeruleus neurons may explain why the induction of certain transcription factors, with potential effects on plasticity and learning, does not occur during sleep.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cirelli, C -- Pompeiano, M -- Tononi, G -- New York, N.Y. -- Science. 1996 Nov 15;274(5290):1211-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Neurosciences Institute, 10640 J. J. Hopkins Drive, San Diego, CA 92121, USA. tononi@nsi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8895474" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/drug effects/physiology ; Animals ; Benzylamines/pharmacology ; Brain/*metabolism ; Cerebral Cortex/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; DNA-Binding Proteins/genetics ; Early Growth Response Protein 1 ; Electroencephalography ; *Gene Expression Regulation ; *Genes, Immediate-Early ; Genes, fos ; Hippocampus/metabolism ; *Immediate-Early Proteins ; Locus Coeruleus/*physiology ; Neurons/*metabolism ; Norepinephrine/metabolism ; Oxidopamine/pharmacology ; Phosphorylation ; Rats ; Sleep ; Sleep Deprivation ; Sympathectomy, Chemical ; Transcription Factors/genetics ; *Wakefulness
    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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