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  • Rats  (282)
  • American Association for the Advancement of Science (AAAS)  (282)
  • Annual Reviews
  • Institute of Physics
  • Nature Publishing Group
  • Periodicals Archive Online (PAO)
  • 2005-2009
  • 1990-1994  (149)
  • 1980-1984  (133)
  • 1992  (77)
  • 1990  (72)
  • 1980  (133)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (282)
  • Annual Reviews
  • Institute of Physics
  • Nature Publishing Group
  • Periodicals Archive Online (PAO)
    • +
Years
  • 2005-2009
  • 1990-1994  (149)
  • 1980-1984  (133)
Year
  • 1
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    A cytosolic protein catalyzes the release of GDP from p21ras (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: The rate of release of guanine nucleotides from the ras proteins (Ras) is extremely slow in the presence of Mg2+. It seemed likely, therefore that a factor might exist to accelerate the release of guanosine diphosphate (GDP), and hence the exchange of GDP for guanosine triphosphate (GTP). Such a factor has now been discovered in rat brain cytosol. Brain cytosol was found to catalyze, by orders of magnitude, the release of guanine nucleotides from recombinant v-H-Ras protein bound with [alpha-32P]GDP. This effect occurred even in the presence of a large excess of Mg2+, but was destroyed by heat or by incubation of the cytosol for an hour at 37 degrees C in the absence of phosphatase inhibitors. The effect was observed with either v-H-Ras or c-H-Ras, but not with p25rab3A, a small G protein with about 30% similarity to Ras. The effect could not be mimicked by addition of recombinant Ras-GAP or purified GEF, a guanine nucleotide exchange factor involved in the regulation of eukaryotic protein synthesis. By gel filtration chromatography, the factor appears to possess a molecular size between 100,000 and 160,000 daltons. This protein (Ras-guanine nucleotide-releasing factor, or Ras-GRF) may be involved in the activation of p21ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolfman, A -- Macara, I G -- CA 43551/CA/NCI NIH HHS/ -- ES 01247/ES/NIEHS NIH HHS/ -- GM 41220/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):67-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics, University of Rochester Medical Center, NY 14642.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2181667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Brain/metabolism ; Cholic Acids ; Cytosol/*metabolism ; Guanine Nucleotides/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Hot Temperature ; Immunosorbent Techniques ; Kinetics ; Magnesium Chloride/pharmacology ; Molecular Weight ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins p21(ras) ; Rats ; Thionucleotides/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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    New transplant method evades immune attack (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skerrett, P J -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1248.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diabetes Mellitus, Experimental/*surgery ; Graft Enhancement, Immunologic ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Rats ; T-Lymphocytes/immunology ; Thymus Gland/surgery ; Transplantation, Heterotopic
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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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    Autophosphorylation of protein kinase C at three separated regions of its primary sequence (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-27
    Description: The major autophosphorylation sites of the rat beta II isozyme of protein kinase C were identified. The modified threonine and serine residues were found in the amino-terminal peptide, the carboxyl-terminal tail, and the hinge region between the regulatory lipid-binding domain and the catalytic kinase domain. Because this autophosphorylation follows an intrapeptide mechanism, extraordinary flexibility of the protein is necessary to phosphorylate the three regions. Comparison of the sequences surrounding the modified residues showed no obvious recognition motif nor any similarity to substrate phosphorylation sites, suggesting that proximity to the active site may be the primary criterion for their phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flint, A J -- Paladini, R D -- Koshland, D E Jr -- DK09765/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 27;249(4967):408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2377895" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Cloning, Molecular ; Isoenzymes/genetics/*metabolism ; Molecular Sequence Data ; Peptide Fragments/isolation & purification/metabolism ; Phosphorylation ; Protein Conformation ; Protein Kinase C/genetics/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Signal Transduction ; Trypsin
    Print ISSN: 0036-8075
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  • 4
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    Protection from chemotherapy-induced alopecia in a rat model (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: Alopecia (hair loss) is among the most distressing side effects of cancer chemotherapy. Little progress has been made, however, in its prevention or treatment, partly because of the lack of suitable experimental model. In recent work on the treatment of myelogenous leukemia in the rat, the following observations were made: (i) treatment of 8-day-old rats with cytosine arabinoside consistently produced alopecia, and (ii) ImuVert, a biologic response modifier derived from the bacterium Serratia marcescens, uniformly produced complete protection against the alopecia. In subsequent experiments, both cyclophosphamide and doxorubicin also produced alopecia in this model, and the doxorubicin-induced alopecia was prevented by treatment with ImuVert. The potential relevance of these observations to chemotherapy-induced alopecia in the clinical setting should be examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussein, A M -- Jimenez, J J -- McCall, C A -- Yunis, A A -- DK07114/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1564-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Miami School of Medicine, FL 33101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218498" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/chemically induced/*prevention & control ; Animals ; Biological Products ; Cytarabine/therapeutic use/*toxicity ; Disease Models, Animal ; Immunologic Factors/*therapeutic use ; Leukemia, Experimental/*drug therapy ; Rats ; Rats, Inbred F344 ; Skin/drug effects/pathology
    Print ISSN: 0036-8075
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  • 5
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    Autoradiographic imaging of phosphoinositide turnover in the brain (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-17
    Description: With [3H]cytidine as a precursor, phosphoinositide turnover can be localized in brain slices by selective autoradiography of the product [3H]cytidine diphosphate diacylglycerol, which is membrane-bound. In the cerebellum, glutamatergic stimulation elicits an increase of phosphoinositide turnover only in Purkinje cells and the molecular layer. In the hippocampus, both glutamatergic and muscarinic cholinergic stimulation increase phosphoinositide turnover, but with distinct localizations. Cholinergic stimulation affects CA1, CA3, CA4, and subiculum, whereas glutamatergic effects are restricted to the subiculum and CA3. Imaging phosphoinositide turnover in brain slices, which are amenable to electrophysiologic studies, will permit a dynamic localized analysis of regulation of this second messenger in response to synaptic stimulation of specific neuronal pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hwang, P M -- Bredt, D S -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- GM-07309/GM/NIGMS NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):802-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975122" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/analogs & derivatives/pharmacology ; Animals ; Autoradiography ; Brain/*metabolism ; Carbachol/pharmacology ; Cerebellum/drug effects/metabolism ; Cycloleucine/analogs & derivatives/pharmacology ; Cytidine/metabolism ; Cytidine Diphosphate Diglycerides/metabolism ; Glutamates/physiology ; Glutamic Acid ; Hippocampus/drug effects/metabolism ; Neomycin/pharmacology ; Phosphatidylinositols/*metabolism ; Pirenzepine/pharmacology ; Purkinje Cells/metabolism ; Rats ; Receptors, Muscarinic/drug effects/physiology ; Tissue Distribution
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  • 6
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    D1 and D2 dopamine receptor-regulated gene expression of striatonigral and striatopallidal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The striatum, which is the major component of the basal ganglia in the brain, is regulated in part by dopaminergic input from the substantia nigra. Severe movement disorders result from the loss of striatal dopamine in patients with Parkinson's disease. Rats with lesions of the nigrostriatal dopamine pathway caused by 6-hydroxydopamine (6-OHDA) serve as a model for Parkinson's disease and show alterations in gene expression in the two major output systems of the striatum to the globus pallidus and substantia nigra. Striatopallidal neurons show a 6-OHDA-induced elevation in their specific expression of messenger RNAs (mRNAs) encoding the D2 dopamine receptor and enkephalin, which is reversed by subsequent continuous treatment with the D2 agonist quinpirole. Conversely, striatonigral neurons show a 6-OHDA-induced reduction in their specific expression of mRNAs encoding the D1 dopamine receptor and substance P, which is reversed by subsequent daily injections of the D1 agonist SKF-38393. This treatment also increases dynorphin mRNA in striatonigral neurons. Thus, the differential effects of dopamine on striatonigral and striatopallidal neurons are mediated by their specific expression of D1 and D2 dopamine receptor subtypes, respectively.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gerfen, C R -- Engber, T M -- Mahan, L C -- Susel, Z -- Chase, T N -- Monsma, F J Jr -- Sibley, D R -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1429-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2147780" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Cerebral Cortex/physiology ; Corpus Striatum/drug effects/*metabolism ; Ergolines/pharmacology ; Gene Expression Regulation ; Globus Pallidus/drug effects/*metabolism ; Hydroxydopamines/pharmacology ; Models, Neurological ; Neurons/drug effects/*metabolism ; Oligonucleotide Probes ; Oxidopamine ; Quinpirole ; RNA, Messenger/drug effects/*genetics ; Rats ; Receptors, Dopamine/*genetics ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Substantia Nigra/drug effects/*metabolism ; Thalamus/physiology
    Print ISSN: 0036-8075
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  • 7
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    Light pulses that shift rhythms induce gene expression in the suprachiasmatic nucleus (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: Lighting cycles synchronize (entrain) mammalian circadian rhythms by altering activity of cells in the suprachiasmatic nucleus (SCN) of the hypothalamus, a circadian pacemaker. Exposure of hamsters and rats to light pulses at those phases of the circadian rhythm during which light can shift the rhythm caused increased immunoreactivity for the product of the immediate-early gene c-fos in cells in the region of the SCN that receives retinal fibers. Light pulses also increased messenger RNA for the Fos protein and for the immediate-early protein NGFI-A in the rat SCN. Similar increases in mRNA for NGFI-A were seen in the SCN of hamsters. Thus cells in this portion of the SCN undergo alterations in gene expression in response to retinal illumination, but only at times in the circadian cycle when light is capable of influencing entrainment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rusak, B -- Robertson, H A -- Wisden, W -- Hunt, S P -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Dalhousie University, Halifax, Nova Scotia, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2112267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Cricetinae ; Darkness ; *Gene Expression ; Light ; Nerve Growth Factors/*genetics ; Proto-Oncogene Proteins/*genetics ; Proto-Oncogene Proteins c-fos ; *Proto-Oncogenes ; RNA, Messenger/*analysis/genetics ; Rats ; Suprachiasmatic Nucleus/*physiology/radiation effects ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 8
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    Molecular cloning and expression of a complementary DNA for inositol 1,4,5-trisphosphate 3-kinase (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-06
    Description: A complementary DNA (cDNA) clone that encodes inositol 1,4,5-trisphosphate 3-kinase was isolated from a rat brain cDNA expression library with the use of monoclonal antibodies. This clone had an open reading frame that would direct the synthesis of a protein consisting of 449 amino acids and with a molecular mass of 49,853 daltons. The putative protein revealed a potential calmodulin-binding site and six regions with amino acid compositions (PEST regions) common to proteins that are susceptible to calpain. Expression of the cDNA in COS cells resulted in an approximately 150-fold increase in inositol 1,4,5-trisphosphate 3-kinase activity of these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, K Y -- Kim, H K -- Lee, S Y -- Moon, K H -- Sim, S S -- Kim, J W -- Chung, H K -- Rhee, S G -- New York, N.Y. -- Science. 1990 Apr 6;248(4951):64-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2157285" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Brain/enzymology ; Calcium/metabolism ; Calmodulin/metabolism ; Calpain/antagonists & inhibitors/pharmacology ; Cell Line ; *Cloning, Molecular ; Codon ; DNA/*genetics ; *Gene Expression ; Molecular Sequence Data ; Molecular Weight ; Phosphotransferases/*genetics/metabolism ; *Phosphotransferases (Alcohol Group Acceptor) ; Plasmids ; Rats ; Transfection
    Print ISSN: 0036-8075
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  • 9
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    Phencyclidine, dizocilpine, and cerebrocortical neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, H L -- Iversen, L L -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Sharp & Dohme Research Laboratories, West Point, PA 19486.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2403696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/drug effects/*ultrastructure ; Dibenzocycloheptenes/administration & dosage/*pharmacology ; Dizocilpine Maleate ; Male ; Neurons/drug effects/*ultrastructure ; Phencyclidine/*pharmacology ; Rats ; Vacuoles/drug effects
    Print ISSN: 0036-8075
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  • 10
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    Identification of a specialized adenylyl cyclase that may mediate odorant detection (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-12-07
    Description: The mammalian olfactory system may transduce odorant information via a G protein-mediated adenosine 3',5'-monophosphate (cAMP) cascade. A newly discovered adenylyl cyclase, termed type III, has been cloned, and its expression was localized to olfactory neurons. The type III protein resides in the sensory neuronal cilia, which project into the nasal lumen and are accessible to airborne odorants. The enzymatic activity of the type III adenylyl cyclase appears to differ from nonsensory cyclases. The large difference seen between basal and stimulated activity for the type III enzyme could allow considerable modulation of the intracellular cAMP concentration. This property may represent one mechanism of achieving sensitivity in odorant perception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bakalyar, H A -- Reed, R R -- 5T32CA09339/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1403-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255909" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/*physiology ; Amino Acid Sequence ; Animals ; Brain/enzymology/physiology ; Cell Line ; Clone Cells ; Cloning, Molecular ; Gene Library ; Glycosylation ; Isoenzymes/genetics/*physiology ; Macromolecular Substances ; Molecular Sequence Data ; Molecular Weight ; Neurons, Afferent/enzymology/physiology ; Nose/enzymology/physiology ; *Odors ; Protein Conformation ; Rats ; *Signal Transduction
    Print ISSN: 0036-8075
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  • 11
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    Endogenous cholecystokinin reduces feeding in young rats (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: The hypothesis that endogenous cholecystokinin (CCK) released from the small intestine during feeding causes satiety was tested in rat pups, 9 to 12 days old. Intragastric administration of soybean trypsin inhibitor, a procedure that releases CCK from the small intestine, decreased the subsequent intake of a test meal. This effect was reversed by prior treatment with MK-329, a selective antagonist of CCK at alimentary-type CCK (CCK-A) receptors. Thus, endogenous, small intestinal CCK can cause satiety in the neonatal rat and this effect involves CCK-A receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weller, A -- Smith, G P -- Gibbs, J -- MH00149/MH/NIMH NIH HHS/ -- MH40010/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1589-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Cornell University Medical College, White Plains, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2321020" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepinones/pharmacology ; Cholecystokinin/antagonists & inhibitors/*physiology ; Devazepide ; Eating/*physiology ; Intestine, Small/*metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Cholecystokinin/drug effects/*physiology
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  • 12
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    High probability opening of NMDA receptor channels by L-glutamate (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: Synaptic plasticity can be triggered by calcium flux into neurons through synaptically activated N-methyl-D-aspartate (NMDA) receptor channels. The amplitude and time course of the resulting intracellular calcium transient depend on the number of open NMDA receptor channels and the kinetics of their activation. Short applications of L-glutamate to outside-out patches from hippocampal neurons in the presence and absence of MK-801 revealed that about 30 percent of L-glutamate-bound channels are open at the peak of the current. This high probability of opening suggests that very few channels are required to guarantee a large, localized postsynaptic calcium transient.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jahr, C E -- NS21419/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):470-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute L474, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Dizocilpine Maleate/pharmacology ; Glutamates/*physiology ; Glutamic Acid ; Hippocampus/physiology ; In Vitro Techniques ; *Ion Channel Gating ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology
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  • 13
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    Syntaxin: a synaptic protein implicated in docking of synaptic vesicles at presynaptic active zones (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: Synaptic vesicles store neurotransmitters that are released during calcium-regulated exocytosis. The specificity of neurotransmitter release requires the localization of both synaptic vesicles and calcium channels to the presynaptic active zone. Two 35-kilodalton proteins (p35 or syntaxins) were identified that interact with the synaptic vesicle protein p65 (synaptotagmin). The p35 proteins are expressed only in the nervous system, are 84 percent identical, include carboxyl-terminal membrane anchors, and are concentrated on the plasma membrane at synaptic sites. An antibody to p35 immunoprecipitated solubilized N-type calcium channels. The p35 proteins may function in docking synaptic vesicles near calcium channels at presynaptic active zones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, M K -- Calakos, N -- Scheller, R H -- 2T32G07365/PHS HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):255-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Physiology, Stanford University Medical Center, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321498" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antigens, Surface ; *Calcium-Binding Proteins ; Electrophoresis, Polyacrylamide Gel ; Immunoblotting ; Membrane Glycoproteins/physiology ; Molecular Sequence Data ; Nerve Tissue Proteins/isolation & purification/*physiology ; Oligonucleotide Probes ; Rats ; Sequence Homology, Nucleic Acid ; Synaptic Transmission/physiology ; Synaptic Vesicles/*physiology ; Synaptotagmin I ; Synaptotagmins ; Syntaxin 1
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  • 14
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    Requirement for the adenovirus type 9 E4 region in production of mammary tumors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-07
    Description: Oncogenic viruses demonstrating a strict tropism for the mammary gland provide special opportunities to study the susceptibility of this tissue to neoplasia. In rats, human adenovirus type 9 (Ad9) elicits mammary fibroadenomas that are similar to common breast tumors in women, as well as phyllodes-like tumors and mammary sarcomas. By constructing recombinant adenoviruses between Ad9 and Ad26 (a related nontumorigenic virus), it was shown that the Ad9 E4 region was absolutely required to produce these mammary tumors. This indicates that an adenovirus gene located outside the classic transforming region (E1) can significantly influence the in vivo oncogenicity of an adenovirus. Consistent with a direct role in mammary gland oncogenesis, the Ad9 E4 region also exhibited transforming properties in vitro. Therefore, the Ad9 E4 region is a viral oncogene specifically involved in mammary gland tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Javier, R -- Raska, K Jr -- Shenk, T -- CA 21196/CA/NCI NIH HHS/ -- CA 41086/CA/NCI NIH HHS/ -- T32 CA09528/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1267-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519063" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/*pathogenicity ; Amino Acid Sequence ; Animals ; Cell Transformation, Neoplastic/*genetics ; Chromosome Mapping ; Female ; Mammary Neoplasms, Experimental/*genetics/*microbiology ; Molecular Sequence Data ; Open Reading Frames/genetics ; Rats ; Rats, Inbred WF ; Sequence Homology, Nucleic Acid
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  • 15
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    Exaggerated carcinogenicity of chemicals (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1992 Jun 19;256(5064):1609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1609271" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butadienes/*toxicity ; *Carcinogenicity Tests ; Haplorhini ; Humans ; Mice ; Neoplasms/*chemically induced ; Rats ; Risk
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  • 16
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    Repression of the insulin-like growth factor II gene by the Wilms tumor suppressor WT1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-31
    Description: The Wilms tumor suppressor gene wt1 encodes a zinc finger DNA binding protein, WT1, that functions as a transcriptional repressor. The fetal mitogen insulin-like growth factor II (IGF-II) is overexpressed in Wilms tumors and may have autocrine effects in tumor progression. The major fetal IGF-II promoter was defined in transient transfection assays as a region spanning from nucleotides -295 to +135, relative to the transcription start site. WT1 bound to multiple sites in this region and functioned as a potent repressor of IGF-II transcription in vivo. Maximal repression was dependent on the presence of WT1 binding sites on each side of the transcriptional initiation site. These findings provide a molecular basis for overexpression of IGF-II in Wilms tumors and suggest that WT1 negatively regulates blastemal cell proliferation by limiting the production of a fetal growth factor in the developing vertebrate kidney.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drummond, I A -- Madden, S L -- Rohwer-Nutter, P -- Bell, G I -- Sukhatme, V P -- Rauscher, F J 3rd -- CA 10817/CA/NCI NIH HHS/ -- CA 47983/CA/NCI NIH HHS/ -- CA 52009/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1323141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*metabolism ; Deoxyribonuclease I/metabolism ; *Gene Expression Regulation, Neoplastic ; Genes, Wilms Tumor/*physiology ; Humans ; Insulin-Like Growth Factor II/*genetics ; Kidney/embryology/metabolism ; Mice ; Molecular Sequence Data ; Promoter Regions, Genetic ; Rats ; Sequence Homology, Nucleic Acid ; Transfection ; WT1 Proteins ; Wilms Tumor/genetics/metabolism ; Zinc Fingers
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  • 17
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    Cholecystokinin antianalgesia: safety cues abolish morphine analgesia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Environmental stimuli that signal the occurrence of aversive or dangerous events activate endogenous opiate analgesia systems. Signals for safety (the nonoccurrence of aversive events) produce the opposite and inhibit environmentally produced analgesia. Stimuli that signal safety are now shown to abolish the analgesic effect of morphine, even when morphine is applied directly to spinal cord. Further, this antiopiate effect occurs because the environmental stimulus leads to release of the neuropeptide cholecystokinin in the spinal cord. This process may contribute to the regulation of pain and the development of opiate tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wiertelak, E P -- Maier, S F -- Watkins, L R -- 5T32MH14617-15/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):830-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589765" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Benzodiazepinones/pharmacology ; Cholecystokinin/*pharmacology ; Injections, Spinal ; Morphine/administration & dosage/antagonists & inhibitors/*pharmacology ; Pain/physiopathology ; *Phenylurea Compounds ; Rats ; Receptors, Cholecystokinin/antagonists & inhibitors/*physiology ; Safety ; Spinal Cord/drug effects/*physiology
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  • 18
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    Chondroitin sulfate as a regulator of neuronal patterning in the retina (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-07
    Description: Highly sulfated proteoglycans are correlated with axon boundaries in the developing central nervous system which suggests that these molecules affect neural pattern formation. In the developing mammalian retina, gradual regression of chondroitin sulfate may help control the onset of ganglion cell differentiation and initial direction of their axons. Changes induced by the removal of chondroitin sulfate from intact retinas in culture confirm the function of chondroitin sulfate in retinal histogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brittis, P A -- Canning, D R -- Silver, J -- New York, N.Y. -- Science. 1992 Feb 7;255(5045):733-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University, Cleveland, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1738848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Differentiation/drug effects ; Cells, Cultured ; Chondroitin Lyases/pharmacology ; Chondroitin Sulfate Proteoglycans/pharmacology ; Chondroitin Sulfates/analysis/*physiology ; Immunohistochemistry ; Rats ; Retina/chemistry/cytology/*embryology ; Retinal Ganglion Cells/chemistry/*cytology ; Tubulin/analysis
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  • 19
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    Activity-dependent decrease in NMDA receptor responses during development of the visual cortex (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-06
    Description: Plasticity of the developing visual system has been regarded as the best model for changes of neuronal connections under the influence of the environment. N-methyl-D-aspartate (NMDA) receptors are crucial for experience-dependent synaptic modifications that occur in the developing visual cortex. NMDA-mediated excitatory postsynaptic currents (EPSCs) in layer IV neurons of the visual cortex lasted longer in young rats than in adult rats, and the duration of the EPSCs became progressively shorter, in parallel with the developmental reduction in synaptic plasticity. This decrease in NMDA receptor-mediated EPSC duration is delayed when the animals are reared in the dark, a condition that prolongs developmental plasticity, and is prevented by treatment with tetrodotoxin, a procedure that inhibits neural activity. Application of L-glutamate to outside-out patches excised from layer IV neurons of young, but not of adult, rats activated prolonged bursts of NMDA channel openings. A modification of the NMDA receptor gating properties may therefore account for the age-dependent decline of visual cortical plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmignoto, G -- Vicini, S -- P01 NS 28130-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 6;258(5084):1007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉FIDIA Georgetown Institute for the Neurosciences, Georgetown University School of Medicine, Washington, DC 20007.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279803" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Aging/physiology ; Animals ; Electric Conductivity ; Glutamates/pharmacology ; Glutamic Acid ; Ion Channel Gating/physiology ; Ion Channels/physiology ; Neuronal Plasticity/physiology ; Neurons/drug effects/physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Synapses/physiology ; Tetrodotoxin/pharmacology ; Visual Cortex/*growth & development/physiology
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  • 20
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    Interleukin-8 as a macrophage-derived mediator of angiogenesis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-11
    Description: Angiogenic factors produced by monocytes-macrophages are involved in the pathogenesis of chronic inflammatory disorders characterized by persistent angiogenesis. The possibility was tested that interleukin-8 (IL-8), which is a cytokine that is chemotactic for lymphocytes and neutrophils, is also angiogenic. Human recombinant IL-8 was potently angiogenic when implanted in the rat cornea and induced proliferation and chemotaxis of human umbilical vein endothelial cells. Angiogenic activity present in the conditioned media of inflamed human rheumatoid synovial tissue macrophages or lipopolysaccharide-stimulated blood monocytes was equally blocked by antibodies to either IL-8 or tumor necrosis factor-alpha. An IL-8 antisense oligonucleotide specifically blocked the production of monocyte-induced angiogenic activity. These data suggest a function for macrophage-derived IL-8 in angiogenesis-dependent disorders such as rheumatoid arthritis, tumor growth, and wound repair.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, A E -- Polverini, P J -- Kunkel, S L -- Harlow, L A -- DiPietro, L A -- Elner, V M -- Elner, S G -- Strieter, R M -- AR30692/AR/NIAMS NIH HHS/ -- AR41492/AR/NIAMS NIH HHS/ -- HL39926/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1798-801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1281554" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/physiopathology ; Base Sequence ; Cell Division/drug effects ; Cells, Cultured ; Chemotaxis/*drug effects ; Cornea/*drug effects/physiology ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects/*physiology ; Fibroblast Growth Factor 2/pharmacology ; Humans ; Interleukin-8/genetics/*pharmacology ; Macrophages/*physiology ; Mice ; Molecular Sequence Data ; Monocytes/physiology ; *Neovascularization, Pathologic ; Oligonucleotides, Antisense/*pharmacology ; Rabbits ; Rats ; Recombinant Proteins/pharmacology ; Synovial Fluid/physiology ; Tumor Necrosis Factor-alpha/genetics ; Umbilical Veins
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  • 21
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    Dendritic spines: convergence of theory and experiment (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, C -- Zador, A -- Brown, T H -- New York, N.Y. -- Science. 1992 May 15;256(5059):973-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computation and Neural Systems Program, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589781" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/physiology/ultrastructure ; Calcium/metabolism ; Dendrites/physiology/*ultrastructure ; Electrophysiology ; Hippocampus/*ultrastructure ; Microscopy, Electron ; Rats ; Synapses/physiology
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  • 22
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    Flow-dependent cytosolic acidification of vascular endothelial cells (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-10-23
    Description: Hemodynamic shear stress affects endothelial cell structure and function, but little is known about the signal transduction mechanisms involved in these processes. The effect of laminar shear stress on cytosolic pH (pHi) was examined in rat aortic endothelial cells cultured in glass capillary tubes. Shear stress forces led to a rapid decrease in pHi (maximal effect 0.09 pH unit at 13.4 dynes per square centimeter). Removal of specific ions or addition of exchange inhibitors suggests that in vascular endothelial cells shear stress forces activate both an alkali extruder, sodium ion-independent chloride-bicarbonate ion exchange, and an acid extruder, sodium-hydrogen ion exchange; the net effect in physiologic buffer with the bicarbonate ion is a decrease in pHi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegelstein, R C -- Cheng, L -- Capogrossi, M C -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicarbonates/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Chloride-Bicarbonate Antiporters ; Cytosol/*physiology ; Endothelium, Vascular/*physiology ; Hydrogen-Ion Concentration ; Membrane Proteins/physiology ; Rats ; Signal Transduction/physiology ; Sodium-Hydrogen Antiporter ; Stress, Mechanical
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  • 23
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    The time course of glutamate in the synaptic cleft (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-27
    Description: The peak concentration and rate of clearance of neurotransmitter from the synaptic cleft are important determinants of synaptic function, yet the neurotransmitter concentration time course is unknown at synapses in the brain. The time course of free glutamate in the cleft was estimated by kinetic analysis of the displacement of a rapidly dissociating competitive antagonist from N-methyl-D-aspartate (NMDA) receptors during synaptic transmission. Glutamate peaked at 1.1 millimolar and decayed with a time constant of 1.2 milliseconds at cultured hippocampal synapses. This time course implies that transmitter saturates postsynaptic NMDA receptors. However, glutamate dissociates much more rapidly from alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Thus, the time course of free glutamate predicts that dissociation contributes to the decay of the AMPA receptor-mediated postsynaptic current.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, J D -- Lester, R A -- Tong, G -- Jahr, C E -- Westbrook, G L -- MH46613/MH/NIMH NIH HHS/ -- NS21419/NS/NINDS NIH HHS/ -- NS26494/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1498-501.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1359647" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Aminoadipic Acid/pharmacology ; Action Potentials/physiology ; Animals ; Cells, Cultured ; Glutamates/*metabolism ; Glutamic Acid ; Hippocampus/cytology/physiology ; Models, Neurological ; Neurons/physiology ; Neurotransmitter Agents/*metabolism ; Piperazines/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/drug effects/physiology ; Synapses/drug effects/*metabolism ; Time Factors
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  • 24
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    Antisense and antigene properties of peptide nucleic acids (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: Peptide nucleic acids (PNAs) are polyamide oligomers that can strand invade duplex DNA, causing displacement of one DNA strand and formation of a D-loop. Binding of either a T10 PNA or a mixed sequence 15-mer PNA to the transcribed strand of a G-free transcription cassette caused 90 to 100 percent site-specific termination of pol II transcription elongation. When a T10 PNA was bound on the nontranscribed strand, site-specific inhibition never exceeded 50 percent. Binding of PNAs to RNA resulted in site-specific termination of both reverse transcription and in vitro translation, precisely at the position of the PNA.RNA heteroduplex. Nuclear microinjection of cells constitutively expressing SV40 large T antigen (T Ag) with either a 15-mer or 20-mer PNA targeted to the T Ag messenger RNA suppressed T Ag expression. This effect was specific in that there was no reduction in beta-galactosidase expression from a coinjected expression vector and no inhibition of T Ag expression after microinjection of a 10-mer PNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanvey, J C -- Peffer, N J -- Bisi, J E -- Thomson, S A -- Cadilla, R -- Josey, J A -- Ricca, D J -- Hassman, C F -- Bonham, M A -- Au, K G -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Glaxo Inc. Research Institute, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics ; Base Sequence ; DNA/*metabolism ; Deoxyribonuclease HindIII/antagonists & inhibitors ; Gene Expression/drug effects ; HeLa Cells ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*metabolism/pharmacology ; Oligonucleotides, Antisense/*metabolism/pharmacology ; *Peptide Nucleic Acids ; Plasmids ; Protein Biosynthesis/drug effects ; RNA/metabolism ; Rabbits ; Rats ; Transcription, Genetic/drug effects
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  • 25
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    Regional variation of extracellular space in the hippocampus (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-10
    Description: The factors responsible for the unusual susceptibility of the hippocampus to seizures and ischemic cell damage are not well understood. The CA1 pyramidal subfield of the hippocampus is particularly vulnerable to seizure activity and damage after ischemia. The possibility was examined that regional differences exist in extracellular volume, which might influence neuronal excitability and response to injury in the hippocampus. CA1 stratum pyramidale exhibited an exceptionally low extracellular volume fraction (EVF) of 0.12, whereas the EVFs of CA3 and dentate were considerably higher--0.18 and 0.15, respectively. The EVF of CA1 stratum pyramidale was reversibly reduced by 30 percent when the extracellular potassium concentration was raised from 3.5 to 8.5 mM, a procedure that induced spontaneous electrographic seizures in CA1. Thus there are regional variations in the properties of the extracellular space in the hippocampus that might underlie the propensity of the CA1 region to develop seizures and to suffer damage after ischemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McBain, C J -- Traynelis, S F -- Dingledine, R -- NS17771/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):674-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2382142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diffusion ; Extracellular Space/drug effects/*physiology ; Hippocampus/anatomy & histology/*physiology/physiopathology ; In Vitro Techniques ; Iontophoresis ; Organ Specificity ; Potassium/pharmacology ; Pyramidal Tracts/drug effects/*physiology ; Quaternary Ammonium Compounds/metabolism ; Rats ; Rats, Inbred Strains ; Seizures/physiopathology
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  • 26
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    HIV-1 coat protein neurotoxicity prevented by calcium channel antagonists (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: Coat protein gp120 from the human immunodeficiency virus type-1 (HIV-1) increased intracellular free calcium and injured rodent retinal ganglion cells and hippocampal neurons in culture. Highly purified recombinant gp120 envelope protein produced these effects in a dose-dependent fashion at picomolar concentrations. Immunoprecipitation with antibody to gp120, but not with control immunoglobulin-containing serum, depleted solutions of the viral envelope protein and also prevented both the rise in intracellular calcium and neuronal toxicity. The gp120-induced increase in intracellular calcium was abrogated by transiently lowering extracellular calcium or by adding the dihydropyridine calcium channel antagonist nimodipine (100 nM). Calcium channel antagonists also prevented gp120-induced neuronal injury. In addition, intracellular stores appeared to contribute substantially to the increase in calcium elicited by gp120. Since increases in intracellular calcium have been associated with neurotoxicity, it is possible that an injurious effect of gp120 on neurons might be related to this mechanism and that treatment with calcium channel antagonists may prove useful in mitigating HIV-1-related neuronal injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dreyer, E B -- Kaiser, P K -- Offermann, J T -- Lipton, S A -- EY 05477/EY/NEI NIH HHS/ -- NS 01395/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):364-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channel Blockers/*pharmacology ; Cells, Cultured ; HIV Envelope Protein gp120/administration & dosage/antagonists & ; inhibitors/*physiology ; HIV-1/*analysis ; Hippocampus/cytology ; Neurons/*drug effects/metabolism ; Nimodipine/pharmacology ; Rats ; Recombinant Proteins/pharmacology ; Retinal Ganglion Cells/drug effects/metabolism
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    Different tumor-derived p53 mutants exhibit distinct biological activities (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-05
    Description: In its wild-type form, the protein p53 can interfere with neoplastic processes. Tumor-derived cells often express mutant p53. Full-length mutant forms of p53 isolated so far from transformed mouse cells exhibit three common properties in vitro: loss of transformation-suppressing activity, gain of pronounced transforming potential, and ability to bind the heat shock protein cognate hsc70. A tumor-derived mouse p53 variant is now described, whose site of mutation corresponds to a hot spot for p53 in human tumors. While absolutely nonsuppressing, it is only weakly transforming and exhibits no detectable hsc70 binding. The data suggest that the ability of a p53 mutant to bind endogenous p53 is not the sole determinant of its oncogenic potential. The data also support the existence of gain-of-function p53 mutants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Halevy, O -- Michalovitz, D -- Oren, M -- R01 CA40099/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 5;250(4977):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218501" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cloning, Molecular ; Humans ; Mice ; *Mutation ; Nuclear Proteins/*genetics ; Plasmids ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Rats ; Transfection ; Tumor Suppressor Protein p53/*genetics/physiology
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    Flunarizine protects neurons from death after axotomy or NGF deprivation (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-15
    Description: Systemically administered flunarizine enhanced neuronal survival in lumbar sensory ganglia in newborn rats after axotomy. Flunarizine-treated rats lost 71 percent fewer neurons than the untreated control rats at the end of 1 week. In cell culture, flunarizine at 30 to 40 microM also prevented neuronal death in nerve growth factor-dependent embryonic sensory and sympathetic neurons after the abrupt withdrawal of neurotrophic support. The drug may cause this effect by acting at an intracellular site, one distinct from its blockade of voltage-dependent calcium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, K M -- Hollowell, J P -- HL20604/HL/NHLBI NIH HHS/ -- NS18071/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1419-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, Washington University School of Medicine, St. Louis, Mo 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Survival/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Flunarizine/administration & dosage/*pharmacology ; Ganglia, Spinal/cytology/embryology ; Ganglia, Sympathetic/cytology/embryology ; Microscopy, Electron, Scanning ; Nerve Crush ; Nerve Growth Factors/administration & dosage/*pharmacology ; Neurons/*cytology/drug effects ; Rats ; Sciatic Nerve/physiology/surgery
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An insulin-stimulated protein kinase similar to yeast kinases involved in cell cycle control (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-06
    Description: A protein kinase characterized by its ability to phosphorylate microtubule-associated protein-2 (MAP2), is thought to be an early intermediate in an insulin-stimulated phosphorylation cascade and in a variety of other mammalian cell responses to extracellular signals. A complementary DNA that encodes this protein serine-threonine kinase has been cloned, and the protein designated extracellular signal-regulated kinase 1 (ERK1). ERK1 has striking similarity to two protein kinases, KSS1 and FUS3, from yeast. The yeast kinases function in an antagonistic manner to regulate the cell cycle in response to mating factors. Thus, ERK1 and the two yeast kinases constitute a family of evolutionarily conserved enzymes involved in regulating the response of eukaryotic cells to extracellular signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulton, T G -- Yancopoulos, G D -- Gregory, J S -- Slaughter, C -- Moomaw, C -- Hsu, J -- Cobb, M H -- DK 01918/DK/NIDDK NIH HHS/ -- DK 34128/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Jul 6;249(4964):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Texas Southwestern Graduate School of Biomedical Sciences, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2164259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Cycle/*physiology ; Cell Line ; Central Nervous System/*enzymology ; DNA/*genetics ; Fibroblasts/enzymology ; Humans ; Insulin/pharmacology ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/genetics/*metabolism ; Rats ; Receptor, Insulin/metabolism ; Yeasts/enzymology
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    Target control of collateral extension and directional axon growth in the mammalian brain (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-12
    Description: Individual neurons in the brain send their axons over considerable distances to multiple targets, but the mechanisms governing this process are unresolved. An amenable system for studying axon outgrowth, branching, and target selection is the mammalian corticopontine projection. This major connection develops from parent corticospinal axons that have already grown past the pons, by a delayed interstitial budding of collateral branches that then grow directly into their target, the basilar pons. When cocultured with explants of developing cortex in three-dimensional collagen matrices, the basilar pons elicits the formation and directional growth of cortical axon collaterals across the intervening matrix. This effect appears to be target-specific and selectively influences neurons in the appropriate cortical layer. These in vitro findings provide evidence that the basilar pons becomes innervated by controlling at a distance the budding and directed ingrowth of cortical axon collaterals through the release of a diffusible, chemotropic molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heffner, C D -- Lumsden, A G -- O'Leary, D D -- EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jan 12;247(4939):217-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2294603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cerebral Cortex/growth & development/*ultrastructure ; Culture Techniques ; Fluorescent Dyes ; Motor Cortex/ultrastructure ; Nerve Growth Factors/physiology ; Neural Pathways/growth & development/ultrastructure ; Pons/*physiology/ultrastructure ; Rats ; Spinal Cord/ultrastructure ; Visual Cortex/ultrastructure
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    Alteration of alpha 1 Na+,K(+)-ATPase 86Rb+ influx by a single amino acid substitution (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-31
    Description: The sodium- and potassium-dependent adenosine triphosphatase (Na+,K(+)-ATPase) maintains the transmembrane Na+ gradient to which is coupled all active cellular transport systems. The R and S alleles of the gene encoding the Na+,K(+)-ATPase alpha 1 subunit isoform were identified in Dahl salt-resistant (DR) and Dahl salt-sensitive (DS) rats, respectively. Characterization of the S allele-specific Na+,K(+)-ATPase alpha 1 complementary DNA identified a leucine substitution of glutamine at position 276. This mutation alters the hydropathy profile of a region in proximity to T3(Na), the trypsin-sensitive site that is only detected in the presence of Na+. This mutation causes a decrease in the rubidium-86 influx of S allele-specific sodium pumps, thus marking a domain in the Na+,K(+)-ATPase alpha subunit important for K+ transport, and supporting the hypothesis of a putative role of these pumps in hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herrera, V L -- Ruiz-Opazo, N -- HL 01967/HL/NHLBI NIH HHS/ -- HL 18318/HL/NHLBI NIH HHS/ -- HL 39267/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1023-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Genetics, Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Membrane/enzymology ; Kidney/enzymology ; Kinetics ; Molecular Sequence Data ; *Mutation ; Polymorphism, Restriction Fragment Length ; Protein Conformation ; Rats ; Rats, Inbred Strains ; Rubidium/*metabolism ; Rubidium Radioisotopes ; Sodium-Potassium-Exchanging ATPase/*genetics/metabolism
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    Molecular characterization of a functional cDNA encoding the rat substance P receptor (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-23
    Description: Substance P is a member of the tachykinin peptide family and participates in the regulation of diverse biological processes. The polymerase chain reaction and conventional library screening were used to isolate a complementary DNA (cDNA) encoding the rat substance P receptor from brain and submandibular gland. By homology analysis, this receptor belongs to the G protein-coupled receptor superfamily. The receptor cDNA was expressed in a mammalian cell line and the ligand binding properties of the encoded receptor were pharmacologically defined by Scatchard analysis and tachykinin peptide displacement as those of a substance P receptor. The distribution of the messenger RNA for this receptor is highest in urinary bladder, submandibular gland, striatum, and spinal cord, which is consistent with the known distribution of substance P receptor binding sites. Thus, this receptor appears to mediate the primary actions of substance P in various brain regions and peripheral tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hershey, A D -- Krause, J E -- NS21937/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 23;247(4945):958-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154852" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain Chemistry ; Cloning, Molecular ; DNA/*genetics/isolation & purification ; GTP-Binding Proteins/metabolism ; Gene Expression ; Intestine, Small/analysis ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; RNA, Messenger/analysis ; Rats ; Receptors, Neurokinin-1 ; Receptors, Neurotransmitter/*genetics ; Sequence Homology, Nucleic Acid ; Submandibular Gland/analysis ; Tissue Distribution ; Urinary Bladder/analysis
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    Light-evoked changes in the interphotoreceptor matrix (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-06-29
    Description: The normal function of vertebrate photoreceptor cells depends on multiple interactions and transfer of substances between the photoreceptors and the retinal pigment epithelium (RPE), but the mechanisms of these interactions are poorly understood. Many are thought to be mediated by the interphotoreceptor matrix (IPM), a complex extracellular matrix that surrounds the photoreceptors and lies between them and the RPE. Histochemical, immunocytochemical, and lectin probes for several IPM constituents revealed that components of the IPM in the rat undergo a major shift in distribution or molecular conformation after the transition between light and dark. In the light, various IPM constituents concentrated in bands at the apical and basal regions of the outer segment zone; in the dark, they distributed much more uniformly throughout the zone. The change in IPM distribution was triggered by the light-dark transition; it was not a circadian event, and it was not driven by a systemic factor. The light-evoked change in IPM distribution may facilitate the transfer of substances between the photoreceptors and the RPE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uehara, F -- Matthes, M T -- Yasumura, D -- LaVail, M M -- EYO1919/EY/NEI NIH HHS/ -- EYO2162/EY/NEI NIH HHS/ -- EYO6842/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1633-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2194288" target="_blank"〉PubMed〈/a〉
    Keywords: Albinism ; Animals ; Darkness ; Extracellular Matrix/physiology ; *Fluorescein-5-isothiocyanate/*analogs & derivatives ; Fluoresceins ; Glycoconjugates/analysis ; Immunoenzyme Techniques ; Immunohistochemistry ; In Vitro Techniques ; Light ; Photoreceptor Cells/*physiology/radiation effects ; Pigment Epithelium of Eye/cytology/*physiology ; Rats ; Rats, Inbred F344 ; Retina/cytology/*physiology/radiation effects ; Rod Cell Outer Segment/physiology ; Sialic Acids/analysis ; Wheat Germ Agglutinins
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    Inhibition of leishmanias but not host macrophages by the antitubulin herbicide trifluralin (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-24
    Description: The dinitroaniline herbicide trifluralin (alpha, alpha, alpha-trifluoro-2,6-dinitro-N, N-dipropyl-p-toluidine), at micromolar concentrations, selectively inhibited both proliferation and differentiation of the parasitic protozoan Leishmania mexicana amazonensis. In vitro, radioactive trifluralin showed specific binding to leishmania tubulin but not to mammalian tubulin. Because herbicides such as trifluralin are economical and are considered safe for man and domesticated animals, they may serve as useful sources of potential antiparasitic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, M M -- Fong, D -- AI 21364/AI/NIAID NIH HHS/ -- CA 49359/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):924-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Rutgers, State University of New Jersey, Piscataway 08855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Leishmania mexicana/drug effects/*growth & development ; Macrophages/drug effects/*physiology ; Protein Binding ; Rats ; Species Specificity ; Toluidines/*pharmacology ; Trifluralin/metabolism/*pharmacology ; Tubulin/metabolism ; *Tubulin Modulators ; Tumor Cells, Cultured/cytology/drug effects
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    Cloning and expression of a developmentally regulated protein that induces mitogenic and neurite outgrowth activity (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-21
    Description: A heparin binding mitogenic protein isolated from bovine uterus shares NH2-terminal amino acid sequence with a protein isolated from newborn rat brain. The cDNA's of the bovine, human, and rat genes have been isolated and encode extraordinarily conserved proteins unrelated to known growth or neurotrophic factors, although identity of nearly 50 percent has been found with the predicted sequence of a retinoic acid induced transcript in differentiating mouse embryonal carcinoma cells. Lysates of COS-7 cells transiently expressing this protein were mitogenic for NRK cells and initiated neurite outgrowth from mixed cultures of embryonic rat brain cells. RNA transcripts encoding this protein were widely distributed in tissues and were developmentally regulated. This protein, previously designated as heparin binding growth factor (HBGF)-8, is now renamed pleiotrophin (PTN) to reflect its diverse activities. PTN may be the first member of a family of developmentally regulated cytokines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Y S -- Milner, P G -- Chauhan, A K -- Watson, M A -- Hoffman, R M -- Kodner, C M -- Milbrandt, J -- Deuel, T F -- CA49712/CA/NCI NIH HHS/ -- HL14147/HL/NHLBI NIH HHS/ -- HL31102/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 21;250(4988):1690-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2270483" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/*physiology/ultrastructure ; Base Sequence ; Brain/*metabolism ; *Carrier Proteins ; Cattle ; Cell Division ; Cell Line ; Cloning, Molecular ; Cytokines/*genetics ; Humans ; Mitogens/*genetics ; Molecular Sequence Data ; Organ Specificity ; Rats ; Sequence Homology, Nucleic Acid ; Transfection
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    Fetal brain grafts and Parkinson's disease (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1990 Dec 7;250(4986):1434-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2255915" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/transplantation ; Animals ; Brain Tissue Transplantation/*physiology ; Disease Models, Animal ; Fetal Tissue Transplantation/*physiology ; Humans ; Parkinson Disease/physiopathology/*surgery ; Rats
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    Cell proliferation in carcinogenesis (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-31
    Description: Chemicals that induce cancer at high doses in animal bioassays often fail to fit the traditional characterization of genotoxins. Many of these nongenotoxic compounds (such as sodium saccharin) have in common the property that they increase cell proliferation in the target organ. A biologically based, computerized description of carcinogenesis was used to show that the increase in cell proliferation can account for the carcinogenicity of nongenotoxic compounds. The carcinogenic dose-response relationship for genotoxic chemicals (such as 2-acetylaminofluorene) was also due in part to increased cell proliferation. Mechanistic information is required for determination of the existence of a threshold for the proliferative (and carcinogenic) response of nongenotoxic chemicals and the estimation of risk for human exposure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, S M -- Ellwein, L B -- CA28015/CA/NCI NIH HHS/ -- CA32513/CA/NCI NIH HHS/ -- CA36727/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):1007-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2204108" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Acetylaminofluorene/metabolism/toxicity ; Animals ; Carcinogens/pharmacology/*toxicity ; Cell Division/*drug effects ; Humans ; Liver/metabolism ; Liver Neoplasms/chemically induced ; Mice ; Mitotic Index/drug effects ; Rats ; Saccharin/toxicity ; Urinary Bladder Neoplasms/chemically induced
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    Secretion of neurotoxins by mononuclear phagocytes infected with HIV-1 (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-12-14
    Description: Mononuclear phagocytes (microglia, macrophages, and macrophage-like giant cells) are the principal cellular targets for human immunodeficiency virus-1 (HIV-1) in the central nervous system (CNS). Since HIV-1 does not directly infect neurons, the causes for CNS dysfunction in acquired immunodeficiency syndrome (AIDS) remain uncertain. HIV-1-infected human monocytoid cells, but not infected human lymphoid cells, released toxic agents that destroy chick and rat neurons in culture. These neurotoxins were small, heat-stable, protease-resistant molecules that act by way of N-methyl-D-aspartate receptors. Macrophages and microglia infected with HIV-1 may produce neurologic disease through chronic secretion of neurotoxic factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Vaca, K -- Noonan, C A -- NS 25637/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Dec 14;250(4987):1593-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2148832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Cell Line ; Cell Survival/*drug effects ; Chick Embryo ; Culture Media/analysis ; HIV-1/*physiology ; Humans ; Intermediate Filaments ; Lymphocytes/microbiology/physiology ; Macrophages/microbiology/physiology ; Monocytes/microbiology/physiology ; N-Methylaspartate/*analogs & derivatives ; Neuroglia/microbiology/physiology ; Neurons/cytology/drug effects/*physiology ; Phagocytes/microbiology/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology ; Spinal Cord/cytology
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    Behavioral effects of progesterone associated with rapid modulation of oxytocin receptors (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-02
    Description: The ventromedial nuclei of the hypothalamus (VMN) are important for the control of feminine mating behavior, and hormone action within these nuclei has been causally related to behavior. Estradiol induces receptors for oxytocin in the VMN and in the area lateral to these nuclei over the course of 1 to 2 days, and progesterone causes, within 30 minutes of its application, a further increase in receptor binding and an expansion of the area covered by these receptors lateral to the VMN. The rapid progesterone effect appears to be a direct and specific effect of this steroid on the receptor or membrane, because it was produced in vitro as well as in vivo and was not mimicked by a variety of other steroids. The effect of progesterone occurred in the posterior part of the VMN, where oxytocin infusion facilitated feminine mating behavior; it did not take place in the anterior part of the VMN, where oxytocin infusion had no effect on mating behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, M -- Coirini, H -- Pfaff, D W -- McEwen, B S -- HD-05751/HD/NICHD NIH HHS/ -- NS-07080/NS/NINDS NIH HHS/ -- TWO4103/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 2;250(4981):691-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173139" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/pharmacology ; Female ; Oxytocin/pharmacology ; Progesterone/*pharmacology ; Rats ; Receptors, Angiotensin/*drug effects/metabolism ; Receptors, Oxytocin ; Sexual Behavior, Animal/*drug effects ; Ventromedial Hypothalamic Nucleus/*drug effects
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    Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-07-13
    Description: The complement system is an important mediator of the acute inflammatory response, and an effective inhibitor would suppress tissue damage in many autoimmune and inflammatory diseases. Such an inhibitor might be found among the endogenous regulatory proteins of complement that block the enzymes that activate C3 and C5. Of these proteins, complement receptor type 1 (CR1; CD35) has the most inhibitory potential, but its restriction to a few cell types limits its function in vivo. This limitation was overcome by the recombinant, soluble human CR1, sCR1, which lacks the transmembrane and cytoplasmic domains. The sCR1 bivalently bound dimeric forms of its ligands, C3b and methylamine-treated C4 (C4-ma), and promoted their inactivation by factor I. In nanomolar concentrations, sCR1 blocked complement activation in human serum by the two pathways. The sCR1 had complement inhibitory and anti-inflammatory activities in a rat model of reperfusion injury of ischemic myocardium, reducing myocardial infarction size by 44 percent. These findings identify sCR1 as a potential agent for the suppression of complement-dependent tissue injury in autoimmune and inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisman, H F -- Bartow, T -- Leppo, M K -- Marsh, H C Jr -- Carson, G R -- Concino, M F -- Boyle, M P -- Roux, K H -- Weisfeldt, M L -- Fearon, D T -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):146-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2371562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology/pathology ; Complement Activation ; Complement C3/antagonists & inhibitors ; Complement C3b Inactivator Proteins/pharmacology ; Complement C4b/antagonists & inhibitors ; Complement C5/antagonists & inhibitors ; Complement Inactivator Proteins/*pharmacology/ultrastructure ; Disease Models, Animal ; Myocardial Reperfusion Injury/*immunology/pathology/prevention & control ; Myocardium/*pathology ; Necrosis ; Rats ; Receptors, Complement/*pharmacology/ultrastructure ; Recombinant Proteins/pharmacology
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  • 41
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    Reversal of diabetes insipidus in Brattleboro rats: intrahypothalamic injection of vasopressin mRNA (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-21
    Description: Messenger RNAs occur within the axons of magnocellular hypothalamic neurons known to secrete oxytocin and vasopressin. In Brattleboro rats, which have a genetic mutation that renders them incapable of vasopressin expression and secretion and thus causes diabetes insipidus, injection into the hypothalamus of purified mRNAs from normal rat hypothalami or of synthetic copies of the vasopressin mRNA leads to selective uptake, retrograde transport, and expression of vasopressin exclusively in the magnocellular neurons. Temporary reversal of their diabetes insipidus (for up to 5 days) can be observed within hours of the injection. Intra-axonal mRNAs may represent an additional category of chemical signals for neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jirikowski, G F -- Sanna, P P -- Maciejewski-Lenoir, D -- Bloom, F E -- MH 47680/MH/NIMH NIH HHS/ -- NS 22347-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):996-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuropharmacology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*genetics/metabolism ; Diabetes Insipidus/*therapy ; Hypothalamus ; RNA, Messenger/administration & dosage ; Rats ; Rats, Brattleboro ; Water-Electrolyte Balance
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    Nitric oxide and arginine-evoked insulin secretion (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vincent, S R -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1376-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455235" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/*pharmacology ; Insulin/*secretion ; Islets of Langerhans/secretion ; Nitric Oxide/*metabolism ; Rats ; Secretory Rate/drug effects
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  • 43
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    MacroH2A, a core histone containing a large nonhistone region (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: A histone, macroH2A, nearly three times the size of conventional H2A histone, was found in rat liver nucleosomes. Its N-terminal third is 64 percent identical to a full-length mouse H2A. However, it also contains a large nonhistone region. This region has a segment that resembles a leucine zipper, a structure known to be involved in dimerization of some transcription factors. Nucleosomes containing macroH2A may have novel functions, possibly involving interactions with other nuclear proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pehrson, J R -- Fried, V A -- CA 06927/CA/NCI NIH HHS/ -- GM 24019/GM/NIGMS NIH HHS/ -- RR 05539/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1398-400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fox Chase Cancer Center, Institute for Cancer Research, Philadelphia, PA 19111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529340" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/chemistry ; Histones/*chemistry/genetics ; Leucine Zippers ; Liver/*ultrastructure ; Macromolecular Substances ; Mice ; Molecular Sequence Data ; Nucleosomes/*chemistry ; Polymerase Chain Reaction ; Rats ; Sequence Homology, Nucleic Acid
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    Synaptotagmin: a calcium sensor on the synaptic vesicle surface (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-15
    Description: Neurons release neurotransmitters by calcium-dependent exocytosis of synaptic vesicles. However, the molecular steps transducing the calcium signal into membrane fusion are still an enigma. It is reported here that synaptotagmin, a highly conserved synaptic vesicle protein, binds calcium at physiological concentrations in a complex with negatively charged phospholipids. This binding is specific for calcium and involves the cytoplasmic domain of synaptotagmin. Calcium binding is dependent on the intact oligomeric structure of synaptotagmin (it is abolished by proteolytic cleavage at a single site). These results suggest that synaptotagmin acts as a cooperative calcium receptor in exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brose, N -- Petrenko, A G -- Sudhof, T C -- Jahn, R -- New York, N.Y. -- Science. 1992 May 15;256(5059):1021-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max-Planck-Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589771" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Calcium/*metabolism/pharmacology ; *Calcium-Binding Proteins ; Cell Membrane/metabolism ; Cytoplasmic Granules/metabolism ; Dansyl Compounds/metabolism ; Energy Transfer ; Exocytosis ; Fluorescent Dyes ; Liposomes/metabolism ; Macromolecular Substances ; Membrane Glycoproteins/chemistry/isolation & purification/*metabolism ; Nerve Tissue Proteins/chemistry/isolation & purification/*metabolism ; Phosphatidylethanolamines/metabolism ; Rats ; Synaptic Vesicles/*metabolism ; Synaptotagmins
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  • 45
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    Calcium-dependent transmitter secretion reconstituted in Xenopus oocytes: requirement for synaptophysin (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-31
    Description: Calcium-dependent glutamate secretion was reconstituted in Xenopus oocytes by injecting the oocyte with total rat cerebellar messenger RNA (mRNA). Co-injection of total mRNA with antisense oligonucleotides to synaptophysin message decreased the expression of synaptophysin in the oocyte and reduced the calcium-dependent secretion. A similar effect on secretion was observed for oocytes injected with total mRNA together with an antibody to rat synaptophysin. These results indicate that synaptophysin is necessary for transmitter secretion and that the oocyte expression system may be useful for dissecting the molecular events associated with the secretory process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alder, J -- Lu, B -- Valtorta, F -- Greengard, P -- Poo, M M -- MH 39327/MH/NIMH NIH HHS/ -- NS 22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):657-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1353905" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Western ; Calcimycin/pharmacology ; Calcium/*pharmacology ; Cerebellum/chemistry ; Fluorescent Antibody Technique ; Gene Expression ; Glutamates/*secretion ; Glutamic Acid ; Kinetics ; Liver/chemistry ; Microscopy, Immunoelectron ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oocytes/*physiology ; RNA, Messenger/genetics ; Rats ; Synaptophysin/genetics/*physiology ; Transfection ; Xenopus
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    Gz-mediated hormonal inhibition of cyclic AMP accumulation (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-17
    Description: Hormones inhibit synthesis of adenosine 3',5'-monophosphate (cAMP) in most cells via receptors coupled to pertussis toxin (PTX)-sensitive guanine nucleotide-binding (G) proteins. Mutationally activated alpha subunits of Gi2 (alpha i2) constitutively inhibit cAMP accumulation when transfected into cells. Cells have now been transfected with mutant alpha subunits of four other G proteins--Gz, a PTX-insensitive G protein of unknown function, and Gi1, Gi3, and G(o), which are PTX-sensitive. Mutant alpha z, alpha i1, and alpha i3 inhibited cAMP accumulation but alpha o did not. Moreover, expression of wild-type alpha z produced cells in which PTX did not block hormonal inhibition of cAMP accumulation. Thus, Gz can trigger an effector pathway in response to hormone receptors that ordinarily interact with PTX-sensitive Gi proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Y H -- Conklin, B R -- Bourne, H R -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347957" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Animals ; Brimonidine Tartrate ; Chorionic Gonadotropin/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/*biosynthesis ; Dinoprostone/pharmacology ; Dopamine/pharmacology ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation/*physiology ; Hormones/*physiology ; In Vitro Techniques ; Lysophospholipids/pharmacology ; Pertussis Toxin ; Quinoxalines/pharmacology ; Rats ; Signal Transduction/physiology ; Transfection ; Virulence Factors, Bordetella/pharmacology
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    An amino acid mutation in a potassium channel that prevents inhibition by protein kinase C (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-03-27
    Description: A slowly activating, voltage-dependent potassium channel protein cloned from rat kidney was expressed in Xenopus oocytes. Two activators of protein kinase C, 1-oleoyl-2-acetyl-rac-glycerol and phorbol 12,13-didecanoate, inhibited the current. This inhibition was blocked by the kinase inhibitor staurosporine. Inhibition of the current was not seen in channels in which Ser103 was replaced by Ala, although other properties of the current were unchanged. These results indicate that inhibition of the potassium current results from direct phosphorylation of the channel subunit protein at Ser103.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busch, A E -- Varnum, M D -- North, R A -- Adelman, J P -- DA03160/DA/NIDA NIH HHS/ -- NS28504/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1705-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553557" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/genetics ; Diglycerides/pharmacology ; Ion Channel Gating ; Membrane Potentials ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Phorbol Esters/pharmacology ; Phosphorylation ; Potassium Channels/*physiology ; Protein Kinase C/*metabolism ; Rats ; Structure-Activity Relationship
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    Do antidepressants promote tumors? (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Jul 3;257(5066):22-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1621088" target="_blank"〉PubMed〈/a〉
    Keywords: Amitriptyline/*toxicity ; Animals ; Breast Neoplasms/drug therapy/prevention & control ; Carcinogens/*toxicity ; Female ; Fluoxetine/*toxicity ; Humans ; Mice ; Neoplasms, Experimental/chemically induced ; Rats ; Tamoxifen/therapeutic use ; United States ; United States Food and Drug Administration
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    Trypsin-sensitive, rapid inactivation of a calcium-activated potassium channel (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-09-18
    Description: Most calcium-activated potassium channels couple changes in intracellular calcium to membrane excitability by conducting a current with a probability that depends directly on submembrane calcium concentration. In rat adrenal chromaffin cells, however, a large conductance, voltage- and calcium-activated potassium channel (BK) undergoes rapid inactivation, suggesting that this channel has a physiological role different than that of other BK channels. The inactivation of the BK channel, like that of the voltage-gated Shaker B potassium channel, is removed by trypsin digestion and channels are blocked by the Shaker B amino-terminal inactivating domain. Thus, this BK channel shares functional and possibly structural homologies with other inactivating voltage-gated potassium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solaro, C R -- Lingle, C J -- New York, N.Y. -- Science. 1992 Sep 18;257(5077):1694-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529355" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Animals ; Calcium/*pharmacology ; Cattle ; Cell Line ; Cell Membrane/physiology ; Chromaffin System/physiology ; Electric Conductivity ; Ion Channel Gating/drug effects/physiology ; Male ; Membrane Potentials/physiology ; Potassium Channels/*physiology ; Rats ; Rats, Inbred Strains ; Trypsin/*pharmacology
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  • 50
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    Mutation of the POU-specific domain of Pit-1 and hypopituitarism without pituitary hypoplasia (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-08-21
    Description: A point mutation in the POU-specific portion of the human gene that encodes the tissue-specific POU-domain transcription factor, Pit-1, results in hypopituitarism, with deficiencies of growth hormone, prolactin, and thyroid-stimulating hormone. In two unrelated Dutch families, a mutation in Pit-1 that altered an alanine in the first putative alpha helix of the POU-specific domain to proline was observed. This mutation generated a protein capable of binding to DNA response elements but unable to effectively activate its known target genes, growth hormone and prolactin. The phenotype of the affected individuals suggests that the mutant Pit-1 protein is competent to initiate other programs of gene activation required for normal proliferation of somatotrope, lactotrope, and thyrotrope cell types. Thus, a mutation in the POU-specific domain of Pit-1 has a selective effect on a subset of Pit-1 target genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfaffle, R W -- DiMattia, G E -- Parks, J S -- Brown, M R -- Wit, J M -- Jansen, M -- Van der Nat, H -- Van den Brande, J L -- Rosenfeld, M G -- Ingraham, H A -- HD24960/HD/NICHD NIH HHS/ -- HD2697/HD/NICHD NIH HHS/ -- NIDDK 18477/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1509263" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Blotting, Northern ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*genetics/metabolism ; Growth Hormone/deficiency ; Humans ; Hypopituitarism/*genetics/pathology ; Mice ; Molecular Sequence Data ; *Mutation ; Nucleic Acid Hybridization ; Pituitary Gland, Anterior/*pathology ; Pituitary Hormones/*deficiency ; Polymerase Chain Reaction ; Prolactin/deficiency ; Rats ; Sequence Homology, Nucleic Acid ; Thyrotropin/deficiency ; Transcription Factor Pit-1 ; Transcription Factors/*genetics/metabolism ; Transfection
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    Calcium-permeable AMPA-kainate receptors in fusiform cerebellar glial cells (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-06-12
    Description: Glutamate-operated ion channels (GluR channels) of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-kainate subtype are found in both neurons and glial cells of the central nervous system. These channels are assembled from the GluR-A, -B, -C, and -D subunits; channels containing a GluR-B subunit show an outwardly rectifying current-voltage relation and low calcium permeability, whereas channels lacking the GluR-B subunit are characterized by a doubly rectifying current-voltage relation and high calcium permeability. Most cell types in the central nervous system coexpress several subunits, including GluR-B. However, Bergmann glia in rat cerebellum do not express GluR-B subunit genes. In a subset of cultured cerebellar glial cells, likely derived from Bergmann glial cells. GluR channels exhibit doubly rectifying current-voltage relations and high calcium permeability, whereas GluR channels of cerebellar neurons have low calcium permeability. Thus, differential expression of the GluR-B subunit gene in neurons and glia is one mechanism by which functional properties of native GluR channels are regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnashev, N -- Khodorova, A -- Jonas, P -- Helm, P J -- Wisden, W -- Monyer, H -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1566-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cell Membrane Permeability ; Cells, Cultured ; Cerebellum/*physiology ; Gene Expression ; Glutamates/physiology ; In Vitro Techniques ; Ion Channel Gating ; Neuroglia/*physiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rats ; Receptors, Kainic Acid ; Receptors, Neurotransmitter/*physiology
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    Control by asparagine residues of calcium permeability and magnesium blockade in the NMDA receptor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: The N-methyl-D-aspartate (NMDA) receptor forms a cation-selective channel with a high calcium permeability and sensitivity to channel block by extracellular magnesium. These properties, which are believed to be important for the induction of long-term changes in synaptic strength, are imparted by asparagine residues in a putative channel-forming segment of the protein, transmembrane 2 (TM2). In the NR1 subunit, replacement of this asparagine by a glutamine residue decreases calcium permeability of the channel and slightly reduces magnesium block. The same substitution in NR2 subunits strongly reduces magnesium block and increases the magnesium permeability but barely affects calcium permeability. These asparagines are in a position homologous to the site in the TM2 region (Q/R site) of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors that is occupied by either glutamine (Q) or arginine (R) and that controls divalent cation permeability of the AMPA receptor channel. Hence AMPA and NMDA receptor channels contain common structural motifs in their TM2 segments that are responsible for some of their ion selectivity and conductance properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnashev, N -- Schoepfer, R -- Monyer, H -- Ruppersberg, J P -- Gunther, W -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1415-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max-Planck-Institut fur Medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1382314" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Asparagine/*chemistry ; Binding Sites ; Calcium/*metabolism/pharmacology ; Cell Line ; Electric Conductivity ; Glutamates/pharmacology ; Glutamic Acid ; Ion Channels/chemistry/*physiology ; Magnesium/metabolism/*pharmacology ; Mice ; Molecular Sequence Data ; Mutagenesis ; Oocytes/metabolism ; Permeability ; Rats ; Receptors, N-Methyl-D-Aspartate/chemistry/genetics/*physiology ; Structure-Activity Relationship ; Transfection ; Xenopus
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    Nitric oxide: a physiologic mediator of penile erection (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: Nitric oxide (NO) is a cytotoxic agent of macrophages, a messenger molecule of neurons, and a vasodilator produced by endothelial cells. NO synthase, the synthetic enzyme for NO, was localized to rat penile neurons innervating the corpora cavernosa and to neuronal plexuses in the adventitial layer of penile arteries. Small doses of NO synthase inhibitors abolished electrophysiologically induced penile erections. These results establish NO as a physiologic mediator of erectile function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnett, A L -- Lowenstein, C J -- Bredt, D S -- Chang, T S -- Snyder, S H -- DA-00266/DA/NIDA NIH HHS/ -- DK-19300/DK/NIDDK NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):401-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1378650" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/biosynthesis ; Animals ; Arginine/analogs & derivatives/pharmacology ; Dose-Response Relationship, Drug ; Male ; Nerve Fibers/metabolism ; *Nitric Oxide ; Nitric Oxide Synthase ; Nitroarginine ; Penile Erection/drug effects/*physiology ; Penis/metabolism ; Rats ; Urethra/metabolism
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    Alzheimer's debate boils over (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1336-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529329" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid beta-Peptides/*metabolism/pharmacology/toxicity ; Animals ; History, 20th Century ; Humans ; Nervous System Diseases/chemically induced/pathology ; Neurons/drug effects/pathology ; Rats ; Research/standards
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    Specific binding of chromosomal protein HMG1 to DNA damaged by the anticancer drug cisplatin (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-04-10
    Description: The mechanism of action of the anticancer compound cis-diamminedichloroplatinum(II) (cisplatin) involves covalent binding to DNA. In an effort to understand the tumor-specific cytotoxicity of such DNA damage, the interactions of these lesions with cellular proteins have been studied. One such protein has been identified as the high-mobility group protein HMG1. Recombinant rat HMG1 binds specifically (dissociation constant 3.7 +/- 2.0 x 10(-7) molar) to DNA containing cisplatin d(GpG) or d(ApG) intrastrand cross-links, which unwind and bend DNA in a specific manner, but not to DNA modified by therapeutically inactive platinum analogs. These results suggest how HMG1 might bind to altered DNA structures and may be helpful in designing new antitumor drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pil, P M -- Lippard, S J -- CA34992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 10;256(5054):234-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/metabolism ; Cisplatin/*pharmacology ; *DNA Damage ; DNA, Neoplasm/drug effects/*metabolism ; HeLa Cells ; High Mobility Group Proteins/*metabolism ; Humans ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*metabolism ; Protein Binding ; Rats ; Recombinant Proteins/metabolism ; Structure-Activity Relationship
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    Cloning and characterization of inducible nitric oxide synthase from mouse macrophages (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-04-10
    Description: Nitric oxide (NO) conveys a variety of messages between cells, including signals for vasorelaxation, neurotransmission, and cytotoxicity. In some endothelial cells and neurons, a constitutive NO synthase is activated transiently by agonists that elevate intracellular calcium concentrations and promote the binding of calmodulin. In contrast, in macrophages, NO synthase activity appears slowly after exposure of the cells to cytokines and bacterial products, is sustained, and functions independently of calcium and calmodulin. A monospecific antibody was used to clone complementary DNA that encoded two isoforms of NO synthase from immunologically activated mouse macrophages. Liquid chromatography-mass spectrometry was used to confirm most of the amino acid sequence. Macrophage NO synthase differs extensively from cerebellar NO synthase. The macrophage enzyme is immunologically induced at the transcriptional level and closely resembles the enzyme in cytokine-treated tumor cells and inflammatory neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, Q W -- Cho, H J -- Calaycay, J -- Mumford, R A -- Swiderek, K M -- Lee, T D -- Ding, A -- Troso, T -- Nathan, C -- AI30165/AI/NIAID NIH HHS/ -- CA43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Apr 10;256(5054):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1373522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/biosynthesis/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Codon ; Enzyme Induction ; Interferon-gamma/pharmacology ; Isoenzymes/biosynthesis/*genetics ; Kinetics ; Lipopolysaccharides ; Macrophages/drug effects/*enzymology ; Mammary Neoplasms, Experimental ; Mice ; Molecular Sequence Data ; Molecular Weight ; Neutrophils/drug effects/enzymology ; Nitric Oxide Synthase ; Oligodeoxyribonucleotides ; Poly A/genetics ; RNA/genetics ; RNA, Messenger ; Rats ; Sequence Homology, Nucleic Acid ; Transcription, Genetic
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    Gene therapy for CF advances (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):289.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549773" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Cystic Fibrosis/*therapy ; Genetic Therapy/*methods ; Genetic Vectors ; Rats ; Transfection
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    High-frequency network oscillation in the hippocampus (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-15
    Description: Pyramidal cells in the CA1 hippocampal region displayed transient network oscillations (200 hertz) during behavioral immobility, consummatory behaviors, and slow-wave sleep. Simultaneous, multisite recordings revealed temporal and spatial coherence of neuronal activity during population oscillations. Participating pyramidal cells discharged at a rate lower than the frequency of the population oscillation, and their action potentials were phase locked to the negative phase of the simultaneously recorded oscillatory field potentials. In contrast, interneurons discharged at population frequency during the field oscillations. Thus, synchronous output of cooperating CA1 pyramidal cells may serve to induce synaptic enhancement in target structures of the hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buzsaki, G -- Horvath, Z -- Urioste, R -- Hetke, J -- Wise, K -- NS02383/NS/NINDS NIH HHS/ -- NS27058/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 May 15;256(5059):1025-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1589772" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal/physiology ; Cell Membrane/physiology ; Electrophysiology ; Hippocampus/*physiology ; Interneurons/physiology ; Male ; Neurons/physiology ; Periodicity ; Pyramidal Tracts/physiology ; Rats ; Sleep/physiology ; Synapses/physiology
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    Hidden messages in genetic maps (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farr, C J -- Goodfellow, P N -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):49.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics Department, University of Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439767" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Conserved Sequence ; Dosage Compensation, Genetic ; Gene Expression Regulation ; *Genome ; Humans ; Mammals/*genetics ; Rats ; *X Chromosome ; *Y Chromosome
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    Roles of SWI1, SWI2, and SWI3 proteins for transcriptional enhancement by steroid receptors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-04
    Description: The SWI1, SWI2, and SWI3 proteins, which are required for regulated transcription of numerous yeast genes, were found also to be essential for rat glucocorticoid receptor function in yeast; the receptor failed to activate transcription in strains with mutations in the SWI1, SWI2, or SWI3 genes. Certain mutations in genes encoding components of chromatin, identified as suppressors of swi mutations, partially relieved the SWI- requirement for receptor function. Immunoprecipitation of glucocorticoid receptor derivatives from wild-type (SWI+) yeast extracts coprecipitated the SWI3 protein; such receptor-SWI3 complexes were not detected in swi1- or swi2- mutant strains, implying that a complex of multiple SWI proteins may associate with the receptor. Prior incubation of a Drosophila embryo transcription extract with the yeast SWI3-specific antibody inhibited receptor function in vitro whereas the antibody had no effect if added after initiation complex formation. Thus, positive regulation by the glucocorticoid receptor in vivo and in vitro appears to require its interaction, at an early step, with one or more SWI proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshinaga, S K -- Peterson, C L -- Herskowitz, I -- Yamamoto, K R -- New York, N.Y. -- Science. 1992 Dec 4;258(5088):1598-604.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco 94143-0448.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1360703" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases ; Animals ; Chromosomal Proteins, Non-Histone ; Cloning, Molecular ; DNA-Binding Proteins/genetics/*metabolism ; Fungal Proteins/genetics/*metabolism ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Glucosephosphate Dehydrogenase/genetics/metabolism ; Nuclear Proteins/genetics/*metabolism ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Rats ; Receptors, Glucocorticoid/*genetics/metabolism ; Receptors, Steroid/*genetics/metabolism ; Saccharomyces cerevisiae/*genetics ; *Saccharomyces cerevisiae Proteins ; TATA Box ; *Trans-Activators ; Transcription Factors/genetics/*metabolism ; *Transcription, Genetic ; Tyrosine Transaminase/genetics/metabolism ; beta-Galactosidase/genetics/metabolism
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    Prevention of autoimmune diabetes in the BB rat by intrathymic islet transplantation at birth (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-29
    Description: Spontaneous diabetes in the BioBreeding (BB) rat, like human type I diabetes, results from the destruction of pancreatic islets by autoreactive T lymphocytes recognizing beta cell-specific antigens. T cell tolerance is in part mediated by interactions of maturing thymocytes with antigens expressed in the thymic microenvironment; islets were therefore implanted into the thymus of neonatal diabetes-prone BB rats to determine whether exposure of T cell precursors to beta cell antigens could influence the development of diabetes. This treatment completely prevented diabetes and insulitis in the native pancreas. The effect may be the result of specific modulation of diabetogenic T cells maturing in an islet-bearing thymus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Posselt, A M -- Barker, C F -- Friedman, A L -- Naji, A -- DK26007/DK/NIDDK NIH HHS/ -- DK34878/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 May 29;256(5061):1321-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1598576" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigens, CD4/analysis ; Antigens, CD8/analysis ; Autoimmune Diseases/genetics/immunology/*prevention & control ; Diabetes Mellitus, Type 1/immunology/*prevention & control ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Lymph Nodes/immunology ; Male ; Pancreas/cytology ; Rats ; Rats, Inbred BB ; Rats, Inbred WF ; T-Lymphocytes/*immunology ; Thymus Gland/cytology ; Thyroid Gland/cytology ; Transplantation, Heterotopic
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    Neuronal domains in developing neocortex (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-31
    Description: The mammalian neocortex consists of a mosaic of columnar units whose development is poorly understood. Optical recordings of brain slices labeled with the fluorescent calcium indicator fura-2 revealed that the neonatal rat cortex was partitioned into distinct domains of spontaneously coactive neurons. In tangential slices, these domains were 50 to 120 micrometers in diameter; in coronal slices they spanned several cortical layers and resembled columns found in the adult cortex. In developing somatosensory cortex, domains were smaller than, and distinct from, the barrels, which represent sensory input from a single vibrissa. The neurons within each domain were coupled by gap junctions. Thus, nonsynaptic communication during cortical development defines discrete multicellular patterns that could presage adult functional architecture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuste, R -- Peinado, A -- Katz, L C -- EY07960/EY/NEI NIH HHS/ -- MH15177/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 31;257(5070):665-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1496379" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Calcium/analysis/metabolism ; Cell Communication ; Cerebral Cortex/cytology/*growth & development/physiology ; Computer Simulation ; Fluorescent Dyes ; Fura-2 ; Image Processing, Computer-Assisted ; Intercellular Junctions/physiology ; Neurons/cytology/*physiology ; Rats ; Tetrodotoxin/pharmacology
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    Bone like plywood (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-03-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1992 Mar 27;255(5052):1638.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biophysical Phenomena ; Biophysics ; Bone and Bones/*ultrastructure ; Calcium Phosphates ; Rats
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    Tapping into nerve conversations (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-05-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, S -- New York, N.Y. -- Science. 1990 May 4;248(4955):555.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2333508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophysiology/*instrumentation ; Hindlimb/innervation ; Microelectrodes ; Nerve Regeneration ; Neurons/*physiology ; Rats ; Spinal Nerves/*physiology
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    Induction of donor-specific unresponsiveness by intrathymic islet transplantation (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-14
    Description: The application of isolated pancreatic islet transplantation for treatment of diabetes mellitus has been hampered by the vulnerability of islet allografts to immunologic rejection. Rat islet allografts that were transplanted into the thymus of recipients treated with a single injection of anti-lymphocyte serum survived indefinitely. A state of donor-specific unresponsiveness was achieved that permitted survival of a second donor strain islet allograft transplanted to an extrathymic site. Maturation of T cell precursors in a thymic microenvironment that is harboring foreign alloantigen may induce the selective unresponsiveness. This model provides an approach for pancreatic islet transplantation and a potential strategy for specific modification of the peripheral immune repertoire.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Posselt, A M -- Barker, C F -- Tomaszewski, J E -- Markmann, J F -- Choti, M A -- Naji, A -- DK26007/DK/NIDDK NIH HHS/ -- DK34878/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1293-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2119056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antilymphocyte Serum ; Blood Glucose/metabolism ; Diabetes Mellitus, Experimental/*surgery ; Graft Enhancement, Immunologic ; Immune Tolerance ; *Islets of Langerhans Transplantation ; Rats ; Rats, Inbred Lew ; Rats, Inbred WF ; T-Lymphocytes/immunology ; Thymus Gland/surgery ; Transplantation, Heterotopic
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    Solution structure of the glucocorticoid receptor DNA-binding domain (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-07-13
    Description: The three-dimensional structure of the DNA-binding domain (DBD) of the glucocorticoid receptor has been determined by nuclear magnetic resonance spectroscopy and distance geometry. The structure of a 71-residue protein fragment containing two "zinc finger" domains is based on a large set of proton-proton distances derived from nuclear Overhauser enhancement spectra, hydrogen bonds in previously identified secondary structure elements, and coordination of two zinc atoms by conserved cysteine residues. The DBD is found to consist of a globular body from which the finger regions extend. A model of the dimeric complex between the DBD and the glucocorticoid response element is proposed. The model is consistent with previous results indicating that specific amino acid residues of the DBD are involved in protein-DNA and protein-protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hard, T -- Kellenbach, E -- Boelens, R -- Maler, B A -- Dahlman, K -- Freedman, L P -- Carlstedt-Duke, J -- Yamamoto, K R -- Gustafsson, J A -- Kaptein, R -- New York, N.Y. -- Science. 1990 Jul 13;249(4965):157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2115209" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/*metabolism ; DNA-Binding Proteins/analysis/*metabolism ; Humans ; Magnetic Resonance Spectroscopy ; Metalloproteins/analysis ; Models, Molecular ; Molecular Sequence Data ; Peptide Fragments/analysis/metabolism ; Protein Conformation ; Rats ; Receptors, Glucocorticoid/*analysis/metabolism ; Regulatory Sequences, Nucleic Acid ; Zinc/analysis
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    Activin-binding protein from rat ovary is follistatin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: Activin, a member of the transforming growth factor beta protein family, was originally isolated from gonadal fluids and stimulates the release of pituitary follicle-stimulating hormone (FSH). Activin has numerous functions in both normal and neoplastic cells. Various cells synthesize activin and have a specific binding site for this peptide. However, the molecular basis for its actions is unknown. A binding protein for activin was purified from rat ovary and was identical to follistatin, a specific inhibitor of FSH release. It is likely that the binding protein participates in the diverse regulatory actions of activin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakamura, T -- Takio, K -- Eto, Y -- Shibai, H -- Titani, K -- Sugino, H -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Frontier Research Program, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2106159" target="_blank"〉PubMed〈/a〉
    Keywords: Activins ; Animals ; *Carrier Proteins ; Cells, Cultured ; Female ; Follicle Stimulating Hormone/secretion ; Inhibins/isolation & purification/*metabolism/pharmacology ; Kinetics ; Molecular Weight ; Ovary/*metabolism ; Pituitary Gland/drug effects/secretion ; Protein Binding ; Rats
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    Phosphorylation of the polymeric immunoglobulin receptor required for its efficient transcytosis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-11
    Description: The endosomal compartment of polarized epithelial cells is a major crossroads for membrane traffic. Proteins entering this compartment from the cell surface are sorted for transport to one of several destinations: recycling to the original cell surface, targeting to lysosomes for degradation, or transcytosis to the opposite surface. The polymeric immunoglobulin receptor (pIgR), which is normally transcytosed from the basolateral to the apical surface, was used as a model to dissect the signals that mediate this sorting event. When exogenous receptor was expressed in Madin-Darby Canine Kidney (MDCK) cells, it was shown that phosphorylation of pIgR at the serine residue at position 664 is required for efficient transcytosis. Replacement of this serine with alanine generated a receptor that is transcytosed only slowly, and appears to be recycled. Conversely, substitution with aspartic acid (which mimics the negative charge of the phosphate group) results in rapid transcytosis. It was concluded that phosphorylation is the signal that directs the pIgR from the endosome into the transcytotic pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casanova, J E -- Breitfeld, P P -- Ross, S A -- Mostov, K E -- R01-AI-25144/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 May 11;248(4956):742-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2110383" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine ; Animals ; Aspartic Acid ; Cell Line ; Cell Membrane/immunology/metabolism ; Endocytosis ; Immunoglobulin A/metabolism ; Kinetics ; Ligands ; Membrane Glycoproteins/metabolism ; Molecular Weight ; Mutation ; Phosphorylation ; Rats ; Receptors, Immunologic ; Secretory Component/genetics/*metabolism ; Serine
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    A borna virus cDNA encoding a protein recognized by antibodies in humans with behavioral diseases (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: Borna disease virus (BDV) causes a rare neurological disease in horses and sheep. The virus has not been classified because neither an infectious particle nor a specific nucleic acid had been identified. To identify the genome of BDV, a subtractive complementary DNA expression library was constructed with polyadenylate-selected RNA from a BDV-infected MDCK cell line. A clone (B8) was isolated that specifically hybridized to RNA isolated from BDV-infected brain tissue and BDV-infected cell lines. This clone hybridized to four BDV-specific positive strand RNAs (10.5, 3.6, 2.1, and 0.85 kilobases) and one negative strand RNA (10.5 kilobases) in BDV-infected rat brain. Nucleotide sequence analysis of the clone suggested that it represented a full-length messenger RNA which contained several open reading frames. In vitro transcription and translation of the clone resulted in the synthesis of the 14- and 24-kilodalton BDV-specific proteins. The 24-kilodalton protein, when translated in vitro from the clone, was recognized by antibodies in the sera of patients (three of seven) with behavioral disorders. This BDV-specific clone will provide the means to isolate the other BDV-specific nucleic acids and to identify the virus responsible for Borna disease. In addition, the significance of BDV or a BDV-related virus as a human pathogen can now be more directly examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉VandeWoude, S -- Richt, J A -- Zink, M C -- Rott, R -- Narayan, O -- Clements, J E -- RR00130/RR/NCRR NIH HHS/ -- RR07002/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Colorado State University, Lab Animal Resources, Fort Collins 80532.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244211" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Viral/*blood ; Borna Disease/*microbiology ; Borna disease virus/*genetics/immunology ; Brain/microbiology ; Cloning, Molecular ; DNA/*genetics ; Fluorescent Antibody Technique ; Humans ; Immunoblotting ; Mental Disorders/*microbiology ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; RNA, Messenger/analysis/genetics ; RNA, Viral/analysis/genetics ; Rats ; Transcription, Genetic ; Viral Proteins/*genetics/immunology
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    L-cysteine, a bicarbonate-sensitive endogenous excitotoxin (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-05-04
    Description: After systemic administration to immature rodents, L-cysteine destroys neurons in the cerebral cortex, hippocampus, thalamus, and striatum, but the underlying mechanism has never been clarified. This neurotoxicity of L-cysteine, in vitro or in vivo, has now been shown to be mediated primarily through the N-methyl-D-aspartate subtype of glutamate receptor (with quisqualate receptor participation at higher concentrations). In addition, the excitotoxic potency of L-cysteine was substantially increased in the presence of physiological concentrations of bicarbonate ion. L-Cysteine is naturally present in the human brain and in the environment, and is much more powerful than beta-N-methylamino-L-alanine, a bicarbonate-dependent excitotoxin, which has been implicated in an adult neurodegenerative disorder endemic to Guam. Thus, the potential involvement of this common sulfur-containing amino acid in neurodegenerative processes affecting the central nervous system warrants consideration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olney, J W -- Zorumski, C -- Price, M T -- Labruyere, J -- DA 05072/DA/NIDA NIH HHS/ -- HD 24237/HD/NICHD NIH HHS/ -- MH 38894/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 May 4;248(4955):596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Washington University School of Medicine, Department of Psychiatry, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2185543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anticonvulsants/pharmacology ; Aspartic Acid/analogs & derivatives/pharmacology ; Bicarbonates/*pharmacology ; Caudate Nucleus/drug effects/*pathology ; Chick Embryo ; Cysteine/pharmacology/*toxicity ; Dibenzocycloheptenes/pharmacology ; Dizocilpine Maleate ; N-Methylaspartate ; Necrosis ; Neurons/drug effects/*pathology ; *Neurotoxins ; Rats ; Rats, Inbred Strains ; Retina/cytology/drug effects ; Retinal Ganglion Cells/cytology/drug effects ; Zinc/pharmacology
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    No pain, no gain? (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holloway, M -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2356468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endorphins/*physiology ; Medulla Oblongata/*physiopathology ; Morphine/administration & dosage ; Pain/*physiopathology ; Rats
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    Underexpression of beta cell high Km glucose transporters in noninsulin-dependent diabetes (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-10-26
    Description: The role of defective glucose transport in the pathogenesis of noninsulin-dependent diabetes (NIDDM) was examined in Zucker diabetic fatty rats, a model of NIDDM. As in human NIDDM, insulin secretion was unresponsive to 20 mM glucose. Uptake of 3-O-methylglucose by islet cells was less than 19% of controls. The beta cell glucose transporter (GLUT-2) immunoreactivity and amount of GLUT-2 messenger RNA were profoundly reduced. Whenever fewer than 60% of beta cells were GLUT-2-positive, the response to glucose was absent and hyperglycemia exceeded 11 mM plasma glucose. We conclude that in NIDDM underexpression of GLUT-2 messenger RNA lowers high Km glucose transport in beta cells, and thereby impairs glucose-stimulated insulin secretion and prevents correction of hyperglycemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, J H -- Ogawa, A -- Chen, L -- Orci, L -- Newgard, C B -- Alam, T -- Unger, R H -- DK02700-30/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 26;250(4980):546-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Diabetes Research, University of Texas, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237405" target="_blank"〉PubMed〈/a〉
    Keywords: 3-O-Methylglucose ; Animals ; Biological Transport ; Diabetes Mellitus/metabolism ; Diabetes Mellitus, Experimental/*metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Female ; *Gene Expression ; Glucose/pharmacology ; Immunoblotting ; Insulin/secretion ; Islets of Langerhans/drug effects/*metabolism ; Kinetics ; Male ; Methylglucosides/metabolism ; Monosaccharide Transport Proteins/*genetics/metabolism ; Obesity ; RNA, Messenger/metabolism ; Rats ; Rats, Inbred Strains ; Rats, Zucker
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    Too many rodent carcinogens: mitogenesis increases mutagenesis (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ames, B N -- Gold, L S -- CA39910/CA/NCI NIH HHS/ -- ES01896/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 31;249(4972):970-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biochemistry and Molecular Biology, University of California, Berkeley.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2136249" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogens ; DNA Damage ; Humans ; *Mitogens ; *Mutation ; Neoplasms/*etiology ; Rats
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    Functional properties of rat brain sodium channels expressed in a somatic cell line (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-16
    Description: Transfection of Chinese hamster ovary cells with complementary DNA encoding the RIIA sodium channel alpha subunit from rat brain led to expression of functional sodium channels with the rapid, voltage-dependent activation and inactivation characteristic of sodium channels in brain neurons. The sodium currents mediated by these transfected channels were inhibited by tetrodotoxin, persistently activated by veratridine, and prolonged by Leiurus alpha-scorpion toxin, indicating that neurotoxin receptor sites 1 through 3 were present in functional form. The RIIA sodium channel alpha subunit cDNA alone is sufficient for stable expression of functional sodium channels with the expected kinetic and pharmacological properties in mammalian somatic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheuer, T -- Auld, V J -- Boyd, S -- Offord, J -- Dunn, R -- Catterall, W A -- NS 15751/NS/NINDS NIH HHS/ -- NS 25704/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Feb 16;247(4944):854-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Cell Line ; Cricetinae ; Cricetulus ; Electric Conductivity ; Female ; Membrane Potentials/drug effects ; Membrane Proteins/genetics/*physiology ; Ovary ; Rats ; Sodium Channels/drug effects/*physiology ; Tetrodotoxin/pharmacology ; *Transfection
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    NKR-P1, a signal transduction molecule on natural killer cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: Natural killer (NK) cells are a subpopulation of large granular lymphocytes characterized by densely staining azurophilic granules. NK cells are able to recognize and lyse various virally infected or neoplastic target cells without previous sensitization or major histocompatibility complex restriction. A 60-kD disulfide-linked dimer, highly expressed on NK cells, was found capable of mediating transmembrane signaling. The gene encoding this signal transduction molecule was cloned and its nucleotide sequence determined. The encoded protein showed significant homology with a number of lectin-related membrane proteins that share receptor characteristics. This protein may function as a receptor able to selectively trigger NK cell activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giorda, R -- Rudert, W A -- Vavassori, C -- Chambers, W H -- Hiserodt, J C -- Trucco, M -- AI 23963/AI/NIAID NIH HHS/ -- AI 26364/AI/NIAID NIH HHS/ -- CA 44977/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pittsburgh Cancer Institute, PA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2399464" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Antigens, Surface/*genetics ; Base Sequence ; Blotting, Southern ; Cloning, Molecular ; Gene Library ; Glycosylation ; Interleukin-2/physiology ; Killer Cells, Natural/immunology/*metabolism ; Molecular Sequence Data ; Rats ; Signal Transduction/*physiology ; Transfection
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    Coding channels in the taste system of the rat (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-28
    Description: Basic taste qualities are thought to be perceived independently, yet discrete neural coding channels have not been demonstrated in the central nervous system. The response profiles of taste cells in the nucleus tractus solitarius (NTS) of the rat were categorized into four groups, and the effects of amiloride, a passive sodium channel blocker, on each were determined. NTS neurons that responded specifically to sodium chloride (NaCl) or to NaCl and sugars were suppressed by amiloride; those broadly sensitive to salts, acids, and bitter stimuli were unaffected. Moreover, the response profile evoked by NaCl lost its distinctiveness after treatment with amiloride, becoming similar to those evoked by acids and quinine. Receptors that respond to sodium must relay their information through independent coding channels to identifiable subgroups of NTS neurons, the activity of which is responsible for the perception of saltiness.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, T R -- Giza, B K -- DK30964/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 28;249(4976):1585-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Delaware, Newark 19716.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2171145" target="_blank"〉PubMed〈/a〉
    Keywords: Amiloride/pharmacology ; Animals ; Chlorides ; Citrates ; Glucose ; Lithium ; Lithium Chloride ; Medulla Oblongata/drug effects/*physiology ; Neurons/drug effects/*physiology ; Rats ; Saccharin ; Salts ; Sensory Receptor Cells/drug effects/physiology ; Sodium Chloride ; Software ; *Taste
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    A family of AMPA-selective glutamate receptors (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-08-03
    Description: Four cloned cDNAs encoding 900-amino acid putative glutamate receptors with approximately 70 percent sequence identity were isolated from a rat brain cDNA library. In situ hybridization revealed differential expression patterns of the cognate mRNAs throughout the brain. Functional expression of the cDNAs in cultured mammalian cells generated receptors displaying alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-selective binding pharmacology (AMPA = quisqualate greater than glutamate greater than kainate) as well as cation channels gated by glutamate, AMPA, and kainate and blocked by 6,7-dinitroquinoxaline-2,3-dione (CNQX).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keinanen, K -- Wisden, W -- Sommer, B -- Werner, P -- Herb, A -- Verdoorn, T A -- Sakmann, B -- Seeburg, P H -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):556-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, University of Heidelberg, F.R.G.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2166337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*metabolism/physiology ; Glutamates/metabolism/pharmacology ; Ibotenic Acid/analogs & derivatives/*pharmacology ; Kainic Acid/pharmacology ; Kinetics ; Molecular Sequence Data ; *Multigene Family ; Oligonucleotide Probes ; Organ Specificity ; Oxadiazoles/pharmacology ; Oxazoles/*pharmacology ; Quisqualic Acid ; RNA, Messenger/analysis/genetics ; Rats ; Receptors, Glutamate ; Receptors, Neurotransmitter/drug effects/*genetics/physiology ; Sequence Homology, Nucleic Acid ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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    Animal carcinogen testing challenged (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Nov 9;250(4982):743-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2237420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Cell Division ; Humans ; Mice ; Mutagenesis ; Neoplasms/chemically induced ; Rats
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    Expression of beta-nerve growth factor receptor mRNA in Sertoli cells downregulated by testosterone (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Nerve growth factor (NGF) is synthesized in male germ cells. The NGF receptor (NGFR) mRNA was found in the Sertoli cells of rat testis. Hypophysectomy increased both NGFR mRNA in testis and the number of NGFR hybridizing cells in seminiferous tubules. This was suppressed by treatment with chorionic gonadotropin or testosterone, but not with follicle-stimulating hormone. The NGFR mRNA also increased after destruction of Leydig cells or blocking of the androgen receptor. This suggests that NGF produced by male germ cells regulates testicular function in an androgen-modulated fashion by mediating an interaction germ and Sertoli cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persson, H -- Ayer-Le Lievre, C -- Soder, O -- Villar, M J -- Metsis, M -- Olson, L -- Ritzen, M -- Hokfelt, T -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):704-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154035" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chorionic Gonadotropin/pharmacology ; DNA Probes ; Down-Regulation/*drug effects ; Follicle Stimulating Hormone/pharmacology ; Gene Expression Regulation/*drug effects ; Hypophysectomy ; Leydig Cells/drug effects/physiology ; Male ; Mesylates/pharmacology ; Nucleic Acid Hybridization ; RNA, Messenger/*genetics ; Rats ; Rats, Inbred Strains ; Receptors, Androgen/physiology ; Receptors, Cell Surface/*genetics ; Receptors, Nerve Growth Factor ; Sertoli Cells/*metabolism ; Testis/metabolism ; Testosterone/*pharmacology
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    Marijuana receptor gene cloned (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Aug 10;249(4969):624-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2166339" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Cloning, Molecular ; Dronabinol/*metabolism ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/*genetics
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  • 81
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    Widespread expression of BDNF but not NT3 by target areas of basal forebrain cholinergic neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-12
    Description: Brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) are homologs of the well-known neurotrophic factor nerve growth factor. The three members of this family display distinct patterns of target specificity. To examine the distribution in brain of messenger RNA for these molecules, in situ hybridization was performed. Cells hybridizing intensely to antisense BDNF probe were located throughout the major targets of the rat basal forebrain cholinergic system, that is, the hippocampus, amygdala, and neocortex. Strongly hybridizing cells were also observed in structures associated with the olfactory system. The distribution of NT3 mRNA in forebrain was much more limited. Within the hippocampus, labeled cells were restricted to CA2, the most medial portion of CA1, and the dentate gyrus. In human hippocampus, cells expressing BDNF mRNA are distributed in a fashion similar to that observed in the rat. These findings point to both basal forebrain cholinergic cells and olfactory pathways as potential central targets for BDNF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Phillips, H S -- Hains, J M -- Laramee, G R -- Rosenthal, A -- Winslow, J W -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):290-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Genentech, South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1688328" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Autoradiography ; Brain/anatomy & histology/*metabolism ; Brain-Derived Neurotrophic Factor ; Computer Simulation ; Gene Expression ; Nerve Growth Factors/*genetics ; Nerve Tissue Proteins/*genetics ; Neurons/*metabolism ; Nucleic Acid Hybridization ; Organ Specificity ; RNA Probes ; RNA, Messenger/*analysis/genetics ; Rats ; Sulfur Radioisotopes
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  • 82
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    2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline: a neuroprotectant for cerebral ischemia (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-02
    Description: 2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX) is an analog of the quinoxalinedione antagonists to the non-N-methyl-D-aspartate (non-NMDA) glutamate receptor. NBQX is a potent and selective inhibitor of binding to the quisqualate subtype of the glutamate receptor, with no activity at the NMDA and glycine sites. NBQX protects against global ischemia, even when administered 2 hours after an ischemic challenge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheardown, M J -- Nielsen, E O -- Hansen, A J -- Jacobsen, P -- Honore, T -- New York, N.Y. -- Science. 1990 Feb 2;247(4942):571-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A/S Ferrosan, CNS Division, Soeborg, Denmark.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2154034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Brain Ischemia/*drug therapy ; Cerebral Cortex/drug effects/*physiology ; Hippocampus/drug effects/*physiology/physiopathology ; Ibotenic Acid/analogs & derivatives/pharmacology ; In Vitro Techniques ; Kainic Acid/pharmacology ; N-Methylaspartate ; Neurons/drug effects/physiology ; Oxadiazoles/pharmacology ; Pyramidal Tracts/drug effects/*physiology/physiopathology ; Quinoxalines/metabolism/pharmacology/*therapeutic use ; Quisqualic Acid ; Rats ; Receptors, Glutamate ; Receptors, Kainic Acid ; Receptors, Neurotransmitter/drug effects/metabolism ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
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  • 83
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    From the tomato to the mouse (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1990 Mar 30;247(4950):1541.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1969680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genetic Diseases, Inborn/*genetics ; *Genetic Linkage ; Humans ; *Multigene Family ; Plants/genetics ; *Polymorphism, Restriction Fragment Length ; Rats
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  • 84
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    Specific acceptance of cardiac allograft after treatment with antibodies to ICAM-1 and LFA-1 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-28
    Description: An indefinite survival of cardiac allografts between fully incompatible mice strains was observed when monoclonal antibodies (MAbs) to intercellular adhesion molecule-1 (ICAM-1) and leukocyte function-associated antigen-1 (LFA-1) were simultaneously administered after the transplantation for 6 days. Mice with long-term surviving cardiac allografts accepted skin grafts from the donor-strain but rejected skin grafts from a third-party strain. Because MAbs to ICAM-1 or LFA-1 alone were insufficient for prolonged tolerance, the two MAbs probably acted synergistically to induce specific unresponsiveness. Thus, ICAM-1----LFA-1 adhesion participates in the induction of allograft rejection and MAbs may be useful as therapeutic agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isobe, M -- Yagita, H -- Okumura, K -- Ihara, A -- New York, N.Y. -- Science. 1992 Feb 28;255(5048):1125-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiac Unit, Massachusetts General Hospital, Boston, 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/administration & dosage/*therapeutic use ; Cell Adhesion Molecules/*immunology ; Cytotoxicity, Immunologic ; Graft Survival ; Heart Transplantation/*immunology/pathology ; Immunity, Cellular ; Immunosuppression ; Intercellular Adhesion Molecule-1 ; Lymphocyte Function-Associated Antigen-1/*immunology ; Mice ; Mice, Inbred Strains ; Rats ; Skin Transplantation/immunology ; Spleen/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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    X-ray laser microscopy of rat sperm nuclei (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-19
    Description: The development of high brightness and short pulse width (〈 200 picoseconds) x-ray lasers now offers biologists the possibility of high-resolution imaging of specimens in an aqueous environment without the blurring effects associated with natural motions and chemical erosion. As a step toward developing the capabilities of this type of x-ray microscopy, a tantalum x-ray laser at 44.83 angstrom wavelength was used together with an x-ray zone plate lens to image both unlabeled and selectively gold-labeled dried rat sperm nuclei. The observed images show approximately 500 angstrom features, illustrate the importance of x-ray microscopy in determining chemical composition, and provide information about the uniformity of sperm chromatin organization and the extent of sperm chromatin hydration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Da Silva, L B -- Trebes, J E -- Balhorn, R -- Mrowka, S -- Anderson, E -- Attwood, D T -- Barbee, T W Jr -- Brase, J -- Corzett, M -- Gray, J -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fractionation ; Cell Nucleus/*ultrastructure ; Chromatin/ultrastructure ; DNA/ultrastructure ; Epididymis/cytology ; Immunohistochemistry ; *Lasers ; Male ; Microscopy/*methods ; Rats ; Spermatozoa/*ultrastructure ; X-Rays
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  • 86
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    Primary structure and functional expression of the beta 1 subunit of the rat brain sodium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Voltage-sensitive sodium channels are responsible for the initiation and propagation of the action potential and therefore are important for neuronal excitability. Complementary DNA clones encoding the beta 1 subunit of the rat brain sodium channel were isolated by a combination of polymerase chain reaction and library screening techniques. The deduced primary structure indicates that the beta 1 subunit is a 22,851-dalton protein that contains a single putative transmembrane domain and four potential extracellular N-linked glycosylation sites, consistent with biochemical data. Northern blot analysis reveals a 1,400-nucleotide messenger RNA in rat brain, heart, skeletal muscle, and spinal cord. Coexpression of beta 1 subunits with alpha subunits increases the size of the peak sodium current, accelerates its inactivation, and shifts the voltage dependence of inactivation to more negative membrane potentials. These results indicate that the beta 1 subunit is crucial in the assembly, expression, and functional modulation of the heterotrimeric complex of the rat brain sodium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isom, L L -- De Jongh, K S -- Patton, D E -- Reber, B F -- Offord, J -- Charbonneau, H -- Walsh, K -- Goldin, A L -- Catterall, W A -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- NS26729/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375395" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/*physiology ; Cloning, Molecular ; DNA/genetics/isolation & purification ; Female ; Kinetics ; Macromolecular Substances ; Membrane Potentials ; Molecular Sequence Data ; Oocytes/physiology ; Polymerase Chain Reaction/methods ; Protein Conformation ; RNA/genetics/isolation & purification ; RNA, Messenger/genetics ; Rats ; Sodium Channels/*genetics/*physiology ; Voltage-Gated Sodium Channel beta-1 Subunit ; Xenopus
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  • 87
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    Inhibition of long-term potentiation by NMDA-mediated nitric oxide release (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: Activation of N-methyl-D-aspartate (NMDA) receptors before tetanic stimulation blocks long-term potentiation (LTP) in the CA1 region of the hippocampus. This NMDA-mediated inhibition of LTP can be reversed by the nitric oxide (NO) inhibitors L-NG-monomethyl-arginine or hemoglobin and mimicked by sodium nitroprusside. These results indicate that the timing of NO release relative to high-frequency activation of CA1 synapses may be an important determinant of LTP generation and suggest that NO may play a positive or negative modulatory role in LTP depending on prior events at the tetanized synapse and the ambient concentration of excitatory amino acids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Izumi, Y -- Clifford, D B -- Zorumski, C F -- AG05681/AG/NIA NIH HHS/ -- MH00964/MH/NIMH NIH HHS/ -- MH45493/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1273-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519065" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/analogs & derivatives/pharmacology ; Electrophysiology ; Hemoglobins/pharmacology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; N-Methylaspartate/*pharmacology ; Nitric Oxide/*metabolism ; Nitroprusside/pharmacology ; Rats ; Time Factors ; omega-N-Methylarginine
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  • 88
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    Carcinogenicity of butadiene (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dankovic, D A -- Stayner, L T -- Smith, R J -- Bailer, A J -- New York, N.Y. -- Science. 1992 Sep 4;257(5075):1330; author reply 1331.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1529327" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butadienes/*toxicity ; Humans ; Mice ; Neoplasms, Experimental/*chemically induced ; Occupational Diseases/chemically induced ; Rats
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  • 89
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    Gating of the cardiac Ca2+ release channel: the role of Na+ current and Na(+)-Ca2+ exchange (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-14
    Description: In cardiac myocytes, calcium influx through the calcium channel is the primary pathway for triggering calcium release. Recently it has been suggested that the calcium-induced calcium release mechanism can also be activated indirectly by the sodium current, which elevates the sodium concentration under the cell membrane, thereby favoring the entry of "trigger" calcium via the sodium-calcium exchanger. To test this hypothesis, sodium current was suppressed by reducing the external sodium concentration or applying tetrodotoxin. At potentials positive to -30 millivolts, calcium release was unaffected. A small calcium release at more negative potentials could be attributed to partial activation of calcium channels, because it was unaltered by replacement of sodium with lithium and was blocked by cadmium. Thus, sodium influx or its accumulation does not initiate calcium release. In addition, sodium-calcium exchange-related calcium release at potentials positive to +80 millivolts has slower kinetics than calcium channel-induced release. Therefore, only the calcium channel gates the fast release of calcium from the sarcoplasmic reticulum in the range of the action potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sham, J S -- Cleemann, L -- Morad, M -- HL-07400/HL/NHLBI NIH HHS/ -- HL-16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 14;255(5046):850-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1311127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/physiology ; Calcium Channels/*physiology ; Heart/*physiology ; In Vitro Techniques ; Ion Channel Gating/*drug effects ; Lithium/pharmacology ; Membrane Potentials ; Rats ; Sodium/*pharmacology ; Tetrodotoxin/pharmacology
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  • 90
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    Widespread dispersion of neuronal clones across functional regions of the cerebral cortex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The cerebral cortex of the mammalian brain has expanded rapidly during the course of evolution and acquired structurally distinguishable areas devoted to separate functions. In some brain regions, topographic restrictions to cell intermixing occur during embryonic development. As a means of examining experimentally whether such restrictions occur during formation of functional subdivisions in the rat neocortex, clonally related neocortical cells were marked by retroviral-mediated transfer of a histochemical marker gene. Clonal boundaries were determined by infection of the developing brain with a library of genetically distinct viruses and amplification of single viral genomes by the polymerase chain reaction. Many clonally related neurons in the cerebral cortex became widely dispersed across functional areas of the cortex. Specification of cortical areas therefore occurs after neurogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walsh, C -- Cepko, C L -- NS 23021/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):434-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain Mapping ; Cerebral Cortex/*cytology/embryology ; Clone Cells ; Genetic Vectors ; Molecular Sequence Data ; Neurons/*cytology ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Rats ; Retroviridae/genetics
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  • 91
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    Neurotransmitter release from synaptotagmin-deficient clonal variants of PC12 cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: Synaptotagmin (p65) is an abundant synaptic vesicle protein of neurons and contains regions similar to the regulatory domain of protein kinase C. These domains are thought to be involved in calcium-dependent interaction with membrane phospholipids during exocytosis. To assess the functional role of synaptotagmin, synaptotagmin-deficient clonal variants of PC12 cells were isolated. All of the variant cells released catecholamine and adenosine triphosphate in response to elevated intracellular concentrations of calcium, which suggests that synaptotagmin is not essential for secretion of catecholamine and adenosine triphosphate from PC12 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoji-Kasai, Y -- Yoshida, A -- Sato, K -- Hoshino, T -- Ogura, A -- Kondo, S -- Fujimoto, Y -- Kuwahara, R -- Kato, R -- Takahashi, M -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1821-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kasel Institute of Life Sciences, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352065" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/secretion ; Animals ; Blotting, Northern ; Blotting, Western ; Calcium/pharmacology ; *Calcium-Binding Proteins ; Cerebellum/metabolism ; Dopamine/secretion ; Ionomycin/pharmacology ; Membrane Glycoproteins/*physiology ; Nerve Tissue Proteins/*physiology ; Neurotransmitter Agents/*secretion ; PC12 Cells ; Prosencephalon/metabolism ; RNA, Messenger/analysis ; Rats ; Synaptotagmin I ; Synaptotagmins
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  • 92
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    Stress-induced facilitation of classical conditioning (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-24
    Description: Stress has been shown to impair subsequent learning. To determine whether stress would impair classical conditioning, rats were exposed to inescapable, low-intensity tail shock and subsequently classically conditioned under freely moving conditions with a brief periorbital shock unconditioned stimulus and a white noise conditioned stimulus. Unexpectedly stressed rats exhibited significantly more conditioned eyeblink responses and the magnitude of their individual responses was also enhanced. These results stand in contrast to the learning deficits typically observed and suggest that stress can enhance the acquisition of discrete conditioned responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shors, T J -- Weiss, C -- Thompson, R F -- AG00093/AG/NIA NIH HHS/ -- AG05500/AG/NIA NIH HHS/ -- AG05514/AG/NIA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 24;257(5069):537-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Princeton University, NJ 08544.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1636089" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Blinking ; Conditioning, Classical/*physiology ; Corticosterone/blood ; Electromyography ; Electroshock ; Learning/physiology ; Male ; Rats ; Rats, Inbred F344 ; Stress, Psychological/*physiopathology
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  • 93
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    Initiation of deregulated growth of multipotent progenitor cells by bcr-abl in vitro (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-08
    Description: Expression of the bcr-abl oncogene in multipotent progenitor cells (MPPCs) is implicated as a key event in the development of chronic myelogenous leukemia. Bone marrow enriched for MPPCs was infected with a retrovirus that carried bcr-abl. The mixed-lineage colonies that resulted were responsive to growth factors and could differentiate. These cells later became growth factor-independent but, when injected into severe combined immunodeficient mice, were not leukemogenic. Thus, the presence of bcr-abl alone does not cause growth factor independence, although it initiates a stepwise process. This system may prove useful in the study of other oncogenes that cause leukemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gishizky, M L -- Witte, O N -- New York, N.Y. -- Science. 1992 May 8;256(5058):836-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/drug effects ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Clone Cells ; Drug Resistance, Microbial/genetics ; Fluorouracil/pharmacology ; Fusion Proteins, bcr-abl/*genetics ; Hematopoietic Cell Growth Factors/pharmacology ; Hematopoietic Stem Cells/*cytology/drug effects/physiology ; Humans ; Interleukin-3/pharmacology ; Macrophages/cytology/drug effects ; Mast Cells/cytology/drug effects ; Mice ; Rats ; Retroviridae/genetics ; Stem Cell Factor ; Transfection
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  • 94
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    Modality-specific retrograde amnesia of fear (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-05-01
    Description: Emotional responses such as fear are rapidly acquired through classical conditioning. This report examines the neural substrate underlying memory of acquired fear. Rats were classically conditioned to fear both tone and context through the use of aversive foot shocks. Lesions were made in the hippocampus either 1, 7, 14, or 28 days after training. Contextual fear was abolished in the rats that received lesions 1 day after fear conditioning. However, rats for which the interval between learning and hippocampal lesions was longer retained significant contextual fear memory. In the same animals, lesions did not affect fear response to the tone at any time. These results indicate that fear memory is not a single process and that the hippocampus may have a time-limited role in associative fear memories evoked by polymodal (contextual) but not unimodal (tone) sensory stimuli.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, J J -- Fanselow, M S -- New York, N.Y. -- Science. 1992 May 1;256(5057):675-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1585183" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia, Retrograde/*etiology/physiopathology ; Animals ; Behavior, Animal/physiology ; Conditioning, Classical/*physiology ; Electroshock ; Fear/*physiology ; Female ; Hippocampus/physiopathology ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Involvement of the N-methyl D-aspartate (NMDA) receptor in synapse elimination during cerebellar development (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: In many instances, the establishment of highly specific neuronal connections during development results from the rearrangement of axonal projections through the trimming of exuberant collaterals or the elimination of functional synapses or both. Although the involvement of the N-methyl D-aspartate (NMDA) subtype of the glutamate receptor has been demonstrated in the shaping of axonal arbors, its participation in the process of selective stabilization of synapses remains an open issue. In this study, the effects of chronic in vivo application of D,L-2-amino-5-phosphonovaleric acid (D,L-APV), a selective antagonist of the NMDA receptor, on the synapse elimination process that takes place in the developing cerebellum of the rat have been analyzed. D,L-APV treatment prevented the regression of supernumerary climbing fiber synapses in 49 percent of the recorded Purkinje cells, while the inactive isomer L-APV was ineffective. Thus, activation of the NMDA receptor is a critical step in the regression of functional synapses during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rabacchi, S -- Bailly, Y -- Delhaye-Bouchaud, N -- Mariani, J -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Pierre and Marie Curie, Institut des Neurosciences, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352066" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Animals, Newborn ; Cerebellum/*growth & development ; Electrophysiology ; Purkinje Cells/drug effects/physiology ; Rats ; Receptors, Glutamate ; Receptors, Neurotransmitter/*physiology ; Synapses/drug effects/*physiology
    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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  • 96
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    The dispersion of neuronal clones across the cerebral cortex (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirkwood, T B -- Price, J -- Grove, E A -- New York, N.Y. -- Science. 1992 Oct 9;258(5080):317-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cerebral Cortex/*cytology ; Clone Cells/*cytology ; Genetic Markers ; Neurons/*cytology ; Rats ; Retroviridae
    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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  • 97
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    Cloning and expression of a rat brain GABA transporter (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-09-14
    Description: A complementary DNA clone (designated GAT-1) encoding a transporter for the neurotransmitter gamma-aminobutyric acid (GABA) has been isolated from rat brain, and its functional properties have been examined in Xenopus oocytes. Oocytes injected with GAT-1 synthetic messenger RNA accumulated [3H]GABA to levels above control values. The transporter encoded by GAT-1 has a high affinity for GABA, is sodium-and chloride-dependent, and is pharmacologically similar to neuronal GABA transporters. The GAT-1 protein shares antigenic determinants with a native rat brain GABA transporter. The nucleotide sequence of GAT-1 predicts a protein of 599 amino acids with a molecular weight of 67 kilodaltons. Hydropathy analysis of the deduced protein suggests multiple transmembrane regions, a feature shared by several cloned transporters; however, database searches indicate that GAT-1 is not homologous to any previously identified proteins. Therefore, GAT-1 appears to be a member of a previously uncharacterized family of transport molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guastella, J -- Nelson, N -- Nelson, H -- Czyzyk, L -- Keynan, S -- Miedel, M C -- Davidson, N -- Lester, H A -- Kanner, B I -- GM 10991/GM/NIGMS NIH HHS/ -- GM 29836/GM/NIGMS NIH HHS/ -- NS 16708/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1303-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975955" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/metabolism ; Carrier Proteins/antagonists & inhibitors/*genetics/metabolism ; Chlorine/physiology ; Cloning, Molecular ; GABA Plasma Membrane Transport Proteins ; Gene Expression ; Membrane Proteins/antagonists & inhibitors/*genetics/metabolism ; *Membrane Transport Proteins ; Microinjections ; Molecular Sequence Data ; Nerve Tissue Proteins/antagonists & inhibitors/*genetics/metabolism ; Oocytes/metabolism ; *Organic Anion Transporters ; Poly A/analysis ; RNA, Messenger/analysis ; Rats ; Sodium/physiology ; Structure-Activity Relationship ; Xenopus ; gamma-Aminobutyric Acid/*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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  • 98
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    Protection against mucoid Pseudomonas aeruginosa in rodent models of endobronchial infections (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-03
    Description: Chronic endobronchial infection with mucoid Pseudomonas aeruginosa accounts for much of the morbidity and mortality in patients with cystic fibrosis (CF). Reduced morbidity is observed when infection is absent. Clinical investigations have implicated opsonizing antibody specific for the mucoid exopolysaccharide (MEP) surrounding these bacteria as a potential immunologic protective mechanism, whereas nonopsonizing antibody to MEP is not protective. Mice and rats immunized with doses of MEP that elicited opsonizing antibody had reduced levels of infection compared with nonimmune controls after intratracheal challenge with mucoid P. aeruginosa enmeshed in agar beads. Doses of MEP that elicited nonopsonizing antibody were not protective. Parallel experiments in which passive transfer of polyclonal and monoclonal opsonizing and nonopsonizing antibody were used yielded similar results. These data indicate that MEP-specific opsonizing antibody can protect against chronic P. aeruginosa infection in this model of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pier, G B -- Small, G J -- Warren, H B -- AI 22534/AI/NIAID NIH HHS/ -- AI 22806/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1990 Aug 3;249(4968):537-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Animal Resource Center, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2116663" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*therapeutic use ; Cystic Fibrosis/complications ; Disease Models, Animal ; Female ; Immunization, Passive ; Lung/pathology ; Polysaccharides, Bacterial/*immunology ; Pseudomonas Infections/*immunology/pathology/prevention & control ; Pseudomonas aeruginosa/immunology ; Rats
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Calcium mobilization and exocytosis after one mechanical stretch of lung epithelial cells (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-11-30
    Description: Deep inflation of the lung stimulates surfactant secretion by unknown mechanisms. The hypothesis that mechanical distension directly stimulates type II cells to secrete surfactant was tested by stretching type II cells cultured on silastic membranes. The intracellular Ca2+ concentration was measured in single cells, before and after stretching. A single stretch of alveolar type II cells caused a transient (less than 60 seconds) increase in cytosolic Ca2+ followed by a sustained (15 to 30 minutes) stimulation of surfactant secretion. Both Ca2+ mobilization and exocytosis exhibited dose-dependence to the magnitude of the stretch-stimulus. Thus, mechanical factors can trigger complex cellular events in nonneuron, nonmuscle cells and may be involved in regulating normal lung functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wirtz, H R -- Dobbs, L G -- HL-24075/HL/NHLBI NIH HHS/ -- HL-34356/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1266-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Institute, University of California, San Francisco 94143-0130.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2173861" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomechanical Phenomena ; Calcium/*metabolism ; Cells, Cultured ; Cyclic AMP/metabolism ; Epithelium/physiology ; *Exocytosis ; Kinetics ; Phosphatidylcholines/secretion ; Proteolipids/pharmacology ; Pulmonary Alveoli/*physiology ; Pulmonary Surfactant-Associated Proteins ; Pulmonary Surfactants/pharmacology/secretion ; Rats ; Surface Properties ; Tetradecanoylphorbol Acetate/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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  • 100
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    Calcium-sensitive cross-bridge transitions in mammalian fast and slow skeletal muscle fibers (1990)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1990-03-02
    Description: The fundamental mechanism underlying the differing rates of tension development in fast and slow mammalian skeletal muscle is still unknown. Now, in skinned (membrane-permeabilized) single fibers it has been shown that the rate of formation of the strongly bound, force-producing cross-bridge between actin and myosin is calcium-sensitive in both fast and slow fibers and that the rate is markedly greater in fast fibers. The transition rates obtained at high calcium concentrations correlated with myosin isoform content, whereas at low calcium concentrations the thin filament regulatory proteins appeared to modulate the rate of tension development, especially in fast fibers. Fiber type-dependent differences in rates of cross-bridge transitions may account for the characteristic rates of tension development in mammalian fast and slow skeletal muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metzger, J M -- Moss, R L -- AR-31806/AR/NIAMS NIH HHS/ -- AR07811/AR/NIAMS NIH HHS/ -- HL-25861/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1088-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, School of Medicine, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2309121" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Calcium/*pharmacology ; Muscle Contraction/*drug effects ; Muscles/drug effects/*physiology ; Myosins/metabolism ; Rats ; Troponin/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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