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  • Rats  (781)
  • National Institutes of Health (U.S.)  (345)
  • American Association for the Advancement of Science (AAAS)  (1,125)
  • American Association of Petroleum Geologists (AAPG)
  • International Union of Crystallography (IUCr)
  • 1990-1994  (573)
  • 1985-1989  (552)
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  • American Association for the Advancement of Science (AAAS)  (1,125)
  • American Association of Petroleum Geologists (AAPG)
  • International Union of Crystallography (IUCr)
  • Springer  (14)
Years
Year
  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 Mar 4;263(5151):1216.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8122099" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Clinical Trials as Topic ; Female ; Humans ; Informed Consent ; *Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Pregnancy ; *Pregnant Women ; Research Subjects ; United States ; *Women's Health
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-14
    Description: An activity that severs stable microtubules is thought to be involved in microtubule reorganization during the cell cycle. Here, a 48-kilodalton microtubule-severing protein was purified from Xenopus eggs and identified as translational elongation factor 1 alpha (EF-1 alpha). Bacterially expressed human EF-1 alpha also displayed microtubule-severing activity in vitro and, when microinjected into fibroblasts, induced rapid and transient fragmentation of cytoplasmic microtubule arrays. Thus, EF-1 alpha, an essential component of the eukaryotic translational apparatus, appears to have a second role as a regulator of cytoskeletal rearrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shiina, N -- Gotoh, Y -- Kubomura, N -- Iwamatsu, A -- Nishida, E -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Molecular Biology, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939665" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Humans ; Microtubules/drug effects/*metabolism ; Molecular Sequence Data ; Molecular Weight ; Oocytes ; Peptide Elongation Factor 1 ; Peptide Elongation Factors/chemistry/isolation & purification/*physiology ; Rats ; Recombinant Proteins/pharmacology ; Ribonucleoproteins/chemistry/isolation & purification/*physiology ; Sepharose/analogs & derivatives/metabolism ; Xenopus laevis
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  • 3
    Publication Date: 1994-06-24
    Description: Two ternary complexes of rat DNA polymerase beta (pol beta), a DNA template-primer, and dideoxycytidine triphosphate (ddCTP) have been determined at 2.9 A and 3.6 A resolution, respectively. ddCTP is the triphosphate of dideoxycytidine (ddC), a nucleoside analog that targets the reverse transcriptase of human immunodeficiency virus (HIV) and is at present used to treat AIDS. Although crystals of the two complexes belong to different space groups, the structures are similar, suggesting that the polymerase-DNA-ddCTP interactions are not affected by crystal packing forces. In the pol beta active site, the attacking 3'-OH of the elongating primer, the ddCTP phosphates, and two Mg2+ ions are all clustered around Asp190, Asp192, and Asp256. Two of these residues, Asp190 and Asp256, are present in the amino acid sequences of all polymerases so far studied and are also spatially similar in the four polymerases--the Klenow fragment of Escherichia coli DNA polymerase I, HIV-1 reverse transcriptase, T7 RNA polymerase, and rat DNA pol beta--whose crystal structures are now known. A two-metal ion mechanism is described for the nucleotidyl transfer reaction and may apply to all polymerases. In the ternary complex structures analyzed, pol beta binds to the DNA template-primer in a different manner from that recently proposed for other polymerase-DNA models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelletier, H -- Sawaya, M R -- Kumar, A -- Wilson, S H -- Kraut, J -- CA17374/CA/NCI NIH HHS/ -- ES06839/ES/NIEHS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1891-903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, San Diego 92093-0317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; DNA/chemistry/metabolism ; DNA Polymerase I/*chemistry/metabolism ; DNA Primers/*chemistry/metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxycytosine Nucleotides/*chemistry/metabolism ; Dideoxynucleotides ; HIV Reverse Transcriptase ; Humans ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Rats ; Recombinant Proteins ; Templates, Genetic ; Thymine Nucleotides/chemistry/metabolism ; Viral Proteins ; Zidovudine/analogs & derivatives/chemistry/metabolism
    Print ISSN: 0036-8075
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  • 4
    Publication Date: 1994-11-11
    Description: The venom of the funnel-web spider Agelenopsis aperta contains several peptides that paralyze prey by blocking voltage-sensitive calcium channels. Two peptides, omega-Aga-IVB (IVB) and omega-Aga-IVC (IVC), have identical amino acid sequences, yet have opposite absolute configurations at serine 46. These toxins had similar selectivities for blocking voltage-sensitive calcium channel subtypes but different potencies for blocking P-type voltage-sensitive calcium channels in rat cerebellar Purkinje cells as well as calcium-45 influx into rat brain synaptosomes. An enzyme purified from venom converts IVC to IVB by isomerizing serine 46, which is present in the carboxyl-terminal tail, from the L to the D configuration. Unlike the carboxyl terminus of IVC, that of IVB was resistant to the major venom protease. These results show enzymatic activities in A. aperta venom being used in an unprecedented strategy for coproduction of necessary neurotoxins that possess enhanced stability and potency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heck, S D -- Siok, C J -- Krapcho, K J -- Kelbaugh, P R -- Thadeio, P F -- Welch, M J -- Williams, R D -- Ganong, A H -- Kelly, M E -- Lanzetti, A J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1065-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NPS Pharmaceuticals Incorporated, Salt Lake City, Utah 84108.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973665" target="_blank"〉PubMed〈/a〉
    Keywords: Agatoxins ; Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Calcium Channel Blockers/chemistry/*metabolism/toxicity ; Calcium Channels/*metabolism ; Isomerases/metabolism ; Molecular Sequence Data ; *Protein Processing, Post-Translational ; Purkinje Cells/metabolism ; Rats ; Serine/*metabolism ; Spider Venoms/chemistry/enzymology/*metabolism/toxicity ; Stereoisomerism ; Structure-Activity Relationship ; Synaptosomes/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-16
    Description: The organization of the hippocampus is generally thought of as a series of cell groups that form a unidirectionally excited chain, regulated by localized inhibitory circuits. With the use of in vivo intracellular labeling, histochemical, and extracellular tracing methods, a longitudinally widespread, inhibitory feedback in rat brain from the CA1 area to the CA3 and hilar regions was observed. This long-range, cross-regional inhibition may allow precise synchronization of population activity by timing the occurrence of action potentials in the principal cells and may contribute to the coordinated induction of synaptic plasticity in distributed networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sik, A -- Ylinen, A -- Penttonen, M -- Buzsaki, G -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1722-4.〈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/8085161" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Dendrites/ultrastructure ; Feedback ; Hippocampus/cytology/*physiology ; Interneurons/*physiology/ultrastructure ; Membrane Potentials ; *Neural Inhibition ; Neural Pathways ; Pyramidal Cells/*physiology/ultrastructure ; Rats ; Synapses/ultrastructure
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1994-12-16
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettit, D L -- Perlman, S -- Malinow, R -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1881-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997883" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Genetic Vectors ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/enzymology/*physiology ; Rats ; Recombinant Proteins/metabolism ; Synaptic Transmission/drug effects/*physiology ; Transfection ; Vaccinia virus/genetics/physiology
    Print ISSN: 0036-8075
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  • 7
    Publication Date: 1994-11-11
    Description: For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present in the limb bud. Members of the neurotrophin family are currently the best candidates for such neurotrophic factors, but inactivation of their receptor genes leads to only partial loss of motoneurons, which suggests that other factors are involved. Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture. GDNF messenger RNA was found in the immediate vicinity of motoneurons during the period of cell death in development. In vivo, GDNF rescues and prevents the atrophy of facial motoneurons that have been deprived of target-derived survival factors by axotomy. GDNF may therefore be a physiological trophic factor for spinal motoneurons. Its potency and specificity in vitro and in vivo also make it a good candidate for treatment of motoneuron disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, C E -- Phillips, H S -- Pollock, R A -- Davies, A M -- Lemeulle, C -- Armanini, M -- Simmons, L -- Moffet, B -- Vandlen, R A -- Simpson LC corrected to Simmons, L -- Koliatsos, V E -- Rosenthal, A -- NS 10580/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1062-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U.382, IBDM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor ; Cell Death ; Cell Survival/drug effects ; Cells, Cultured ; Ciliary Neurotrophic Factor ; Face/innervation ; Glial Cell Line-Derived Neurotrophic Factor ; Growth Inhibitors/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Molecular Sequence Data ; Motor Neurons/*cytology/drug effects ; Muscle Fibers, Skeletal/*metabolism ; Nerve Growth Factors/analysis/biosynthesis/genetics/*pharmacology ; Nerve Tissue Proteins/*analysis/biosynthesis/genetics/*pharmacology ; Neurons, Afferent/cytology/drug effects ; Peripheral Nerves/*metabolism ; RNA, Messenger/analysis/genetics ; Rats ; Schwann Cells/metabolism
    Print ISSN: 0036-8075
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  • 8
    Publication Date: 1994-09-09
    Description: Endogenous DNA adducts may contribute to the etiology of human genetic disease and cancer. One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde. A sensitive mass spectrometric method permitted detection and quantitation of the major malondialdehyde-DNA adduct, a pyrimidopurinone derived from deoxyguanosine. DNA from disease-free human liver was found to contain 5400 adducts per cell, a frequency comparable to that of adducts formed by exogenous carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhary, A K -- Nokubo, M -- Reddy, G R -- Yeola, S N -- Morrow, J D -- Blair, I A -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- GM42056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A. B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt University School of Medicine, Nashville, TN 37232-0146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079172" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Carbon Tetrachloride/toxicity ; DNA/*chemistry ; DNA Damage ; Deoxyguanosine/*analogs & derivatives/analysis/*metabolism ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Lipid Peroxidation ; Liver/*chemistry ; Male ; Malondialdehyde/*metabolism ; Rats ; Rats, Sprague-Dawley
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1345.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073266" target="_blank"〉PubMed〈/a〉
    Keywords: *Embryo, Mammalian ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; *Research ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messing, R B -- Gust, L D -- Petersen, D W -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1518-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Chloroform/administration & dosage/*toxicity ; Female ; Humans ; Kidney Neoplasms/*chemically induced ; Rats ; Risk Factors ; *Water Supply
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fochtmann, L J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):953.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973669" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; National Institutes of Health (U.S.) ; *Research ; Research Personnel/*economics ; *Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1371-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073270" target="_blank"〉PubMed〈/a〉
    Keywords: Centers for Disease Control and Prevention (U.S.) ; Drug Approval ; Drug Industry ; Humans ; Institute of Medicine (U.S.) ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States ; *Vaccines ; World Health Organization
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  • 13
    Publication Date: 1994-01-14
    Description: The vagus nerve exerts a profound influence on the heart, regulating the heart rate and rhythm. An extensive vagal innervation of the cardiac ventricles and the central origin and extent of this innervation was demonstrated by transynaptic transport of pseudorabies virus with a virulent and two attenuated pseudorabies viral strains. The neurons that innervate the ventricles are numerous, and their distribution within the nucleus ambiguus and dorsal motor nucleus of the vagus is similar to that of neurons innervating other cardiac targets, such as the sino-atrial node. These data provide a neuroanatomical correlate to the physiological influence of the vagus nerve on ventricular function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Standish, A -- Enquist, L W -- Schwaber, J S -- MH-43787/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):232-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Computation Group, E. I. DuPont de Nemours & Co., Wilmington, DE 19880-0323.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Heart Ventricles/*innervation/microbiology ; Herpesvirus 1, Suid/pathogenicity/*physiology ; Interneurons/cytology ; Medulla Oblongata/*anatomy & histology/microbiology ; Motor Neurons/cytology ; Neural Pathways ; Rats ; Rats, Wistar ; Vagus Nerve/*anatomy & histology/microbiology ; Virulence
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  • 14
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1475-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Fear/physiology ; Humans ; Learning/physiology ; Motor Cortex/physiology ; Nerve Growth Factors/physiology ; Nerve Net/*physiology ; Neural Pathways/physiology ; Neuronal Plasticity/*physiology ; Pain/physiopathology ; Rats ; Synapses/physiology
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  • 15
    Publication Date: 1994-04-01
    Description: Several types of calcium channels found in the central nervous system are possible participants in triggering neurotransmitter release. Synaptic transmission between hippocampal CA3 and CA1 neurons was mediated by N-type calcium channels, together with calcium channels whose pharmacology differs from that of L- and P-type channels but resembles that of the Q-type channel encoded by the alpha 1A subunit gene. Blockade of either population of channels strongly increased enhancement of synaptic transmission with repetitive stimuli. Even after complete blockade of N-type channels, transmission was strongly modulated by stimulation of neurotransmitter receptors or protein kinase C. These findings suggest a role for alpha 1A subunits in synaptic transmission and support the idea that neurotransmitter release may depend on multiple types of calcium channels under physiological conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, D B -- Randall, A -- Tsien, R W -- MH48108-02/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):107-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7832825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects/*physiology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Peptides/pharmacology ; Phorbol 12,13-Dibutyrate/pharmacology ; Protein Kinase C/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholinergic/metabolism ; Receptors, GABA-B/metabolism ; Receptors, Glutamate/metabolism ; Receptors, Purinergic P1/metabolism ; Spider Venoms/pharmacology ; *Synaptic Transmission/drug effects ; omega-Agatoxin IVA ; omega-Conotoxin GVIA ; *omega-Conotoxins
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  • 16
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):603-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Learning/*physiology ; Memory/physiology ; Rats ; Sleep/*physiology ; Sleep, REM/physiology
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 May 6;264(5160):772-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171331" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy ; Amyotrophic Lateral Sclerosis/drug therapy ; Animals ; Clinical Trials as Topic ; Humans ; Insulin-Like Growth Factor I/therapeutic use ; Nerve Growth Factors/*therapeutic use ; Nerve Tissue Proteins/*therapeutic use ; Nervous System Diseases/*drug therapy ; Neurons/drug effects ; Parkinson Disease/drug therapy ; Peripheral Nervous System Diseases/drug therapy ; Rats
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):600-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303261" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Control Groups ; Double-Blind Method ; Federal Government ; *Fetal Research ; *Fetal Tissue Transplantation ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; Parkinson Disease/*surgery ; Peer Review, Research ; Research Subjects ; Research Support as Topic ; Risk Assessment ; United States
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
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  • 20
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monro, A M -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*statistics & numerical data ; Carcinogens/*administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Mice ; Mutagenicity Tests ; Neoplasms/*chemically induced ; Rats ; Risk Assessment
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  • 22
    Publication Date: 1994-12-02
    Description: In many mammalian species, the placenta is the site of synthesis of proteins in the prolactin and growth hormone family. Analysis of two such proteins, proliferin (PLF) and proliferin-related protein (PRP), revealed that they are potent regulators of angiogenesis; PLF stimulated and PRP inhibited endothelial cell migration in cell culture and neovascularization in vivo. The mouse placenta secretes an angiogenic activity during the middle of pregnancy that corresponds primarily to PLF, but later in gestation releases a factor that inhibits angiogenesis, which was identified as PRP. Incubation of placental tissue with PLF led to the specific binding of this hormone to capillary endothelial cells. Thus PLF and PRP may regulate the initiation and then the cessation of placental neovascularization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, D -- Volpert, O V -- Bouck, N -- Linzer, D I -- CA52750/CA/NCI NIH HHS/ -- HD24518/HD/NICHD NIH HHS/ -- HD29962/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Movement/drug effects ; Cornea/blood supply ; Culture Techniques ; Endothelium, Vascular/*cytology/drug effects/metabolism ; Female ; Fibroblast Growth Factor 2/pharmacology ; Glycoproteins/metabolism/*pharmacology ; Growth Substances/metabolism/*pharmacology ; Intercellular Signaling Peptides and Proteins ; *Neovascularization, Pathologic ; Placenta/*blood supply ; Pregnancy ; Pregnancy Proteins/*pharmacology ; Rats
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  • 23
    Publication Date: 1994-11-11
    Description: The decay of excitatory postsynaptic currents in central neurons mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors is likely to be shaped either by receptor desensitization or by offset after removal of glutamate from the synaptic cleft. Native AMPA receptors show desensitization time constants of 1 to about 10 milliseconds, but the underlying molecular determinants of these large differences are unknown. Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower. Cerebellar granule cells switch their expression of GluR-D splice variants from mostly flip forms in early stages to predominantly flop forms in the adult rat brain. These findings suggest that rapid desensitization of AMPA receptors can be regulated by the expression and alternative splicing of GluR-D gene transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosbacher, J -- Schoepfer, R -- Monyer, H -- Burnashev, N -- Seeburg, P H -- Ruppersberg, J P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1059-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/7973663" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cloning, Molecular ; Glutamic Acid/*pharmacology ; In Situ Hybridization ; Oocytes ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/drug effects/genetics/*physiology ; Recombinant Proteins ; Synaptic Transmission ; Xenopus laevis
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  • 24
    Publication Date: 1994-08-12
    Description: Dynamin I is a nerve terminal phosphoprotein with intrinsic guanosine triphosphatase (GTPase) activity that is required for endocytosis. Upon depolarization and synaptic vesicle recycling, dynamin I undergoes a rapid dephosphorylation. Dynamin I was found to be a specific high-affinity substrate for calcineurin in vitro. At low concentrations, calcineurin dephosphorylated dynamin I that had been phosphorylated by protein kinase C. The dephosphorylation inhibited dynamin I GTPase activity in vitro and after depolarization of nerve terminals. The effect in nerve terminals was prevented by the calcineurin inhibitor cyclosporin A. This suggests that in nerve terminals, calcineurin serves as a Ca(2+)-sensitive switch for depolarization-evoked synaptic vesicle recycling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, J P -- Sim, A T -- Robinson, P J -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):970-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Unit, John Hunter Hospital, NSW, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin ; Calcium/metabolism ; Calmodulin-Binding Proteins/metabolism/*pharmacology ; Cyclosporine/pharmacology ; Dynamin I ; Dynamins ; Endocytosis ; GTP Phosphohydrolases/*antagonists & inhibitors/metabolism ; Nerve Endings/enzymology/*metabolism ; Phosphoprotein Phosphatases/metabolism/*pharmacology ; Phosphorylation ; Rats ; Synaptic Vesicles/*metabolism ; Synaptosomes/enzymology/*metabolism
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  • 25
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈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/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 26
    Publication Date: 1994-01-28
    Description: As changes in synaptic strength are thought to be critical for learning and memory, it would be useful to monitor the activity of individual identified synapses on mammalian central neurons. Calcium imaging of cortical neurons grown in primary culture was used to visualize the activation of individual postsynaptic elements by miniature excitatory synaptic currents elicited by spontaneous quantal release. This approach revealed that the probability of spontaneous activity differed among synapses on the same dendrite. Furthermore, synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, T H -- Baraban, J M -- Wier, W G -- Blatter, L A -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):529-32.〈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/7904774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cerebral Cortex ; Dendrites/*metabolism ; Glutamates/pharmacology ; Glutamic Acid ; Kinetics ; Microelectrodes ; Neuronal Plasticity ; Neurons/*physiology ; Phorbol Esters/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
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  • 27
    Publication Date: 1994-12-09
    Description: Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). A potential animal model of CF, the CFTR-/- mouse, has had limited utility because most mice die from intestinal obstruction during the first month of life. Human CFTR (hCFTR) was expressed in CFTR-/- mice under the control of the rat intestinal fatty acid-binding protein gene promoter. The mice survived and showed functional correction of ileal goblet cell and crypt cell hyperplasia and cyclic adenosine monophosphate-stimulated chloride secretion. These results support the concept that transfer of the hCFTR gene may be a useful strategy for correcting physiologic defects in patients with CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, L -- Dey, C R -- Wert, S E -- DuVall, M D -- Frizzell, R A -- Whitsett, J A -- DK38518/DK/NIDDK NIH HHS/ -- HL49004/HL/NHLBI NIH HHS/ -- HL51832/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, OH 45229-3039.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Carrier Proteins/genetics ; Chlorides/metabolism ; Colforsin/pharmacology ; Colon/chemistry/pathology ; Cystic Fibrosis/genetics/metabolism/pathology/*therapy ; Cystic Fibrosis Transmembrane Conductance Regulator ; Disease Models, Animal ; Fatty Acid-Binding Proteins ; Gene Expression ; *Genetic Therapy ; Humans ; Intestinal Mucosa/chemistry/*pathology/secretion ; Intestine, Small/chemistry/pathology ; Membrane Proteins/analysis/*genetics/physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Promoter Regions, Genetic ; RNA, Messenger/analysis/genetics ; Rats ; Recombinant Proteins/biosynthesis ; *Tumor Suppressor Proteins
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  • 28
    Publication Date: 1994-12-09
    Description: AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor channels mediate the fast component of excitatory postsynaptic currents in the central nervous system. Site-selective nuclear RNA editing controls the calcium permeability of these channels, and RNA editing at a second site is shown here to affect the kinetic aspects of these channels in rat brain. In three of the four AMPA receptor subunits (GluR-B, -C, and -D), intronic elements determine a codon switch (AGA, arginine, to GGA, glycine) in the primary transcripts in a position termed the R/G site, which immediately precedes the alternatively spliced modules "flip" and "flop." The extent of editing at this site progresses with brain development in a manner specific for subunit and splice form, and edited channels possess faster recovery rates from desensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lomeli, H -- Mosbacher, J -- Melcher, T -- Hoger, T -- Geiger, J R -- Kuner, T -- Monyer, H -- Higuchi, M -- Bach, A -- Seeburg, P H -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1709-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992055" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Brain/embryology/*metabolism ; Cell Nucleus/metabolism ; Exons ; Glutamic Acid/pharmacology ; Glycine/genetics ; Introns ; Kinetics ; Membrane Potentials ; Molecular Sequence Data ; Oocytes ; PC12 Cells ; Patch-Clamp Techniques ; *RNA Editing ; Rats ; Rats, Wistar ; Receptors, AMPA/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Xenopus
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-25
    Description: Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, M -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, 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/8134839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/*metabolism ; Calcium/*metabolism ; Cell Communication ; Cells, Cultured ; Electric Stimulation ; Excitatory Amino Acid Antagonists ; Gap Junctions/physiology ; Kynurenic Acid/pharmacology ; Neurons/drug effects/*metabolism ; Nifedipine/pharmacology ; Octanols/pharmacology ; Prosencephalon/*cytology/embryology ; Rats ; *Signal Transduction ; Synapses/metabolism ; Tetrodotoxin/pharmacology
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-19
    Description: Repeated high-frequency trains of stimuli induce long-term potentiation (LTP) in the CA1 region that persists for up to 8 hours in hippocampal slices and for days in intact animals. This long time course has made LTP an attractive model for certain forms of long-term memory in the mammalian brain. A hallmark of long-term memory in the intact animal is a requirement for transcription, and thus whether the late phase of LTP (L-LTP) requires transcription was investigated here. With the use of different inhibitors, it was found in rat hippocampal slices that the induction of L-LTP [produced either by tetanic stimulation or by application of the cyclic adenosine monophosphate (cAMP) analog Sp-cAMPS (Sp-cyclic adenosine 3',5'-monophosphorothioate)] was selectively prevented when transcription was blocked immediately after tetanization or during application of cAMP. As with behavioral memory, this requirement for transcription had a critical time window. Thus, the late phase of LTP in the CA1 region requires transcription during a critical period, perhaps because cAMP-inducible genes must be expressed during this period.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nguyen, P V -- Abel, T -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066450" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/analogs & derivatives/metabolism/pharmacology ; Dactinomycin/pharmacology ; Dichlororibofuranosylbenzimidazole/pharmacology ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Pyramidal Cells/metabolism ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; *Transcription, Genetic/drug effects
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saundry, P D -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):185.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146642" target="_blank"〉PubMed〈/a〉
    Keywords: *Environment ; *Government Agencies ; National Institutes of Health (U.S.) ; United States
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  • 32
    Publication Date: 1994-06-24
    Description: Structures of the 31-kilodalton catalytic domain of rat DNA polymerase beta (pol beta) and the whole 39-kilodalton enzyme were determined at 2.3 and 3.6 angstrom resolution, respectively. The 31-kilodalton domain is composed of fingers, palm, and thumb subdomains arranged to form a DNA binding channel reminiscent of the polymerase domains of the Klenow fragment of Escherichia coli DNA polymerase I, HIV-1 reverse transcriptase, and bacteriophage T7 RNA polymerase. The amino-terminal 8-kilodalton domain is attached to the fingers subdomain by a flexible hinge. The two invariant aspartates found in all polymerase sequences and implicated in catalytic activity have the same geometric arrangement within structurally similar but topologically distinct palms, indicating that the polymerases have maintained, or possibly re-evolved, a common nucleotidyl transfer mechanism. The location of Mn2+ and deoxyadenosine triphosphate in pol beta confirms the role of the invariant aspartates in metal ion and deoxynucleoside triphosphate binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawaya, M R -- Pelletier, H -- Kumar, A -- Wilson, S H -- Kraut, J -- CA17374/CA/NCI NIH HHS/ -- ES06839/ES/NIEHS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1930-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, San Diego 92093-0317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cloning, Molecular ; Crystallization ; Crystallography, X-Ray ; DNA/metabolism ; DNA Polymerase I/*chemistry/metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxyadenine Nucleotides/chemistry/metabolism ; Deoxycytosine Nucleotides/chemistry/metabolism ; Dideoxynucleotides ; HIV Reverse Transcriptase ; Protein Folding ; Protein Structure, Secondary ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Rats ; Recombinant Proteins/chemistry ; Viral Proteins
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  • 33
    Publication Date: 1994-12-09
    Description: Circadian rhythms of mammals are timed by an endogenous clock with a period of about 24 hours located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Light synchronizes this clock to the external environment by daily adjustments in the phase of the circadian oscillation. The mechanism has been thought to involve the release of excitatory amino acids from retinal afferents to the SCN. Brief treatment of rat SCN in vitro with glutamate (Glu), N-methyl-D-aspartate (NMDA), or nitric oxide (NO) generators produced lightlike phase shifts of circadian rhythms. The SCN exhibited calcium-dependent nitric oxide synthase (NOS) activity. Antagonists of NMDA or NOS pathways blocked Glu effects in vitro, and intracerebroventricular injection of a NOS inhibitor in vivo blocked the light-induced resetting of behavioral rhythms. Together, these data indicate that Glu release, NMDA receptor activation, NOS stimulation, and NO production link light activation of the retina to cellular changes within the SCN mediating the phase resetting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, J M -- Chen, D -- Weber, E T -- Faiman, L E -- Rea, M A -- Gillette, M U -- NS22155/NS/NINDS NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1713-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527589" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Biological Clocks/drug effects/*physiology ; Circadian Rhythm/drug effects/*physiology ; Glutamic Acid/*metabolism/pharmacology ; In Vitro Techniques ; Light ; N-Methylaspartate/pharmacology ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent/physiology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Retina/physiology ; Signal Transduction ; Suprachiasmatic Nucleus/drug effects/metabolism/*physiology
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  • 34
    Publication Date: 1994-09-09
    Description: The role of the low-affinity neurotrophin receptor (p75NTR) in signal transduction is undefined. Nerve growth factor can activate the sphingomyelin cycle, generating the putative-lipid second messenger ceramide. In T9 glioma cells, addition of a cell-permeable ceramide analog mimicked the effects of nerve growth factor on cell growth inhibition and process formation. This signaling pathway appears to be mediated by p75NTR in T9 cells and NIH 3T3 cells overexpressing p75NTR. Expression of an epidermal growth factor receptor-p75NTR chimera in T9 cells imparted to epidermal growth factor the ability to activate the sphingomyelin cycle. These data demonstrate that p75NTR is capable of signaling independently of the trk neurotrophin receptor (p140trk) and that ceramide may be a mediator in neurotrophin biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dobrowsky, R T -- Werner, M H -- Castellino, A M -- Chao, M V -- Hannun, Y A -- AG05531/AG/NIA NIH HHS/ -- GM43825/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Cell Biology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079174" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Astrocytes/cytology/*metabolism ; Ceramides/metabolism/pharmacology ; Epidermal Growth Factor/pharmacology ; Glioblastoma ; Mice ; Nerve Growth Factors/pharmacology ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Sphingomyelins/*metabolism ; Tumor Cells, Cultured
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  • 35
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1555-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dopamine/metabolism ; Drug and Narcotic Control ; Humans ; Limbic System/drug effects/metabolism ; *Nicotine/pharmacology ; Rats ; Receptors, Cholinergic/drug effects/metabolism ; *Smoking ; *Substance-Related Disorders ; United States ; *United States Food and Drug Administration
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  • 36
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seachrist, L -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/chemically induced/prevention & control ; Endometrial Neoplasms/chemically induced ; Female ; Humans ; Liver Neoplasms, Experimental/chemically induced ; Rats ; Tamoxifen/therapeutic use/*toxicity
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  • 37
    Publication Date: 1994-11-25
    Description: One therapeutic approach to treating Parkinson's disease is to convert endogenous striatal cells into levo-3,4-dihydroxyphenylalanine (L-dopa)-producing cells. A defective herpes simplex virus type 1 vector expressing human tyrosine hydroxylase was delivered into the partially denervated striatum of 6-hydroxydopamine-lesioned rats, used as a model of Parkinson's disease. Efficient behavioral and biochemical recovery was maintained for 1 year after gene transfer. Biochemical recovery included increases in both striatal tyrosine hydroxylase enzyme activity and in extracellular dopamine concentrations. Persistence of human tyrosine hydroxylase was revealed by expression of RNA and immunoreactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉During, M J -- Naegele, J R -- O'Malley, K L -- Geller, A I -- EY09749/EY/NEI NIH HHS/ -- NS06208/NS/NINDS NIH HHS/ -- NS28227/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1399-403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7669103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Corpus Striatum/*enzymology/metabolism ; Denervation ; Disease Models, Animal ; Dopamine/metabolism ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Humans ; Levodopa/metabolism ; Male ; Molecular Sequence Data ; *Motor Activity ; Neurons/enzymology ; Parkinson Disease/metabolism/*therapy ; Rats ; Rats, Sprague-Dawley ; Simplexvirus/*genetics ; Tyrosine 3-Monooxygenase/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 38
    Publication Date: 1994-01-28
    Description: Fusion of BERH-2 rat hepatocellular carcinoma cells with activated B cells produced hybrid cells that lost their tumorigenicity and became immunogenic. Syngeneic rats injected with BERH-2-B hybrid cells became resistant to challenge with parental BERH-2 cells, and rats with established BERH-2 hepatomas were cured by subsequent injection of BERH-2-B cells. Both CD4+ and CD8+ cells were essential for the induction of protective immunity; however, only CD8+ cells were required for the eradication of BERH-2 tumors. The generation of hybrid tumor cells that elicit antitumor immune responses may be a useful strategy for cancer immunotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Y -- Wu, M -- Chen, H -- Wang, X -- Liu, G -- Li, G -- Ma, J -- Sy, M S -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):518-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumor Immunology and Biotherapy Center, Eastern Institute of Hepatobiliary Surgery, Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7507262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD80/analysis ; B-Lymphocytes/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cell Fusion ; Female ; Histocompatibility Antigens Class II/analysis ; Hybrid Cells/*immunology ; Immunotherapy, Active ; Liver Neoplasms, Experimental/*immunology/prevention & control/therapy ; Lymphocyte Activation ; Neoplasm Transplantation ; Rats ; Rats, Wistar ; T-Lymphocyte Subsets/immunology ; Tumor Cells, Cultured ; Vaccination ; Vaccines/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 39
    Publication Date: 1994-09-02
    Description: A beta 1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM). Thus, physiological factors which induce A beta amyloid formation could provide clues to the pathogenesis of the disease. It has been shown that human A beta specifically and saturably binds zinc. Here, concentrations of zinc above 300 nM rapidly destabilized human A beta 1-40 solutions, inducing tinctorial amyloid formation. However, rat A beta 1-40 binds zinc less avidly and is immune to these effects, perhaps explaining the scarcity with which these animals form cerebral A beta amyloid. These data suggest a role for cerebral zinc metabolism in the neuropathogenesis of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bush, A I -- Pettingell, W H -- Multhaup, G -- d Paradis, M -- Vonsattel, J P -- Gusella, J F -- Beyreuther, K -- Masters, C L -- Tanzi, R E -- R01 AG11899-01/AG/NIA NIH HHS/ -- R01 NS30428-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics and Aging, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073293" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/etiology/*metabolism ; Amyloid beta-Peptides/chemistry/*metabolism ; Animals ; Brain/metabolism ; Edetic Acid/pharmacology ; Humans ; Kinetics ; Mice ; Peptide Fragments/chemistry/*metabolism ; Rats ; Solubility ; Zinc/*metabolism/pharmacology
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: When the sympathetic nerves that innervate rat sweat glands reach their targets, they are induced to switch from using norepinephrine as their neurotransmitter to acetylcholine. Catecholamines (such as norepinephrine) released by nerves growing to the sweat gland induce this phenotypic conversion by stimulating production of a cholinergic differentiation factor [sweat gland factor (SGF)] by gland cells. Here, culture of gland cells with sympathetic, but not sensory, neurons induced SGF production. Blockage of alpha 1- or beta-adrenergic receptors prevented acquisition of the cholinergic phenotype in sympathetic neurons co-cultured with sweat glands, and sweat glands from sympathectomized animals lacked SGF. Thus, reciprocal instructive interactions, mediated in part by small molecule neurotransmitters, direct the development of this synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habecker, B A -- Landis, S C -- NS-023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1602-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4975.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Glycoproteins/*biosynthesis ; Molecular Sequence Data ; Neuregulins ; Neurons/cytology/physiology ; Neurons, Afferent/cytology/physiology ; Parasympathetic Nervous System/cytology/*physiology ; Phenotype ; Rats ; Receptors, Adrenergic/*physiology ; Sweat Glands/cytology/*innervation/metabolism ; Sympathectomy ; Sympathetic Nervous System/cytology/*physiology
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):863.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052838" target="_blank"〉PubMed〈/a〉
    Keywords: *Government Agencies ; National Institutes of Health (U.S.) ; *Peer Review, Research ; United States
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1530.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202706" target="_blank"〉PubMed〈/a〉
    Keywords: Antiviral Agents/*adverse effects/therapeutic use ; Arabinofuranosyluracil/adverse effects/*analogs & derivatives/therapeutic use ; Clinical Trials as Topic/*standards ; Drug-Induced Liver Injury ; Federal Government ; Government Regulation ; Hepatitis B/*drug therapy ; Humans ; National Institutes of Health (U.S.) ; Pancreatic Diseases/chemically induced ; *Research Subjects ; United States ; United States Food and Drug Administration
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maruyama, Y -- Fontanesi, J -- Porter, A T -- Wierzbicki, J G -- Gaspar, L -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):714-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Boron Neutron Capture Therapy ; Brain Neoplasms/*radiotherapy ; Californium/*therapeutic use ; Humans ; Neutron Capture Therapy/*methods ; Rats
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, C -- New York, N.Y. -- Science. 1994 May 20;264(5162):1077.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178164" target="_blank"〉PubMed〈/a〉
    Keywords: *Academies and Institutes/economics ; *Biotechnology ; *Drug Industry/economics ; Financing, Government ; National Institutes of Health (U.S.) ; *Research ; Research Support as Topic ; United States
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasselmo, N -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):453.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290944" target="_blank"〉PubMed〈/a〉
    Keywords: *Antilymphocyte Serum/therapeutic use ; *Drugs, Investigational ; Humans ; Minnesota ; National Institutes of Health (U.S.) ; Research/*standards ; Research Support as Topic ; *Schools, Medical ; United States
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  • 46
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flam, F -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Boron Neutron Capture Therapy ; Brain Neoplasms/*radiotherapy ; Clinical Trials as Topic ; Ethics, Medical ; Female ; Glioblastoma/*radiotherapy ; Humans ; Investigational New Drug Application ; Rats ; United States ; United States Food and Drug Administration
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: Mitogen-activated protein kinases (MAPKs) are rapidly activated in response to stimulation of diverse receptor types. MAPKs are positively regulated by phosphorylation on threonine and tyrosine by MAP kinase or extracellular signal-regulated kinase (ERK) kinases (MEKs). MEK kinase (MEKK) is part of a family of serine-threonine protein kinases that phosphorylate and activate MEKs independently of Raf. MEKK was rapidly and persistently activated in response to stimulation of resting PC12 cells with epidermal growth factor (EGF). Nerve growth factor (NGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA) also activated MEKK, although to a lesser degree than did EGF. Activation of MEKK and B-Raf in response to EGF was inhibited by expression of dominant negative N17Ras. Expression of oncogenic Ras resulted in activation of MEKK. Stimulation of synthesis of cyclic adenosine 3',5'-monophosphate abolished activation of MEKK and B-Raf by EGF, NGF, and TPA. Thus, Ras simultaneously controls the activation of members of the Raf and MEKK families of protein kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lange-Carter, C A -- Johnson, G L -- CA58157/CA/NCI NIH HHS/ -- DK37871/DK/NIDDK NIH HHS/ -- GM30324/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1458-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Basic Sciences, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073291" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/metabolism ; Enzyme Activation ; Epidermal Growth Factor/pharmacology ; *Genes, ras ; MAP Kinase Kinase 1 ; *Mitogen-Activated Protein Kinase Kinases ; Nerve Growth Factors/*pharmacology ; PC12 Cells ; Phosphorylation ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Tetradecanoylphorbol Acetate/pharmacology
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1839.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009201" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/immunology ; Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; *Clinical Trials as Topic ; Humans ; National Institutes of Health (U.S.) ; United States
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  • 49
    Publication Date: 1994-02-04
    Description: Increased discharge activity of mesopontine cholinergic neurons participates in the production of electroencephalographic (EEG) arousal; such arousal diminishes as a function of the duration of prior wakefulness or of brain hyperthermia. Whole-cell and extracellular recordings in a brainstem slice show that mesopontine cholinergic neurons are under the tonic inhibitory control of endogenous adenosine, a neuromodulator released during brain metabolism. This inhibitory tone is mediated postsynaptically by an inwardly rectifying potassium conductance and by an inhibition of the hyperpolarization-activated current. These data provide a coupling mechanism linking neuronal control of EEG arousal with the effects of prior wakefulness, brain hyperthermia, and the use of the adenosine receptor blockers caffeine and theophylline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rainnie, D G -- Grunze, H C -- McCarley, R W -- Greene, R W -- R01 MH039683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard University, Brockton, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303279" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Arousal/*physiology ; Calcium/metabolism ; Electric Conductivity ; *Electroencephalography/drug effects ; Female ; Frontal Lobe/physiology ; In Vitro Techniques ; Male ; Membrane Potentials ; Neurons/*physiology ; Parasympathetic Nervous System/*physiology ; Potassium/metabolism ; Rats
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  • 50
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1800-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522343" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Cell Line ; Central Nervous System/*cytology ; Ganglia, Spinal/cytology ; Myelin Proteins/pharmacology/*physiology ; Myelin-Associated Glycoprotein ; Nerve Regeneration/*physiology ; Neurites/physiology ; Neurons/*physiology ; Neurons, Afferent/physiology ; Rats
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1690-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209247" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Alcoholism/genetics ; Animals ; *Behavior, Animal ; Crosses, Genetic ; Drosophila/genetics ; Drosophila Proteins ; Genes ; Genes, Insect ; Genetic Markers ; Genetic Techniques ; *Genetics, Behavioral/methods ; Humans ; Learning ; Mice ; Nuclear Proteins/genetics ; Period Circadian Proteins ; Rats
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  • 52
    Publication Date: 1994-12-09
    Description: Growth factors activate mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs) and Jun kinases (JNKs). Although the signaling cascade from growth factor receptors to ERKs is relatively well understood, the pathway leading to JNK activation is more obscure. Activation of JNK by epidermal growth factor (EGF) or nerve growth factor (NGF) was dependent on H-Ras activation, whereas JNK activation by tumor necrosis factor alpha (TNF-alpha) was Ras-independent. Ras activates two protein kinases, Raf-1 and MEK (MAPK, or ERK, kinase) kinase (MEKK). Raf-1 contributes directly to ERK activation but not to JNK activation, whereas MEKK participated in JNK activation but caused ERK activation only after overexpression. These results demonstrate the existence of two distinct Ras-dependent MAPK cascades--one initiated by Raf-1 leading to ERK activation, and the other initiated by MEKK leading to JNK activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minden, A -- Lin, A -- McMahon, M -- Lange-Carter, C -- Derijard, B -- Davis, R J -- Johnson, G L -- Karin, M -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1719-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California at San Diego, La Jolla 92093-0636.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992057" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Enzyme Activation/drug effects ; Epidermal Growth Factor/pharmacology ; Genes, ras ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; Mice ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinases ; Nerve Growth Factors/pharmacology ; PC12 Cells ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; ras Proteins/*pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 53
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-29
    Description: Simultaneous recordings were made from large ensembles of hippocampal "place cells" in three rats during spatial behavioral tasks and in slow-wave sleep preceding and following these behaviors. Cells that fired together when the animal occupied particular locations in the environment exhibited an increased tendency to fire together during subsequent sleep, in comparison to sleep episodes preceding the behavioral tasks. Cells that were inactive during behavior, or that were active but had non-overlapping spatial firing, did not show this increase. This effect, which declined gradually during each post-behavior sleep session, may result from synaptic modification during waking experience. Information acquired during active behavior is thus re-expressed in hippocampal circuits during sleep, as postulated by some theories of memory consolidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, M A -- McNaughton, B L -- MH46823/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):676-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson 85724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036517" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Hippocampus/*physiology ; Male ; Memory/*physiology ; Models, Neurological ; Motor Activity/physiology ; Nerve Net/physiology ; Neurons/*physiology ; Pyramidal Cells/physiology ; Rats ; Rats, Inbred F344 ; Reaction Time/physiology ; Sleep/*physiology ; Spatial Behavior/physiology
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Aug 5;265(5173):735.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047878" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; *Clinical Trials as Topic ; Humans ; National Institutes of Health (U.S.) ; United States ; World Health Organization
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  • 55
    Publication Date: 1994-02-18
    Description: Clonidine, an antihypertensive drug, binds to alpha 2-adrenergic and imidazoline receptors. The endogenous ligand for imidazoline receptors may be a clonidine-displacing substance, a small molecule isolated from bovine brain. This clonidine-displacing substance was purified and determined by mass spectroscopy to be agmatine (decarboxylated arginine), heretofore not detected in brain. Agmatine binds to alpha 2-adrenergic and imidazoline receptors and stimulates release of catecholamines from adrenal chromaffin cells. Its biosynthetic enzyme, arginine decarboxylase, is present in brain. Agmatine, locally synthesized, is an endogenous agonist at imidazoline receptors, a noncatecholamine ligand at alpha 2-adrenergic receptors and may act as a neurotransmitter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, G -- Regunathan, S -- Barrow, C J -- Eshraghi, J -- Cooper, R -- Reis, D J -- HL18974/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):966-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neuroscience, 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/7906055" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/drug effects/metabolism ; Agmatine/chemistry/isolation & purification/*metabolism/pharmacology ; Animals ; Binding Sites ; Brain/enzymology/metabolism ; *Brain Chemistry ; Carboxy-Lyases/metabolism ; Cattle ; Cerebral Cortex/metabolism ; Clonidine/analogs & derivatives/metabolism ; Epinephrine/metabolism ; Imidazoline Receptors ; Neurotransmitter Agents/metabolism ; Norepinephrine/metabolism ; Rats ; Receptors, Adrenergic, alpha/metabolism ; Receptors, Drug/metabolism
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansen, A S -- Loewy, A D -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):121-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Heart Ventricles/*innervation/microbiology ; Herpesvirus 1, Suid/*physiology ; Medulla Oblongata/*anatomy & histology/microbiology ; Neural Pathways ; Neurons/*cytology/microbiology ; Rats ; Vagus Nerve/*anatomy & histology/microbiology
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  • 57
    Publication Date: 1994-10-28
    Description: PHAS-I is a heat-stable protein (relative molecular mass approximately 12,400) found in many tissues. It is rapidly phosphorylated in rat adipocytes incubated with insulin or growth factors. Nonphosphorylated PHAS-I bound to initiation factor 4E (eIF-4E) and inhibited protein synthesis. Serine-64 in PHAS-I was rapidly phosphorylated by mitogen-activated (MAP) kinase, the major insulin-stimulated PHAS-I kinase in adipocyte extracts. Results obtained with antibodies, immobilized PHAS-I, and a messenger RNA cap affinity resin indicated that PHAS-I did not bind eIF-4E when serine-64 was phosphorylated. Thus, PHAS-I may be a key mediator of the stimulation of protein synthesis by the diverse group of agents and stimuli that activate MAP kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, T A -- Kong, X -- Haystead, T A -- Pause, A -- Belsham, G -- Sonenberg, N -- Lawrence, J C Jr -- AR41180/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Pharmacology, 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/7939721" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/metabolism ; Animals ; *Carrier Proteins ; Insulin/*pharmacology ; Mice ; Mitogen-Activated Protein Kinase 1 ; Peptide Initiation Factors/isolation & purification/*metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; *Protein Biosynthesis ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Recombinant Proteins/metabolism ; Serine/metabolism
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  • 58
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-03-18
    Description: Cultured embryonic cortical neurons from rats were used to explore mechanisms of activity-dependent neuronal survival. Cell survival was increased by the activation of voltage-sensitive calcium channels (VSCCs) but not by activation of N-methyl-D-aspartate receptors. These effects correlated with the expression of brain-derived neurotrophic factor (BDNF) induced by these two classes of calcium channels. Antibodies to BDNF (which block intracellular signaling by BDNF, but not by nerve growth factor, NT3, or NT4/5) reduced the survival of cortical neurons and reversed the VSCC-mediated increase in survival. Thus, endogenous BDNF is a trophic factor for cortical neurons whose expression is VSCC-regulated and that functions in the VSCC-dependent survival of these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, A -- Carnahan, J -- Greenberg, M E -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1618-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7907431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Brain-Derived Neurotrophic Factor ; Calcium Channels/*physiology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Cerebral Cortex/*cytology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Embryo, Mammalian ; Glutamates/pharmacology ; Glutamic Acid ; N-Methylaspartate/pharmacology ; Nerve Growth Factors/biosynthesis/genetics/immunology/*physiology ; Nerve Tissue Proteins/biosynthesis/genetics/immunology/*physiology ; Neurons/*cytology ; Phosphorylation ; Potassium Chloride/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Signal Transduction
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  • 59
    Publication Date: 1994-11-25
    Description: Although several ion channels have been reported to be directly modulated by calcium-calmodulin, they have not been conclusively shown to bind calmodulin, nor are the modulatory mechanisms understood. Study of the olfactory cyclic nucleotide-activated cation channel, which is modulated by calcium-calmodulin, indicates that calcium-calmodulin directly binds to a specific domain on the amino terminus of the channel. This binding reduces the effective affinity of the channel for cyclic nucleotides, apparently by acting on channel gating, which is tightly coupled to ligand binding. The data reveal a control mechanism that resembles those underlying the regulation of enzymes by calmodulin. The results also point to the amino-terminal part of the olfactory channel as an element for gating, which may have general significance in the operation of ion channels with similar overall structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, M -- Chen, T Y -- Ahamed, B -- Li, J -- Yau, K W -- EY 06837/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1348-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Baltimore, MD.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526466" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcium/*metabolism ; Calmodulin/*metabolism ; Cell Line ; Cyclic AMP/*metabolism ; Cyclic GMP/*metabolism ; Humans ; *Ion Channel Gating ; Ion Channels/chemistry/*metabolism ; Molecular Sequence Data ; Olfactory Receptor Neurons/metabolism ; Peptides/metabolism ; Protein Structure, Secondary ; Rats ; Recombinant Fusion Proteins/metabolism
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glanz, J -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1174.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066457" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Epilepsy/physiopathology/*therapy ; Hippocampus/*physiopathology ; Humans ; *Nonlinear Dynamics ; Rats
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  • 61
    Publication Date: 1994-08-05
    Description: Neurons in the primary visual cortex of the cat are selectively activated by stimuli with particular orientations. This selectivity can be disrupted by the application of antagonists of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) to a local region of the cortex. In order to determine whether inhibitory inputs are necessary for a single cortical neuron to show orientation selectivity, GABA receptors were blocked intracellularly during whole cell recording. Although the membrane potential, spontaneous activity, subfield antagonism, and directional selectivity of neurons were altered after they were perfused internally with the blocking solution, 18 out of 18 neurons remained selective for stimulus orientation. These results indicate that excitatory inputs are sufficient to generate orientation selectivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, S -- Toth, L -- Sheth, B -- Sur, M -- EY06363/EY/NEI NIH HHS/ -- EY07023/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047882" target="_blank"〉PubMed〈/a〉
    Keywords: 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid/pharmacology ; Animals ; Cats ; Cesium/pharmacology ; Electric Stimulation ; Evoked Potentials/drug effects/physiology ; Female ; Fluorides/pharmacology ; Form Perception/physiology ; In Vitro Techniques ; Muscimol/pharmacology ; Neural Inhibition/drug effects/*physiology ; Neurons/drug effects/*physiology ; Orientation/physiology ; Photic Stimulation ; Picrotoxin/pharmacology ; Rats ; Visual Cortex/*cytology/drug effects/physiology
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  • 62
    Publication Date: 1994-12-23
    Description: A synthetic combinatorial library containing 52,128,400 D-amino acid hexapeptides was used to identify a ligand for the mu opioid receptor. The peptide, Ac-rfwink-NH2, bears no resemblance to any known opioid peptide. Simulations using molecular dynamics, however, showed that three amino acid moieties have the same spatial orientation as the corresponding pharmacophoric groups of the opioid peptide PLO17. Ac-rfwink-NH2 was shown to be a potent agonist at the mu receptor and induced long-lasting analgesia in mice. Analgesia produced by intraperitoneally administered Ac-rfwink-NH2 was blocked by intracerebroventricular administration of naloxone, demonstrating that this peptide may cross the blood-brain barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dooley, C T -- Chung, N N -- Wilkes, B C -- Schiller, P W -- Bidlack, J M -- Pasternak, G W -- Houghten, R A -- DA-000138/DA/NIDA NIH HHS/ -- DA-02615/DA/NIDA NIH HHS/ -- DA-03742/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):2019-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Torrey Pines Institute for Molecular Studies, San Diego, CA 92121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801131" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Analgesics/chemistry/metabolism/*pharmacology ; Animals ; Brain/metabolism ; Dose-Response Relationship, Drug ; Endorphins/pharmacology ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- ; Enkephalin, D-Penicillamine (2,5)- ; Enkephalins/metabolism ; Guinea Pigs ; Injections, Intraventricular ; Male ; Mice ; Models, Molecular ; Molecular Sequence Data ; Naloxone/administration & dosage/pharmacology ; Opioid Peptides/chemistry/metabolism/*pharmacology ; Pain Measurement ; Protein Conformation ; Rats ; Receptors, Opioid, mu/agonists/metabolism ; Stereoisomerism
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1538-41.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202708" target="_blank"〉PubMed〈/a〉
    Keywords: Biomarkers ; Editorial Policies ; Education, Medical, Continuing ; Federal Government ; Female ; Government Regulation ; Humans ; Male ; Meta-Analysis as Topic ; National Institutes of Health (U.S.) ; Random Allocation ; Randomized Controlled Trials as Topic/*standards/statistics & numerical data ; Scientific Misconduct ; United States ; United States Food and Drug Administration
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 May 6;264(5160):766-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171330" target="_blank"〉PubMed〈/a〉
    Keywords: Acetaldehyde/pharmacology ; Animals ; Humans ; Muscle, Smooth, Vascular/drug effects ; *Nicotine/analogs & derivatives/pharmacology ; Rats ; *Research ; *Smoking/adverse effects ; *Substance-Related Disorders ; United States
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1800-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997873" target="_blank"〉PubMed〈/a〉
    Keywords: *Biotechnology ; Chromosome Mapping ; DNA Repair ; DNA, Complementary/*genetics ; *Databases, Factual ; Gene Expression ; *Genome, Human ; Human Genome Project ; Humans ; National Institutes of Health (U.S.) ; Private Sector ; Public Sector ; Sequence Analysis, DNA ; United States
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunlap, K -- Luebke, J I -- Turner, T J -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):828-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channel Blockers/*pharmacology ; Calcium Channels/drug effects/*physiology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; *Neurosecretion/drug effects ; Peptides/pharmacology ; Rats ; Spider Venoms/pharmacology ; Synaptic Transmission/drug effects/*physiology ; omega-Agatoxin IVA ; *omega-Conotoxins
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1524, 1526-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202702" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Breast Neoplasms/*prevention & control ; *Clinical Trials as Topic ; Coronary Disease/prevention & control ; Endometrial Neoplasms/chemically induced ; Female ; Humans ; Informed Consent ; Lipids/blood ; Middle Aged ; National Institutes of Health (U.S.) ; Risk Factors ; Tamoxifen/adverse effects/*therapeutic use ; United States
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1081.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108723" target="_blank"〉PubMed〈/a〉
    Keywords: Academic Medical Centers/*economics ; Education, Medical, Graduate/economics ; Financing, Government ; *Health Care Reform ; Humans ; National Institutes of Health (U.S.) ; Preventive Medicine/economics ; *Research Support as Topic ; Schools, Medical ; United States
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  • 69
    Publication Date: 1994-05-13
    Description: Growth factor receptor-bound protein 2 (Grb2) links tyrosine-phosphorylated proteins to a guanine nucleotide releasing factor of the son of sevenless (Sos) class by attaching to the former by its Src homology 2 (SH2) moiety and to the latter by its SH3 domains. An isoform of grb2 complementary DNA (cDNA) was cloned that has a deletion in the SH2 domain. The protein encoded by this cDNA, Grb3-3, did not bind to phosphorylated epidermal growth factor receptor (EGFR) but retained functional SH3 domains and inhibited EGF-induced transactivation of a Ras-responsive element. The messenger RNA encoding Grb3-3 was expressed in high amounts in the thymus of rats at an age when massive negative selection of thymocytes occurs. Microinjection of Grb3-3 into Swiss 3T3 fibroblasts induced apoptosis. These findings indicate that Grb3-3, by acting as a dominant negative protein over Grb2 and by suppressing proliferative signals, may trigger active programmed cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fath, I -- Schweighoffer, F -- Rey, I -- Multon, M C -- Boiziau, J -- Duchesne, M -- Tocque, B -- New York, N.Y. -- Science. 1994 May 13;264(5161):971-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry sur Seine, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178156" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; *Apoptosis ; Base Sequence ; Cloning, Molecular ; Epidermal Growth Factor/pharmacology ; GRB2 Adaptor Protein ; Humans ; Mice ; Molecular Sequence Data ; Proteins/*genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Receptor, Epidermal Growth Factor/*metabolism ; T-Lymphocytes/cytology ; Thymus Gland/metabolism ; Transcriptional Activation/drug effects ; Transfection
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):199.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939646" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; Financing, Government ; Government Agencies ; Health Care Reform ; *Human Genome Project/economics/organization & administration ; Humans ; National Institutes of Health (U.S.) ; United States
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  • 71
    Publication Date: 1994-04-29
    Description: An elastomeric stamp, containing defined features on the micrometer scale, was used to imprint gold surfaces with specific patterns of self-assembled monolayers of alkanethiols and, thereby, to create islands of defined shape and size that support extracellular matrix protein adsorption and cell attachment. Through this technique, it was possible to place cells in predetermined locations and arrays, separated by defined distances, and to dictate their shape. Limiting the degree of cell extension provided control over cell growth and protein secretion. This method is experimentally simple and highly adaptable. It should be useful for applications in biotechnology that require analysis of individual cells cultured at high density or repeated access to cells placed in specified locations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singhvi, R -- Kumar, A -- Lopez, G P -- Stephanopoulos, G N -- Wang, D I -- Whitesides, G M -- Ingber, D E -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):696-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biotechnology Processing Engineering Center, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171320" target="_blank"〉PubMed〈/a〉
    Keywords: Albumins/secretion ; Amino Acid Sequence ; Animals ; Cell Adhesion ; Cell Differentiation ; Cell Division ; *Cell Size ; Cells, Cultured/*cytology/metabolism ; Culture Media ; *Cytological Techniques ; Dimethylpolysiloxanes ; Gold ; Liver/*cytology ; Molecular Sequence Data ; Rats ; Silicones ; Sulfhydryl Compounds
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-02
    Description: Insulin stimulation was found to promote association of the alpha v beta 3 integrin (a vitronectin receptor) with insulin receptor substrate-1 (IRS-1), an intracellular protein that mediates insulin signaling by binding other signaling molecules, including growth factor receptor-bound protein 2 (Grb2) and phosphatidylinositol-3' kinase. Insulin-treated cells expressing the alpha v beta 3 integrin showed 2.5 times more DNA synthesis when plated on vitronectin than on other substrates, whereas cells expressing another vitronectin receptor, alpha v beta 5, did not show this difference. The association between integrin and IRS-1 may be a mechanism for the synergistic action of growth factor and extracellular matrix receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vuori, K -- Ruoslahti, E -- CA 28896/CA/NCI NIH HHS/ -- CA 30199/CA/NCI NIH HHS/ -- CA 42507/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1576-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, La Jolla Cancer Research Foundation, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527156" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Collagen ; DNA/biosynthesis ; Glycoproteins ; Humans ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Integrins/*metabolism ; Molecular Sequence Data ; Phosphoproteins/*metabolism ; Phosphorylation ; Rats ; Receptor, Insulin ; Receptors, Cytoadhesin/*metabolism ; Receptors, Vitronectin ; Transfection ; Tumor Cells, Cultured ; Vitronectin
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baier, H -- Bonhoeffer, F -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1541-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Entwicklungsbiologie, Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Caenorhabditis elegans ; *Caenorhabditis elegans Proteins ; Cell Movement ; Chick Embryo ; Cloning, Molecular ; Helminth Proteins/genetics/metabolism ; Nerve Growth Factors/chemistry/genetics/*physiology ; *Nerve Tissue Proteins ; Rats ; Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-16
    Description: In our report "Activation of Raf as a result of recruitment to the plasma membrane" (3 June, p. 1463) (1), panels E and F of figure 1 on page 1464 were incorrect. The correct photographs appear below. In addition, the [See figure in the PDF file] second sentence of the legend to figure 1 should have read, "The Raf constructs were tagged at the COOH-terminus with a Glu-Glu epitope (MEYMPME) (24) for c-Raf, or at the NH(2)-terminus with both the Glu-Glu and the Myc (MEQKLISEEDL) (23) epitopes for RafCAAX"; the next-to-the-last sentence of the legend to figure 1 should have read, "The c-Raf constructs in (A through D) are Glu-Glu-tagged and were detected by using an anti Glu-Glu antibody, and the RafCAAX and Raf6QCAAX constructs used in E and F were detected by using the antibody to Raf COOH-terminal peptide"; and the third sentence of note 26 should have read, "After blocking with 5% milk in phosphate-buffered saline (M-PBS), cells were incubated with a mouse monoclonal antibody to Glu-Glu or a rabbit polyclonal antibody to a 20-amino acid COOH-terminal peptide of Raf-1 (Santa Cruz Biotechnology, Santa Cruz, California), washed, and incubated with donkey antibodies to mouse or rabbit IgG combined with Texas Red (Jackson) in M-PBS, washed, and mounted in FITC-Guard (Testog)."〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ballou, W R -- Diggs, C L -- Landry, S -- Hall, B F -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1792.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7864993" target="_blank"〉PubMed〈/a〉
    Keywords: Government Agencies ; Humans ; International Cooperation ; *Malaria Vaccines ; National Institutes of Health (U.S.) ; *Research ; United States ; World Health Organization
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  • 75
    Publication Date: 1994-01-21
    Description: Mechanistic information and structure-based design methods have been used to design a series of nonpeptide cyclic ureas that are potent inhibitors of human immunodeficiency virus (HIV) protease and HIV replication. A fundamental feature of these inhibitors is the cyclic urea carbonyl oxygen that mimics the hydrogen-bonding features of a key structural water molecule. The success of the design in both displacing and mimicking the structural water molecule was confirmed by x-ray crystallographic studies. Highly selective, preorganized inhibitors with relatively low molecular weight and high oral bioavailability were synthesized.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, P Y -- Jadhav, P K -- Eyermann, C J -- Hodge, C N -- Ru, Y -- Bacheler, L T -- Meek, J L -- Otto, M J -- Rayner, M M -- Wong, Y N -- New York, N.Y. -- Science. 1994 Jan 21;263(5145):380-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology Research, DuPont Merck Pharmaceutical Company, Wilmington, DE 19880.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8278812" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Azepines/*chemistry/metabolism/pharmacokinetics/pharmacology ; Binding Sites ; Biological Availability ; Cell Line ; Crystallography, X-Ray ; Dogs ; *Drug Design ; Drug Evaluation, Preclinical ; HIV Protease/chemistry/metabolism ; HIV Protease Inhibitors/*chemistry/metabolism/pharmacokinetics/pharmacology ; HIV-1/drug effects/physiology ; Hydrogen Bonding ; Models, Molecular ; Molecular Conformation ; Molecular Weight ; Rats ; Recombinant Proteins/chemistry/metabolism ; Urea ; Virus Replication/drug effects
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):23-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016652" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/*legislation & jurisprudence ; France ; HIV/isolation & purification ; Humans ; National Institutes of Health (U.S.) ; *Patents as Topic ; Scientific Misconduct ; United States
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikulski, B A -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):221-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146650" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; *Financing, Government ; National Institutes of Health (U.S.) ; *Research Support as Topic ; Science/*economics ; United States
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  • 78
    Publication Date: 1994-09-16
    Description: Sodium ion (Na+) channels, which initiate the action potential in electrically excitable cells, are the molecular targets of local anesthetic drugs. Site-directed mutations in transmembrane segment S6 of domain IV of the Na+ channel alpha subunit from rat brain selectively modified drug binding to resting or to open and inactivated channels when expressed in Xenopus oocytes. Mutation F1764A, near the middle of this segment, decreased the affinity of open and inactivated channels to 1 percent of the wild-type value, resulting in almost complete abolition of both the use-dependence and voltage-dependence of drug block, whereas mutation N1769A increased the affinity of the resting channel 15-fold. Mutation I1760A created an access pathway for drug molecules to reach the receptor site from the extracellular side. The results define the location of the local anesthetic receptor site in the pore of the Na+ channel and identify molecular determinants of the state-dependent binding of local anesthetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ragsdale, D S -- McPhee, J C -- Scheuer, T -- Catterall, W A -- P01-HL44948/HL/NHLBI NIH HHS/ -- R01-NS15751/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1724-8.〈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/8085162" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Anesthetics, Local/metabolism/*pharmacology ; Animals ; Binding Sites ; Etidocaine/metabolism/*pharmacology ; Lidocaine/analogs & derivatives/metabolism/pharmacology ; Mutagenesis, Site-Directed ; Oocytes ; Rats ; Sodium Channels/chemistry/*drug effects/genetics/metabolism ; Xenopus
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikulski, B -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):192-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146645" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets ; *Financing, Government ; Government Agencies/*economics ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States ; United States Food and Drug Administration
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):738.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047879" target="_blank"〉PubMed〈/a〉
    Keywords: Angioplasty, Balloon ; Animals ; Arterial Occlusive Diseases/*therapy ; Cell Division ; *Genetic Therapy ; Muscle, Smooth, Vascular/cytology ; Rats ; Recurrence ; Swine ; Thymidine Kinase/genetics
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Widner, H -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):737.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303281" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; *Fetal Tissue Transplantation ; Humans ; National Institutes of Health (U.S.) ; Nerve Tissue/embryology/*transplantation ; Parkinson Disease/*surgery ; Research Support as Topic ; United States
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):463.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290949" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines/therapeutic use ; Acquired Immunodeficiency Syndrome/*therapy ; Clinical Trials as Topic ; Government Agencies ; Humans ; National Institutes of Health (U.S.) ; Peer Review, Research ; Recombinant Proteins/therapeutic use ; *Research Support as Topic ; United States ; Vaccines, Synthetic
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- Marshall, E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):313.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023149" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Serodiagnosis/*economics ; France ; HIV/isolation & purification ; Humans ; International Cooperation ; National Institutes of Health (U.S.) ; *Patents as Topic ; United States
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):466.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Hippocampus ; Learning/physiology ; Long-Term Potentiation/*physiology ; Memory/*physiology ; Neurons/physiology ; Nitric Oxide/*physiology ; Rats ; Synapses/*physiology
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1631.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644652" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Federal Government ; Fetal Diseases/*therapy ; *Fetal Research ; *Genetic Therapy ; *Germ Cells ; Government ; Humans ; National Institutes of Health (U.S.) ; *Public Policy ; *Research ; United States
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  • 86
    Publication Date: 1994-01-07
    Description: Transforming growth factor beta (TGF-beta) is a multifunctional factor that regulates many aspects of cellular functions. TGF-beta signals through a heteromeric complex of the type I and type II TGF-beta receptors. However, the molecular mechanism of signal transduction by this receptor complex remains unresolved. The type II receptor belongs to a transmembrane receptor serine-threonine kinase family. A new member of this receptor family (R4) was identified and shown to be a functional TGF-beta type I receptor on the basis of its ability to restore a TGF-beta-induced gene response in mutant cell lines lacking endogenous type I receptor. Both ligand binding and signaling of the R4 protein were dependent on the presence of a functional type II receptor. The type I receptor has an intrinsic serine-threonine kinase activity, which was essential for signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bassing, C H -- Yingling, J M -- Howe, D J -- Wang, T -- He, W W -- Gustafson, M L -- Shah, P -- Donahoe, P K -- Wang, X F -- DK45746/DK/NIDDK NIH HHS/ -- NICHD T32HD07396/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 7;263(5143):87-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8272871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Gene Expression Regulation ; Genes, Reporter ; Mutagenesis, Site-Directed ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Transforming Growth Factor beta/*metabolism ; *Signal Transduction ; Transfection ; Transforming Growth Factor beta/*metabolism/pharmacology
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-06-17
    Description: Behavioral and pharmacological responses of selectively bred and inbred rodent lines have been analyzed to elucidate many features of drug sensitivity and the adverse effects of drugs, the underlying mechanisms of drug tolerance and dependence, and the motivational states underlying drug reward and aversion. Genetic mapping of quantitative trait loci (QTLs) has been used to identify provisional chromosomal locations of genes influencing such pharmacological responses. Recent advances in transgenic technology, representational difference analysis, and other molecular methods now make feasible the positional cloning of QTLs that influence sensitivity to drugs of abuse. This marks a new period of synthesis in pharmacogenetic research, in which networks of drug-related behaviors, their underlying pharmacological, physiological, and biochemical mechanisms, and particular genomic regions of interest are being identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, J C -- Belknap, J K -- Buck, K J -- AA06243/AA/NIAAA NIH HHS/ -- AA08621/AA/NIAAA NIH HHS/ -- DA05228/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1715-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Service, Veterans Administration (VA) Medical Center, Portland, OR 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209252" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/*genetics ; Animals ; Animals, Genetically Modified ; Chromosome Mapping ; *Disease Models, Animal ; Ethanol/pharmacology ; Genetic Techniques ; Mice ; Mice, Inbred Strains ; Oligonucleotides, Antisense/pharmacology ; Rats ; Rats, Inbred Strains ; Reward ; Substance-Related Disorders/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-08-05
    Description: Retinotopic map development in nonmammalian vertebrates appears to be controlled by molecules that guide or restrict retinal axons to correct locations in their targets. However, the retinotopic map in the superior colliculus (SC) of the rat is developed instead by a topographic bias in collateral branching and arborization. Temporal retinal axons extending across alternating membranes from the topographically correct rostral SC or the incorrect caudal SC of embryonic rats preferentially branch on rostral membranes. Branching preference is due to an inhibitory phosphatidylinositol-linked molecule in the caudal SC. Thus, position-encoding membrane-bound molecules may establish retinotopic maps in mammals by regulating axon branching, not by directing axon growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roskies, A L -- O'Leary, D D -- NEI RO1 EY07025/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):799-803.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Salk Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carbocyanines ; Cells, Cultured ; Embryonic and Fetal Development/physiology ; Fluorescent Dyes ; Phosphatidylinositol Diacylglycerol-Lyase ; Phosphoric Diester Hydrolases ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/*physiology ; Superior Colliculi/embryology
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  • 89
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-10-14
    Description: Mitogen-activated protein kinases (MAP kinases) are common components of signaling pathways induced by diverse growth stimuli. Although the guanidine nucleotide-binding Ras proteins are known to be upstream activators of MAP kinases, the extent to which MAP kinases directly contribute to the mitogenic effect of Ras is as yet undefined. In this study, inhibition of MAP kinases by the MAP kinase phosphatase MKP-1 blocked the induction of DNA synthesis in quiescent rat embryonic fibroblast REF-52 cells by an activated mutant of Ras, V12Ras. These results suggest an essential role for activation of MAP kinases in the transition from the quiescent to the DNA replication phase of the eukaryotic cell cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, H -- Tonks, N K -- Bar-Sagi, D -- CA53840/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):285-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, NY 11724-2208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors ; *Cell Cycle Proteins ; Cell Line ; DNA/*biosynthesis ; Dual Specificity Phosphatase 1 ; Enzyme Activation ; G0 Phase ; HeLa Cells ; Humans ; Immediate-Early Proteins/*metabolism/pharmacology ; JNK Mitogen-Activated Protein Kinases ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinases ; Molecular Sequence Data ; Mutation ; *Phosphoprotein Phosphatases ; Protein Phosphatase 1 ; Protein Tyrosine Phosphatases/*metabolism/pharmacology ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Rats ; S Phase ; Signal Transduction ; Transfection ; ras Proteins/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1994 Dec 23;266(5193):1949.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11644654" target="_blank"〉PubMed〈/a〉
    Keywords: *Cloning, Organism ; Deception ; *Embryo Research ; Embryo, Mammalian ; Ethical Review ; Ethics ; Ethics Committees ; Ethics Committees, Research ; Federal Government ; Government ; Government Regulation ; Humans ; National Institutes of Health (U.S.) ; Organizational Policy ; *Research ; Research Personnel ; *Scientific Misconduct ; Social Control, Formal ; United States ; Universities
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  • 91
    Publication Date: 1994-06-10
    Description: The alpha 1-adrenergic receptors activate a phospholipase C enzyme by coupling to members of the large molecular size (approximately 74 to 80 kilodaltons) G alpha h family of guanosine triphosphate (GTP)-binding proteins. Rat liver G alpha h is now shown to be a tissue transglutaminase type II (TGase II). The transglutaminase activity of rat liver TGase II expressed in COS-1 cells was inhibited by the nonhydrolyzable GTP analog guanosine 5'-O-(3-thiotriphosphate) or by alpha 1-adrenergic receptor activation. Rat liver TGase II also mediated alpha 1-adrenergic receptor stimulation of phospholipase C activity. Thus, G alpha h represents a new class of GTP-binding proteins that participate in receptor signaling and may be a component of a complex regulatory network in which receptor-stimulated GTP binding switches the function of G alpha h from transglutamination to receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakaoka, H -- Perez, D M -- Baek, K J -- Das, T -- Husain, A -- Misono, K -- Im, M J -- Graham, R M -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1593-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiovascular Biology, Cleveland Clinic Foundation, OH 44195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7911253" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Epinephrine/pharmacology ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guinea Pigs ; Inositol Phosphates/metabolism ; Liver/enzymology ; Molecular Sequence Data ; Prazosin/pharmacology ; Rats ; Receptors, Adrenergic, alpha/genetics/*metabolism ; *Signal Transduction ; Transfection ; Transglutaminases/chemistry/genetics/*metabolism ; Type C Phospholipases/metabolism
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):362-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153617" target="_blank"〉PubMed〈/a〉
    Keywords: *Anti-Bacterial Agents/pharmacology/therapeutic use ; Centers for Disease Control and Prevention (U.S.) ; Drug Approval ; *Drug Resistance, Microbial ; Financing, Government ; Humans ; National Institutes of Health (U.S.) ; *Research Support as Topic ; United States
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  • 93
    Publication Date: 1994-11-11
    Description: Optical imaging with high spatial and temporal resolution of neural activity in rat cortical slices was used to investigate the dynamics of signal transmission through neural connections in the visual cortex. When inhibition due to gamma-aminobutyric acid was slightly suppressed, horizontal propagation of excitation in both the supra- and infragranular layers became prominent. This propagation was not affected by vertical cuts in either the supra- or infragranular layer, which suggests that excitation is at least partially conveyed horizontally by reciprocal vertical connections between neurons in these layers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanifuji, M -- Sugiyama, T -- Murase, K -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1057-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Information Science, Fukui University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/analogs & derivatives/pharmacology ; Electric Stimulation ; Electrodes ; In Vitro Techniques ; Light ; Rats ; Visual Cortex/*physiology ; Visual Pathways/*physiology ; gamma-Aminobutyric Acid/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-05-20
    Description: Long-term depression (LTD) is an activity-dependent decrease in synaptic efficacy that together with its counterpart, long-term potentiation, is thought to be an important cellular mechanism for learning and memory in the mammalian brain. The induction of LTD in hippocampal CA1 pyramidal neurons in neonatal rats is shown to depend on postsynaptic calcium ion entry through L-type voltage-gated calcium channels paired with the activation of metabotropic glutamate receptors. Although induced postsynaptically, LTD is due to a long-term decrease in transmitter release from presynaptic terminals. This suggests that LTD is likely to require the production of a retrograde messenger.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolshakov, V Y -- Siegelbaum, S A -- New York, N.Y. -- Science. 1994 May 20;264(5162):1148-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Howard Hughes Medical Institute, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909958" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Electric Stimulation ; Hippocampus/*physiology ; Long-Term Potentiation ; *Neuronal Plasticity ; Nitrendipine/pharmacology ; Presynaptic Terminals/*physiology ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/metabolism ; Synaptic Transmission/drug effects
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  • 95
    Publication Date: 1994-08-26
    Description: Estrogen and progesterone modulate gene expression in rodents by activation of intracellular receptors in the hypothalamus, which regulate neuronal networks that control female sexual behavior. However, the neurotransmitter dopamine has been shown to activate certain steroid receptors in a ligand-independent manner. A dopamine receptor stimulant and a D1 receptor agonist, but not a D2 receptor agonist, mimicked the effects of progesterone in facilitating sexual behavior in female rats. The facilitory effect of the neurotransmitter was blocked by progesterone receptor antagonists, a D1 receptor antagonist, or antisense oligonucleotides to the progesterone receptor. The results suggest that in rodents neurotransmitters may regulate in vivo gene expression and behavior by means of cross-talk with steroid receptors in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, S K -- Allen, J M -- Clark, J H -- Blaustein, J D -- O'Malley, B W -- MH-00885/MH/NIMH NIH HHS/ -- NS 19327/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 26;265(5176):1246-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7915049" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/drug effects ; Animals ; Base Sequence ; Benzazepines/pharmacology ; Dopamine/*physiology ; Dopamine Agents/administration & dosage/pharmacology ; Estradiol/analogs & derivatives/pharmacology ; Female ; Hypothalamus/drug effects/*physiology ; Injections, Intraventricular ; Male ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Posture ; Progesterone/pharmacology/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Progesterone/genetics/*physiology ; Sexual Behavior, Animal/drug effects/*physiology
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  • 96
    Publication Date: 1994-04-15
    Description: A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Afar, D E -- Goga, A -- McLaughlin, J -- Witte, O N -- Sawyers, C L -- CA 01551/CA/NCI NIH HHS/ -- CA 53867/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):424-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, University of California-Los Angeles 90024-1489.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153630" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line ; *Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*genetics/physiology ; GRB2 Adaptor Protein ; Gene Expression ; *Genes, abl ; *Genes, myc ; Genetic Complementation Test ; Molecular Sequence Data ; Phosphorylation ; Point Mutation ; Proteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics/physiology ; Rats ; Retroviridae/physiology ; Signal Transduction ; Transfection ; Tyrosine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-23
    Description: During tactile learning there is a transformation in the way the primary somatosensory cortex integrates, represents, and distributes information from the skin. To define this transformation, the site of earliest modification has been identified in rat somatosensory cortex after a change in sensory experience. Afferent activity was manipulated by clipping all except two whiskers on one side of the snout ("whisker pairing"), and the receptive fields of neurons at different cortical depths were mapped 24 hours later. Neurons in layer IV, the target of the primary thalamic pathway, were unaltered, whereas neurons located above and below layer IV showed significant changes. These changes were similar to those that occur in layer IV after longer periods of whisker pairing. The findings support the hypothesis that the layers of cortex contribute differently to plasticity. Neurons in the supragranular and infragranular layers respond rapidly to changes in sensory experience and may contribute to subsequent modification in layer IV.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diamond, M E -- Huang, W -- Ebner, F F -- NS-25907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1885-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sciences and Biomedical Technologies, University of Udine, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091215" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Afferent Pathways ; Animals ; Male ; *Neuronal Plasticity ; Neurons, Afferent/*physiology ; Rats ; Somatosensory Cortex/*physiology ; Thalamic Nuclei/physiology ; Vibrissae/*innervation
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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-12-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1634-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992040" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; *Embryo Research ; *Embryo, Mammalian ; Federal Government ; Financing, Government ; *Guidelines as Topic ; Humans ; National Institutes of Health (U.S.) ; *Research ; *Research Embryo Creation ; Research Support as Topic ; United States
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-04-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Apr 8;264(5156):196-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8146646" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; *Nicotine ; Rats ; Smoking ; *Substance-Related Disorders ; Tobacco Use Disorder/etiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-07-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036507" target="_blank"〉PubMed〈/a〉
    Keywords: Advisory Committees ; Clinical Protocols ; Ethical Review ; Federal Government ; Genetic Therapy/*legislation & jurisprudence ; *Government Regulation ; Humans ; National Institutes of Health (U.S.) ; United States ; United States Food and Drug Administration
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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