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  • In Vitro Techniques  (286)
  • American Association for the Advancement of Science (AAAS)  (286)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
  • 1990-1994  (170)
  • 1985-1989  (116)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (286)
  • American Chemical Society (ACS)
  • National Academy of Sciences
  • PANGAEA
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Year
  • 1
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    Abnormal fear response and aggressive behavior in mutant mice deficient for alpha-calcium-calmodulin kinase II (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Mice deficient for the gene encoding alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII knockout mice) provide a promising tool to link behavioral and cellular abnormalities with a specific molecular lesion. The heterozygous mouse exhibited a well-circumscribed syndrome of behavioral abnormalities, consisting primarily of a decreased fear response and an increase in defensive aggression, in the absence of any measured cognitive deficits. Unlike the heterozygote, the homozygote displayed abnormal behavior in all paradigms tested. At the cellular level, both extracellular and whole-cell patch clamp recordings indicated that serotonin release in putative serotonergic neurons of the dorsal raphe was reduced. Thus, alpha-CaMKII knockout mice, in particular the heterozygote, may provide a model for studying the molecular and cellular basis underlying emotional disorders involving fear and aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C -- Rainnie, D G -- Greene, R W -- Tonegawa, S -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939668" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Animals ; Behavior, Animal ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/deficiency/genetics/*physiology ; *Fear ; Fluoxetine/pharmacology ; Gene Dosage ; Heterozygote ; Homozygote ; In Vitro Techniques ; Membrane Potentials ; Mice ; Mice, Knockout ; Mutation ; Neurons/metabolism ; Patch-Clamp Techniques ; Raphe Nuclei/metabolism ; Serotonin/metabolism/pharmacology ; Synaptic Transmission/drug effects
    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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    Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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  • 3
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    Reduction in viscosity of cystic fibrosis sputum in vitro by gelsolin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-18
    Description: Obstruction of airways by viscous sputum causes lung damage in patients with cystic fibrosis (CF). Sputum samples from CF patients were shown to contain filamentous actin. Human plasma gelsolin, a protein that severs actin filaments, rapidly decreased the viscosity of CF sputum samples in vitro. Gc globulin and deoxyribonuclease I, proteins that sequester monomeric actin but do not sever actin filaments, were less efficient than gelsolin in diminishing sputum viscosity. These results suggest that gelsolin may have therapeutic potential as a mucolytic agent in CF patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vasconcellos, C A -- Allen, P G -- Wohl, M E -- Drazen, J M -- Janmey, P A -- Stossel, T P -- AR38910/AR/NIAMS NIH HHS/ -- HL19170/HL/NHLBI NIH HHS/ -- HL19429/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):969-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8310295" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*analysis/chemistry ; Adult ; Cystic Fibrosis/*metabolism ; Deoxyribonuclease I/metabolism ; Gelsolin/*pharmacology ; Humans ; In Vitro Techniques ; Sputum/chemistry/*drug effects ; Viscosity ; Vitamin D-Binding Protein/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: Repetitive activation of hippocampal mossy fibers evokes a long-term potentiation (LTP) of synaptic responses in pyramidal cells in the CA3 region that is independent of N-methyl-D-aspartate receptor activation. Previous results suggest that the site for both the induction and expression of this form of LTP is presynaptic. Experimental elevation of cyclic adenosine 3',5'-monophosphate (cAMP) both mimics and interferes with tetanus-induced mossy fiber LTP, and blockers of the cAMP cascade block mossy fiber LTP. It is proposed that calcium entry into the presynaptic terminal may activate Ca(2+)-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisskopf, M G -- Castillo, P E -- Zalutsky, R A -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1878-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; *Carbazoles ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Glutamates/metabolism/pharmacology ; Glutamic Acid ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Indoles/pharmacology ; Isoquinolines/pharmacology ; *Long-Term Potentiation/drug effects ; Models, Biological ; Nerve Fibers/*physiology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/physiology ; Pyrroles/pharmacology ; *Sulfonamides ; Synaptic Transmission/drug effects
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  • 5
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    Roles of N-type and Q-type Ca2+ channels in supporting hippocampal synaptic transmission (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 6
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    Requirement of a critical period of transcription for induction of a late phase of LTP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 7
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    Resetting the biological clock: mediation of nocturnal circadian shifts by glutamate and NO (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 8
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    Adenosine inhibition of mesopontine cholinergic neurons: implications for EEG arousal (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 9
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    Orientation selectivity of cortical neurons during intracellular blockade of inhibition (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 10
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    Long-term potentiation: evidence against an increase in transmitter release probability in the CA1 region of the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: It is widely accepted that N-methyl-D-aspartate (NMDA)-receptor-dependent long-term potentiation (LTP) in the CA1 region of the hippocampus is triggered postsynaptically, but there is considerable debate as to the site at which the increase in synaptic strength is expressed. The irreversible open-channel blocking action of the NMDA receptor antagonist MK-801 has been used to test whether the probability of transmitter release (Pr) is increased during LTP. Although the rate of decline of the amplitude of the NMDA receptor-mediated excitatory postsynaptic current (EPSC) in the presence of MK-801 strongly depends on Pr, the rate of decline of the EPSC evoked at synapses expressing LTP is identical to that observed at synapses not expressing LTP. These findings are difficult to reconcile with models in which the expression of LTP is due to an increase in Pr.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manabe, T -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1888-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Guinea Pigs ; Hippocampus/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation ; Male ; Neurotransmitter Agents/*metabolism ; Receptors, AMPA/antagonists & inhibitors/physiology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; Synapses/physiology
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  • 11
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    Identification of calcium channels that control neurosecretion (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 12
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    Calcium and inositol 1,4,5-trisphosphate-induced Ca2+ release (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Combettes, L -- Champeil, P -- New York, N.Y. -- Science. 1994 Aug 5;265(5173):813-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8047889" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism/physiology ; Egtazic Acid/pharmacology ; Feedback/physiology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate/*physiology ; Sheep
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  • 13
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    Role of NO production in NMDA receptor-mediated neurotransmitter release in cerebral cortex (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-18
    Description: L-Glutamate and norepinephrine are examples of a major excitatory neurotransmitter and a neuromodulator in the cerebral cortex, respectively. Little is known of how chemical signaling between the anatomically distinct chemical pathways occurs. Specific activation of the N-methyl-D-aspartate (NMDA) class of glutamate receptor in synaptosomal preparations from guinea pig cerebral cortex caused release of both of these chemicals, and this release was blocked by agents that inhibit nitric oxide (NO) production or remove NO from the extracellular space. Furthermore, neurotransmitter release correlated with cortical NO production after NMDA receptor stimulation. These results suggest that NO production and its extracellular movement may be links in the pathway from NMDA receptor activation to changes in chemical signaling in surrounding synaptic terminals in the cerebral cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montague, P R -- Gancayco, C D -- Winn, M J -- Marchase, R B -- Friedlander, M J -- EY05116/EY/NEI NIH HHS/ -- EY06714/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 18;263(5149):973-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Research Center, University of Alabama at Birmingham 35294-0021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7508638" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors ; Animals ; Arginine/analogs & derivatives/pharmacology ; Cerebral Cortex/drug effects/*metabolism ; Glutamates/*metabolism ; Glutamic Acid ; Guinea Pigs ; In Vitro Techniques ; Indazoles/pharmacology ; Male ; N-Methylaspartate/pharmacology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine ; Norepinephrine/*metabolism ; Potassium Chloride/pharmacology ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synaptosomes/drug effects/*metabolism ; omega-N-Methylarginine
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  • 14
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    Rearrangements of synaptic connections in visual cortex revealed by laser photostimulation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-08
    Description: Assessing patterns of synaptic connections in the developing mammalian neocortex has relied primarily on anatomical studies. In a physiological approach described here, the patterns of synaptic connections in slices of developing ferret visual cortex were determined with scanning laser photostimulation. Functional synaptic inputs to pyramidal cells in cortical layers 2 and 3 originating from sites close to the neuronal cell body appeared at least 2 weeks before eye opening, prior to the formation of long-range horizontal connections. Extensive long-range horizontal connections appeared in the next 10 days of development. The number of local connections peaked at the time of eye opening; the number of these connections subsequently declined to the level found in the adult while the specificity of long-distance connections increased. Thus, the relative influence of local connections on the activity of layer 2 and layer 3 neurons declines as the cortex matures while the influence of longer range connections increases substantially.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalva, M B -- Katz, L C -- EY07960/EY/NEI NIH HHS/ -- T32-6M08441/PHS HHS/ -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):255-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7912852" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Brain Mapping ; Ferrets ; Glutamates/pharmacology ; Glutamic Acid ; In Vitro Techniques ; Light ; Ocular Physiological Phenomena ; Photic Stimulation ; Pyramidal Cells/physiology ; Receptors, Glutamate/physiology ; Synapses/*physiology ; Visual Cortex/growth & development/*physiology
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  • 15
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    Horizontal propagation of excitation in rat visual cortical slices revealed by optical imaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 16
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    Release of adenosine by activation of NMDA receptors in the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Adenosine is present in the mammalian brain in large amounts and has potent effects on neuronal activity, but its role in neural signaling is poorly understood. The glutamate receptor agonist N-methyl-D-aspartate (NMDA) caused a presynaptic depression of excitatory synaptic transmission in the CA1 region of guinea pig hippocampal slices. This depression was blocked by an adenosine A1 receptor antagonist, which suggests that activation of the NMDA subtype of glutamate receptor raises the concentration of extracellular adenosine, which acts on presynaptic inhibitory A1 receptors. Strong tetanic stimulation caused a heterosynaptic inhibition that was blocked by both NMDA and A1 receptor antagonists. Enkephalin, which selectively inhibits interneurons, antagonized the heterosynaptic inhibition. These findings suggest that synaptically released glutamate activates NMDA receptors, which in turn releases adenosine, at least in part from interneurons, that acts at a distance to inhibit presynaptically the release of glutamate from excitatory synapses. Thus, interneurons may mediate a widespread purinergic presynaptic inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manzoni, O J -- Manabe, T -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California at San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916485" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Adenosine/*metabolism ; Animals ; Electric Stimulation ; Enkephalins/pharmacology ; GABA-B Receptor Antagonists ; Glutamates/metabolism ; Glutamic Acid ; Guinea Pigs ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; Interneurons/drug effects/*metabolism ; Male ; N-Methylaspartate/pharmacology ; Neural Inhibition/drug effects ; Organophosphorus Compounds/pharmacology ; Receptors, N-Methyl-D-Aspartate/drug effects/*metabolism ; Synapses/*metabolism ; Synaptic Transmission/drug effects ; Theophylline/analogs & derivatives/pharmacology
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  • 17
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    Locally distributed synaptic potentiation in the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-01-28
    Description: The long-lasting increase in synaptic strength known as long-term potentiation has been advanced as a potential physiological mechanism for many forms of both developmental and adult neuronal plasticity. In many models of plasticity, intercellular communication has been proposed to account for observations in which simultaneously active neurons are strengthened together. The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger. This distributed potentiation provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuman, E M -- Madison, D V -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):532-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford Medical School, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290963" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/metabolism ; Diffusion ; Electric Stimulation ; In Vitro Techniques ; Long-Term Potentiation/*physiology ; Nitric Oxide/*metabolism ; Pyramidal Cells/*physiology ; Synapses/*physiology ; Synaptic Transmission/*physiology
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  • 18
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    Endothelial NOS and the blockade of LTP by NOS inhibitors in mice lacking neuronal NOS (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-22
    Description: Long-term potentiation (LTP) is a persistent increase in synaptic strength implicated in certain forms of learning and memory. In the CA1 region of the hippocampus, LTP is thought to involve the release of one or more retrograde messengers from the postsynaptic cell that act on the presynaptic terminal to enhance transmitter release. One candidate retrograde messenger is the membrane-permeant gas nitric oxide (NO), which in the brain is released after activation of the neuronal-specific NO synthase isoform (nNOS). To assess the importance of NO in hippocampal synaptic plasticity, LTP was examined in mice where the gene encoding nNOS was disrupted by gene targeting. In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal except for a slight reduction in comparison to that in wild-type mice and was blocked by NOS inhibitors, just as it was in wild-type mice. Immunocytochemical studies indicate that in the nNOS- mice as in wild-type mice, the endothelial form of NOS (eNOS) is expressed in CA1 neurons. These findings suggest that eNOS, rather than nNOS, generates NO within the postsynaptic cell during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Dell, T J -- Huang, P L -- Dawson, T M -- Dinerman, J L -- Snyder, S H -- Kandel, E R -- Fishman, M C -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- MH-45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):542-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518615" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/genetics/*metabolism ; Animals ; Arginine/*analogs & derivatives/pharmacology ; Electric Stimulation ; Endothelium/enzymology ; Hippocampus/drug effects/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Mice ; Mutation ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine ; Pyramidal Cells/drug effects/enzymology/*physiology ; Synaptic Transmission/drug effects
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  • 19
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    GTP hydrolysis in protein synthesis: two for Tu? (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schimmel, P -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1264-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446896" target="_blank"〉PubMed〈/a〉
    Keywords: Energy Metabolism ; Escherichia coli ; Guanosine Triphosphate/*metabolism ; In Vitro Techniques ; *Peptide Chain Elongation, Translational ; Peptide Elongation Factor Tu/*metabolism ; Ribosomes/*metabolism
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  • 20
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    Higher level organization of individual gene transcription and RNA splicing (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-26
    Description: Visualization of fibronectin and neurotensin messenger RNAs within mammalian interphase nuclei was achieved by fluorescence hybridization with genomic, complementary DNA, and intron-specific probes. Unspliced transcripts accumulated in one or two sites per nucleus. Fibronectin RNA frequently accumulated in elongated tracks that overlapped and extended well beyond the site of transcription. Splicing appears to occur directly within this RNA track, as evidenced by an unambiguous spatial separation of intron-containing and spliced transcripts. Excised introns for neurotensin RNA appear free to diffuse. The transcription and processing site of the fibronectin gene localized to the nuclear interior and was associated with larger transcript domains in over 88 percent of the cells. These results support a view of nuclear function closely integrated with structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xing, Y -- Johnson, C V -- Dobner, P R -- Lawrence, J B -- R01 HG00251/HG/NHGRI NIH HHS/ -- R01 HL33307/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1326-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Massachusetts Medical Center, Worcester 01655.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446901" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/metabolism/*ultrastructure ; Fibronectins/genetics ; Gene Expression ; In Vitro Techniques ; Introns ; Microscopy, Fluorescence ; Neurotensin/genetics ; PC12 Cells ; Poly A/metabolism ; *RNA Processing, Post-Transcriptional ; RNA Splicing ; RNA, Messenger/*metabolism ; Rats ; Spliceosomes/metabolism ; *Transcription, Genetic
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  • 21
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    A mechanism for virilization of female spotted hyenas in utero (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-25
    Description: Female spotted hyenas exhibit male-like genitalia and dominance over males. Hyena ovarian tissues incubated in vitro produced large quantities of the steroid hormone precursor androstenedione. The activity of aromatase, which converts androstenedione to estrogen, was one-twentieth as great in hyena versus human placental homogenates. In comparison, the activity of 17 beta-hydroxysteroid dehydrogenase, which converts androstenedione to testosterone, was equal in the two homogenates. The limited aromatase activity may allow the hyena placenta to convert high circulating concentrations of androstenedione to testosterone, which results in virilization of the fetal external genitalia and possibly destruction of fetal ovarian follicles. Androstenedione production by residual ovarian stromal cells during reproductive life accounts for the epigenetic transmission of virilization in female spotted hyenas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcinkaya, T M -- Siiteri, P K -- Vigne, J L -- Licht, P -- Pavgi, S -- Frank, L G -- Glickman, S E -- CA-39825/CA/NCI NIH HHS/ -- MH-39917/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1929-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics, Gynecology, University of California School of Medicine, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391165" target="_blank"〉PubMed〈/a〉
    Keywords: 17-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Aromatase/*metabolism ; Carnivora/embryology/*metabolism ; Corpus Luteum/metabolism ; Estradiol/biosynthesis ; Female ; Humans ; In Vitro Techniques ; Luteinizing Hormone/pharmacology ; Male ; Ovary/*metabolism ; Placenta/enzymology/*metabolism ; Pregnancy ; Progesterone/biosynthesis ; *Sex Differentiation ; Testosterone/*biosynthesis
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  • 22
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    Effects of cAMP simulate a late stage of LTP in hippocampal CA1 neurons (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: Hippocampal long-term potentiation (LTP) is thought to serve as an elementary mechanism for the establishment of certain forms of explicit memory in the mammalian brain. As is the case with behavioral memory, LTP in the CA1 region has stages: a short-term early potentiation lasting 1 to 3 hours, which is independent of protein synthesis, precedes a later, longer lasting stage (L-LTP), which requires protein synthesis. Inhibitors of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) blocked L-LTP, and analogs of cAMP induced a potentiation that blocked naturally induced L-LTP. The action of the cAMP analog was blocked by inhibitors of protein synthesis. Thus, activation of PKA may be a component of the mechanism that generates L-LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frey, U -- Huang, Y Y -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1661-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8389057" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects/physiology ; Animals ; Cyclic AMP/*physiology ; Hippocampus/cytology/drug effects/*physiology ; In Vitro Techniques ; Male ; Memory/physiology ; Neurons/drug effects/*physiology ; Protein Kinases/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/physiology ; Second Messenger Systems/physiology ; Time Factors
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  • 23
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    Interleukin-1 type II receptor: a decoy target for IL-1 that is regulated by IL-4 (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-07-23
    Description: Interleukin-1 (IL-1) interacts with cells through two types of binding molecules, IL-1 type I receptor (IL-1R I) and IL-1R II. The function of IL-1R II is unknown. In studies using monoclonal antibodies, IL-1 prolonged the in vitro survival of polymorphonuclear cells (PMN) through IL-1R I, and IL-4 antagonized the action of IL-1 by inducing expression and release of IL-1R II. Dexamethasone also induced expression and release of the IL-1R II in PMN. These results, together with the effect of antibodies to IL-1R on IL-1-induced production of cytokines in monocytes, indicate that IL-1 acts on myelomonocytic cells through IL-1R I and that IL-1R II inhibits IL-1 activity by acting as a decoy target for IL-1. The existence of multiple pathways of regulation emphasizes the need for tight control of IL-1 action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colotta, F -- Re, F -- Muzio, M -- Bertini, R -- Polentarutti, N -- Sironi, M -- Giri, J G -- Dower, S K -- Sims, J E -- Mantovani, A -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):472-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Daniela e Catullo Borgomainerio, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8332913" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Survival/immunology ; Dexamethasone/pharmacology ; Humans ; In Vitro Techniques ; Interleukin-1/*physiology ; Interleukin-4/*physiology ; Molecular Weight ; Monocytes/physiology ; Neutrophils/*physiology ; Receptors, Interleukin-1/classification/drug effects/*physiology
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  • 24
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    Dormancy of inhibitory interneurons in a model of temporal lobe epilepsy (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-01-01
    Description: In humans temporal lobe epilepsy (TLE) is characterized by recurrent seizures, neuronal hyperexcitability, and selective loss of certain neuronal populations in the hippocampus. Animal models of the condition indicate that a diminution of inhibition mediated by gamma-aminobutyric acid (GABA) accounts for the altered function, and it has been hypothesized that the diminution arises because GABAergic basket interneurons are "dormant" as a result of their being disconnected from excitatory inputs. In hippocampal slices, inhibitory postsynaptic potentials (IPSPs) were elicited in CA1 pyramidal cells by activation of basket cells; responses from an animal model of TLE were compared to those from control tissue. IPSPs evoked indirectly by activation of terminals that then excited basket cells were reduced in the epileptic tissue, whereas IPSPs evoked by direct activation of basket cells, when excitatory neurotransmission was blocked, were not different from controls. These results provide support for the "dormant basket cell" hypothesis and have implications for the pathophysiology and treatment of human TLE.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bekenstein, J W -- Lothman, E W -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):97-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8093417" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Action Potentials ; Animals ; Baclofen/analogs & derivatives/pharmacology ; Electric Stimulation ; Epilepsy, Temporal Lobe/*physiopathology ; Evoked Potentials ; Hippocampus/*physiology/*physiopathology ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; Male ; Membrane Potentials ; Picrotoxin/pharmacology ; Pyramidal Tracts/drug effects/*physiology ; Quinoxalines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Status Epilepticus/*physiopathology
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  • 25
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    Complexes of Ras.GTP with Raf-1 and mitogen-activated protein kinase kinase (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-11
    Description: The guanosine triphosphate (GTP)-binding protein Ras functions in regulating growth and differentiation; however, little is known about the protein interactions that bring about its biological activity. Wild-type Ras or mutant forms of Ras were covalently attached to an insoluble matrix and then used to examine the interaction of signaling proteins with Ras. Forms of Ras activated either by mutation (Gly12Val) or by binding of the GTP analog, guanylyl-imidodiphosphate (GMP-PNP) interacted specifically with Raf-1 whereas an effector domain mutant, Ile36Ala, failed to interact with Raf-1. Mitogen-activated protein kinase (MAP kinase) activity was only associated with activated forms of Ras. The specific interaction of activated Ras with active MAP kinase kinase (MAPKK) was confirmed by direct assays. Thus the forming of complexes containing MAPKK activity and Raf-1 protein are dependent upon the activity of Ras.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moodie, S A -- Willumsen, B M -- Weber, M J -- Wolfman, A -- CA 39076/CA/NCI NIH HHS/ -- CA 40042/CA/NCI NIH HHS/ -- GM 41220/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Jun 11;260(5114):1658-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cleveland Clinic Foundation, OH 44106.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8503013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Guanosine Triphosphate/*metabolism ; Guanylyl Imidodiphosphate/metabolism ; In Vitro Techniques ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase Kinases ; Mutation ; Phosphorylation ; Protein Binding ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Proto-Oncogene Proteins p21(ras)/*metabolism ; Rats ; Signal Transduction/physiology
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    Nitric oxide and carbon monoxide produce activity-dependent long-term synaptic enhancement in hippocampus (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-25
    Description: Nitric oxide (NO) and carbon monoxide (CO) may act as retrograde messages for long-term potentiation (LTP) in the hippocampus. Zinc protoporphyrin IX, an inhibitor of the enzyme that produces CO, blocked induction of LTP in the CA1 region of hippocampal slices. Application of either NO or CO to slices produced a rapid and long-lasting increase in the size of evoked synaptic potentials if, and only if, the application occurred at the same time as weak tetanic stimulation. This long-term enhancement was spatially restricted to synapses from active presynaptic fibers and appeared to involve mechanisms utilized by LTP, occluding the subsequent induction of LTP by strong tetanic stimulation. The enhancement by NO and CO was not blocked by an N-methyl-D-aspartate (NMDA) receptor blocker, suggesting that NO and CO act downstream from the NMDA receptor. Also, CO produced long-term enhancement when paired with low-frequency stimulation. These results are consistent with the hypothesis that NO and CO, either alone or in combination, serve as retrograde messages that produce activity-dependent presynaptic enhancement during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhuo, M -- Small, S A -- Kandel, E R -- Hawkins, R D -- AG08702/AG/NIA NIH HHS/ -- MH45923/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1946-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8100368" target="_blank"〉PubMed〈/a〉
    Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione ; Animals ; Carbon Monoxide/*pharmacology ; Electric Stimulation ; Guinea Pigs ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Male ; Membrane Potentials/drug effects ; Nitric Oxide/*pharmacology ; Protoporphyrins/pharmacology ; Quinoxalines/pharmacology ; Signal Transduction/drug effects ; Synapses/drug effects/*physiology
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    The role of water in hemoglobin function and stability (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bulone, D -- San Biagio, P L -- Palma-Vittorelli, M B -- Palma, M U -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1335-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446903" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Hemoglobins/*chemistry ; Humans ; In Vitro Techniques ; Solvents ; Thermodynamics ; Water/chemistry
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    Feedback regulation mechanisms for the control of GTP cyclohydrolase I activity (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-04
    Description: Guanosine triphosphate (GTP) cyclohydrolase I, the rate-limiting enzyme in the biosynthesis of tetrahydrobiopterin (BH4), is subject to feedback inhibition by BH4, a cofactor for phenylalanine hydroxylase. Inhibition was found to depend specifically on BH4 and the presence of another protein (p35). The inhibition occurred through BH4-dependent complex formation between p35 protein and GTP cyclohydrolase I. Furthermore, the inhibition was specifically reversed by phenylalanine, and, in conjunction with p35, phenylalanine reduced the cooperativity of GTP cyclohydrolase I. These findings also provide a molecular basis for high plasma BH4 concentrations observed in patients with hyperphenylalaninemia caused by phenylalanine hydroxylase deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harada, T -- Kagamiyama, H -- Hatakeyama, K -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1507-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Osaka Medical College, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Factors/physiology ; Biopterin/analogs & derivatives/physiology ; Chromatography, Gel ; Feedback ; GTP Cyclohydrolase/antagonists & inhibitors/*metabolism ; Humans ; In Vitro Techniques ; Liver/metabolism ; Phenylalanine/physiology ; Phenylalanine Hydroxylase/metabolism ; Protein Binding ; Rats ; Recombinant Proteins/metabolism ; Tissue Extracts
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    Peptide translocation by variants of the transporter associated with antigen processing (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-12-24
    Description: Major histocompatibility complex (MHC) class I molecules associate with peptides that are delivered from the cytosol to the lumen of the endoplasmic reticulum by the transporter associated with antigen processing (TAP). Liver microsomes of SHR and Lewis rats, which express different alleles of TAP (cim(b) and cim(a), respectively), accumulate different sets of peptides. Use of MHC congenic rats assigned this difference to the MHC, independent of the class I products expressed. Both the cim(a) and cim(b) TAP complexes translocate peptides with a hydrophobic carboxyl terminus, but translocation of peptides with a carboxyl-terminal His, Lys, or Arg residue is unique to cim(a). Thus, the specificity of the TAP peptide translocator restricts the peptides available for antigen presentation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heemels, M T -- Schumacher, T N -- Wonigeit, K -- Ploegh, H L -- R01 AI3 3456-01/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2059-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266106" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Alleles ; Amino Acid Sequence ; Animals ; Antigen Presentation/*physiology ; Biological Transport/physiology ; Carrier Proteins/genetics/*physiology ; Histocompatibility Antigens Class I/physiology ; Histocompatibility Antigens Class II/genetics/*physiology ; In Vitro Techniques ; Microsomes, Liver/metabolism ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Rats ; Rats, Inbred BN ; Rats, Inbred Lew ; Rats, Inbred SHR ; Substrate Specificity
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    Cellular mechanisms of a synchronized oscillation in the thalamus (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-07-16
    Description: Spindle waves are a prototypical example of synchronized oscillations, a common feature of neuronal activity in thalamic and cortical systems in sleeping and waking animals. Spontaneous spindle waves recorded from slices of the ferret lateral geniculate nucleus were generated by rebound burst firing in relay cells. This rebound burst firing resulted from inhibitory postsynaptic potentials arriving from the perigeniculate nucleus, the cells of which were activated by burst firing in relay neurons. Reduction of gamma-aminobutyric acidA (GABAA) receptor-mediated inhibition markedly enhanced GABAB inhibitory postsynaptic potentials in relay cells and subsequently generated a slowed and rhythmic population activity resembling that which occurs during an absence seizure. Pharmacological block of GABAB receptors abolished this seizure-like activity but not normal spindle waves, suggesting that GABAB antagonists may be useful in the treatment of absence seizures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Krosigk, M -- Bal, T -- McCormick, D A -- New York, N.Y. -- Science. 1993 Jul 16;261(5119):361-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, 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/8392750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baclofen/analogs & derivatives/pharmacology ; Bicuculline/pharmacology ; Calcium/metabolism ; Epilepsy, Absence/physiopathology ; Ferrets ; Geniculate Bodies/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Neurons/drug effects/*physiology ; Potassium/metabolism ; Receptors, Amino Acid/physiology ; Receptors, GABA-A/drug effects/*physiology ; Receptors, Glutamate/physiology ; Receptors, Kainic Acid ; Receptors, N-Methyl-D-Aspartate/physiology
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    Common forms of synaptic plasticity in the hippocampus and neocortex in vitro (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-06-04
    Description: Activity-dependent synaptic plasticity in the superficial layers of juvenile cat and adult rat visual neocortex was compared with that in adult rat hippocampal field CA1. Stimulation of neocortical layer IV reliably induced synaptic long-term potentiation (LTP) and long-term depression (LTD) in layer III with precisely the same types of stimulation protocols that were effective in CA1. Neocortical LTP and LTD were specific to the conditioned pathway and, as in the hippocampus, were dependent on activation of N-methyl-D-aspartate receptors. These results provide strong support for the view that common principles may govern experience-dependent synaptic plasticity in CA1 and throughout the superficial layers of the mammalian neocortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirkwood, A -- Dudek, S M -- Gold, J T -- Aizenman, C D -- Bear, M F -- New York, N.Y. -- Science. 1993 Jun 4;260(5113):1518-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8502997" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Aging/physiology ; Animals ; Cats ; Cerebral Cortex/*physiology ; Electric Stimulation ; Hippocampus/*physiology ; In Vitro Techniques ; Neural Pathways/physiology ; Neuronal Plasticity/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology
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    Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-10-29
    Description: Spontaneous local increases in the concentration of intracellular calcium, called "calcium sparks," were detected in quiescent rat heart cells with a laser scanning confocal microscope and the fluorescent calcium indicator fluo-3. Estimates of calcium flux associated with the sparks suggest that calcium sparks result from spontaneous openings of single sarcoplasmic reticulum (SR) calcium-release channels, a finding supported by ryanodine-dependent changes of spark kinetics. At resting intracellular calcium concentrations, these SR calcium-release channels had a low rate of opening (approximately 0.0001 per second). An increase in the calcium content of the SR, however, was associated with a fourfold increase in opening rate and resulted in some sparks triggering propagating waves of increased intracellular calcium concentration. The calcium spark is the consequence of elementary events underlying excitation-contraction coupling and provides an explanation for both spontaneous and triggered changes in the intracellular calcium concentration in the mammalian heart.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, H -- Lederer, W J -- Cannell, M B -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):740-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235594" target="_blank"〉PubMed〈/a〉
    Keywords: Aniline Compounds ; Animals ; Calcium/metabolism/*physiology ; Calcium Channels/drug effects/physiology ; Fluorescent Dyes ; In Vitro Techniques ; Ion Channel Gating/physiology ; Microscopy, Fluorescence/methods ; Models, Biological ; Muscle Proteins/drug effects/physiology ; Myocardial Contraction/*physiology ; Myocardium/metabolism ; Rats ; Ryanodine/pharmacology ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/metabolism ; Xanthenes
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    A functional role for GTP-binding proteins in synaptic vesicle cycling (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-19
    Description: The squid giant synapse was used to test the hypothesis that guanosine-5'-triphosphate (GTP)-binding proteins regulate the local distribution of synaptic vesicles within nerve terminals. Presynaptic injection of the nonhydrolyzable GTP analog GTP gamma S irreversibly inhibited neurotransmitter release without changing either the size of the calcium signals produced by presynaptic action potentials or the number of synaptic vesicles docked at presynaptic active zones. Neurotransmitter release was also inhibited by injection of the nonhydrolyzable guanosine diphosphate (GDP) analog GDP beta S but not by injection of AIF4-. These results suggest that a small molecular weight GTP-binding protein directs the docking of synaptic vesicles that occurs before calcium-dependent neurotransmitter release. Depletion of undocked synaptic vesicles by GTP gamma S indicates that additional GTP-binding proteins function in the terminal at other steps responsible for synaptic vesicle replenishment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hess, S D -- Doroshenko, P A -- Augustine, G J -- NS-21624/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1169-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8438167" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum/pharmacology ; *Aluminum Compounds ; Animals ; Calcium/metabolism ; Decapodiformes ; *Fluorides ; Fluorine/pharmacology ; GTP-Binding Proteins/*physiology ; Ganglia/physiology ; Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology ; Guanosine Diphosphate/analogs & derivatives/metabolism/pharmacology ; Guanosine Triphosphate/metabolism ; In Vitro Techniques ; Kinetics ; Models, Neurological ; Nerve Endings/physiology/ultrastructure ; Signal Transduction/drug effects ; Synaptic Vesicles/drug effects/*physiology/ultrastructure ; Thionucleotides/pharmacology ; Time Factors
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    The cell's nucleus shapes up (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, M -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1257-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Cell Nucleus/*ultrastructure ; Gene Expression Regulation ; In Vitro Techniques ; Nuclear Matrix/*ultrastructure ; *RNA Processing, Post-Transcriptional ; RNA Splicing ; RNA, Messenger/genetics/metabolism ; Rats ; Spliceosomes/metabolism/ultrastructure
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    A putative ATP-activated Na+ channel involved in sperm-induced fertilization (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-07-23
    Description: Extracellular application of adenosine triphosphate (ATP) to defolliculated Xenopus laevis oocytes activated a saturating inward current with a maximal amplitude E(max) of 2.4 +/- 0.2 microamperes and an apparent Michaelis constant of 197.6 micromolar. The current was carried predominantly by sodium ions and potently inhibited by amiloride, guanosine triphosphate (GTP), and its nonhydrolyzable analogs guanosine 5'-[beta,gamma-imido]triphosphate (GppNHp) and guanosine 5'-O-(3-thiotriphosphate). Likewise, in vitro fertilization using mature eggs and Xenopus sperm was inhibited by amiloride, GTP, and GppNHp. Hence, an ATP receptor on the egg membrane may be the recipient target for ATP originating in sperm, suggesting that an ATP-induced increase in sodium permeability mediates the initial sperm to egg signal in the fertilization process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupitz, Y -- Atlas, D -- New York, N.Y. -- Science. 1993 Jul 23;261(5120):484-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Hebrew University of Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8392753" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/analogs & derivatives/pharmacology/*physiology ; Amiloride/pharmacology ; Animals ; Female ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; In Vitro Techniques ; Male ; Membrane Potentials/physiology ; Oocytes/physiology ; Receptors, Purinergic/drug effects/physiology ; Sodium Channels/*physiology ; Sperm-Ovum Interactions/*physiology ; Xenopus laevis
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    Activation of exocytosis by the heterotrimeric G protein Gi3 (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-12-03
    Description: Secretagogues of rat peritoneal mast cells, such as mastoparan and compound 48/80, induce mast cell exocytosis by activating directly the guanosine triphosphate-binding proteins that are required for exocytosis. The introduction of a synthetic peptide that corresponds to the carboxyl-terminal end sequence of G alpha i3 into the cells specifically blocked this secretion. Similar results were obtained when antibodies to this peptide were introduced. The G alpha i3 was located in both the Golgi and the plasma membrane, but only the latter source of G alpha i3 appeared to be essential for secretion. These results indicate that G alpha i3 functions to control regulated exocytosis in mast cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aridor, M -- Rajmilevich, G -- Beaven, M A -- Sagi-Eisenberg, R -- New York, N.Y. -- Science. 1993 Dec 3;262(5139):1569-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Weizmann Institute of Science, Department of Chemical Immunology, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7504324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Exocytosis/drug effects/*physiology ; GTP-Binding Proteins/analysis/drug effects/*physiology ; Histamine Release/drug effects ; In Vitro Techniques ; Mast Cells/chemistry/drug effects/secretion ; Molecular Sequence Data ; Peptide Fragments/pharmacology ; Rats ; Subcellular Fractions/chemistry ; Virulence Factors, Bordetella/pharmacology
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    A mixed-valent polyiron oxo complex that models the biomineralization of the ferritin core (1993)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1993-02-26
    Description: A novel polyiron oxo complex, [FeIII4FeII8(O)2(OCH3)18(O2CCH3)6(CH3OH) 4.67] (1), has been prepared from ferrous acetate and lithium methoxide in methanol by slow addition of dioxygen. The three-dimensional close-packed layered structure found in 1 closely mimics that proposed for the inorganic core in the iron storage protein ferritin. The Mossbauer spectra of 1 reveal superparamagnetic relaxation at temperatures below 15 K, a property characteristic of the ferritin core. The small size and mixed-valent nature of 1 suggest that it is a reasonable model for intermediates formed in the biomineralization of iron during ferritin core formation. A related compound, with the same iron-oxygen framework found in 1 but containing only two ferric ions, has also been structurally characterized. Because the clusters exhibit properties of both discrete molecules and extended solids, they are representative of a new class of nanometer-sized compounds that bridge the molecular solid-state boundary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taft, K L -- Papaefthymiou, G C -- Lippard, S J -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1302-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8446898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ferritins/chemistry/*ultrastructure ; Horses ; Humans ; In Vitro Techniques ; Iron/*chemistry ; Models, Molecular ; Spectrum Analysis
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    The cloning of PIG-A, a component in the early step of GPI-anchor biosynthesis (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-02-26
    Description: The glycosylphosphatidylinositol (GPI) anchor is a membrane attachment structure of many proteins and occurs in a wide variety of eukaryotes from yeasts to mammals. The structure of the core of the GPI anchor is conserved in protozoa and mammals and so is its biosynthetic pathway. A complementary DNA encoding a human protein termed PIG-A (phosphatidylinositol glycan-class A) was cloned. PIG-A was necessary for synthesis of N-acetylglucosaminyl-phosphatidylinositol, the very early intermediate in GPI-anchor biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyata, T -- Takeda, J -- Iida, Y -- Yamada, N -- Inoue, N -- Takahashi, M -- Maeda, K -- Kitani, T -- Kinoshita, T -- New York, N.Y. -- Science. 1993 Feb 26;259(5099):1318-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunoregulation, Osaka University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7680492" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/metabolism ; Antigens, CD55 ; Antigens, CD59 ; Antigens, Surface/metabolism ; Antigens, Thy-1 ; Cloning, Molecular ; DNA/genetics ; Genetic Complementation Test ; Glycosylphosphatidylinositols/*biosynthesis ; HeLa Cells ; Humans ; In Vitro Techniques ; Membrane Glycoproteins/metabolism ; Membrane Proteins/*genetics/metabolism ; Mice ; Molecular Sequence Data ; Solubility ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Optical analysis of synaptic vesicle recycling at the frog neuromuscular junction (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-10
    Description: The fluorescent dyes FM1-43 and RH414 label motor nerve terminals in an activity-dependent fashion that involves dye uptake by synaptic vesicles that are recycling. This allows optical monitoring of vesicle recycling in living nerve terminals to determine how recycled vesicles reenter the vesicle pool. The results suggest that recycled vesicles mix with the pool morphologically and functionally. One complete cycle of release of transmitter, recycling of a vesicle, and rerelease of transmitter appears to take about 1 minute.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Betz, W J -- Bewick, G S -- NS10207/NS/NINDS NIH HHS/ -- NS23466/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 10;255(5041):200-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Colorado School of Medicine, Denver 80262.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553547" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Evoked Potentials ; Fluorescent Dyes ; In Vitro Techniques ; Microscopy, Fluorescence ; Motor Neurons/physiology ; Neuromuscular Junction/*physiology/ultrastructure ; Pyridinium Compounds ; *Quaternary Ammonium Compounds ; Ranidae ; Synaptic Vesicles/*physiology/ultrastructure ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    High probability opening of NMDA receptor channels by L-glutamate (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: Synaptic plasticity can be triggered by calcium flux into neurons through synaptically activated N-methyl-D-aspartate (NMDA) receptor channels. The amplitude and time course of the resulting intracellular calcium transient depend on the number of open NMDA receptor channels and the kinetics of their activation. Short applications of L-glutamate to outside-out patches from hippocampal neurons in the presence and absence of MK-801 revealed that about 30 percent of L-glutamate-bound channels are open at the peak of the current. This high probability of opening suggests that very few channels are required to guarantee a large, localized postsynaptic calcium transient.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jahr, C E -- NS21419/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):470-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute L474, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346477" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cells, Cultured ; Dizocilpine Maleate/pharmacology ; Glutamates/*physiology ; Glutamic Acid ; Hippocampus/physiology ; In Vitro Techniques ; *Ion Channel Gating ; Rats ; Receptors, N-Methyl-D-Aspartate/*physiology
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    Neural computing in cancer drug development: predicting mechanism of action (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-16
    Description: Described here are neural networks capable of predicting a drug's mechanism of action from its pattern of activity against a panel of 60 malignant cell lines in the National Cancer Institute's drug screening program. Given six possible classes of mechanism, the network misses the correct category for only 12 out of 141 agents (8.5 percent), whereas linear discriminant analysis, a standard statistical technique, misses 20 out of 141 (14.2 percent). The success of the neural net indicates several things. (i) The cell line response patterns are rich in information about mechanism. (ii) Appropriately designed neural networks can make effective use of that information. (iii) Trained networks can be used to classify prospectively the more than 10,000 agents per year tested by the screening program. Related networks, in combination with classical statistical tools, will help in a variety of ways to move new anticancer agents through the pipeline from in vitro studies to clinical application.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weinstein, J N -- Kohn, K W -- Grever, M R -- Viswanadhan, V N -- Rubinstein, L V -- Monks, A P -- Scudiero, D A -- Welch, L -- Koutsoukos, A D -- Chiausa, A J -- New York, N.Y. -- Science. 1992 Oct 16;258(5081):447-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Mathematical Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411538" target="_blank"〉PubMed〈/a〉
    Keywords: Alkylating Agents ; *Antineoplastic Agents/classification ; Databases, Factual ; *Drug Design ; Drug Evaluation, Preclinical ; Growth Inhibitors ; Humans ; In Vitro Techniques ; Neural Networks (Computer) ; Tumor Cells, Cultured/drug effects
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    The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-21
    Description: The fms-like tyrosine kinase (Flt) is a transmembrane receptor in the tyrosine kinase family. Expression of flt complementary DNA in COS cells conferred specific, high-affinity binding of vascular endothelial growth factor, also known as vascular permeability factor (VEGF-VPF), a factor that induces vascular permeability when injected in the guinea pig skin and stimulates endothelial cell proliferation. Expression of Flt in Xenopus laevis oocytes caused the oocytes to release calcium in response to VEGF-VPF. These findings show that flt encodes a receptor for VEGF-VPF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Vries, C -- Escobedo, J A -- Ueno, H -- Houck, K -- Ferrara, N -- Williams, L T -- P01 HL-43821/HL/NHLBI NIH HHS/ -- R01 HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):989-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Cross-Linking Reagents ; Endothelial Growth Factors/*physiology ; Enzyme Activation ; Humans ; In Vitro Techniques ; Lymphokines/*physiology ; Proto-Oncogene Proteins/genetics/*physiology ; Receptors, Cell Surface/*genetics ; Signal Transduction ; Transfection ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1 ; Vascular Endothelial Growth Factors ; Xenopus laevis
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    Immunoglobulin A-induced shift of Epstein-Barr virus tissue tropism (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: Increased immunoglobulin A (IgA) antibodies to the Epstein-Barr virus (EBV) appear months to years before the clinical onset of nasopharyngeal carcinoma and define populations at high risk for this EBV-associated epithelial cancer common in south China. In the human HT-29 epithelial cell line, polymeric IgA (pIgA) specific for EBV promoted infection of the otherwise refractory epithelial cells. When bound to pIgA, EBV entered epithelial cells through secretory component-mediated IgA transport but no longer infected B lymphocytes. Such an immune-induced shift in EBV tissue tropism provides a paradigm for endogenous spread of EBV in the immune host that predicts infectious sequelae of epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sixbey, J W -- Yao, Q Y -- CA21765/CA/NCI NIH HHS/ -- CA38877/CA/NCI NIH HHS/ -- CA52258/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1578-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectious Diseases, St. Jude Children's Research Hospital, TN 38101-0318.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312750" target="_blank"〉PubMed〈/a〉
    Keywords: B-Lymphocytes/immunology/microbiology ; Base Sequence ; Epithelium/*microbiology ; Gene Products, env ; Herpesvirus 4, Human/*pathogenicity ; Humans ; Immunoglobulin A/*immunology ; In Vitro Techniques ; Infectious Mononucleosis/immunology ; Lymphocyte Activation/immunology ; Molecular Sequence Data ; Nasopharyngeal Neoplasms/immunology ; Secretory Component/physiology
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    A freeze-frame view of eukaryotic transcription during elongation and capping of nascent mRNA (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-21
    Description: Ribonuclease footprinting of nascent messenger RNA within ternary complexes of vaccinia RNA polymerase revealed an RNA binding site that encompasses an 18-nucleotide RNA segment. The dimensions of the binding site did not change as the polymerase moved along the template. Capping of the 5' end of the RNA was cotranscriptional and was confined to nascent chains 31 nucleotides or greater in length. Purified capping enzyme formed a binary complex with RNA polymerase in solution in the absence of nucleic acid. These findings suggest a mechanism for cotranscriptional establishment of messenger RNA identity in eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hagler, J -- Shuman, S -- GM42498/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):983-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Biology, Sloan-Kettering Institute, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546295" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell-Free System ; DNA/chemistry ; Eukaryotic Cells ; In Vitro Techniques ; Molecular Sequence Data ; *RNA Caps ; RNA Polymerase II/metabolism ; RNA, Messenger/*biosynthesis ; Templates, Genetic ; Terminator Regions, Genetic ; Transcription Factors/physiology ; *Transcription, Genetic ; Vaccinia virus
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    Overlapping but nonidentical binding sites on CD2 for CD58 and a second ligand CD59 (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-26
    Description: The interaction of the T cell glycoprotein CD2 with one ligand, CD58, contributes to T cell function. We have identified CD59, a glycoprotein with complement-inhibitory function, as a second physiological ligand for CD2. Antibodies to CD59 inhibit CD2-dependent T cell activation in murine T cell hybridomas expressing human CD2. In an in vitro binding assay with purified CD58 and CD59, CD2+ cells bind not only immobilized CD58 but also CD59. With two complementary approaches, it was demonstrated that the binding sites on CD2 for CD58 and CD59 are overlapping but nonidentical. These observations suggest that direct interactions between CD2 and both CD58 and CD59 contribute to T cell activation and adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hahn, W C -- Menu, E -- Bothwell, A L -- Sims, P J -- Bierer, B E -- AI28554/AI/NIAID NIH HHS/ -- HL36061/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1805-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pediatric Oncology, Dana-Farber Cancer Institute, and Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1377404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*metabolism ; Antigens, CD2 ; Antigens, CD58 ; Antigens, CD59 ; Antigens, Differentiation, T-Lymphocyte/*metabolism ; Binding Sites ; Dose-Response Relationship, Drug ; Humans ; Hybridomas ; Immunity, Cellular ; In Vitro Techniques ; Membrane Glycoproteins/*metabolism ; Mice ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Immunologic/*metabolism ; T-Lymphocytes/immunology
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    Probing protein stability with unnatural amino acids (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-06-26
    Description: Unnatural amino acid mutagenesis, in combination with molecular modeling and simulation techniques, was used to probe the effect of side chain structure on protein stability. Specific replacements at position 133 in T4 lysozyme included (i) leucine (wt), norvaline, ethylglycine, and alanine to measure the cost of stepwise removal of methyl groups from the hydrophobic core, (ii) norvaline and O-methyl serine to evaluate the effects of side chain solvation, and (iii) leucine, S,S-2-amino-4-methylhexanoic acid, and S-2-amino-3-cyclopentylpropanoic acid to measure the influence of packing density and side chain conformational entropy on protein stability. All of these factors (hydrophobicity, packing, conformational entropy, and cavity formation) significantly influence protein stability and must be considered when analyzing any structural change to proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mendel, D -- Ellman, J A -- Chang, Z -- Veenstra, D L -- Kollman, P A -- Schultz, P G -- GM-08388-02/GM/NIGMS NIH HHS/ -- GM-29072/GM/NIGMS NIH HHS/ -- NIH-RR-1081/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 26;256(5065):1798-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1615324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*physiology ; Enzyme Stability ; In Vitro Techniques ; Muramidase/*chemistry ; Mutagenesis, Site-Directed ; Spectrum Analysis ; T-Phages/*enzymology ; Thermodynamics
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    A multifunctional aqueous channel formed by CFTR (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: The cystic fibrosis gene product (CFTR) is a complex protein that functions as an adenosine 3,5-monophosphate (cAMP)-stimulated ion channel and possibly as a regulator of intracellular processes. In order to determine whether the CFTR molecule contains a functional aqueous pathway, anion, water, and urea transport were measured in Xenopus oocytes expressing CFTR. Cyclic AMP agonists induced a Cl- conductance of 94 microsiemens and an increase in water permeability of 4 x 10(-4) centimeter per second that was inhibited by a Cl- channel blocker and was dependent on anion composition. CFTR has a calculated single channel water conductance of 9 x 10(-13) cubic centimeter per second, suggesting a pore-like aqueous pathway. Oocytes expressing CFTR also showed cAMP-stimulated transport of urea but not the larger solute sucrose. Thus CFTR contains a cAMP-stimulated aqueous pore that can transport anions, water, and small solutes. The results also provide functional evidence for water movement through an ion channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasegawa, H -- Skach, W -- Baker, O -- Calayag, M C -- Lingappa, V -- Verkman, A S -- DK35124/DK/NIDDK NIH HHS/ -- DK43840/DK/NIDDK NIH HHS/ -- HL42368/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1477-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0532.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279809" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Biological Transport/physiology ; Chlorides/metabolism ; Cyclic AMP/physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Female ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Molecular Sequence Data ; Oocytes ; Urea/metabolism ; Water/metabolism ; Xenopus
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    Potocytosis: sequestration and transport of small molecules by caveolae (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, R G -- Kamen, B A -- Rothberg, K G -- Lacey, S W -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):410-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1310359" target="_blank"〉PubMed〈/a〉
    Keywords: Carrier Proteins/physiology ; Cell Membrane/*physiology/ultrastructure ; Cells, Cultured ; *Endocytosis ; Folate Receptors, GPI-Anchored ; Folic Acid/metabolism ; Glycolipids/physiology ; Glycosylphosphatidylinositols ; In Vitro Techniques ; Membrane Glycoproteins/physiology ; Phosphatidylinositols/physiology ; Receptors, Cell Surface/physiology
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    Antisense and antigene properties of peptide nucleic acids (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: Peptide nucleic acids (PNAs) are polyamide oligomers that can strand invade duplex DNA, causing displacement of one DNA strand and formation of a D-loop. Binding of either a T10 PNA or a mixed sequence 15-mer PNA to the transcribed strand of a G-free transcription cassette caused 90 to 100 percent site-specific termination of pol II transcription elongation. When a T10 PNA was bound on the nontranscribed strand, site-specific inhibition never exceeded 50 percent. Binding of PNAs to RNA resulted in site-specific termination of both reverse transcription and in vitro translation, precisely at the position of the PNA.RNA heteroduplex. Nuclear microinjection of cells constitutively expressing SV40 large T antigen (T Ag) with either a 15-mer or 20-mer PNA targeted to the T Ag messenger RNA suppressed T Ag expression. This effect was specific in that there was no reduction in beta-galactosidase expression from a coinjected expression vector and no inhibition of T Ag expression after microinjection of a 10-mer PNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanvey, J C -- Peffer, N J -- Bisi, J E -- Thomson, S A -- Cadilla, R -- Josey, J A -- Ricca, D J -- Hassman, C F -- Bonham, M A -- Au, K G -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1481-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Glaxo Inc. Research Institute, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279811" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/genetics ; Base Sequence ; DNA/*metabolism ; Deoxyribonuclease HindIII/antagonists & inhibitors ; Gene Expression/drug effects ; HeLa Cells ; Humans ; In Vitro Techniques ; Molecular Sequence Data ; Oligodeoxyribonucleotides/*metabolism/pharmacology ; Oligonucleotides, Antisense/*metabolism/pharmacology ; *Peptide Nucleic Acids ; Plasmids ; Protein Biosynthesis/drug effects ; RNA/metabolism ; Rabbits ; Rats ; Transcription, Genetic/drug effects
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    Functional transcription elongation complexes from synthetic RNA-DNA bubble duplexes (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: A synthetic RNA-DNA bubble duplex construct intended to mimic the nucleic acid framework of a functional transcription elongation complex was designed and assembled. The construct consisted of a double-stranded DNA duplex of variable length (the template and nontemplate strands) containing an internal noncomplementary DNA "bubble" sequence. The 3' end of an RNA oligonucleotide that is partially complementary to the template DNA strand was hybridized within the DNA bubble to form an RNA-DNA duplex with a non-complementary 5'-terminal RNA tail. The addition of either Escherichia coli or T7 RNA polymerase to this construct formed a complex that synthesized RNA with good efficiency from the hybridized RNA primer in a template-directed and processive manner, and displayed other features of a normal promoter-initiated transcription elongation complex. Other such constructs can be designed to examine many of the functional and regulatory properties of transcription systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daube, S S -- von Hippel, P H -- GM-15792/GM/NIGMS NIH HHS/ -- GM-29158/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1320-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1280856" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA/genetics ; DNA-Directed RNA Polymerases/*metabolism ; Escherichia coli/enzymology/genetics ; In Vitro Techniques ; Molecular Sequence Data ; Nucleic Acid Hybridization ; *Promoter Regions, Genetic ; RNA/genetics ; Structure-Activity Relationship ; Templates, Genetic ; *Transcription, Genetic
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    Impaired long-term potentiation, spatial learning, and hippocampal development in fyn mutant mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-18
    Description: Mice with mutations in four nonreceptor tyrosine kinase genes, fyn, src, yes, and abl, were used to study the role of these kinases in long-term potentiation (LTP) and in the relation of LTP to spatial learning and memory. All four kinases were expressed in the hippocampus. Mutations in src, yes, and abl did not interfere with either the induction or the maintenance of LTP. However, in fyn mutants, LTP was blunted even though synaptic transmission and two short-term forms of synaptic plasticity, paired-pulse facilitation and post-tetanic potentiation, were normal. In parallel with the blunting of LTP, fyn mutants showed impaired spatial learning, consistent with a functional link between LTP and learning. Although fyn is expressed at mature synapses, its lack of expression during development resulted in an increased number of granule cells in the dentate gyrus and of pyramidal cells in the CA3 region. Thus, a common tyrosine kinase pathway may regulate the growth of neurons in the developing hippocampus and the strength of synaptic plasticity in the mature hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, S G -- O'Dell, T J -- Karl, K A -- Stein, P L -- Soriano, P -- Kandel, E R -- AG08702/AG/NIA NIH HHS/ -- HD24875/HD/NICHD NIH HHS/ -- MH45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Dec 18;258(5090):1903-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1361685" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Acetylcholinesterase/analysis ; Animals ; Brain/cytology/*physiology ; Cerebral Cortex/cytology/physiology ; Electric Stimulation ; Genes, abl ; Genes, src ; Hippocampus/drug effects/growth & development/*physiology ; In Vitro Techniques ; *Learning ; Mice ; Mice, Neurologic Mutants ; Neurons/drug effects/*physiology ; Protein-Tyrosine Kinases/*genetics/metabolism ; Proto-Oncogene Proteins/*genetics/metabolism ; Proto-Oncogene Proteins c-fyn ; Proto-Oncogene Proteins c-yes ; Pyramidal Tracts/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Space Perception ; Synapses/physiology ; *src-Family Kinases
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    Tumor necrosis factor-alpha activates the sphingomyelin signal transduction pathway in a cell-free system (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-03-27
    Description: The mechanism of tumor necrosis factor (TNF)-alpha signaling is unknown. TNF-alpha signaling may involve sphingomyelin hydrolysis to ceramide by a sphingomyelinase and stimulation of a ceramide-activated protein kinase. In a cell-free system, TNF-alpha induced a rapid reduction in membrane sphingomyelin content and a quantitative elevation in ceramide concentrations. Ceramide-activated protein kinase activity also increased. Kinase activation was mimicked by addition of sphingomyelinase but not by phospholipases A2, C, or D. Reconstitution of this cascade in a cell-free system demonstrates tight coupling to the receptor, suggesting this is a signal transduction pathway for TNF-alpha.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dressler, K A -- Mathias, S -- Kolesnick, R N -- 1 F32 GM14207-01/GM/NIGMS NIH HHS/ -- R0-1-CA-42385/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1715-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1313189" target="_blank"〉PubMed〈/a〉
    Keywords: Cell-Free System ; Ceramides/*physiology ; Enzyme Activation ; Humans ; In Vitro Techniques ; Phosphorylation ; Protein Kinases/*metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Receptors, Cell Surface/*physiology ; Receptors, Tumor Necrosis Factor ; Second Messenger Systems ; Signal Transduction/*drug effects ; Sphingomyelin Phosphodiesterase/*physiology ; Sphingomyelins/*physiology ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha/*pharmacology
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    Identification of the integrin VLA-2 as a receptor for echovirus 1 (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-03-27
    Description: Cell surface receptors for echovirus, a common human pathogen, were identified with monoclonal antibodies that protected susceptible cells from infection with echovirus 1. These monoclonal antibodies, which prevented virus attachment to specific receptor sites, recognized the alpha and beta subunits of the integrin VLA-2 (alpha 2 beta 1), a receptor for collagen and laminin. RD rhabdomyosarcoma cells expressed little VLA-2, did not bind to 35S-labeled virus, and resisted infection until transfected with complementary DNA encoding the alpha 2 subunit of VLA-2. Thus, integrins, adhesion receptors important in interactions between cells and with the extracellular matrix, can mediate virus attachment and infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bergelson, J M -- Shepley, M P -- Chan, B M -- Hemler, M E -- Finberg, R W -- AI 20382/AI/NIAID NIH HHS/ -- GM 38903/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1718-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553561" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Cytopathogenic Effect, Viral ; Enterovirus B, Human/*metabolism ; HeLa Cells ; Humans ; In Vitro Techniques ; Molecular Weight ; Receptors, Very Late Antigen/*metabolism ; Receptors, Virus/chemistry/*metabolism
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    Gz-mediated hormonal inhibition of cyclic AMP accumulation (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-17
    Description: Hormones inhibit synthesis of adenosine 3',5'-monophosphate (cAMP) in most cells via receptors coupled to pertussis toxin (PTX)-sensitive guanine nucleotide-binding (G) proteins. Mutationally activated alpha subunits of Gi2 (alpha i2) constitutively inhibit cAMP accumulation when transfected into cells. Cells have now been transfected with mutant alpha subunits of four other G proteins--Gz, a PTX-insensitive G protein of unknown function, and Gi1, Gi3, and G(o), which are PTX-sensitive. Mutant alpha z, alpha i1, and alpha i3 inhibited cAMP accumulation but alpha o did not. Moreover, expression of wild-type alpha z produced cells in which PTX did not block hormonal inhibition of cAMP accumulation. Thus, Gz can trigger an effector pathway in response to hormone receptors that ordinarily interact with PTX-sensitive Gi proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, Y H -- Conklin, B R -- Bourne, H R -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347957" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-Agonists/pharmacology ; Animals ; Brimonidine Tartrate ; Chorionic Gonadotropin/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/*biosynthesis ; Dinoprostone/pharmacology ; Dopamine/pharmacology ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation/*physiology ; Hormones/*physiology ; In Vitro Techniques ; Lysophospholipids/pharmacology ; Pertussis Toxin ; Quinoxalines/pharmacology ; Rats ; Signal Transduction/physiology ; Transfection ; Virulence Factors, Bordetella/pharmacology
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    Transcription factor IID mutants defective for interaction with transcription factor IIA (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-28
    Description: Transcription factor IID (TFIID) recognizes the TATA element of promoters transcribed by RNA polymerase II (RNAPII) and serves as the base for subsequent association by other general transcription factors and RNAPII. The carboxyl-terminal domain of TFIID is highly conserved and contains an imperfect repetition of a 60-amino acid sequence. These repeats are separated by a region rich in basic amino acids. Mutagenesis of the lysines in this region resulted in a conditioned phenotype in vivo, and the mutant proteins were defective for interactions with transcription factor IIA in vitro. Binding of TFIID to DNA was unaffected. These results suggest that the basic domain of TFIID is important for protein-protein interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buratowski, S -- Zhou, H -- R29-GM46498/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 28;255(5048):1130-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546314" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Fungal Proteins/genetics/metabolism ; Humans ; In Vitro Techniques ; Macromolecular Substances ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; RNA Polymerase II/metabolism ; Saccharomyces cerevisiae ; Transcription Factor TFIIA ; Transcription Factor TFIID ; Transcription Factors/*genetics/*metabolism ; *Transcription, Genetic
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    Calcium-permeable AMPA-kainate receptors in fusiform cerebellar glial cells (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-06-12
    Description: Glutamate-operated ion channels (GluR channels) of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-kainate subtype are found in both neurons and glial cells of the central nervous system. These channels are assembled from the GluR-A, -B, -C, and -D subunits; channels containing a GluR-B subunit show an outwardly rectifying current-voltage relation and low calcium permeability, whereas channels lacking the GluR-B subunit are characterized by a doubly rectifying current-voltage relation and high calcium permeability. Most cell types in the central nervous system coexpress several subunits, including GluR-B. However, Bergmann glia in rat cerebellum do not express GluR-B subunit genes. In a subset of cultured cerebellar glial cells, likely derived from Bergmann glial cells. GluR channels exhibit doubly rectifying current-voltage relations and high calcium permeability, whereas GluR channels of cerebellar neurons have low calcium permeability. Thus, differential expression of the GluR-B subunit gene in neurons and glia is one mechanism by which functional properties of native GluR channels are regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnashev, N -- Khodorova, A -- Jonas, P -- Helm, P J -- Wisden, W -- Monyer, H -- Seeburg, P H -- Sakmann, B -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1566-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cell Membrane Permeability ; Cells, Cultured ; Cerebellum/*physiology ; Gene Expression ; Glutamates/physiology ; In Vitro Techniques ; Ion Channel Gating ; Neuroglia/*physiology ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rats ; Receptors, Kainic Acid ; Receptors, Neurotransmitter/*physiology
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    Tyrosyl phosphorylation and activation of MAP kinases by p56lck (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-14
    Description: T cell signaling via the CD4 surface antigen is mediated by the associated tyrosyl protein kinase p56lck. The 42-kilodalton mitogen-activated protein (MAP) kinase (p42mapk) was tyrosyl-phosphorylated and activated after treatment of the murine T lymphoma cell line 171CD4+, which expresses CD4, with antibody to CD3. Treatment of the CD4-deficient cell line 171 with the same antibody did not result in phosphorylation or activation of p42mapk. Purified p56lck both tyrosyl-phosphorylated and stimulated the seryl-threonyl phosphotransferase activity of purified p44mpk, a MAP kinase isoform from sea star oocytes. A synthetic peptide modeled after the putative regulatory phosphorylation site in murine p42mapk (Tyr185) was phosphorylated by p56lck with a similar Vmax, but a fivefold lower Michaelis constant (Km) than a peptide containing the Tyr394 autophosphorylation site from p56lck. MAP kinases may participate in protein kinase cascades that link Src family protein-tyrosyl kinases to seryl-threonyl kinases such as those encoded by rsk and raf, which are putative substrates of MAP kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ettehadieh, E -- Sanghera, J S -- Pelech, S L -- Hess-Bienz, D -- Watts, J -- Shastri, N -- Aebersold, R -- R126604/PHS HHS/ -- New York, N.Y. -- Science. 1992 Feb 14;255(5046):853-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biomedical Research Centre, University of British Columbia, Vancouver, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1311128" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD3 ; Antigens, Differentiation, T-Lymphocyte/physiology ; Calcium-Calmodulin-Dependent Protein Kinases ; Cell Line ; Glycogen Synthase Kinase 3 ; In Vitro Techniques ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Lymphoma, T-Cell ; Mice ; Molecular Sequence Data ; Oncogene Proteins, Viral/*physiology ; Phosphorylation ; Protein Kinases/*physiology ; Protein-Tyrosine Kinases/*physiology ; Receptors, Antigen, T-Cell/physiology ; Signal Transduction/*physiology ; T-Lymphocytes/physiology
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    Role of beta gamma subunits of G proteins in targeting the beta-adrenergic receptor kinase to membrane-bound receptors (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-08-28
    Description: The rate and extent of the agonist-dependent phosphorylation of beta 2-adrenergic receptors and rhodopsin by beta-adrenergic receptor kinase (beta ARK) are markedly enhanced on addition of G protein beta gamma subunits. With a model peptide substrate it was demonstrated that direct activation of the kinase could not account for this effect. G protein beta gamma subunits were shown to interact directly with the COOH-terminal region of beta ARK, and formation of this beta ARK-beta gamma complex resulted in receptor-facilitated membrane localization of the enzyme. The beta gamma subunits of transducin were less effective at both enhancing the rate of receptor phosphorylation and binding to the COOH-terminus of beta ARK, suggesting that the enzyme preferentially binds specific beta gamma complexes. The beta gamma-mediated membrane localization of beta ARK serves to intimately link receptor activation to beta ARK-mediated desensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pitcher, J A -- Inglese, J -- Higgins, J B -- Arriza, J L -- Casey, P J -- Kim, C -- Benovic, J L -- Kwatra, M M -- Caron, M G -- Lefkowitz, R J -- 4R37-HL16039/HL/NHLBI NIH HHS/ -- GM 44944/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1264-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Research Institute, Department of Medicine, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1325672" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cattle ; *Cyclic AMP-Dependent Protein Kinases ; Dose-Response Relationship, Drug ; Escherichia coli ; GTP-Binding Proteins/*physiology ; Gene Expression Regulation/drug effects ; In Vitro Techniques ; Molecular Sequence Data ; Phosphorylation ; Protein Kinases/*pharmacology ; Protein Processing, Post-Translational ; Receptors, Adrenergic, beta/*drug effects/*metabolism ; Recombinant Fusion Proteins ; Rhodopsin/metabolism ; Time Factors ; Virulence Factors, Bordetella/pharmacology ; beta-Adrenergic Receptor Kinases
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    Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-17
    Description: The paucity of virus-laden CD4+ cells in individuals infected with human immunodeficiency virus type-1 (HIV-1) contrasts with the greatly reduced numbers and function of these lymphocytes. A pathway is described whereby dendritic cells carry HIV-1 to uninfected T cells, amplifying the cytopathic effects of small amounts of virus. After exposure to HIV-1, dendritic cells continue to present superantigens and antigens, forming clusters with T cells that are driven to replicate. Infection of the dendritic cells cannot be detected, but the clustered T cells form syncytia, release virions, and die. Carriage of HIV-1 by dendritic cells may facilitate the lysis and loss of antigen specific CD4+ T cells in acquired immunodeficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cameron, P U -- Freudenthal, P S -- Barker, J M -- Gezelter, S -- Inaba, K -- Steinman, R M -- AI 24775/AI/NIAID NIH HHS/ -- MOI-RR00102/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):383-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cellular Physiology and Immunology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1352913" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/drug therapy/*transmission ; Animals ; Antigen-Presenting Cells/immunology ; CD4-Positive T-Lymphocytes/*immunology/*microbiology ; Cell Separation ; Dendritic Cells/*immunology/*microbiology ; Flow Cytometry ; HIV Core Protein p24/biosynthesis ; HIV Long Terminal Repeat/physiology ; HIV-1/*pathogenicity ; In Vitro Techniques ; Lymphocyte Culture Test, Mixed ; Mice ; Microscopy, Electron ; Polymerase Chain Reaction ; Zidovudine/pharmacology
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    Triple helix-specific ligands (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-06-19
    Description: A triple helix is formed upon binding of an oligodeoxynucleotide to the major groove of duplex DNA. A benzo[e]pyridoindole derivative (BePI) strongly stabilized this structure and showed preferential binding to a triplex rather than to a duplex. Energy transfer experiments suggest that BePI intercalates within the triple helix. Sequence-specific inhibition of transcription initiation of a specific gene by Escherichia coli RNA polymerase by a triplex-forming oligodeoxynucleotide is strongly enhanced when the triplex is stabilized by BePI. Upon irradiation with ultraviolet light, BePI induces covalent modifications of the target within the triple helix structure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mergny, J L -- Duval-Valentin, G -- Nguyen, C H -- Perrouault, L -- Faucon, B -- Rougee, M -- Montenay-Garestier, T -- Bisagni, E -- Helene, C -- New York, N.Y. -- Science. 1992 Jun 19;256(5064):1681-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Biophysique, Institut National de la Sante et de la Recherche Medicale, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1609278" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Carbolines/metabolism ; DNA/genetics/*metabolism ; DNA-Directed RNA Polymerases/genetics/metabolism ; Escherichia coli/*genetics ; Hot Temperature ; In Vitro Techniques ; *Ligands ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Transcription, Genetic
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    The cytosensor microphysiometer: biological applications of silicon technology (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-09-25
    Description: A silicon-based device, dubbed a microphysiometer, can be used to detect and monitor the response of cells to a variety of chemical substances, especially ligands for specific plasma membrane receptors. The microphysiometer measures the rate of proton excretion from 10(4) to 10(6) cells. This article gives an overview of experiments currently being carried out with this instrument with emphasis on receptors with seven transmembrane helices and tyrosine kinase receptors. As a scientific instrument, the microphysiometer can be thought of as serving two distinct functions. In terms of detecting specific molecules, selected biological cells in this instrument serve as detectors and amplifiers. The microphysiometer can also investigate cell function and biochemistry. A major application of this instrument may prove to be screening for new receptor ligands. In this respect, the microphysiometer appears to offer significant advantages over other techniques.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McConnell, H M -- Owicki, J C -- Parce, J W -- Miller, D L -- Baxter, G T -- Wada, H G -- Pitchford, S -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1906-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329199" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology ; *Cell Physiological Phenomena ; Cells, Cultured ; Culture Media ; HIV Infections/physiopathology ; Humans ; *Hydrogen-Ion Concentration ; In Vitro Techniques ; Potentiometry/*instrumentation ; Receptors, Cell Surface/physiology ; Silicon
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    Modulation of activity of the promoter of the human MDR1 gene by Ras and p53 (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-24
    Description: Drug resistance in human cancer is associated with overexpression of the multidrug resistance (MDR1) gene, which confers cross-resistance to hydrophobic natural product cytotoxic drugs. Expression of the MDR1 gene can occur de novo in human cancers in the absence of drug treatment. The promoter of the human MDR1 gene was shown to be a target for the c-Ha-Ras-1 oncogene and the p53 tumor suppressor gene products, both of which are associated with tumor progression. The stimulatory effect of c-Ha-Ras-1 was not specific for the MDR1 promoter alone, whereas a mutant p53 specifically stimulated the MDR1 promoter and wild-type p53 exerted specific repression. These results imply that the MDR1 gene could be activated during tumor progression associated with mutations in Ras and p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chin, K V -- Ueda, K -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):459-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346476" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Cell Line ; Drug Resistance ; *Gene Expression Regulation ; Genes, Tumor Suppressor ; Genes, ras ; In Vitro Techniques ; Membrane Glycoproteins/*genetics ; Mice ; P-Glycoprotein ; *Promoter Regions, Genetic ; Proto-Oncogene Proteins p21(ras)/*physiology ; Transcription, Genetic ; Tumor Suppressor Protein p53/*physiology
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    Generation of neurons and astrocytes from isolated cells of the adult mammalian central nervous system (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-27
    Description: Neurogenesis in the mammalian central nervous system is believed to end in the period just after birth; in the mouse striatum no new neurons are produced after the first few days after birth. In this study, cells isolated from the striatum of the adult mouse brain were induced to proliferate in vitro by epidermal growth factor. The proliferating cells initially expressed nestin, an intermediate filament found in neuroepithelial stem cells, and subsequently developed the morphology and antigenic properties of neurons and astrocytes. Newly generated cells with neuronal morphology were immunoreactive for gamma-aminobutyric acid and substance P, two neurotransmitters of the adult striatum in vivo. Thus, cells of the adult mouse striatum have the capacity to divide and differentiate into neurons and astrocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, B A -- Weiss, S -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1707-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Calgary Faculty of Medicine, Alberta, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1553558" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*cytology ; Cell Division/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Corpus Striatum/*cytology ; Culture Media, Serum-Free ; Epidermal Growth Factor/pharmacology ; Fluorescent Antibody Technique ; Glial Fibrillary Acidic Protein/metabolism ; In Vitro Techniques ; Intermediate Filament Proteins/metabolism ; Intermediate Filaments/metabolism ; Mice ; *Nerve Tissue Proteins ; Nestin ; Neurons/*cytology ; Phosphopyruvate Hydratase/metabolism
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    Selective role of N-type calcium channels in neuronal migration (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Analysis of neuronal migration in mouse cerebellar slice preparations by a laser scanning confocal microscope revealed that postmitotic granule cells initiate their migration only after the expression of N-type calcium channels on their plasmalemmal surface. Furthermore, selective blockade of these channels by addition of omega-conotoxin to the incubation medium curtailed cell movement. In contrast, inhibitors of L- and T-type calcium channels, as well as those of sodium and potassium channels, had no effect on the rate of granule cell migration. These results suggest that N-type calcium channels, which have been predominantly associated with neurotransmitter release in adult brain, also play a transient but specific developmental role in directed migration of immature neurons before the establishment of their synaptic circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komuro, H -- Rakic, P -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, 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/1323145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Calcium Channels/drug effects/*physiology ; Cell Movement/drug effects ; Cells, Cultured ; Cerebellum/cytology/*physiology ; In Vitro Techniques ; Kinetics ; Mice ; Mollusk Venoms/pharmacology ; Neurons/cytology/drug effects/*physiology ; Peptides, Cyclic/pharmacology ; Time Factors ; *omega-Conotoxins
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    Maternal-effect selfish genes in flour beetles (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-04-03
    Description: A previously unknown class of dominant, maternal-effect lethal M factors was found to be widespread in natural populations of the flour beetle, Tribolium castaneum, collected on several continents. Such factors are integrated into the host chromosomes at variable locations and show the remarkable property of self-selection by maternal-effect lethality to all hatchlings that do not inherit a copy of the factor itself. Offspring are rescued by either paternally or maternally inherited copies. The M-bearing chromosome is thereby perpetuated at the expense of its non-M homolog. M factors that map to different regions of the genome do not rescue one another's maternal-effect lethality. Factors expressing these properties are predicted to spread in a population, even in the absence of any additional selective advantage. Similar factors also occur in the related species T. confusum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beeman, R W -- Friesen, K S -- Denell, R E -- New York, N.Y. -- Science. 1992 Apr 3;256(5053):89-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Grain Marketing Research Laboratory, U.S. Department of Agriculture, Manhattan, KS 66502.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1566060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beetles/*genetics ; Crosses, Genetic ; Female ; Fertility/genetics ; *Genes, Dominant ; *Genes, Lethal ; Genotype ; In Vitro Techniques ; Phenotype ; *Sex Differentiation ; Zygote/physiology
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    Inhibition of long-term potentiation by NMDA-mediated nitric oxide release (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-08-28
    Description: Activation of N-methyl-D-aspartate (NMDA) receptors before tetanic stimulation blocks long-term potentiation (LTP) in the CA1 region of the hippocampus. This NMDA-mediated inhibition of LTP can be reversed by the nitric oxide (NO) inhibitors L-NG-monomethyl-arginine or hemoglobin and mimicked by sodium nitroprusside. These results indicate that the timing of NO release relative to high-frequency activation of CA1 synapses may be an important determinant of LTP generation and suggest that NO may play a positive or negative modulatory role in LTP depending on prior events at the tetanized synapse and the ambient concentration of excitatory amino acids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Izumi, Y -- Clifford, D B -- Zorumski, C F -- AG05681/AG/NIA NIH HHS/ -- MH00964/MH/NIMH NIH HHS/ -- MH45493/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1273-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1519065" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/analogs & derivatives/pharmacology ; Electrophysiology ; Hemoglobins/pharmacology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; N-Methylaspartate/*pharmacology ; Nitric Oxide/*metabolism ; Nitroprusside/pharmacology ; Rats ; Time Factors ; omega-N-Methylarginine
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    The size of gating charge in wild-type and mutant Shaker potassium channels (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-03-27
    Description: The high sensitivity of voltage-gated ion channels to changes in membrane potential implies that the process of channel opening is accompanied by large charge movements. Previous estimates of the total charge displacement, q, have been deduced from the voltage dependence of channel activation and have ranged from 4 to 8 elementary charges (e0). A more direct measurement of q in Drosophila melanogaster Shaker 29-4 potassium channels yields a q value of 12.3 e0. A similar q value is obtained from mutated Shaker channels having reduced voltage sensitivity. These results can be explained by a model for channel activation in which the equilibria of voltage-dependent steps are altered in the mutant channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schoppa, N E -- McCormack, K -- Tanouye, M A -- Sigworth, F J -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1712-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Physiology, 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/1553560" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Mutational Analysis ; Drosophila melanogaster ; Electric Conductivity ; In Vitro Techniques ; *Ion Channel Gating ; Membrane Potentials ; Oocytes ; Potassium Channels/*physiology ; Structure-Activity Relationship
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    Hebbian depression of isolated neuromuscular synapses in vitro (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-06-12
    Description: Modulation of synaptic efficacy may depend on the temporal correlation between pre- and postsynaptic activities. At isolated neuromuscular synapses in culture, repetitive postsynaptic application of acetylcholine pulses alone or in the presence of asynchronous presynaptic activity resulted in immediate and persistent synaptic depression, whereas synchronous pre- and postsynaptic coactivation had no effect. This synaptic depression was a result of a reduction of evoked transmitter release, but induction of the depression requires a rise in postsynaptic cytosolic calcium concentration. Thus, Hebbian modulation operates at isolated peripheral synapses in vitro, and transsynaptic retrograde interaction appears to be an underlying mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dan, Y -- Poo, M M -- NS 22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1570-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Columbia University, New York, NY 10027.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317971" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; In Vitro Techniques ; Neural Inhibition ; Neuromuscular Junction/*physiology ; *Synaptic Transmission ; Xenopus laevis
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    Phosphorylation-independent modulation of L-type calcium channels by magnesium-nucleotide complexes (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-07-10
    Description: Free magnesium ions and magnesium-nucleotide complexes can exert opposite effects on many fundamental cellular processes. Although increases in the intracellular concentration of magnesium ions inhibit the L-type calcium current in heart cells, magnesium-adenosine triphosphate complexes (MgATP) would be expected to increase the current by promoting channel phosphorylation. Rapid increases in the intracellular concentration of MgATP induced by flash photolysis of caged magnesium or caged ATP resulted in enhanced calcium current. The increase in calcium current was not prevented by blocking phosphorylation, revealing a previously unrecognized direct regulatory action of the magnesium-nucleotide complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, B -- Backx, P H -- Marban, E -- HL 07227/HL/NHLBI NIH HHS/ -- HL 36957/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321495" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/analogs & derivatives/*pharmacology ; Adenylyl Imidodiphosphate/pharmacology ; Animals ; Barium/metabolism ; Calcium/metabolism ; Calcium Channels/*drug effects ; *Carrier Proteins ; In Vitro Techniques ; *Intracellular Signaling Peptides and Proteins ; Isoproterenol/pharmacology ; Magnesium/*pharmacology ; Myocardium/metabolism ; Peptide Fragments/pharmacology ; Peptides/pharmacology ; Phosphorylation ; Time Factors
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    Gating of the cardiac Ca2+ release channel: the role of Na+ current and Na(+)-Ca2+ exchange (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-02-14
    Description: In cardiac myocytes, calcium influx through the calcium channel is the primary pathway for triggering calcium release. Recently it has been suggested that the calcium-induced calcium release mechanism can also be activated indirectly by the sodium current, which elevates the sodium concentration under the cell membrane, thereby favoring the entry of "trigger" calcium via the sodium-calcium exchanger. To test this hypothesis, sodium current was suppressed by reducing the external sodium concentration or applying tetrodotoxin. At potentials positive to -30 millivolts, calcium release was unaffected. A small calcium release at more negative potentials could be attributed to partial activation of calcium channels, because it was unaltered by replacement of sodium with lithium and was blocked by cadmium. Thus, sodium influx or its accumulation does not initiate calcium release. In addition, sodium-calcium exchange-related calcium release at potentials positive to +80 millivolts has slower kinetics than calcium channel-induced release. Therefore, only the calcium channel gates the fast release of calcium from the sarcoplasmic reticulum in the range of the action potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sham, J S -- Cleemann, L -- Morad, M -- HL-07400/HL/NHLBI NIH HHS/ -- HL-16152/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 14;255(5046):850-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1311127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/physiology ; Calcium Channels/*physiology ; Heart/*physiology ; In Vitro Techniques ; Ion Channel Gating/*drug effects ; Lithium/pharmacology ; Membrane Potentials ; Rats ; Sodium/*pharmacology ; Tetrodotoxin/pharmacology
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    Sporogonic development of a malaria parasite in vitro (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The sporogonic cycle of the avian malaria parasite Plasmodium gallinaceum was completed in vitro. Ookinetes (motile zygotes) were seeded onto a murine basement membrane-like gel (Matrigel) in coculture with Drosophila melanogaster cells (Schneider's L2). Transformation into oocysts as well as subsequent growth and differentiation were observed in parasites attached to Matrigel and depended on the presence of L2 cells. Sporozoites were first observed on day 10 in culture. Specific circumsporozoite protein antigenicity was identified in mature oocysts and in sporozoites. It is now possible to follow the entire life cycle of Plasmodium in vitro.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warburg, A -- Miller, L H -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):448-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Malaria Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734521" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Protozoan/metabolism ; Cells, Cultured ; Drosophila melanogaster/cytology ; Extracellular Matrix ; In Vitro Techniques ; Microscopy, Electron ; Plasmodium/*growth & development/ultrastructure ; *Protozoan Proteins
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    Polymerase II promoter activation: closed complex formation and ATP-driven start site opening (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-24
    Description: Studies on bacterial RNA polymerases have divided the initiation pathway into three steps, namely (i) promoter binding to form the closed complex; (ii) DNA melting to form an open complex, and (iii) messenger RNA initiation. Potassium permanganate was used to detect DNA melting by mammalian RNA polymerase II in vitro. Closed complexes formed in a rate-limiting step that was stimulated by the activator GAL4-VP16. Adenosine triphosphate was then hydrolyzed to rapidly melt the DNA within the closed complex to form an open complex. Addition of nucleoside triphosphates resulted in the melted bubble moving away from the start site, completing initiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, W -- Carey, M -- Gralla, J D -- GM35754/GM/NIGMS NIH HHS/ -- GM46424/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):450-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, Los Angeles 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1310361" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Base Sequence ; DNA/chemistry/*metabolism ; DNA-Binding Proteins ; Fungal Proteins/metabolism ; HeLa Cells ; Humans ; In Vitro Techniques ; Manganese/chemistry ; *Manganese Compounds ; Molecular Sequence Data ; Oxides/chemistry ; *Promoter Regions, Genetic ; RNA Polymerase II/*metabolism ; Regulatory Sequences, Nucleic Acid ; *Saccharomyces cerevisiae Proteins ; Simplexvirus/genetics ; Templates, Genetic ; Trans-Activators ; Transcription Factors/physiology ; Transcription, Genetic
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    Interactions of small nuclear RNA's with precursor messenger RNA during in vitro splicing (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-09-25
    Description: Precursor messenger RNA splicing requires multiple factors including U1, U2, U4, U5, and U6 small nuclear RNA's. The crosslinking reagent psoralen was used to analyze the interactions of these RNA's with an adenovirus precursor messenger RNA in HeLa nuclear extract. An endogenous U2-U4-U6 crosslinkable complex dissociated upon incubation with precursor messenger RNA. During splicing, U1, U2, U5, and U6 became crosslinked to precursor messenger RNA and U2, U5, and U6 became crosslinked to excised lariat intron. U2 also formed a doubly crosslinked complex with U6 and precursor messenger RNA. The U1, U5, and U6 crosslinks to the precursor messenger RNA mapped to intron sequences near the 5' splice site, whereas the U2 crosslink mapped to the branch site. The kinetics of crosslink formation and disappearance delineates a temporal pathway for the action of small RNA's in the spliceosome. Potential base pairing interactions between conserved sequences in the small nuclear RNA's and precursor messenger RNA at the sites of crosslinking suggest that the 5' splice site is defined in several steps prior to the first cleavage event.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wassarman, D A -- Steitz, J A -- GM26154/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1918-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry, Yale University School of Medicine, Haven, CT 06536.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411506" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Base Sequence ; Cell Nucleus/metabolism ; Cross-Linking Reagents ; HeLa Cells ; Humans ; In Vitro Techniques ; Macromolecular Substances ; Molecular Sequence Data ; RNA Precursors/metabolism ; *RNA Splicing ; RNA, Messenger/*metabolism ; RNA, Small Nuclear/*metabolism ; Ribonucleoproteins, Small Nuclear/*metabolism/ultrastructure
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    Analytical chemists push the cellular envelope (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amato, I -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):925-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1312253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/chemistry/*physiology ; Electrophysiology ; In Vitro Techniques ; Microelectrodes ; Neurobiology/methods ; Synaptic Transmission
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    Activation of a plant gene by T-DNA tagging: auxin-independent growth in vitro (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-20
    Description: A transferred DNA (T-DNA) tagging vector with the potential to produce dominant mutations was used with cocultured Agrobacterium tumefaciens and protoplasts to tag genes involved in the action of the plant growth substance auxin. Transgenic calli were selected for their ability to grow in the absence of auxin in the culture media. From one experiment, 12 calli that displayed this phenotype were recovered, of which 11 were able to regenerate into plants. In one plant studied in detail, protoplast division in the absence of auxin genetically cosegregated with a single T-DNA insert. A messenger RNA encoded by a 6.4-kilobase sequence of plant genomic DNA rescued from the mutant is overexpressed relative to untransformed plants. The genomic DNA, as well as a cognate complementary DNA, once transfected into protoplasts promote growth and cell division in vitro in the absence of exogenously added auxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, H -- Czaja, I -- Lubenow, H -- Schell, J -- Walden, R -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1350-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Agriculture, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455228" target="_blank"〉PubMed〈/a〉
    Keywords: Agrobacterium tumefaciens/genetics ; Amino Acid Sequence ; Cloning, Molecular ; *Gene Expression Regulation ; Genes, Plant ; *Genetic Vectors ; In Vitro Techniques ; Indoleacetic Acids/*genetics ; Molecular Sequence Data ; Plants, Genetically Modified/*genetics/growth & development ; Restriction Mapping
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    Actin filament dynamics in living glial cells imaged by atomic force microscopy (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-09-25
    Description: Observation of filamentous actin (F-actin) in living cells is currently limited to the resolution of the light microscope. Higher resolution procedures require sample fixation and preclude dynamic studies. The atomic force microscope (AFM) can image and manipulate samples at very high, sometimes atomic resolution by scanning a fine tip over the surface of interest and detecting physical interactions between the tip and sample. This study demonstrates that F-actin can be readily resolved in living cells with the AFM and that the dynamic properties of F-actin are easily observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, E -- Haydon, P G -- Sakaguchi, D S -- New York, N.Y. -- Science. 1992 Sep 25;257(5078):1944-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology and Genetics, Iowa State University, Ames 50011.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411511" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*ultrastructure ; Actins/*physiology ; Animals ; *Cell Movement ; Cells, Cultured ; In Vitro Techniques ; Membrane Fluidity ; Microscopy/*methods ; Neuroglia/*ultrastructure ; Xenopus laevis
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    DNA polymerase beta and DNA synthesis in Xenopus oocytes and in a nuclear extract (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-16
    Description: The identities of the DNA polymerases required for conversion of single-strand (ss) M13 DNA to double-strand (ds) M13 DNA were examined both in injected Xenopus laevis oocytes and in an oocyte nuclear extract. Inhibitors and antibodies specific to DNA polymerases alpha and beta were used. In nuclear extracts, inhibition by the antibody to polymerase beta could be reversed by purified polymerase beta. The polymerase beta inhibitors, dideoxythymidine triphosphate (ddTTP) and dideoxycytidine triphosphate (ddCTP), also blocked DNA synthesis and indicated that polymerase beta is involved in the conversion of ssDNA to dsDNA. These results also may have particular significance for emerging evidence of an ssDNA replication mode in eukaryotic cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jenkins, T M -- Saxena, J K -- Kumar, A -- Wilson, S H -- Ackerman, E J -- New York, N.Y. -- Science. 1992 Oct 16;258(5081):475-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1411545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphidicolin/pharmacology ; Cell Nucleus/*metabolism ; Cell-Free System ; DNA Polymerase I/*metabolism ; DNA Polymerase II/metabolism ; *DNA Replication ; DNA, Single-Stranded/metabolism ; Dideoxynucleosides/pharmacology ; In Vitro Techniques ; Oocytes ; Xenopus laevis
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    Peptide binding by chaperone SecB: implications for recognition of nonnative structure (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: The molecular basis for recognition of nonnative proteins by the molecular chaperone SecB was investigated with an in vitro assay based on the protection of SecB from proteolysis when a ligand is bound. The SecB tetramer has multiple binding sites for positively charged peptides. When the peptide binding sites are occupied, the complex undergoes a conformational change to expose hydrophobic sites that bind the fluorescent probe 1-anilinonaphthalene-8-sulfonate. A model is proposed for interaction of nonnative polypeptides with both hydrophilic and hydrophobic sites on SecB.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Randall, L L -- GM29798/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):241-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Washington State University, Pullman 99164-4660.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1631545" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*metabolism ; Binding Sites/physiology ; Electrophoresis, Polyacrylamide Gel ; In Vitro Techniques ; Models, Chemical ; Molecular Sequence Data ; Osmolar Concentration ; Peptides/*metabolism ; Protein Conformation
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    Regulation of protein serine-threonine phosphatase type-2A by tyrosine phosphorylation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: Extracellular signals that promote cell growth activate cascades of protein kinases. The kinases are dephosphorylated and deactivated by a single type-2A protein phosphatase. The catalytic subunit of type-2A protein phosphatase was phosphorylated by tyrosine-specific protein kinases. Phosphorylation was enhanced in the presence of the phosphatase inhibitor okadaic acid, consistent with an autodephosphorylation reaction. More than 90% of the activity of phosphatase 2A was lost when thioadenosine triphosphate was used to produce a thiophosphorylated protein resistant to autodephosphorylation. Phosphorylation in vitro occurred exclusively on Tyr307. Phosphorylation was catalyzed by p60v-src, p56lck, epidermal growth factor receptors, and insulin receptors. Transient deactivation of phosphatase 2A might enhance transmission of cellular signals through kinase cascades within cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- Martin, B L -- Brautigan, D L -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1261-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology and Medicine, Brown University, Providence, RI 02912.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1325671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ethers, Cyclic/pharmacology ; Gene Expression Regulation/drug effects/*physiology ; Humans ; In Vitro Techniques ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Okadaic Acid ; Oncogene Protein pp60(v-src)/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation/drug effects ; Protein Phosphatase 2 ; Protein-Tyrosine Kinases/physiology ; Rabbits ; Receptor, Epidermal Growth Factor/physiology ; Receptor, Insulin/physiology ; Thionucleotides/pharmacology ; Tyrosine/*metabolism
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  • 80
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    Structural evidence for induced fit as a mechanism for antibody-antigen recognition (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-02-21
    Description: The three-dimensional structure of a specific antibody (Fab 17/9) to a peptide immunogen from influenza virus hemagglutinin [HA1(75-110)] and two independent crystal complexes of this antibody with bound peptide (TyrP100-LeuP108) have been determined by x-ray crystallographic techniques at 2.0 A, 2.9 A, and 3.1 A resolution, respectively. The nonapeptide antigen assumes a type I beta turn in the antibody combining site and interacts primarily with the Fab hypervariable loops L3, H2, and H3. Comparison of the bound and unbound Fab structures shows that a major rearrangement in the H3 loop accompanies antigen binding. This conformational change results in the creation of a binding pocket for the beta turn of the peptide, allowing TyrP105 to be accommodated. The conformation of the peptide bound to the antibody shows similarity to its cognate sequence in the HA1, suggesting a possible mechanism for the cross-reactivity of this Fab with monomeric hemagglutinin. The structures of the free and antigen bound antibodies demonstrate the flexibility of the antibody combining site and provide an example of induced fit as a mechanism for antibody-antigen recognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rini, J M -- Schulze-Gahmen, U -- Wilson, I A -- AI-23498/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 21;255(5047):959-65.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1546293" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/ultrastructure ; *Antigen-Antibody Reactions ; Hemagglutinins, Viral/*immunology ; Hydrogen Bonding ; Immunoglobulin Fab Fragments/*ultrastructure ; Immunoglobulin G/ultrastructure ; In Vitro Techniques ; Influenza A virus/immunology ; Mice ; Models, Molecular ; Molecular Sequence Data ; Motion ; Peptides/chemistry/immunology ; Protein Binding ; Protein Conformation ; X-Ray Diffraction
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    DNA binding activity of recombinant SRY from normal males and XY females (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The protein encoded by the human testis determining gene, SRY, contains a high mobility group (HMG) box related to that present in the T cell-specific, DNA-binding protein TCF-1. Recombinant SRY protein was able to bind to the same core sequence AACAAAG recognized by TCF-1 in a sequence dependent manner. In five XY females point mutations were found in the region encoding the HMG box. In four cases DNA binding activity of mutant SRY protein was negligible; in the fifth case DNA binding was reduced. These results imply that the DNA binding activity of SRY is required for sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harley, V R -- Jackson, D I -- Hextall, P J -- Hawkins, J R -- Berkovitz, G D -- Sockanathan, S -- Lovell-Badge, R -- Goodfellow, P N -- MC_U117562207/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):453-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Molecular Genetics Laboratory, Imperial Cancer Research Fund, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA-Binding Proteins/*metabolism ; Female ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Male ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Oligonucleotide Probes ; Recombinant Proteins/metabolism ; Sequence Alignment ; Sex-Determining Region Y Protein ; Transcription Factors/metabolism
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  • 82
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    Induction of broadly cross-reactive cytotoxic T cells recognizing an HIV-1 envelope determinant (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-17
    Description: An immunodominant determinant for cytotoxic T lymphocytes (CTLs) exists in the hypervariable portion of human immunodeficiency virus-1 (HIV-1) gp160. Three mouse CTL lines (specific for isolates MN, RF, and IIIB) were examined for recognition of homologous determinants from distinct isolates. Only MN-elicited CTLs showed extensive interisolate cross-reactivity. Residue 325 played a critical role in specificity, with MN-elicited CTLs responding to peptides with an aromatic or cyclic residue and IIIB-induced cells recognizing peptides with an aliphatic residue at this position. CTL populations with broad specificities were generated by restimulation of IIIB-gp160 primed cells with MN-type peptides that have an aliphatic substitution at 325. This represents an approach to synthetic vaccines that can generate broadly cross-reactive CTLs capable of effector function against a wide range of HIV isolates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, H -- Nakagawa, Y -- Pendleton, C D -- Houghten, R A -- Yokomuro, K -- Germain, R N -- Berzofsky, J A -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):333-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Nippon Medical School, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1372448" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/immunology ; Amino Acid Sequence ; Animals ; Cell Line ; Cross Reactions ; Epitopes/immunology ; Gene Products, env/genetics/*immunology ; HIV Antigens/immunology ; HIV Envelope Protein gp160 ; HIV-1/*immunology ; In Vitro Techniques ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Protein Precursors/genetics/*immunology ; Sequence Homology, Nucleic Acid ; T-Lymphocytes, Cytotoxic/*immunology ; Vaccination
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    Inhibition of myeloid differentiation by the helix-loop-helix protein Id (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-27
    Description: Id is a helix-loop-helix (HLH) protein that represses activity of several basic helix-loop-helix (bHLH) proteins involved in cell type--specific transcription and cell lineage commitment. The myeloid precursor cell line 32DC13(G) expressed Id messenger RNA, which was transiently decreased when cells were induced to terminally differentiate with granulocyte--colony-stimulating factor. Concomitant with the decrease of Id messenger RNA was the appearance in nuclear extracts of DNA binding proteins that recognized a canonical E-box motif, a DNA binding site for some bHLH proteins. Constitutive expression of an Id complementary DNA in 32DC13(G) cells blocked their ability to differentiate and to induce E-box-binding activity. These results suggest that Id and, hence, bHLH proteins function in the process of myeloid differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kreider, B L -- Benezra, R -- Rovera, G -- Kadesch, T -- CA 10815/CA/NCI NIH HHS/ -- CA 21124/CA/NCI NIH HHS/ -- CA 25875/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Mar 27;255(5052):1700-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1372755" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Differentiation/*drug effects ; Cells, Cultured ; DNA-Binding Proteins/*physiology ; Gene Expression ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoiesis/*drug effects ; In Vitro Techniques ; Inhibitor of Differentiation Protein 1 ; Interleukin-3/pharmacology ; Macromolecular Substances ; RNA, Messenger/genetics ; *Repressor Proteins ; *Transcription Factors
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  • 84
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    Transcription factor loading on the MMTV promoter: a bimodal mechanism for promoter activation (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-20
    Description: The mouse mammary tumor virus (MMTV) promoter attains a phased array of six nucleosomes when introduced into rodent cells. This architecture excludes nuclear factor 1/CCAAT transcription factor (NF1/CTF) from the promoter before glucocorticoid treatment and hormone-dependent access of nucleolytic agents to promoter DNA. In contrast, when the promoter was transiently introduced into cells, NF1/CTF was bound constitutively and nucleolytic attack was hormone-independent. Thus, induction at this promoter was a bimodal process involving receptor-dependent remodeling of chromatin that allows NF1/CTF loading and direct receptor-mediated recruitment of additional transcription factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Archer, T K -- Lefebvre, P -- Wolford, R G -- Hager, G L -- New York, N.Y. -- Science. 1992 Mar 20;255(5051):1573-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hormone Action and Oncogenesis Section, Laboratory of Molecular Virology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1347958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *CCAAT-Enhancer-Binding Proteins ; DNA, Viral/physiology ; DNA-Binding Proteins/physiology ; Dexamethasone/pharmacology ; *Gene Expression Regulation, Viral ; Glucocorticoids/physiology ; In Vitro Techniques ; Mammary Tumor Virus, Mouse/*genetics ; Molecular Sequence Data ; NFI Transcription Factors ; Nuclear Proteins ; Nucleosomes/physiology ; Polymorphism, Restriction Fragment Length ; Promoter Regions, Genetic/*physiology ; Restriction Mapping ; Rodentia/*genetics ; Transcription Factors/*physiology ; Transfection ; Y-Box-Binding Protein 1
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    The ability of certain SIV vaccines to provoke reactions against normal cells (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langlois, A J -- Weinhold, K J -- Matthews, T J -- Greenberg, M L -- Bolognesi, D P -- New York, N.Y. -- Science. 1992 Jan 17;255(5042):292-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1549775" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; Cross Reactions ; Humans ; Immune Sera/immunology ; In Vitro Techniques ; Macaca ; Simian Immunodeficiency Virus/*immunology ; Vaccines, Inactivated/*immunology
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  • 86
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    Calcium entry through kainate receptors and resulting potassium-channel blockade in Bergmann glial cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-12
    Description: Glutamate receptors, the most abundant excitatory transmitter receptors in the brain, are not restricted to neurons; they have also been detected on glial cells. Bergmann glial cells in mouse cerebellar slices revealed a kainate-type glutamate receptor with a sigmoid current-to-voltage relation, as demonstrated with the patch-clamp technique. Calcium was imaged with fura-2, and a kainate-induced increase in intracellular calcium concentration was observed, which was blocked by the non-N-methyl-D-aspartate (NMDA) glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and by low concentrations of external calcium, indicating that there was an influx of calcium through the kainate receptor itself. The entry of calcium led to a marked reduction in the resting (passive) potassium conductance of the cell. Purkinje cells, which have glutamatergic synapses, are closely associated with Bergmann glial cells and therefore may provide a functionally important stimulus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, T -- Moller, T -- Berger, T -- Schnitzer, J -- Kettenmann, H -- New York, N.Y. -- Science. 1992 Jun 12;256(5063):1563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Calcium/*metabolism ; Cerebellum/*physiology ; Electric Conductivity ; In Vitro Techniques ; *Ion Channel Gating ; Ionomycin/pharmacology ; Kainic Acid/pharmacology ; Mice ; Neuroglia/*physiology ; Potassium Channels/*metabolism ; Receptors, Kainic Acid ; Receptors, Neurotransmitter/*metabolism
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    Polyamine depletion and drug-induced chromosomal damage: new results (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tofilon, P J -- Deen, D F -- Marton, L J -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1378.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455236" target="_blank"〉PubMed〈/a〉
    Keywords: Carmustine/toxicity ; Cell Death ; Cells, Cultured ; *DNA Damage ; In Vitro Techniques ; Polyamines/*metabolism ; Sister Chromatid Exchange/drug effects
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    The role of GABAB receptor activation in absence seizures of lethargic (lh/lh) mice (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-27
    Description: Lethargic (lh/lh) mice, which function as an animal model of absence seizures, have spontaneous seizures that have behavioral and electrographic features and anticonvulsant sensitivity similar to those of human absence seizures. Antagonists of the gamma-aminobutyric acidB (GABAB) receptor suppressed these seizures in lethargic mice, whereas agonists of GABAB receptors exacerbated them. Furthermore, GABAB receptor binding and synaptically evoked GABAB receptor-mediated inhibition of N-methyl-D-aspartate responses were selectively increased in lh/lh mice. Therefore, enhanced GABAB receptor-mediated synaptic responses may underlie absence seizures in lh/lh mice, and GABAB receptor antagonists hold promise as anticonvulsants for absence seizures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hosford, D A -- Clark, S -- Cao, Z -- Wilson, W A Jr -- Lin, F H -- Morrisett, R A -- Huin, A -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):398-401.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University, Durham, NC.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/pharmacology ; Baclofen/analogs & derivatives/pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Electroencephalography ; Electrophysiology ; Epilepsy, Absence/drug therapy/*physiopathology ; Hippocampus/drug effects/physiology ; In Vitro Techniques ; Mice ; Mice, Inbred Strains ; Organophosphorus Compounds/pharmacology ; Picrotoxin/pharmacology ; Quinoxalines/pharmacology ; Receptors, GABA-A/*physiology ; Receptors, N-Methyl-D-Aspartate/metabolism
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  • 89
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    GnRH-induced Ca2+ oscillations and rhythmic hyperpolarizations of pituitary gonadotropes (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-01-24
    Description: Secretion of gonadotropic hormones from pituitary gonadotropes in response to gonadotropin-releasing hormone (GnRH) is essential for regulation of reproductive potential. Gonadotropes from male rats exhibited an unusual form of cellular excitation that resulted from periodic membrane hyperpolarization. GnRH induced an oscillatory release of intracellular Ca2+ via a guanosine triphosphate (GTP) binding protein-coupled phosphoinositide pathway and hyperpolarized the gonadotrope periodically by opening apamin-sensitive Ca(2+)-activated K+ (SK) channels. Each hyperpolarization was terminated by firing of a few action potentials that may result from removal of inactivation from voltage-gated Na+ and Ca2+ channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, A -- Hille, B -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):462-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734523" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apamin/pharmacology ; Calcium/*metabolism ; Cells, Cultured ; GTP-Binding Proteins/physiology ; Gonadotropin-Releasing Hormone/*physiology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate/physiology ; Membrane Potentials ; Periodicity ; Pituitary Gland, Anterior/cytology/*physiology ; Potassium Channels/physiology ; Rats
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    Encoding of a homolog of the IFN-gamma receptor by myxoma virus (1992)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1992-11-20
    Description: Many poxvirus-encoded virulence factors have been identified as proteins that are secreted from infected cells. The major secreted protein (37 kilodaltons) from cells infected with myxoma virus is encoded by the M-T7 open reading frame. This protein has significant sequence similarity to the human and mouse receptors for interferon-gamma (IFN-gamma). Furthermore, the myxoma M-T7 protein specifically binds rabbit IFN-gamma and inhibits the biological activity of extracellular IFN-gamma, one of the key regulatory cytokines in the host immune response against viral infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, C -- Mossman, K -- McFadden, G -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1369-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Alberta, Edmonton, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1455233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cloning, Molecular ; *Genes, Viral ; In Vitro Techniques ; Interferon-gamma/metabolism ; Molecular Sequence Data ; Myxoma virus/*genetics/pathogenicity ; Protein Binding ; Rabbits ; Receptors, Interferon/*genetics ; Restriction Mapping ; Sequence Alignment ; Sequence Homology, Amino Acid ; Viral Interference ; Viral Proteins/*genetics ; Viral Structural Proteins/*genetics
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  • 91
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    Mediation of responses to calcium in taste cells by modulation of a potassium conductance (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-04-05
    Description: Calcium salts are strong taste stimuli in vertebrate animals. However, the chemosensory transduction mechanisms for calcium are not known. In taste buds of Necturus maculosus (mud puppy), calcium evokes depolarizing receptor potentials by acting extracellularly on the apical ends of taste cells to block a resting potassium conductance. Therefore, divalent cations elicit receptor potentials in taste cells by modulating a potassium conductance rather than by permeating the cell membrane, the mechanism utilized by monovalent cations such as sodium and potassium ions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bigiani, A R -- Roper, S D -- 2 POI NS 20486/NS/NINDS NIH HHS/ -- 2 RO1 NS24107/NS/NINDS NIH HHS/ -- 5 RO1 AG06557/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1991 Apr 5;252(5002):126-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2011748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cadmium/pharmacology ; Calcium/*physiology ; Electric Conductivity ; In Vitro Techniques ; Membrane Potentials ; Necturus ; Potassium/*physiology ; Potassium Channels/*physiology ; Taste/*physiology ; Tetraethylammonium Compounds/pharmacology ; Tongue/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Receptor-induced conformation change of the immunosuppressant cyclosporin A (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wuthrich, K -- von Freyberg, B -- Weber, C -- Wider, G -- Traber, R -- Widmer, H -- Braun, W -- New York, N.Y. -- Science. 1991 Nov 15;254(5034):953-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molekularbiologie und Biophysik, Eidgenossische Technische Hochschule-Honggerberg, Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1948082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Isomerases/*ultrastructure ; Carrier Proteins/*ultrastructure ; *Cyclosporine/chemistry ; Hydrogen Bonding ; In Vitro Techniques ; Ligands ; Magnetic Resonance Spectroscopy ; Molecular Conformation ; Molecular Structure ; Peptidylprolyl Isomerase ; Protein Binding
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 93
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    Lysyl oxidase and rrg messenger RNA (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-08-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kenyon, K -- Contente, S -- Trackman, P C -- Tang, J -- Kagan, H M -- Friedman, R M -- P01 HL13262/HL/NHLBI NIH HHS/ -- R01 CA37351-04A1/CA/NCI NIH HHS/ -- R37 AR18880/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Aug 16;253(5021):802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1678898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blotting, Northern ; Cell Line ; *Cell Transformation, Neoplastic ; Gene Expression ; *Genes, Tumor Suppressor ; In Vitro Techniques ; Mice ; Protein-Lysine 6-Oxidase/*physiology ; RNA, Messenger/genetics
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  • 94
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    Function of the homeodomain protein GHF1 in pituitary cell proliferation (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: Mutations that cause pituitary dwarfism in the mouse reside in the gene encoding the transcription factor growth hormone factor 1 (GHF1 or pit1). These dwarf mice (dw and dwJ) are deficient in growth hormone (GH) and prolactin (PRL) synthesis and exhibit pituitary hypoplasia, suggesting a stem cell defect. With antisense oligonucleotide technology, a cell culture model of this genetic defect was developed. Specific inhibition of GHF1 synthesis by complementary oligonucleotides led to a marked decrease in GH and PRL expression and to a marked decrease in proliferation of somatotrophic cell lines. These results provide direct evidence that the homeodomain protein GHF1 is required not only for the establishment and maintenance of the differentiated phenotype but for cell proliferation as well.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castrillo, J L -- Theill, L E -- Karin, M -- DK38527/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):197-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1677216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antisense Elements (Genetics) ; Base Sequence ; *Cell Division ; Cells, Cultured ; DNA/biosynthesis ; DNA-Binding Proteins/*physiology ; Dwarfism/genetics ; Gene Expression Regulation ; *Genes, Homeobox ; Growth Hormone/genetics ; In Vitro Techniques ; Mice ; Molecular Sequence Data ; Pituitary Gland/*cytology/physiology ; Prolactin/genetics ; Transcription Factor Pit-1 ; Transcription Factors/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Recognition of self antigens by skin-derived T cells with invariant gamma delta antigen receptors (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-06-07
    Description: Thy-1+ dendritic epidermal T cells (dECs) express invariant gamma delta antigen receptors and are found in intimate contact with keratinocytes in murine epidermis--thus raising the possibility that keratinocytes express a ligand for the antigen receptor of these T cells. Thy-1+ dECs were stimulated to produce lymphokines by interaction with keratinocytes in vitro. This stimulation was mediated through the dEC antigen receptor and did not appear to be restricted by the major histocompatibility complex. Thus, dECs can recognize self antigens and may participate in immune surveillance for cellular damage rather than for foreign antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Havran, W L -- Chien, Y H -- Allison, J P -- AI26942/AI/NIAID NIH HHS/ -- CA40041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1430-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1828619" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*immunology ; Cell Line ; Dendrites/immunology ; Epidermis ; *Immunity, Cellular ; In Vitro Techniques ; Interleukin-2/secretion ; Keratinocytes/physiology ; Mice ; Mice, Inbred BALB C ; Receptors, Antigen, T-Cell/*physiology ; Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocytes/*immunology
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  • 96
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    Excitatory synaptic responses mediated by GABAA receptors in the hippocampus (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-09-20
    Description: Gamma-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the cortex. Activation of postsynaptic GABAA receptors hyperpolarizes cells and inhibits neuronal activity. Synaptic responses mediated by GABAA receptors also strongly excited hippocampal neurons. This excitatory response was recorded in morphologically identified interneurons in the presence of 4-aminopyridine or after elevation of extracellular potassium concentrations. The synaptic excitation sustained by GABAA receptors synchronized the activity of inhibitory interneurons. This synchronized discharge of interneurons in turn elicited large-amplitude inhibitory postsynaptic potentials in pyramidal and granule cells. Excitatory synaptic responses mediated by GABAA receptors may thus provide a mechanism for the recruitment of GABAergic interneurons through their recurrent connections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michelson, H B -- Wong, R K -- New York, N.Y. -- Science. 1991 Sep 20;253(5026):1420-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, State University of New York, Brooklyn 11203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1654594" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Aminopyridine/pharmacology ; Animals ; Atropine/*pharmacology ; Evoked Potentials/drug effects ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Neurons/drug effects/*physiology ; Propranolol/*pharmacology ; Receptors, GABA-A/drug effects/*physiology ; Synapses/drug effects/*physiology
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  • 97
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    Stereospecific effects of inhalational general anesthetic optical isomers on nerve ion channels (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-10-18
    Description: Although it is generally agreed that general anesthetics ultimately act on neuronal ion channels, there is considerable controversy over whether this occurs by direct binding to protein or secondarily by nonspecific perturbation of lipids. Very pure optical isomers of the inhalational general anesthetic isoflurane exhibited clear stereoselectivity in their effects on particularly sensitive ion channels in identified molluscan central nervous system neurons. At the human median effect dose (ED50) for general anesthesia, the (+)-isomer was about twofold more effective than the (-)-isomer both in eliciting the anesthetic-activated potassium current IK(An) and in inhibiting a current mediated by neuronal nicotinic acetylcholine receptors. For inhibiting the much less sensitive transient potassium current IA, the (-)-isomer was marginally more potent than the (+)-isomer. Both isomers were equally effective at disrupting lipid bilayers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Franks, N P -- Lieb, W R -- GM 41609/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Oct 18;254(5030):427-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Blackett Laboratory, Imperial College of Science, Technology & Medicine, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925602" target="_blank"〉PubMed〈/a〉
    Keywords: Anesthesia, Inhalation ; Anesthetics, Dissociative ; Animals ; In Vitro Techniques ; Isoflurane/*pharmacology ; Lipid Bilayers/chemistry ; Lymnaea ; Neurons/*drug effects/metabolism ; Potassium Channels/*drug effects ; Receptors, Nicotinic/drug effects ; Stereoisomerism ; Thermodynamics
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  • 98
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    Requirement of heparan sulfate for bFGF-mediated fibroblast growth and myoblast differentiation (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-06-21
    Description: Basic fibroblast growth factor (bFGF) binds to heparan sulfate proteoglycans at the cell surface and to receptors with tyrosine kinase activity. Prevention of binding between cell surface heparan sulfate and bFGF (i) substantially reduces binding of fibroblast growth factor to its cell-surface receptors, (ii) blocks the ability of bFGF to support the growth of Swiss 3T3 fibroblasts, and (iii) induces terminal differentiation of MM14 skeletal muscle cells, which is normally repressed by fibroblast growth factor. These results indicate that cell surface heparan sulfate is directly involved in bFGF cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapraeger, A C -- Krufka, A -- Olwin, B B -- 5T32H007118/PHS HHS/ -- AR39467/AR/NIAMS NIH HHS/ -- HD21881/HD/NICHD NIH HHS/ -- R01 AR039467/AR/NIAMS NIH HHS/ -- R01 HD021881/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 21;252(5013):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Wisconsin, Madison 53706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1646484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cell Line ; Chlorates/pharmacology ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*cytology ; Heparitin Sulfate/*physiology ; In Vitro Techniques ; Mice ; Muscles/*cytology ; Polysaccharide-Lyases/pharmacology ; Protein Binding ; Receptors, Cell Surface/metabolism ; Structure-Activity Relationship
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  • 99
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    Demonstration that CFTR is a chloride channel by alteration of its anion selectivity (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-12
    Description: Expression of the cystic fibrosis transmembrane conductance regulator (CFTR) generates adenosine 3',5'-monophosphate (cAMP)-regulated chloride channels, indicating that CFTR is either a chloride channel or a chloride channel regulator. To distinguish between these possibilities, basic amino acids in the putative transmembrane domains were mutated. The sequence of anion selectivity of cAMP-regulated channels in cells containing either endogenous or recombinant CFTR was bromide greater than chloride greater than iodide greater than fluoride. Mutation of the lysines at positions 95 or 335 to acidic amino acids converted the selectivity sequence to iodide greater than bromide greater than chloride greater than fluoride. These data indicate that CFTR is a cAMP-regulated chloride channel and that lysines 95 and 335 determine anion selectivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Gregory, R J -- Thompson, S -- Souza, D W -- Paul, S -- Mulligan, R C -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1712984" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chloride Channels ; Chlorides/*physiology ; Cyclic AMP/physiology ; Cystic Fibrosis/physiopathology ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA Mutational Analysis ; Electric Conductivity ; HeLa Cells ; Humans ; In Vitro Techniques ; Ion Channels/genetics/*physiology ; Membrane Glycoproteins/genetics/physiology ; Membrane Potentials ; Membrane Proteins/genetics/*physiology ; Molecular Sequence Data ; Transfection
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  • 100
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    Requirement of nuclear prolactin for interleukin-2--stimulated proliferation of T lymphocytes (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-07-05
    Description: Prolactin (PRL) is necessary for the proliferation of cloned T lymphocytes in response to interleukin-2 (IL-2). Translocation of PRL into the nucleus occurs during IL-2--stimulated mitogenesis. Therefore, the function of intranuclear PRL in T cell proliferation was tested. Eukaryotic expression vectors were prepared to express wild-type PRL [PRL(WT)], PRL that lacks the signal sequence for translocation into the endoplasmic reticulum [PRL(ER-)], and chimeric PRL in which the signal peptide was replaced with the sequence that directs the nuclear translocation of the SV40 large T antigen [PRL(NT+)]. Expression of these constructs in a T cell line (Nb2) responsive to PRL and IL-2 resulted in localization of PRL in the extracellular milieu, cytoplasm, or nucleus, respectively. Stimulation with IL-2 alone resulted in a five- to tenfold increase in the incorporation of [3H]thymidine by cells expressing PRL(NT+) or PRL(WT) as compared to PRL(ER-) or the parental Nb2 cells. Only the PRL(NT+) clone proliferated continuously with IL-2 stimulation in the presence of antiserum to PRL. These results demonstrate that nuclear PRL is necessary for IL-2--stimulated proliferation and suggest that a peptide hormone can function in the nucleus without binding to its cell surface receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clevenger, C V -- Altmann, S W -- Prystowsky, M B -- GM-13901/GM/NIGMS NIH HHS/ -- GM-36962/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 5;253(5015):77-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2063207" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport, Active ; Cell Cycle/drug effects ; Cell Nucleus/metabolism ; Drug Synergism ; Genetic Vectors ; In Vitro Techniques ; Interleukin-2/pharmacology ; Lymphocyte Activation/*drug effects ; Molecular Sequence Data ; Prolactin/pharmacokinetics/*pharmacology ; Rats ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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