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  • American Association for the Advancement of Science (AAAS)  (7)
  • American Chemical Society (ACS)
  • Copernicus
  • 2010-2014  (7)
  • 1980-1984
  • 1975-1979
  • 2010  (7)
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  • 2010-2014  (7)
  • 1980-1984
  • 1975-1979
Year
  • 1
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    Spiroindolones, a potent compound class for the treatment of malaria (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Recent reports of increased tolerance to artemisinin derivatives--the most recently adopted class of antimalarials--have prompted a need for new treatments. The spirotetrahydro-beta-carbolines, or spiroindolones, are potent drugs that kill the blood stages of Plasmodium falciparum and Plasmodium vivax clinical isolates at low nanomolar concentration. Spiroindolones rapidly inhibit protein synthesis in P. falciparum, an effect that is ablated in parasites bearing nonsynonymous mutations in the gene encoding the P-type cation-transporter ATPase4 (PfATP4). The optimized spiroindolone NITD609 shows pharmacokinetic properties compatible with once-daily oral dosing and has single-dose efficacy in a rodent malaria model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050001/" 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/PMC3050001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rottmann, Matthias -- McNamara, Case -- Yeung, Bryan K S -- Lee, Marcus C S -- Zou, Bin -- Russell, Bruce -- Seitz, Patrick -- Plouffe, David M -- Dharia, Neekesh V -- Tan, Jocelyn -- Cohen, Steven B -- Spencer, Kathryn R -- Gonzalez-Paez, Gonzalo E -- Lakshminarayana, Suresh B -- Goh, Anne -- Suwanarusk, Rossarin -- Jegla, Timothy -- Schmitt, Esther K -- Beck, Hans-Peter -- Brun, Reto -- Nosten, Francois -- Renia, Laurent -- Dartois, Veronique -- Keller, Thomas H -- Fidock, David A -- Winzeler, Elizabeth A -- Diagana, Thierry T -- R01 AI059472/AI/NIAID NIH HHS/ -- R01 AI059472-04/AI/NIAID NIH HHS/ -- R01 AI059472-05/AI/NIAID NIH HHS/ -- R01AI059472/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1175-80. doi: 10.1126/science.1193225.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Tropical and Public Health Institute, Parasite Chemotherapy, CH-4002 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813948" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/antagonists & inhibitors/chemistry/genetics/metabolism ; Animals ; Antimalarials/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Cell Line ; Drug Discovery ; Drug Resistance ; Erythrocytes/parasitology ; Female ; Genes, Protozoan ; Humans ; Indoles/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Malaria/*drug therapy/parasitology ; Male ; Mice ; Models, Molecular ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Mutation ; Parasitic Sensitivity Tests ; Plasmodium berghei/*drug effects ; Plasmodium falciparum/*drug effects/genetics/growth & development ; Plasmodium vivax/*drug effects/growth & development ; Protein Synthesis Inhibitors/administration & ; dosage/chemistry/pharmacokinetics/pharmacology ; Protozoan Proteins/biosynthesis/chemistry/genetics/metabolism ; Rats ; Rats, Wistar ; Spiro Compounds/administration & dosage/chemistry/pharmacokinetics/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    The calcium store sensor, STIM1, reciprocally controls Orai and CaV1.2 channels (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Calcium signals, pivotal in controlling cell function, can be generated by calcium entry channels activated by plasma membrane depolarization or depletion of internal calcium stores. We reveal a regulatory link between these two channel subtypes mediated by the ubiquitous calcium-sensing STIM proteins. STIM1 activation by store depletion or mutational modification strongly suppresses voltage-operated calcium (Ca(V)1.2) channels while activating store-operated Orai channels. Both actions are mediated by the short STIM-Orai activating region (SOAR) of STIM1. STIM1 interacts with Ca(V)1.2 channels and localizes within discrete endoplasmic reticulum/plasma membrane junctions containing both Ca(V)1.2 and Orai1 channels. Hence, STIM1 interacts with and reciprocally controls two major calcium channels hitherto thought to operate independently. Such coordinated control of the widely expressed Ca(V)1.2 and Orai channels has major implications for Ca(2+) signal generation in excitable and nonexcitable cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601900/" 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/PMC3601900/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Youjun -- Deng, Xiaoxiang -- Mancarella, Salvatore -- Hendron, Eunan -- Eguchi, Satoru -- Soboloff, Jonathan -- Tang, Xiang D -- Gill, Donald L -- AI058173/AI/NIAID NIH HHS/ -- HL55426/HL/NHLBI NIH HHS/ -- R01 AI058173/AI/NIAID NIH HHS/ -- R01 HL055426/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):105-9. doi: 10.1126/science.1191086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Cardiovascular Research Center, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Calcium Channels, L-Type/*metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Glycoproteins/chemistry/genetics/*metabolism ; Muscle, Smooth, Vascular/cytology ; Mutant Proteins/metabolism ; Myocytes, Smooth Muscle/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; Rats ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    A gating charge transfer center in voltage sensors (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-03
    Description: Voltage sensors regulate the conformations of voltage-dependent ion channels and enzymes. Their nearly switchlike response as a function of membrane voltage comes from the movement of positively charged amino acids, arginine or lysine, across the membrane field. We used mutations with natural and unnatural amino acids, electrophysiological recordings, and x-ray crystallography to identify a charge transfer center in voltage sensors that facilitates this movement. This center consists of a rigid cyclic "cap" and two negatively charged amino acids to interact with a positive charge. Specific mutations induce a preference for lysine relative to arginine. By placing lysine at specific locations, the voltage sensor can be stabilized in different conformations, which enables a dissection of voltage sensor movements and their relation to ion channel opening.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2869078/" 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/PMC2869078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tao, Xiao -- Lee, Alice -- Limapichat, Walrati -- Dougherty, Dennis A -- MacKinnon, Roderick -- GM43949/GM/NIGMS NIH HHS/ -- NS 34407/NS/NINDS NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 GM043949/GM/NIGMS NIH HHS/ -- R01 GM043949-20/GM/NIGMS NIH HHS/ -- R37 NS034407/NS/NINDS NIH HHS/ -- R37 NS034407-15/NS/NINDS NIH HHS/ -- R37 NS034407-15S1/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 2;328(5974):67-73. doi: 10.1126/science.1185954.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neurobiology and Biophysics, Rockefeller University, Howard Hughes Medical Institute, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360102" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Arginine/chemistry ; Binding Sites ; Crystallography, X-Ray ; Electric Capacitance ; *Ion Channel Gating ; Kv1.2 Potassium Channel/*chemistry/*metabolism ; Lysine/chemistry ; Models, Molecular ; Molecular Sequence Data ; Patch-Clamp Techniques ; Phenylalanine/chemistry ; Protein Conformation ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Shab Potassium Channels/*chemistry/*metabolism ; Shaker Superfamily of Potassium Channels/chemistry/metabolism ; Tryptophan/chemistry ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cell biology. How to STIMulate calcium channels (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133971/" 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/PMC3133971/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cahalan, Michael D -- R37 NS014609/NS/NINDS NIH HHS/ -- R37 NS014609-33/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):43-4. doi: 10.1126/science.1196348.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of California, Irvine, CA 92697, USA. mcahalan@uci.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channel Blockers/metabolism ; Calcium Channels/*metabolism ; Calcium Channels, L-Type/chemistry/*metabolism ; Calcium Signaling ; Cell Membrane/*metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Lymphocytes/metabolism ; Membrane Glycoproteins/chemistry/*metabolism ; Membrane Proteins/chemistry/*metabolism ; Neoplasm Proteins/chemistry/*metabolism ; Neurons/metabolism ; Protein Structure, Tertiary ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Paradoxical false memory for objects after brain damage (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Poor memory after brain damage is usually considered to be a result of information being lost or rendered inaccessible. It is assumed that such memory impairment must be due to the incorrect interpretation of previously encountered information as being novel. In object recognition memory experiments with rats, we found that memory impairment can take the opposite form: a tendency to treat novel experiences as familiar. This impairment could be rescued with the use of a visual-restriction procedure that reduces interference. Such a pattern of data can be explained in terms of a recent representational-hierarchical view of cognition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McTighe, Stephanie M -- Cowell, Rosemary A -- Winters, Boyer D -- Bussey, Timothy J -- Saksida, Lisa M -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1408-10. doi: 10.1126/science.1194780.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Psychology, University of Cambridge, Cambridge CB2 3EB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127256" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/physiopathology ; Animals ; Brain Injuries/*physiopathology ; Brain Mapping ; Cognition ; Darkness ; Male ; *Memory ; Memory Disorders/*physiopathology ; Models, Neurological ; Neural Pathways/physiology ; Random Allocation ; Rats ; *Recognition (Psychology) ; Sensory Deprivation ; Temporal Lobe/*injuries/*physiopathology ; Vision, Ocular
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Dynamic Ca2+-dependent stimulation of vesicle fusion by membrane-anchored synaptotagmin 1 (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: In neurons, synaptotagmin 1 (Syt1) is thought to mediate the fusion of synaptic vesicles with the plasma membrane when presynaptic Ca2+ levels rise. However, in vitro reconstitution experiments have failed to recapitulate key characteristics of Ca2+-triggered membrane fusion. Using an in vitro single-vesicle fusion assay, we found that membrane-anchored Syt1 enhanced Ca2+ sensitivity and fusion speed. This stimulatory activity of membrane-anchored Syt1 dropped as the Ca2+ level rose beyond physiological levels. Thus, Syt1 requires the membrane anchor to stimulate vesicle fusion at physiological Ca2+ levels and may function as a dynamic presynaptic Ca2+ sensor to control the probability of neurotransmitter release.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994549/" 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/PMC2994549/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Han-Ki -- Yang, Yoosoo -- Su, Zengliu -- Hyeon, Changbong -- Lee, Tae-Sun -- Lee, Hong-Won -- Kweon, Dae-Hyuk -- Shin, Yeon-Kyun -- Yoon, Tae-Young -- R01 GM051290/GM/NIGMS NIH HHS/ -- R01 GM051290-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 May 7;328(5979):760-3. doi: 10.1126/science.1187722.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, KAIST, Daejeon 305-701, South Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Magnesium/metabolism ; *Membrane Fusion ; Membrane Lipids/metabolism ; Neurotransmitter Agents/metabolism ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Rats ; SNARE Proteins/metabolism ; Synaptic Vesicles/*physiology ; Synaptotagmin I/chemistry/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    The asynchronous state in cortical circuits (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-30
    Description: Correlated spiking is often observed in cortical circuits, but its functional role is controversial. It is believed that correlations are a consequence of shared inputs between nearby neurons and could severely constrain information decoding. Here we show theoretically that recurrent neural networks can generate an asynchronous state characterized by arbitrarily low mean spiking correlations despite substantial amounts of shared input. In this state, spontaneous fluctuations in the activity of excitatory and inhibitory populations accurately track each other, generating negative correlations in synaptic currents which cancel the effect of shared input. Near-zero mean correlations were seen experimentally in recordings from rodent neocortex in vivo. Our results suggest a reexamination of the sources underlying observed correlations and their functional consequences for information processing.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861483/" 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/PMC2861483/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Renart, Alfonso -- de la Rocha, Jaime -- Bartho, Peter -- Hollender, Liad -- Parga, Nestor -- Reyes, Alex -- Harris, Kenneth D -- DC-005787-01A1/DC/NIDCD NIH HHS/ -- DC009947/DC/NIDCD NIH HHS/ -- MH073245/MH/NIMH NIH HHS/ -- R01 DC009947/DC/NIDCD NIH HHS/ -- R01 DC009947-02/DC/NIDCD NIH HHS/ -- R01 MH073245/MH/NIMH NIH HHS/ -- R01 MH073245-05/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):587-90. doi: 10.1126/science.1179850.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA. arenart@andromeda.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110507" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Algorithms ; Animals ; Cerebral Cortex/cytology/*physiology ; Computer Simulation ; Excitatory Postsynaptic Potentials ; Inhibitory Postsynaptic Potentials ; *Models, Neurological ; Nerve Net/*physiology ; Neural Inhibition ; Neural Pathways/*physiology ; Neurons/*physiology ; Rats ; Rats, Sprague-Dawley ; Synapses/*physiology ; *Synaptic Potentials ; Synaptic Transmission
    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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