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  • 1
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    Regulation of chloride channels by protein kinase C in normal and cystic fibrosis airway epithelia (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: Apical membrane chloride channels control chloride secretion by airway epithelial cells. Defective regulation of these channels is a prominent characteristic of cystic fibrosis. In normal intact cells, activation of protein kinase C (PKC) by phorbol ester either stimulated or inhibited chloride secretion, depending on the physiological status of the cell. In cell-free membrane patches, PKC also had a dual effect: at a high calcium concentration, PKC inactivated chloride channels; at a low calcium concentration, PKC activated chloride channels. In cystic fibrosis cells, PKC-dependent channel inactivation was normal, but activation was defective. Thus it appears that PKC phosphorylates and regulates two different sites on the channel or on an associated membrane protein, one of which is defective in cystic fibrosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, M -- McCann, J D -- Anderson, M P -- Clancy, J P -- Liedtke, C M -- Nairn, A C -- Greengard, P -- Welsch, M J -- DK27651/DK/NIDDK NIH HHS/ -- HL29851/HL/NHLBI NIH HHS/ -- HL42385/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Membrane Transport, 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/2472006" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/physiology ; Chloride Channels ; Chlorides/*physiology ; Cystic Fibrosis/*physiopathology ; Enzyme Activation ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Protein Kinase C/*physiology ; Respiratory Physiological Phenomena ; Respiratory System/cytology/*physiopathology ; Tetradecanoylphorbol Acetate/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Demonstration that CFTR is a chloride channel by alteration of its anion selectivity (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Generation of cAMP-activated chloride currents by expression of CFTR (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-08
    Description: Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis. In order to evaluate its function, CFTR was expressed in HeLa, Chinese hamster ovary (CHO), and NIH 3T3 fibroblast cells, and anion permeability was assessed with a fluorescence microscopic assay and the whole-cell patch-clamp technique. Adenosine 3',5'-monophosphate (cAMP) increased anion permeability and chloride currents in cells expressing CFTR, but not in cells expressing a mutant CFTR (delta F508) or in nontransfected cells. The simplest interpretation of these observations is that CFTR is itself a cAMP-activated chloride channel. The alternative interpretation, that CFTR directly or indirectly regulates chloride channels, requires that these cells have endogenous cryptic, chloride channels that are stimulated by cAMP only in the presence of CFTR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Rich, D P -- Gregory, R J -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Feb 8;251(4994):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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/1704151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chloride Channels ; Chlorides/*metabolism ; Cricetinae ; Cyclic AMP/*physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Humans ; Membrane Proteins/*metabolism/*physiology ; Mice ; Mutation ; Recombinant Proteins ; Structure-Activity Relationship
    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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    Correction (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-12-11
    Description: In the final preparation of the manuscript of our report "Regulation by ATP and ADP of CFTR chloride channels that contain mutant nucleotide-binding domains" (18 Sept., p. 1701) (1), we inadvertently plotted the data for figure 1C with an incorrect x axis: MgATP was plotted on the x axis instead of P(o). We did not immediately notice the error, which was brought to our attention by Charles Venglarik and Robert Bridges, because the shape of the two curves is similiar. The correct plot is shown in the figure below. In both plots the data do not fit a straight [See figure in the PDF file] line, which supports our interpretation that more than one site may be involved with adenosine triphosphate (ATP) regulation of the cystic fibrosis transmembrane conductance regulator (CFTR). We regret any inconvenience this may have caused.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welsh, M J -- Anderson, M P -- New York, N.Y. -- Science. 1992 Dec 11;258(5089):1719.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17831643" target="_blank"〉PubMed〈/a〉
    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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    Effect of deleting the R domain on CFTR-generated chloride channels (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-07-12
    Description: The cystic fibrosis transmembrane conductance regulator (CFTR), which forms adenosine 3',5'-monophosphate (cAMP)-regulated chloride channels, is defective in patients with cystic fibrosis. This protein contains two putative nucleotide binding domains (NBD1 and NBD2) and an R domain. CFTR in which the R domain was deleted (CFTR delta R) conducted chloride independently of the presence of cAMP. However, sites within CFTR other than those deleted also respond to cAMP, because the chloride current of CFTR delta R increased further in response to cAMP stimulation. In addition, deletion of the R domain suppressed the inactivating effect of a mutation in NBD2 (but not NBD1), a result which suggests that NBD2 interacts with the channel through the R domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rich, D P -- Gregory, R J -- Anderson, M P -- Manavalan, P -- Smith, A E -- Welsh, M J -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):205-7.〈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/1712985" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Chloride Channels ; Chlorides/*physiology ; Cyclic AMP/physiology ; Cystic Fibrosis ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA Mutational Analysis ; Electric Conductivity ; HeLa Cells ; Humans ; In Vitro Techniques ; Ion Channel Gating ; Ion Channels/chemistry/*physiology ; Membrane Potentials ; Membrane Proteins/chemistry/*physiology ; Nitrates/metabolism ; Structure-Activity Relationship ; 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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  • 6
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    Regulation by ATP and ADP of CFTR chloride channels that contain mutant nucleotide-binding domains (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-09-18
    Description: Regulation of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is unusual in that phosphorylated channels require cytosolic adenosine triphosphate (ATP) to open. The CFTR contains two regions predicted to be nucleotide-binding domains (NBDs); site-directed mutations in each NBD have now been shown to alter the relation between ATP concentration and channel activity, which indicates that ATP stimulates the channel by direct interaction with both NBDs. The two NBDs are not, however, functionally equivalent: adenosine diphosphate (ADP) competitively inhibited the channel by interacting with NBD2 but not by interacting with NBD1. Four cystic fibrosis-associated mutations in the NBDs reduced absolute chloride channel activity, and one mutation also decreased the potency with which ATP stimulates channel activity. Dysfunction of ATP-dependent stimulation through the NBDs may be the basis for defective CFTR chloride channel activity in some cystic fibrosis patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, M P -- Welsh, M J -- New York, N.Y. -- Science. 1992 Sep 18;257(5077):1701-4.〈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/1382316" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/*pharmacology ; Adenosine Triphosphate/*pharmacology ; Amino Acid Sequence ; Animals ; Binding Sites/genetics ; Binding, Competitive ; Cell Line ; Chloride Channels ; Cyclic AMP/pharmacology ; Cystic Fibrosis/*genetics ; Cystic Fibrosis Transmembrane Conductance Regulator ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Nucleotides/*metabolism ; Protein Kinases/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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    Transplanted hypothalamic neurons restore leptin signaling and ameliorate obesity in db/db mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-26
    Description: Evolutionarily old and conserved homeostatic systems in the brain, including the hypothalamus, are organized into nuclear structures of heterogeneous and diverse neuron populations. To investigate whether such circuits can be functionally reconstituted by synaptic integration of similarly diverse populations of neurons, we generated physically chimeric hypothalami by microtransplanting small numbers of embryonic enhanced green fluorescent protein-expressing, leptin-responsive hypothalamic cells into hypothalami of postnatal leptin receptor-deficient (db/db) mice that develop morbid obesity. Donor neurons differentiated and integrated as four distinct hypothalamic neuron subtypes, formed functional excitatory and inhibitory synapses, partially restored leptin responsiveness, and ameliorated hyperglycemia and obesity in db/db mice. These experiments serve as a proof of concept that transplanted neurons can functionally reconstitute complex neuronal circuitry in the mammalian brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770458/" 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/PMC3770458/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czupryn, Artur -- Zhou, Yu-Dong -- Chen, Xi -- McNay, David -- Anderson, Matthew P -- Flier, Jeffrey S -- Macklis, Jeffrey D -- DKR37-28082/PHS HHS/ -- K02 NS054674/NS/NINDS NIH HHS/ -- NS054674/NS/NINDS NIH HHS/ -- NS057444/NS/NINDS NIH HHS/ -- NS070295/NS/NINDS NIH HHS/ -- NS41590/NS/NINDS NIH HHS/ -- NS45523/NS/NINDS NIH HHS/ -- NS49553/NS/NINDS NIH HHS/ -- R01 NS041590/NS/NINDS NIH HHS/ -- R01 NS045523/NS/NINDS NIH HHS/ -- R01 NS049553/NS/NINDS NIH HHS/ -- R01 NS057444/NS/NINDS NIH HHS/ -- R21 NS070295/NS/NINDS NIH HHS/ -- R37 DK028082/DK/NIDDK NIH HHS/ -- R37 NS041590/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 25;334(6059):1133-7. doi: 10.1126/science.1209870.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell and Regenerative Biology, and Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22116886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/analysis ; Body Weight ; Cell Shape ; Electrophysiological Phenomena ; Excitatory Postsynaptic Potentials ; Glucose/administration & dosage ; Hypothalamus/*cytology/metabolism ; Hypothalamus, Middle/*cytology/metabolism/*physiopathology ; Inhibitory Postsynaptic Potentials ; Insulin/administration & dosage/blood ; Leptin/administration & dosage/*metabolism ; Membrane Potentials ; Mice ; Mice, Obese ; Neurogenesis ; Neurons/cytology/*physiology/*transplantation ; Obesity/metabolism/*physiopathology/*therapy ; Receptors, Leptin/*metabolism ; Signal Transduction ; 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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  • 8
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    Depositional Sequences and Hydrocarbon Exploration in Wilcox Group, South Texas: ABSTRACT (1988)
    American Association of Petroleum Geologists
    Details
    Publication Date: 1988-01-01
    Print ISSN: 0149-1423
    Electronic ISSN: 1943-2674
    Topics: Geosciences
    Published by American Association of Petroleum Geologists
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  • 9
    Electronic Resource
    Electronic Resource
    The Young's modulus of silica beads/epoxy composites: Experiments and simulations (1994)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 75 (1994), S. 1442-1455 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The effect of particulate volume fraction vp and diameter dp on the composite Young's modulus Ec is studied both experimentally, using a silica bead/epoxy system, as well as with the help of computer simulations. The experimental and simulation results show that for a given particulate size, the overall Ec vs vp curve displays a concave upward shape and not a linear shape. This superlinear trend of the data implies that the average strain normalized to the applied strain λ=ε¯p/εc transferred to the particulates increases with volume fraction. The above finding is explained in terms of a mean-field picture, where a single particle interacts with an effective medium consisting of the remaining particles embedded in the matrix. As the modulus of the effective medium surrounding a reference particle increases with vp, the modulus mismatch between the reference particulate and the medium is consequently reduced. This leads to an overall increase in the normalized average strain λ transferred to each particulate as vp is increased. The experimental results using silica particulates with various sizes dp, as well as the simulation results, show that smaller particulates provide an increased composite modulus as compared to larger particulates, at constant vp. General equations are developed, which relate the composite modulus to the average particle stress or strain, given only information about the volume fraction and the Young's modulus of each of the phases present.Through the application of these relations, it is found that smaller particulates display a greater amount of normalized average strain λ transferred than larger particulates. The effect of particulate Young's modulus Ep in combination with particulate size on the resulting Ec is also studied using simulations only. It is found that for a low particulate to matrix modulus ratio Ep/Em, the particulate size has very little influence on Ec. Moreover, the shape of the Ec vs vp curve can be well approximated by a straight line up to large values of vp. On the other hand, as the ratio Ep/Em is increased, the superlinear trend of the composite modulus Ec vs vp data is more apparent. This results in a smaller range of the Ec vs vp curve, which can be approximated by a linear function. It is also found that the extent of this linear region also decreases with particle size.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.356378
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of volume fraction and morphology of reinforcing phases in composites (1994)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 75 (1994), S. 1155-1170 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Computer modeling has been employed to study the effect of volume fraction and morphology of second-phase constituents on composite stiffness and strength. It is found that the efficiency of load transfer to the second-phase constituent increases with volume fraction vf for particulate composites. For aligned short-fiber composites, the efficiency of load transfer reaches a limiting value with increasing volume fraction for homogeneous fiber dispersions, while for fiber distributions which allow for fiber-rich and matrix-rich regions, the efficiency of load transfer decreases. The saturation or decrease in load transfer efficiency is due to fiber confinement, by which the interfiber matrix material is constrained by the presence of neighboring fibers. Hence, the amount of shear tractions and load transferred to a given fiber is altered by the local fiber distribution, as compared to the case of an isolated fiber (dilute limit). The strength of brittle particulate composites is reduced for most particulate volume fractions considered, while the strength of aligned short-fiber composites with a homogeneous fiber dispersion is marginally increased only for vf(approximately-greater-than)0.2. The composite strength has a downward concave shape, as a function of vf. This is accounted for by both the saturation in load transfer due to fiber confinement and the lower composite strain at failure (embrittlement) as vf is increased. The strength of viscoelastic aligned short-fiber composites with a homogeneous fiber dispersion displays a higher strength at high fiber volume fractions, as compared to a perfectly brittle matrix, which suggests that matrix toughness plays a key role in the strengthening of short-fiber composites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.356501
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