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  • Articles  (30)
  • Kinetics  (30)
  • 1985-1989  (30)
  • 1987  (30)
  • Science. 235(4795): 1495-8.  (1)
  • Science. 235(4796): 1644-8.  (1)
  • Science. 236(4797): 68-9.  (1)
  • Science. 236(4798): 183-6.  (1)
  • Science. 236(4799): 324-7.  (1)
  • Science. 236(4801): 558-63.  (1)
  • Science. 236(4801): 586-9.  (1)
  • Science. 236(4802): 714-8.  (1)
  • Science. 236(4804): 944-7.  (1)
  • Science. 236(4806): 1295-9.  (1)
  • Science. 236(4806): 1311-5.  (1)
  • Science. 236(4807): 1460-3.  (1)
  • Science. 237(4814): 500-6.  (1)
  • Science. 237(4816): 777-9.  (1)
  • Science. 237(4817): 909-13.  (1)
  • Science. 237(4822): 1618-20.  (1)
  • Science. 238(4825): 373-6.  (1)
  • Science. 238(4826): 486-91.  (1)
  • Science. 238(4826): 533-6.  (1)
  • Science. 238(4827): 638-44.  (1)
  • 25
Collection
  • Articles  (30)
Source
Keywords
Publisher
Years
  • 1985-1989  (30)
Year
Journal
Topic
  • 1
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    Sodium-calcium exchange in heart: membrane currents and changes in [Ca2+]i (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: Recordings have been made of changes in intracellular calcium ion concentration ([Ca2+]i) that can be attributed to the operation of an electrogenic, voltage-dependent sodium-calcium (Na-Ca) exchanger in mammalian heart cells. Guinea pig ventricular myocytes under voltage clamp were perfused internally with fura-2, a fluorescent Ca2+-indicator, and changes in [Ca2+]i and membrane current that resulted from Na-Ca exchange were identified through the use of various organic channel blockers and impermeant ions. Depolarization of cells elicited slow increases in [Ca2+]i, with the maximum increase depending on internal [Na+], external [Ca2+], and membrane voltage. Repolarization was associated with net Ca2+ efflux and a decline in the inward current that developed instantaneously upon repolarization. The relation between [Ca2+]i and current was linear, and the slope was made steeper by hyperpolarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barcenas-Ruiz, L -- Beuckelmann, D J -- Wier, W G -- HL29473/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1720-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Maryland School of Medicine, Baltimore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Carrier Proteins/*physiology ; Cell Membrane/physiology ; Guinea Pigs ; Heart/*physiology ; In Vitro Techniques ; Kinetics ; Membrane Potentials ; Sodium-Calcium Exchanger ; Ventricular Function
    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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    Transformation of rat fibroblasts by FSV rapidly increases glucose transporter gene transcription (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-20
    Description: Elevation of glucose transport is an alteration common to most virally induced tumors. Rat fibroblasts transformed with wild-type or a temperature-sensitive Fujinami sarcoma virus (FSV) were studied in order to determine the mechanisms underlying the increased transport. Five- to tenfold increases in total cellular glucose transporter protein in response to transformation were accompanied by similar increases in transporter messenger RNA levels. This, in turn, was preceded by an absolute increase in the rate of glucose transporter gene transcription within 30 minutes after shift of the temperature-sensitive FSV-transformed cells to the permissive temperature. The transporter messenger RNA levels in transformed fibroblasts were higher than those found in proliferating cells maintained at the nonpermissive temperature. The activation of transporter gene transcription by transformation represents one of the earliest known effects of oncogenesis on the expression of a gene encoding a protein of well-defined function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birnbaum, M J -- Haspel, H C -- Rosen, O M -- AM35430-01/AM/NIADDK NIH HHS/ -- DK 35158/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1495-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3029870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses ; Cell Division ; Cell Line ; *Cell Transformation, Viral ; Fibroblasts ; Gene Expression Regulation ; Kinetics ; Monosaccharide Transport Proteins/*genetics ; RNA, Messenger/genetics ; Rats ; Transcription, Genetic
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  • 3
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    A novel thyroid hormone receptor encoded by a cDNA clone from a human testis library (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-06
    Description: The c-erbA gene belongs to a multigene family that encodes transcriptional regulatory proteins including the v-erbA oncogene product, steroid hormone receptors, and the vitamin D3 receptor. A v-erbA DNA probe encoding the DNA-binding region of the v-erbA protein was used to screen a human complementary DNA testis library. One of the clones isolated, erbA-T-1, was found to encode a 490-amino acid protein (erbA-T). The erbA-T polypeptide shows high homology with the proteins encoded by both the chicken c-erbA and the human c-erbA-beta genes but is most closely related to the chicken gene. The chicken c-erbA and the human c-erbA-beta genes encode high-affinity receptors for thyroid hormone, and here it is shown that the erbA-T protein binds specifically to 3,5,3'-triiodo-L-thyronine with a dissociation constant of 3.8 +/- 0.2 x 10(-10) M. These data imply that more than one thyroid hormone receptor exists in humans and that these receptors might have different tissue- and gene-activating specificities.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benbrook, D -- Pfahl, M -- DK-35083/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):788-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, La Jolla Cancer Research Foundation, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672126" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; *Cloning, Molecular ; DNA/*metabolism ; *Genes ; Humans ; Kinetics ; Male ; Protein Biosynthesis ; *Proto-Oncogenes ; Receptors, Thyroid Hormone/*genetics/metabolism ; Testis/*metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 4
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    Antiarthritic gold compounds effectively quench electronically excited singlet oxygen (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-03
    Description: Although certain gold [Au(I)] compounds have been used effectively in the treatment of rheumatoid arthritis for some years, the molecular basis for such therapeutic action has been unclear. One possible mechanism of the action of Au(I) compounds is that they protect unsaturated membrane lipids and proteins against oxidative degradation caused by activated phagocytes that are not properly regulated. In this study it has been shown that superoxide ion (O-2.), a product of activated phagocytes, can be oxidized to electronically excited singlet oxygen (O1(2)delta g), an agent that is capable of peroxidation of unsaturated fatty acid derivatives. It has also been shown that antiarthritic Au(I) compounds are effective deactivators of O1(2)delta g with quenching constants on the order of 10(7) M-1 sec-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corey, E J -- Mehrotra, M M -- Khan, A U -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):68-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563489" target="_blank"〉PubMed〈/a〉
    Keywords: Arthritis, Rheumatoid/drug therapy ; *Auranofin ; Chemistry, Physical ; Humans ; Kinetics ; Lipid Peroxides ; *Oxygen ; Physicochemical Phenomena
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  • 5
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    Protein kinase C contains a pseudosubstrate prototope in its regulatory domain (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-18
    Description: The regulatory domain of protein kinase C contains an amino acid sequence between residues 19 and 36 that resembles a substrate phosphorylation site in its distribution of basic residue recognition determinants. The corresponding synthetic peptide (Arg19-Phe-Ala-Arg-Lys-Gly-Ala25-Leu-Arg-Gln-Lys-Asn-Val-His -Glu-Val-Lys-Asn36) acts as a potent substrate antagonist with an inhibitory constant of 147 +/- 9 nM. It is a specific inhibitor of protein kinase C and inhibits both autophosphorylation and protein substrate phosphorylation. Substitution of Ala25 with serine transforms the pseudosubstrate into a potent substrate. These results demonstrate that the conserved region of the regulatory domain (residues 19 to 36) of protein kinase C has the secondary structural features of a pseudosubstrate and may be responsible for maintaining the enzyme in the inactive form in the absence of allosteric activators such as phospholipids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉House, C -- Kemp, B E -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1726-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Melbourne, Repatriation General Hospital, West Heidelberg, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686012" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Homeostasis ; Kinetics ; Myosin-Light-Chain Kinase/metabolism ; Protein Kinase C/*metabolism ; Substrate Specificity
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  • 6
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    Identification of nuclear receptors for VIP on a human colonic adenocarcinoma cell line (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: Vasoactive intestinal peptide (VIP) is a neuropeptide with broad tissue distribution. Although its precise function is unknown, it is thought to exert its effect, at least in part, by interacting with cell surface receptors. Nuclear receptors for VIP have now been identified by specific binding of 125I-labeled VIP to nuclei of a human colonic adenocarcinoma cell line (HT29) and by cross-linking of 125I-labeled VIP to its receptor on intact nuclei. In contrast, 125I-labeled transferrin shows only background binding to nuclei but significant binding to intact cells. Purity of the isolated nuclei was further substantiated by electron microscopy. The apparent molecular sizes of the VIP--cross-linked nuclear and cell surface receptors are similar but not identical.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Omary, M B -- Kagnoff, M F -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department 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/2825352" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*metabolism/ultrastructure ; Cell Line ; Cell Nucleus/*metabolism/ultrastructure ; Colonic Neoplasms/*metabolism/ultrastructure ; Humans ; Kinetics ; Microscopy, Electron ; Receptors, Gastrointestinal Hormone/*metabolism ; Receptors, Vasoactive Intestinal Peptide ; Vasoactive Intestinal Peptide/*metabolism
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  • 7
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    Regulation of bcl-2 proto-oncogene expression during normal human lymphocyte proliferation (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: The bcl-2 and c-myc proto-oncogenes are brought into juxtaposition with the immunoglobulin heavy chain locus in particular B-cell lymphomas, resulting in high levels of constitutive accumulation of their messenger RNAs. Precisely how the products of the bcl-2 and c-myc genes contribute to tumorigenesis is unknown, but observations that c-myc expression is rapidly induced in nonneoplastic lymphocytes upon stimulation of proliferation raise the possibility that this proto-oncogene is involved in the control of normal cellular growth. In addition to c-myc, the bcl-2 proto-oncogene also was expressed in normal human B and T lymphocytes after stimulation with appropriate mitogens. Comparison of the regulation of the expression of these proto-oncogenes demonstrated marked differences and provided evidence that, in contrast to c-myc, levels of bcl-2 messenger RNA are regulated primarily through transcriptional mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reed, J C -- Tsujimoto, Y -- Alpers, J D -- Croce, C M -- Nowell, P C -- CA-42232/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1295-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3495884" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Proteins/biosynthesis/drug effects ; Cycloheximide/pharmacology ; Gene Expression Regulation/*drug effects ; Humans ; Interleukin-2/pharmacology ; Kinetics ; Lymphocyte Activation/*drug effects ; Phytohemagglutinins/pharmacology ; Proto-Oncogenes/*drug effects ; RNA, Messenger/blood/drug effects ; Transcription, Genetic/drug effects
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  • 8
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    Regional changes in calcium underlying contraction of single smooth muscle cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-27
    Description: The role of calcium in regulating the contractile state of smooth muscle has been investigated by measuring calcium and contraction in single smooth muscle cells with the calcium-sensitive dye fura-2 and the digital imaging microscope. The concentration of free calcium in the cytoplasm increased after stimulation of the cells by depolarization with high potassium or by application of carbachol. Changes in calcium always preceded contraction. The increase in calcium induced by these stimuli was limited to less than 1 microM. Calcium within the nucleus was also subject to a limitation of its rise during contraction. Intranuclear calcium rose from 200 nM at rest to no more than 300 nM while cytoplasmic calcium rose to over 700 nM. These apparent ceilings for both cytoplasmic and intranuclear calcium may result either from negative feedback of calcium on cytoplasmic and nuclear calcium channel gating mechanisms, respectively, or from the presence of calcium pumps that are strongly activated at the calcium ceilings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, D A -- Becker, P L -- Fay, F S -- AM07807/AM/NIADDK NIH HHS/ -- HL-14523/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 27;235(4796):1644-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103219" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzofurans ; Bufo marinus ; Calcium/*metabolism ; Carbachol/pharmacology ; Electric Stimulation ; Fura-2 ; Kinetics ; *Muscle Contraction ; Muscle, Smooth/*metabolism ; Potassium/pharmacology ; Software ; Spectrometry, Fluorescence
    Print ISSN: 0036-8075
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  • 9
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    Direct demonstration of macula densa-mediated renin secretion (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-25
    Description: An in vitro method has been used to examine whether secretion of renin from the juxtaglomerular apparatus is affected by changes in the sodium chloride concentration of the tubular fluid at the macula densa. Single juxtaglomerular apparatuses were microdissected from rabbits and the tubule segment containing the macula densa was perfused, while simultaneously the entire juxtaglomerular apparatus was superfused, and the fluid was collected for renin measurement. In this preparation, in which influences from renal nerves and local hemodynamic effects are eliminated, a decrease in the tubular sodium chloride concentration at the macula densa results in a prompt stimulation of the renin release rate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skott, O -- Briggs, J P -- DK37448/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1618-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Extracellular Space/physiology ; In Vitro Techniques ; Juxtaglomerular Apparatus/cytology/*secretion/ultrastructure ; Kinetics ; Rabbits ; Renin/*secretion ; Sodium Chloride/physiology
    Print ISSN: 0036-8075
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  • 10
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    Interferon-gamma and B cell stimulatory factor-1 reciprocally regulate Ig isotype production (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: Gamma interferon (IFN-gamma) and B cell stimulatory factor-1 (BSF-1), also known as interleukin-4, are T cell-derived lymphokines that have potent effects on B cell proliferation and differentiation. They are often secreted by distinct T cell clones. It is now shown that IFN-gamma stimulates the expression of immunoglobulin (Ig) of the IgG2a isotype and inhibits the production of IgG3, IgG1, IgG2b, and IgE. By contrast, BSF-1 has powerful effects in promoting switching to the expression of IgG1 and IgE but markedly inhibits IgM, IgG3, IgG2a, and IgG2b. These results indicate that BSF-1 and IFN-gamma as well as the T cells that produce them may act as reciprocal regulatory agents in the determination of Ig isotype responses. The effects of IFN-gamma and BSF-1 on isotype expression are independent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snapper, C M -- Paul, W E -- New York, N.Y. -- Science. 1987 May 22;236(4804):944-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; B-Lymphocytes/drug effects/*immunology ; Cricetinae ; Growth Substances/*pharmacology ; Immunoglobulin Isotypes/*biosynthesis ; Interferon-gamma/immunology/*pharmacology ; Interleukin-4 ; Kinetics ; Lymphocyte Activation ; Lymphokines/*pharmacology ; Mice ; Mice, Inbred DBA ; Recombinant Proteins/*pharmacology
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  • 11
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    The catalytic role of the active site aspartic acid in serine proteases (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: The role of the aspartic acid residue in the serine protease catalytic triad Asp, His, and Ser has been tested by replacing Asp102 of trypsin with Asn by site-directed mutagenesis. The naturally occurring and mutant enzymes were produced in a heterologous expression system, purified to homogeneity, and characterized. At neutral pH the mutant enzyme activity with an ester substrate and with the Ser195-specific reagent diisopropylfluorophosphate is approximately 10(4) times less than that of the unmodified enzyme. In contrast to the dramatic loss in reactivity of Ser195, the mutant trypsin reacts with the His57-specific reagent, tosyl-L-lysine chloromethylketone, only five times less efficiently than the unmodified enzyme. Thus, the ability of His57 to react with this affinity label is not severely compromised. The catalytic activity of the mutant enzyme increases with increasing pH so that at pH 10.2 the kcat is 6 percent that of trypsin. Kinetic analysis of this novel activity suggests this is due in part to participation of either a titratable base or of hydroxide ion in the catalytic mechanism. By demonstrating the importance of the aspartate residue in catalysis, especially at physiological pH, these experiments provide a rationalization for the evolutionary conservation of the catalytic triad.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Craik, C S -- Roczniak, S -- Largman, C -- Rutter, W J -- GM 10765/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):909-13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3303334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asparagine ; *Aspartic Acid ; Binding Sites ; Catalysis ; *Endopeptidases ; Hydrogen-Ion Concentration ; Kinetics ; Rats ; Serine Endopeptidases ; Structure-Activity Relationship ; Substrate Specificity
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  • 12
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    Insulin rapidly increases diacylglycerol by activating de novo phosphatidic acid synthesis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: The mechanisms whereby insulin increases diacylglycerol in BC3H-1 myocytes were examined. When [3H]arachidonate labeling of phospholipids was used as an indicator of phospholipase C activation, transient increases in [3H]diacylglycerol were observed between 0.5 and 10 minutes after the onset of insulin treatment. With [3H]glycerol labeling as an indicator of de novo phospholipid synthesis, [3H]diacylglycerol was increased maximally at 1 minute and remained elevated for 20 minutes. [3H]Glycerol-labeled diacylglycerol was largely derived directly from phosphatidic acid. Insulin increased de novo phosphatidic acid synthesis within 5 to 10 seconds; within 1 minute, this synthesis was 60 times greater than that of controls. Thus, the initial increase in diacylglycerol is due to both increased hydrolysis of phospholipids and a burst of de novo phosphatidic acid synthesis. After 5 to 10 minutes, de novo phosphatidic acid synthesis continues as a major source of diacylglycerol. Both phospholipid effects of insulin seem important for generating diacylglycerol and other phospholipid-derived intracellular signaling substances.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farese, R V -- Konda, T S -- Davis, J S -- Standaert, M L -- Pollet, R J -- Cooper, D R -- AM18608/AM/NIADDK NIH HHS/ -- HD22248/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):586-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107122" target="_blank"〉PubMed〈/a〉
    Keywords: Arachidonic Acid ; Arachidonic Acids/metabolism ; Cell Line ; Diglycerides/*metabolism ; Enzyme Activation ; Glycerides/*metabolism ; Glycerol/metabolism ; Insulin/*pharmacology ; Kinetics ; Muscles/drug effects/*metabolism ; Phosphatidic Acids/*biosynthesis ; Phosphatidylinositols/metabolism ; Phospholipids/metabolism ; Type C Phospholipases/metabolism
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  • 13
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    The dynamics of free calcium in dendritic spines in response to repetitive synaptic input (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: Increased levels of intracellular calcium at either pre- or postsynaptic sites are thought to precede changes in synaptic strength. Thus, to induce long-term potentiation in the hippocampus, periods of intense synaptic stimulation would have to transiently raise the levels of cytosolic calcium at postsynaptic sites--dendritic spines in the majority of cases. Since direct experimental verification of this hypothesis is not possible at present, calcium levels have been studied by numerically solving the appropriate electro-diffusion equations for two different postsynaptic structures. Under the assumption that voltage-dependent calcium channels are present on dendritic spines, free intracellular calcium in spines can reach micromolar levels after as few as seven spikes in 20 milliseconds. Moreover, a short, but high-frequency, burst of presynaptic activity is more effective in raising levels of calcium and especially of the calcium-calmodulin complex than sustained low-frequency activity. This behavior is different from that seen at the soma of a typical vertebrate neuron.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gamble, E -- Koch, C -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1311-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3495885" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Biological Transport, Active ; Calcium/*metabolism ; Cerebral Cortex/physiology ; Dendrites/*metabolism/physiology ; Ganglia, Sympathetic/physiology ; Kinetics ; Membrane Potentials ; Models, Neurological ; Neuronal Plasticity ; Rana catesbeiana ; Synapses/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Purification and properties of Drosophila heat shock activator protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Drosophila heat shock activator protein, a rare transacting factor which is induced upon heat shock to bind specifically to the heat shock regulatory sequence in vivo, has been purified from shocked cells to more than 95 percent homogeneity by sequence-specific duplex oligonucleotide affinity chromatography. The purified protein has a relative molecular mass of 110 kilodaltons, binds to the regulatory sequence with great affinity and specificity, and strongly stimulates transcription of the Drosophila hsp70 gene. Studies with this regulatory protein should lead to an understanding of the biochemical pathway underlying the heat shock phenomenon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, C -- Wilson, S -- Walker, B -- Dawid, I -- Paisley, T -- Zimarino, V -- Ueda, H -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1247-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685975" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Drosophila/*genetics ; *Genes ; *Genes, Regulator ; Heat-Shock Proteins/*genetics ; Kinetics ; Molecular Weight
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  • 15
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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  • 16
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    Computer simulations of the diffusion of a substrate to an active site of an enzyme (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-12
    Description: Computer simulations of the diffusion of a substrate to an enzyme active site were performed. They included the detailed shape of the protein and an accurate description of its electrostatic potential. Application of the method to the diffusion of the superoxide anion to the protein superoxide dismutase revealed that the electric field of the enzyme enhances the association rate of the anion by a factor of 30 or more. Calculated changes in the association rate as a function of ionic strength and amino acid modification paralleled the observed behavior. Design principles of superoxide dismutase are considered with respect to insights provided by the simulations. A possible means of enhancing the enzyme turnover rate through site-directed mutagenesis is proposed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharp, K -- Fine, R -- Honig, B -- GM30518/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 12;236(4807):1460-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3589666" target="_blank"〉PubMed〈/a〉
    Keywords: *Binding Sites ; *Computer Simulation ; Diffusion ; Enzymes/*metabolism ; Kinetics ; Mathematics ; Mutation ; Superoxide Dismutase/metabolism
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  • 17
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    Skeletal muscle as the potential power source for a cardiovascular pump: assessment in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-17
    Description: Skeletal muscle ventricles (SMVs) were constructed from canine latissimus dorsi and connected to a totally implantable mock circulation device. The SMVs, stimulated by an implantable pulse generator, pumped continuously for up to 8 weeks in free-running beagle dogs. Systolic pressures produced by the SMVs, initially of 139 +/- 7.2 mmHg and after 1 month of continuous pumping of 107 +/- 7 mmHg, were comparable to normal physiologic pressures in the adult beagles (114 +/- 21 mmHg). After 2 weeks of continuous pumping, the mean stroke work of the SMVs was 0.4 X 10(6) ergs, a performance that compares favorably with the animal's cardiac ventricles. This study shows that canine skeletal muscle which has not received prior training or electrical conditioning can perform sustained work at the high levels needed for an auxiliary cardiovascular pump. It might be possible eventually to use such muscle pumps in humans to assist the failing circulation and to provide support in children with certain types of congenital heart defects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Acker, M A -- Hammond, R L -- Mannion, J D -- Salmons, S -- Stephenson, L W -- HLBI 34778/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):324-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2951849" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Blood Circulation ; Blood Pressure ; *Cardiovascular Physiological Phenomena ; Dogs ; Kinetics ; Models, Biological ; Muscles/enzymology/*physiology ; Myosins/metabolism
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  • 18
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    Genetic reconstitution of functional acetylcholine receptor channels in mouse fibroblasts (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: Foreign genes can be stably integrated into the genome of a cell by means of DNA-mediated gene transfer techniques, and large quantities of homogenous cells that continuously express these gene products can then be isolated. Such an expression system can be used to study the functional consequences of introducing specific mutations into genes and to study the expressed protein in the absence of cellular components with which it is normally in contact. All four Torpedo acetylcholine receptor (AChR) subunit complementary DNA's were introduced into the genome of a mouse fibroblast cell by DNA-mediated gene transfer. A clonal cell line that stably produced high concentrations of correctly assembled cell surface AChR's and formed proper ligand-gated ion channels was isolated. With this new expression system, recombinant DNA, biochemical, pharmacological, and electrophysiological techniques were combined to study Torpedo AChR's in a single intact system. The physiological and pharmacological profiles of Torpedo AChR's expressed in mouse fibroblast cells differ in some details from those described earlier, and may provide a more accurate reflection of the properties of this receptor in its natural environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claudio, T -- Green, W N -- Hartman, D S -- Hayden, D -- Paulson, H L -- Sigworth, F J -- Sine, S M -- Swedlund, A -- NS 07102/NS/NINDS NIH HHS/ -- NS 21501/NS/NINDS NIH HHS/ -- NS 21714/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1688-94.〈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/3686008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/physiology ; Fibroblasts/metabolism ; *Genes ; Kinetics ; Mice ; Receptors, Cholinergic/*genetics/metabolism ; Torpedo ; *Transfection
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  • 19
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    Efflux of chloroquine from Plasmodium falciparum: mechanism of chloroquine resistance (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Chloroquine-resistant Plasmodium falciparum accumulate significantly less chloroquine than susceptible parasites, and this is thought to be the basis of their resistance. However, the reason for the lower accumulation of chloroquine was unknown. The resistant parasite has now been found to release chloroquine 40 to 50 times more rapidly than the susceptible parasite, although their initial rates of chloroquine accumulation are the same. Verapamil and two other calcium channel blockers, as well as vinblastine and daunomycin, each slowed the release and increased the accumulation of chloroquine by resistant (but not susceptible) Plasmodium falciparum. These results suggest that a higher rate of chloroquine release explains the lower chloroquine accumulation, and thus the resistance observed in resistant Plasmodium falciparum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krogstad, D J -- Gluzman, I Y -- Kyle, D E -- Oduola, A M -- Martin, S K -- Milhous, W K -- Schlesinger, P H -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1283-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, 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/3317830" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Calcium Channel Blockers/pharmacology ; Chloroquine/*metabolism/pharmacology ; Daunorubicin/pharmacology ; Drug Resistance ; Kinetics ; Plasmodium falciparum/drug effects/genetics/*metabolism ; Vinblastine/pharmacology
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  • 20
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    Rapid stimulation of diacylglycerol production in Xenopus oocytes by microinjection of H-ras p21 (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: The p21 products of ras proto-oncogenes are thought to be important components in pathways regulating normal cell proliferation and differentiation. These proteins acquire transforming properties as a result of activating lesions that convert ras genes to oncogenes in a wide array of malignancies. In Xenopus laevis oocytes, microinjection of transforming ras p21 is a potent inducer of maturation, whereas microinjection of a monoclonal antibody to ras p21 inhibits normal maturation induced by hormones. The phosphoinositide pathway is a ubiquitous system that appears to play a key role in diverse cellular functions. By use of the Xenopus oocyte system, it was possible to quantitate the effects of ras p21 microinjection on individual components of the phosphoinositide pathway. Within 20 minutes of microinjection, levels of phosphatidylinositol 4,5-bisphosphate, inositol 1-phosphate, and inositol bisphosphate increased 1.5- to 2-fold. The most striking effects were on diacylglycerol, which increased 5-fold under the same conditions. In contrast, the normal ras p21 protein induced no detectable alteration in any of the metabolites analyzed. The earliest effects of the transforming p21 on phosphoinositol turnover were observable within 2 minutes, implying a very rapid effect of ras p21 on the enzymes involved in phospholipid metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacal, J C -- de la Pena, P -- Moscat, J -- Garcia-Barreno, P -- Anderson, P S -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):533-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diglycerides/*biosynthesis ; Female ; Glycerides/*biosynthesis ; Glycerol/metabolism ; Inositol/metabolism ; Inositol Phosphates/biosynthesis ; Kinetics ; Microinjections ; Oocytes/drug effects/*metabolism ; Phosphatidylinositol 4,5-Diphosphate ; Phosphatidylinositols/biosynthesis/*metabolism ; Proto-Oncogene Proteins/*pharmacology ; Proto-Oncogene Proteins p21(ras) ; Xenopus laevis
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  • 21
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    Promotion of tubulin assembly by aluminum ion in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-10
    Description: It has been proposed that aluminum ion is a contributing factor in a variety of neurological diseases. In many of these diseases, aberrations in the cytoskeleton have been noted. The effects of aluminum ion on the in vitro assembly of tubulin into microtubules has been examined by determining the association constants for the metal ion-guanosine triphosphate-tubulin ternary complex required for polymerization. The association constant for aluminum ion was approximately 10(7) times that of magnesium ion, the physiological mediator of microtubule assembly. In addition, aluminum ion at 4.0 X 10(-10) mole per liter competed effectively with magnesium ion for support of tubulin polymerization when magnesium ion falls below 1.0 millimole per liter. The microtubules produced by aluminum ion were indistinguishable from those produced by magnesium ion when viewed by electron microscopy, and they showed identical critical tubulin concentrations for assembly and sensitivities to cold-induced depolymerization. However, the rate of guanosine triphosphate hydrolysis and the sensitivity to calcium ion-induced depolymerization, critical regulatory processes of microtubules in vivo, were markedly lower for aluminum ion microtubules than for magnesium ion microtubules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macdonald, T L -- Humphreys, W G -- Martin, R B -- AM 32453/AM/NIADDK NIH HHS/ -- ES 03181/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):183-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3105058" target="_blank"〉PubMed〈/a〉
    Keywords: Aluminum/*pharmacology ; Animals ; Calcium/pharmacology ; Cattle ; GTP-Binding Proteins/metabolism ; Guanosine Triphosphate/metabolism ; In Vitro Techniques ; Kinetics ; Magnesium/metabolism ; Microtubules/*metabolism ; Morphogenesis/drug effects ; Protein Binding/drug effects ; Tubulin/*metabolism
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  • 22
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    Delay time of hemoglobin S polymerization prevents most cells from sickling in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-31
    Description: A laser photolysis technique has been developed to assess the quantitative significance of the delay time of hemoglobin S gelation to the pathophysiology of sickle cell disease. Changes in the saturation of hemoglobin S with carbon monoxide produced by varying the intensity of a photolytic laser beam were used to simulate changes in the saturation of oxyhemoglobin S produced by variations in oxygen pressure. The presence of polymer at steady-state saturation with carbon monoxide was determined by measurement of the kinetics of gelation after complete photodissociation. The kinetics are a very sensitive probe for polymer since small amounts of polymerized hemoglobin increase the rate of nucleation sufficiently to eliminate the delay period. First, the equilibrium gelation properties of partially photodissociated carbonmonoxyhemoglobin S were shown to be the same as partially oxygenated hemoglobin S, and the method was then used to determine the effect of saturation on the formation and disappearance of polymers in individual sickle cells. The saturation at which polymers first formed upon deoxygenation was much lower than the saturation at which polymers disappeared upon reoxygenation. The results indicate that at venous saturations with oxygen, gelation takes place in most cells at equilibrium, but is prevented from occurring in vivo because the delay times are sufficiently long that most cells return to the lungs and are reoxygenated before polymerization has begun.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mozzarelli, A -- Hofrichter, J -- Eaton, W A -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):500-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603036" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/*blood ; Biopolymers ; Carbon Monoxide/blood ; Erythrocytes, Abnormal/*metabolism ; Gels ; Hemoglobin, Sickle/*metabolism ; Humans ; Kinetics ; Lasers ; Light ; Oxygen/blood ; Photolysis ; Scattering, Radiation ; Spectrophotometry
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  • 23
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    Computer-aided molecular design (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: Theoretical chemistry, as implemented on fast computers, is beginning to yield accurate predictions of the thermodynamic and kinetic properties of large molecular assemblies. In addition to providing detailed insights into the origins of molecular activity, theoretical calculations can be used to design new molecules with specific properties. This article describes two types of calculations that show special promise as design tools, the thermodynamic cycle-perturbation method and the Brownian reactive dynamics method. These methods can be applied to calculate equilibrium and rate constants that describe many aspects of molecular recognition, stability, and reactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCammon, J A -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):486-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Houston, TX 77004.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3310236" target="_blank"〉PubMed〈/a〉
    Keywords: Chemistry/*methods ; *Computers ; Diffusion ; Electrochemistry ; Kinetics ; Thermodynamics
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  • 24
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    Molecular dynamics of a cytochrome c-cytochrome b5 electron transfer complex (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-06
    Description: Cytochrome c and cytochrome b5 form an electrostatically associated electron transfer complex. Computer models of this and related complexes that were generated by docking the x-ray structures of the individual proteins have provided insight into the specificity and mechanism of electron transfer reactions. Previous static modeling studies were extended by molecular dynamics simulations of a cytochrome c-cytochrome b5 intermolecular complex. The simulations indicate that electrostatic interactions at the molecular interface results in a flexible association complex that samples alternative interheme geometries and molecular conformations. Many of these transient geometries appear to be more favorable for electron transfer than those formed in the initial model complex. Of particular interest is a conformational change that occurred in phenylalanine 82 of cytochrome c that allowed the phenyl side chain to bridge the two cytochrome heme groups.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wendoloski, J J -- Matthew, J B -- Weber, P C -- Salemme, F R -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):794-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Research and Development Department, E. I. du Pont de Nemours and Company, Wilmington, DE 19898.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2823387" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Graphics ; Cytochrome b Group/*metabolism ; Cytochrome c Group/*metabolism ; Cytochromes b5 ; Electron Transport ; Kinetics ; Models, Molecular ; Protein Binding ; Protein Conformation
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  • 25
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    Acylation of proteins with myristic acid occurs cotranslationally (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Several proteins of viral and cellular origin are acylated with myristic acid early during their biogenesis. To investigate the possibility that myristylation occurred cotranslationally, the BC3H1 muscle cell line, which contains a broad array of myristylated proteins, was pulse-labeled with [3H]myristic acid. Nascent polypeptide chains covalently associated with transfer RNA were isolated subsequently by ion-exchange chromatography. [3H]Myristate was attached to nascent chains through an amide linkage and was identified by thin-layer chromatography after its release from nascent chains by acid methanolysis. Inhibition of cellular protein synthesis with puromycin resulted in cessation of [3H]myristate-labeling of nascent chains, in agreement with the dependence of this modification on protein synthesis in vivo. These data represent a direct demonstration that myristylation of proteins is a cotranslational modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilcox, C -- Hu, J S -- Olson, E N -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1275-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Hospital and Tumor Institute at Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685978" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Animals ; Cell Line ; Kinetics ; Methionine/metabolism ; Muscles ; Myristic Acid ; Myristic Acids/*metabolism ; *Protein Biosynthesis ; Proteins/*genetics/metabolism ; Sulfur Radioisotopes ; Tritium
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  • 26
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    Linkage of functional and structural heterogeneity in proteins: dynamic hole burning in carboxymyoglobin (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-16
    Description: Inhomogeneous broadening of the 760-nanometer photoproduct band of carboxymyoglobin at cryogenic temperatures has been demonstrated with a dynamic hole burning technique. Line-shape changes and frequency shifts in this spectral band are generated by ligand recombination and are shown not to be the result of structural relaxation below 60 K. The observation of dynamic hole burning exposes the relation between the structural disorder responsible for the inhomogeneous broadening and the well-known distributed ligand rebinding kinetics. The findings provide direct evidence for the functional relevance of conformational substrates in myoglobin rebinding. In addition, a general protocol for evaluating the relative contributions of structural relaxation and hole burning to the spectral changes accompanying rebinding in hemeproteins is presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Campbell, B F -- Chance, M R -- Friedman, J M -- HL-18708/HL/NHLBI NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AT&T Bell Laboratories, Murray Hill, NJ 07974.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Monoxide/metabolism ; Kinetics ; Myoglobin/*metabolism ; Photochemistry ; Protein Binding ; Protein Conformation ; Spectrophotometry ; Spectrophotometry, Infrared ; Temperature
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    Left-handed DNA in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-06
    Description: Left-handed DNA is shown to exist and elicit a biological response in Escherichia coli. A plasmid encoding the gene for a temperature-sensitive Eco RI methylase (MEco RI) was cotransformed with different plasmids containing inserts that had varying capacities to form left-handed helices or cruciforms with a target Eco RI site in the center or at the ends of the inserts. Inhibition of methylation in vivo was found for the stable inserts with the longest left-handed (presumably Z) helices. In vitro methylation with the purified MEco RI agreed with the results in vivo. Supercoil-induced changes in the structure of the primary helix in vitro provided confirmation that left-handed helices were responsible for this behavior. The presence in vivo of left-handed inserts elicits specific deletions and plasmid incompatibilities in certain instances.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaworski, A -- Hsieh, W T -- Blaho, J A -- Larson, J E -- Wells, R D -- GM 30822/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):773-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, School of Medicine, University of Alabama, Birmingham 35294.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3313728" target="_blank"〉PubMed〈/a〉
    Keywords: Cloning, Molecular ; DNA/*genetics ; DNA, Superhelical/genetics ; Escherichia coli/enzymology/*genetics ; Kinetics ; Methyltransferases/genetics/metabolism ; *Nucleic Acid Conformation ; *Plasmids ; *Site-Specific DNA-Methyltransferase (Adenine-Specific)
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    Actin polymerization and ATP hydrolysis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-30
    Description: F-actin is the major component of muscle thin filaments and, more generally, of the microfilaments of the dynamic, multifunctional cytoskeletal systems of nonmuscle eukaryotic cells. Polymeric F-actin is formed by reversible noncovalent self-association of monomeric G-actin. To understand the dynamics of microfilament systems in cells, the dynamics of polymerization of pure actin must be understood. The following model has emerged from recent work. During the polymerization process, adenosine 5'-triphosphate (ATP) that is bound to G-actin is hydrolyzed to adenosine 5'-diphosphate (ADP) that is bound to F-actin. The hydrolysis reaction occurs on the F-actin subsequent to the polymerization reaction in two steps: cleavage of ATP followed by the slower release of inorganic phosphate (Pi). As a result, at high rates of filament growth a transient cap of ATP-actin subunits exists at the ends of elongating filaments, and at steady state a stabilizing cap of ADP.Pi-actin subunits exists at the barbed ends of filaments. Cleavage of ATP results in a highly stable filament with bound ADP.Pi, and release of Pi destabilizes the filament. Thus these two steps of the hydrolytic reaction provide potential mechanisms for regulating the monomer-polymer transition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korn, E D -- Carlier, M F -- Pantaloni, D -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):638-44.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672117" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology ; Actins/*physiology ; Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Animals ; Cytoskeleton/*physiology ; Humans ; Hydrolysis ; Kinetics ; Polymers ; Protein Binding
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 29
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    Heparin promotes the inactivation of antithrombin by neutrophil elastase (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: Heparin is an acceleratory cofactor for antithrombin, a circulating inhibitor of blood coagulation enzymes. The presence of heparin on blood vessel walls is believed to contribute to the nonthrombogenic properties of those surfaces. In apparent opposition to this function, heparin was found to greatly accelerate the in vitro inactivation of antithrombin by neutrophil elastase. Inactivation rates in solution were potentiated several hundredfold by specific heparin fractions with anticoagulant activity. Although the data suggest that a heparin-antithrombin complex is essential for the inactivation by elastase to occur, the enzyme itself interacts tightly with heparin. These results suggest a mechanism which, if operating in vivo, could lead to a localized neutralization of the anticoagulant function of heparin at the endothelial surface.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jordan, R E -- Kilpatrick, J -- Nelson, R M -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):777-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3649921" target="_blank"〉PubMed〈/a〉
    Keywords: Antithrombin III/antagonists & inhibitors/*metabolism ; Endothelium/metabolism ; Heparin/metabolism/*pharmacology ; Humans ; Kinetics ; Neutrophils/*enzymology ; Pancreatic Elastase/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 30
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    Assembly of clathrin-coated pits onto purified plasma membranes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-01
    Description: During receptor-mediated endocytosis, coated pits invaginate to form coated vesicles, clathrin and associated proteins dissociate from the vesicle membrane, and these proteins form new coated pits at the cell surface. As a means of elucidating molecular mechanisms that govern the function of coated pits, the assembly phase of this cycle was reconstituted by incubating purified membranes that were treated to remove endogenous coated pits with cytoplasm extracted from cultured cells. The in vitro assembly of coated pits on these membranes satisfactorily mimics many features of coated pit formation in the intact cell. These studies indicate that: the membranes contain a limited number of coated pit assembly sites that bind clathrin with high affinity; the half-time for assembly is 5 minutes both at 4 degrees C and 37 degrees C; during assembly, proteins with molecular sizes of 180, 110, and 36 kilodaltons are recruited to the plasma membrane; and assembly is not dependent on adenosine triphosphate, but this nucleotide triggers a temperature-dependent loss of coated pits that are assembled in the absence of adenosine triphosphate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, M S -- Mahaffey, D T -- Brodsky, F M -- Anderson, R G -- HL 20948/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 1;236(4801):558-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2883727" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Cell Membrane/metabolism/*ultrastructure ; Clathrin/*metabolism ; Coated Pits, Cell-Membrane/drug effects/*physiology/ultrastructure ; Endocytosis ; Endosomes/*physiology ; Humans ; Kinetics ; Membrane Proteins/metabolism ; Microscopy, Electron ; Molecular Weight ; Temperature
    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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