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  • Rats  (68)
  • *Biological Evolution
  • Models, Molecular
  • American Association for the Advancement of Science (AAAS)  (91)
  • American Meteorological Society
  • MDPI Publishing
  • 1995-1999
  • 1985-1989  (91)
  • 1987  (91)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (91)
  • American Meteorological Society
  • MDPI Publishing
  • Springer  (1)
Years
  • 1995-1999
  • 1985-1989  (91)
Year
  • 1
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    Long-term neuropathological and neurochemical effects of nucleus basalis lesions in the rat (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-13
    Description: The long-term effects of excitotoxic lesions in the nucleus basalis magnocellularis of the rat were found to mimic several neuropathological and chemical changes associated with Alzheimer's disease. Neuritic plaque-like structures, neurofibrillary changes, and neuronal atrophy or loss were observed in the frontoparietal cortex, hippocampus, amygdala, and entorhinal cortex 14 months after the lesions were made. Cholinergic markers in neocortex were reduced, while catecholamine and indoleamine metabolism was largely unaffected at this time. Bilateral lesions of the nucleus basalis magnocellularis increased somatostatin and neuropeptide Y in the cortex of the rat by at least 138 and 284 percent, respectively, suggesting a functional interaction between cholinergic and peptidergic neurons that may differ from that in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arendash, G W -- Millard, W J -- Dunn, A J -- Meyer, E M -- HD 17933/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 13;238(4829):952-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of South Florida, Tampa 33620.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890210" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Animals ; Biogenic Amines/metabolism ; Brain/metabolism/*pathology ; Cerebral Cortex/metabolism/*pathology ; Choline/metabolism ; Choline O-Acetyltransferase/metabolism ; Male ; Neuropeptide Y/analysis ; Olivary Nucleus/*physiology ; Organ Specificity ; Rats ; Rats, Inbred Strains ; Somatostatin/analysis
    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 visual cycle operates via an isomerase acting on all-trans retinol in the pigment epithelium (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-26
    Description: Thirty years have elapsed since Wald and his colleagues showed that 11-cis retinal was isomerized to all-trans when rhodopsin was bleached, yet little has been understood about the reverse process that generates 11-cis retinal for rhodopsin regeneration. It is not known whether the isomerization is enzyme-mediated, whether it occurs in the pigment epithelium or in the retina, or whether retinal, retinol, or a retinyl ester is the vitamin A compound that is isomerized. Radiolabeled all-trans retinol and high-performance liquid chromatography have now been used to demonstrate the existence of an eye-specific, membrane-bound enzyme (retinol isomerase) that converts all-trans to 11-cis retinol in the dark. Retinol isomerase is concentrated in the pigment epithelium; this localization clarifies the role of this tissue in rhodopsin regeneration and explains the need to transfer all-trans retinol from the rod outer segments to the pigment epithelium during the visual cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridges, C D -- Alvarez, R A -- New York, N.Y. -- Science. 1987 Jun 26;236(4809):1678-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura ; Choroid/enzymology ; Chromatography, High Pressure Liquid ; Dark Adaptation ; Hot Temperature ; In Vitro Techniques ; Isomerases/antagonists & inhibitors/*metabolism ; Light ; Liver/enzymology ; Phenylmethylsulfonyl Fluoride/pharmacology ; Pigment Epithelium of Eye/*enzymology ; Rats ; Retina/enzymology ; Trypsin ; Vitamin A/*metabolism ; *cis-trans-Isomerases
    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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  • 3
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    A new prosomatostatin-derived peptide reveals a pattern for prohormone cleavage at monobasic sites (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: Cleavage of the peptide bonds of preprosomatostatin at basic residues near the carboxyl terminus yields somatostatin-14, somatostatin-28, and somatostatin-28 (1-12). However, little is known about the molecular forms derived from the amino terminal portion of the precursor, even though this part of the prohormone is highly conserved through evolution. By using an antibody against the amino terminus of prosomatostatin, a decapeptide with the structure Ala-Pro-Ser-Asp-Pro-Arg-Leu-Arg-Gln-Phe, corresponding to preprosomatostatin (25-34), was isolated from the endocrine portion of the rat stomach, the gastric antrum. The antral decapeptide may represent a bioactive product generated from prosomatostatin after a monobasic cleavage similar to that involved in the formation of somatostatin-28. In fact, a monobasic cleavage requires two basic residues and a domain containing nonpolar amino acids such as alanine or leucine, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benoit, R -- Ling, N -- Esch, F -- AM I88II/AM/NIADDK NIH HHS/ -- HD 09690/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1126-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Montreal General Hospital Research Institute, Department of Medicine, McGill University, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2891188" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Hydrolysis ; Immunologic Techniques ; Peptide Fragments/physiology ; Protein Precursors/immunology/*physiology ; Protein Processing, Post-Translational ; Rats ; Somatostatin/immunology/*physiology ; Stomach/*physiology ; Structure-Activity Relationship
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1 (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Intraperitoneal administration of human recombinant interleukin-1 (IL-1) to rats can increase blood levels of corticosterone and adrenocorticotropic hormone (ACTH). The route by which IL-1 affects pituitary-adrenal activity is unknown. That the IL-1-induced pituitary-adrenal activation involves an increased secretion of corticotropin-releasing factor (CRF) is indicated by three lines of evidence. First, immunoneutralization of CRF markedly attenuated the IL-1-induced increase of ACTH blood levels. Second, after blockade of fast axonal transport in hypothalamic neurons by colchicine, IL-1 administration decreased the CRF immunostaining in the median eminence, indicating an enhanced release of CRF in response to IL-1. Third, IL-1 did not stimulate ACTH release from primary cultures of anterior pituitary cells. These data further support the notion of the existence of an immunoregulatory feedback circuit between the immune system and the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkenbosch, F -- van Oers, J -- del Rey, A -- Tilders, F -- Besedovsky, H -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Medical Faculty, Free University, Amsterdam, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443979" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Adrenocorticotropic Hormone/secretion ; Animals ; Axonal Transport/drug effects ; Colchicine/pharmacology ; Corticotropin-Releasing Hormone/immunology/*physiology ; Fluorescent Antibody Technique ; Hypothalamus/*metabolism ; Immune Sera/pharmacology ; Interleukin-1/*physiology ; Male ; Median Eminence/metabolism ; Neurons/*metabolism ; Pituitary Gland, Anterior/physiology ; Rats ; Rats, Inbred Strains
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  • 5
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    Release of multiple hormones by a direct action of interleukin-1 on pituitary cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Exposure to bacterial endotoxins has long been known to stimulate the release of anterior pituitary hormones; administration of endotoxin was at one time a common clinical test of anterior pituitary function. Endotoxin is a potent stimulus for production of the endogenous pyrogenic protein, interleukin-1 (IL-1), by macrophages and monocytes. The possibility that IL-1 has a direct effect on the secretion of hormones by rat pituitary cells in a monolayer culture was investigated. Recombinant human IL-1 beta stimulated the secretion of adrenocorticotropic hormone, luteinizing hormone, growth hormone, and thyroid-stimulating hormone. Increased hormone secretion into culture supernatants was found with IL-1 concentrations ranging from 10(-9) M to 10(-12) M. Prolactin secretion by the monolayers was inhibited by similar doses. These concentrations of IL-1 are within the range reported for IL-1 in serum, suggesting that IL-1 generated peripherally by mononuclear immune cells may act directly on anterior pituitary cells to modulate hormone secretion in vivo. Incubation of IL-1 solutions with antibody to IL-1 neutralized these actions. These pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernton, E W -- Beach, J E -- Holaday, J W -- Smallridge, R C -- Fein, H G -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):519-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropsychiatry, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821620" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Cells, Cultured ; Dinoprostone ; Female ; Growth Hormone/secretion ; Humans ; Infection/physiopathology ; Inflammation/physiopathology ; Interleukin-1/*physiology ; Luteinizing Hormone/secretion ; Pituitary Gland, Anterior/*secretion ; Pituitary Hormones, Anterior/*secretion ; Prolactin/secretion ; Prostaglandins E/secretion ; Rats ; Rats, Inbred Strains ; Recombinant Proteins/pharmacology ; Thyrotropin/secretion
    Print ISSN: 0036-8075
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  • 6
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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
    Print ISSN: 0036-8075
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  • 7
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    The adenovirus major late transcription factor activates the rat gamma-fibrinogen promoter (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The major late transcription factor (MLTF) is a 46-kilodalton polypeptide that specifically binds to and activates transcription from the major late promoter of adenovirus. The presence of this promoter-specific transcription factor in uninfected HeLa cell extracts suggests that MLTF is also involved in the transcription of cellular genes. This report demonstrates that MLTF specifically stimulates transcription of the rat gamma-fibrinogen gene through a high-affinity binding site. Stimulation of transcription by MLTF was not dependent on the exact position of the MLTF binding site with respect either to the transcription initiation site or to adjacent promoter elements. These results suggest that one of the cellular functions of MLTF is to control gamma-fibrinogen gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chodosh, L A -- Carthew, R W -- Morgan, J G -- Crabtree, G R -- Sharp, P A -- P01-CA42063/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):684-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672119" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; DNA-Binding Proteins/*genetics ; Fibrinogen/*genetics ; *Gene Expression Regulation ; *Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; Rats ; Regulatory Sequences, Nucleic Acid ; Transcription Factors/*genetics ; Transcription, Genetic ; Viral Proteins/genetics
    Print ISSN: 0036-8075
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  • 8
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    erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-10
    Description: A wide variety of human tumors contain an amplified or overexpressed erbB-2 gene, which encodes a growth factor receptor-like protein. When erbB-2 complementary DNA was expressed in NIH/3T3 cells under the control of the SV40 promoter, the gene lacked transforming activity despite expression of detectable levels of the erbB-2 protein. A further five- to tenfold increase in its expression under influence of the long terminal repeat of Moloney murine leukemia virus was associated with activation of erbB-2 as a potent oncogene. The high levels of the erbB-2 product associated with malignant transformation of NIH/3T3 cells were observed in human mammary tumor cells that overexpressed this gene. These findings demonstrate a new mechanism for acquisition of oncogenic properties by genes encoding growth factor receptor-like proteins and provide a functional basis for the role of their overexpression in the development of human malignancies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Fiore, P P -- Pierce, J H -- Kraus, M H -- Segatto, O -- King, C R -- Aaronson, S A -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):178-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2885917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Line ; *Cell Transformation, Neoplastic/genetics ; DNA/genetics ; Fibroblasts/*metabolism ; Gene Expression Regulation ; Genes, Viral ; Humans ; Mice ; Moloney murine leukemia virus/genetics ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/biosynthesis/genetics/*physiology ; Rats ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; Receptors, Cell Surface/genetics ; Recombinant Fusion Proteins/biosynthesis/genetics/physiology ; Simian virus 40/genetics ; Tumor Stem Cell Assay
    Print ISSN: 0036-8075
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  • 9
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    Generation of a hybrid sequence-specific single-stranded deoxyribonuclease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-04
    Description: The relatively nonspecific single-stranded deoxyribonuclease, staphylococcal nuclease, was selectively fused to an oligonucleotide binding site of defined sequence to generate a hybrid enzyme. A cysteine was substituted for Lys116 in the enzyme by oligonucleotide-directed mutagenesis and coupled to an oligonucleotide that contained a 3'-thiol. The resulting hybrid enzyme cleaved single-stranded DNA at sites adjacent to the oligonucleotide binding site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corey, D R -- Schultz, P G -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1401-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685986" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA, Single-Stranded/metabolism ; Hydrolysis ; Micrococcal Nuclease/*genetics/metabolism ; Models, Molecular ; Mutation ; Protein Conformation ; Staphylococcus aureus/enzymology/genetics ; Substrate Specificity
    Print ISSN: 0036-8075
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  • 10
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    X-ray holograms at improved resolution: a study of zymogen granules (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: X-ray holography offers the possibility of three-dimensional microscopy with resolution higher than that of the light microscope and with contrast based on x-ray edges. In principle, the method is especially advantageous for biological samples if x-rays in the wavelength region between the carbon and oxygen K edges are used. However, until now the achieved resolution has not exceeded that of the light microscope because of the poor coherence properties of the x-ray sources and the low resolution of the detectors that were available. With a recently developed x-ray source based on an undulator on an electron storage ring, and high resolution x-ray resist, a hologram has been recorded at about 400-angstrom resolution. The experiment utilized x-rays with wavelengths of 24.7 angstroms and required a 1-hour exposure of the pancreatic zymogen granules under study.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Howells, M -- Jacobsen, C -- Kirz, J -- Feder, R -- McQuaid, K -- Rothman, S -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):514-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for X-ray Optics, Lawrence Berkeley Laboratory, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659925" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytoplasmic Granules/enzymology/*ultrastructure ; *Enzyme Precursors ; Holography/*methods ; Microscopy, Electron ; Pancreas/ultrastructure ; Rats ; X-Rays
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  • 11
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    Functional analysis of a complementary DNA for the 50-kilodalton subunit of calmodulin kinase II (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: The calcium-calmodulin-dependent protein kinase II is a major component of brain synaptic junctions and has been proposed to play a variety of important roles in brain function. A complementary DNA representing a portion of the smaller 50-kilodalton subunit of the rat brain enzyme has been cloned and sequenced. The calmodulin-binding region has been identified and a synthetic analog prepared that binds calmodulin with high affinity in the presence of calcium. Like the 50-kilodalton kinase polypeptide, the concentration of the messenger RNA varies both neuroanatomically and during postnatal development of the brain. The broad tissue and species cross-reactivity of the complementary DNA suggests that the 50-kilodalton subunit found in rat brain is evolutionarily conserved and is the product of a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanley, R M -- Means, A R -- Ono, T -- Kemp, B E -- Burgin, K E -- Waxham, N -- Kelly, P T -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):293-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037704" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Amino Acid Sequence ; Animals ; Base Sequence ; Biological Assay ; Brain/enzymology/growth & development ; Calcium-Calmodulin-Dependent Protein Kinases ; Cloning, Molecular ; DNA/genetics ; Protein Kinases/*genetics ; RNA, Messenger/genetics ; Rats ; Species Specificity
    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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  • 12
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    A Mab to a unique cerebellar neuron generated by immunosuppression and rapid immunization (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: The cerebellar cortex is perhaps the best characterized structure in the mammalian central nervous system. Although the major cerebellar cell classes are well known, a new class of cerebellar cortical neuron has now been identified with a monoclonal antibody (Mab) generated by a procedure for rapid immunization and selective immunosuppression of antibody responses. This procedure generates a high frequency of immunoglobulin G-class antibodies of desired specificity, and has allowed the generation of two antibodies that recognize subsets of cerebellar cortical neurons. One of these antibodies defines a previously unrecognized class of cerebellar neuron. The distribution and antigenic characteristics of this neuron suggest that it has a distinct role in cerebellar circuitry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hockfield, S -- R01 EY06511/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):67-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603010" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn/immunology ; Antibodies, Monoclonal/*immunology ; Cerebellar Cortex/cytology/*immunology ; Immune Tolerance ; Mice ; Mice, Inbred BALB C/immunology ; Rats
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  • 13
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    Slow transport of tubulin in the neurites of differentiated PC12 cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-16
    Description: In order to study the rate and form of tubulin transport in cultured neuronal cells, the fluorescence recovery after the photobleaching of a fluorescent tubulin analog has been followed within the neuritic processes of differentiated PC12 cells. In these cells, as in peripheral axons, tubulin is transported in coherent, nondiffusing waves at two different slow rates that are within the range of the slow components a and b of axonal transport measured in vivo. Finally, it appears that most, if not all, of the tubulin analog is moving out these processes. Thus, slow neuroplasmic transport in cultured neuron-like cells is a good model of axonal transport, in which experimental manipulations of the system can be performed that would be difficult in the whole animal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keith, C H -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):337-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Biological Transport ; Neurons/*metabolism ; Pheochromocytoma ; Rats ; Spectrometry, Fluorescence ; Tubulin/*metabolism ; Video Recording
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  • 14
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    My close cousin the chimpanzee (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):273-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3116670" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Biological Evolution ; DNA/genetics ; Dental Enamel/anatomy & histology ; Gait ; Haplorhini/anatomy & histology/*genetics ; Humans ; Metacarpophalangeal Joint/anatomy & histology ; Molar ; Nucleic Acid Hybridization ; Pan troglodytes/anatomy & histology/*genetics ; Sequence Homology, Nucleic Acid
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  • 15
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    Four legs bad, two legs good (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):969-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3823869" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology ; *Biological Evolution ; Foot ; Gait ; Humans ; *Locomotion
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  • 16
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    The unmasking of mitochondrial Eve (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Oct 2;238(4823):24-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3116666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; DNA, Mitochondrial/*genetics ; Haplorhini/*genetics
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  • 17
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    Chemistry in the image of biology (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):611-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672114" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Phenomena ; *Chemistry ; Models, Molecular ; *Nobel Prize
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  • 18
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    Physiological role of silent receptors of atrial natriuretic factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: A ring-deleted analog of atrial natriuretic factor--des[Gln18, Ser19, Gly20, Leu21, Gly22] ANF4-23-NH2 (C-ANF4-23)--binds with high affinity to approximately 99% of ANF receptors in the isolated perfused rat kidney. In this preparation, C-ANF4-23 is devoid of detectable renal effects and does not antagonize any of the known renal hemodynamic and natriuretic actions of biologically active ANF1-28. In contrast, both C-ANF4-23 and ANF1-28 increase sodium excretion and decrease blood pressure in intact anesthetized rats. This apparent contradiction is resolved by the finding that the ring-deleted analog markedly increases plasma levels of endogenous immunoreactive ANF in the rat. The results show that the majority of the renal receptors of ANF are biologically silent. This new class of receptors may serve as specific peripheral storage-clearance binding sites, acting as a hormonal buffer system to modulate plasma levels of ANF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maack, T -- Suzuki, M -- Almeida, F A -- Nussenzveig, D -- Scarborough, R M -- McEnroe, G A -- Lewicki, J A -- AM-14241/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):675-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2823385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/analogs & derivatives/*physiology ; Binding, Competitive ; Cyclic GMP/physiology ; Glomerular Filtration Rate ; Kidney/*physiology ; Kidney Cortex/metabolism ; Kidney Medulla/metabolism ; Natriuresis ; Rats ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Structure-Activity Relationship
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  • 19
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    Structure of MHC protein solved (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):613-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3313727" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens ; Binding Sites ; *HLA Antigens ; Humans ; Models, Molecular ; Protein Conformation
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  • 20
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    Trophic stimulation of cultured neurons from neonatal rat brain by epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-02
    Description: Epidermal growth factor (EGF) is a potent polypeptide mitogen originally isolated from the adult male mouse submaxillary gland. It also acts as a gastrointestinal hormone. EGF-immunoreactive material has recently been identified within neuronal fibers and terminals in rodent brain. In the present study, EGF was found to enhance survival and process outgrowth of primary cultures of subneocortical telencephalic neurons of neonatal rat brain in a dose-dependent manner. This effect was observed with EGF concentrations as low as 100 picograms per milliliter (0.016 nanomolar) and was dependent on the continuous presence of EGF in the medium. Similar effects were observed with basic fibroblast growth factor, but several other growth-promoting substances, including other mitogens for glial elements, were without effect. Thus EGF, in addition to its mitogenic and hormonal activities, may act as a neurite elongation and maintenance factor for select neurons of the rodent central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, R S -- Kornblum, H I -- Leslie, F M -- Bradshaw, R A -- NS19319/NS/NINDS NIH HHS/ -- NS19964/NS/NINDS NIH HHS/ -- T32-CA0905A/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 2;238(4823):72-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, College of Medicine, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/*cytology ; Cell Survival/drug effects ; Cells, Cultured ; Epidermal Growth Factor/*physiology ; Growth Substances/pharmacology ; Rats
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  • 21
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    Accelerated healing of incisional wounds in rats induced by transforming growth factor-beta (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: The role of polypeptide growth factors in the processes of inflammation and repair was investigated by analyzing the influence of transforming growth factor-beta (TGF-beta), applied directly to linear incisions made through rat dorsal skin. A dose-dependent, direct stimulatory effect of a single application of TGF-beta on the breaking strength of healing incisional wounds was demonstrated. An increase in maximum wound strength of 220 percent of control was observed at 5 days; the healing rate was accelerated by approximately 3 days for at least 14 days after production of the wound and application of TGF-beta. These increases in wound strength were accompanied by an increased influx of mononuclear cells and fibroblasts and by marked increases in collagen deposition at the site of application of TGF-beta. TGF-beta is thus a potent pharmacologic agent that can accelerate wound healing in rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustoe, T A -- Pierce, G F -- Thomason, A -- Gramates, P -- Sporn, M B -- Deuel, T F -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1333-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2442813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Substances/*pharmacology ; Male ; Peptides/*pharmacology ; Rats ; Rats, Inbred Strains ; Staining and Labeling ; Transforming Growth Factors ; Wound Healing/*drug effects ; Wounds, Penetrating/*pathology
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  • 22
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    Expression and properties of two types of protein kinase C: alternative splicing from a single gene (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-29
    Description: Two complementary DNA's, encoding the complete sequences of 671 and 673 amino acids for subspecies of rat brain protein kinase C, were expressed in COS 7 cells. The complementary DNA sequence analysis predicted that the two enzymes are derived from different ways of splicing and differ from each other only in the short ranges of their carboxyl-terminal regions. Both enzymes showed typical characteristics of protein kinase C that responded to Ca2+, phospholipid, and diacylglycerol. The enzymes showed practically identical physical and kinetic properties and were indistinguishable from one of the several subspecies of protein kinase C that occurs in rat brain but not in untransfected COS 7 cells. Partial analysis of the genomic structure confirmed that these two subspecies of protein kinase C resulted indeed from alternative splicing of a single gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ono, Y -- Kikkawa, U -- Ogita, K -- Fujii, T -- Kurokawa, T -- Asaoka, Y -- Sekiguchi, K -- Ase, K -- Igarashi, K -- Nishizuka, Y -- New York, N.Y. -- Science. 1987 May 29;236(4805):1116-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/enzymology ; Chromatography, High Pressure Liquid ; DNA/genetics ; Nucleic Acid Hybridization ; Protein Kinase C/*genetics/metabolism ; RNA Splicing ; Rabbits ; Rats
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  • 23
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    Decreased TRH receptor mRNA activity precedes homologous downregulation: assay in oocytes (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: Ligand-induced decrease in cell-surface receptor number (homologous downregulation) is often due to rapid receptor internalization. Thyrotropin-releasing hormone (TRH), however, causes a slow downregulation of TRH receptors (TRH-Rs), with a half-time of approximately 12 hours, in GH3 rat pituitary cells. The mechanism of TRH-R downregulation was studied by monitoring TRH-evoked depolarizing currents in Xenopus oocytes injected with GH3 cell RNA as a bioassay for TRH-R messenger RNA (mRNA) activity. In GH3 cells, TRH caused a rapid decrease in TRH-R mRNA activity to 15 percent of control within 3 hours. Because the half-life of TRH-R mRNA activity in control cells was approximately 3 hours, the rapid decrease in mRNA activity was not due to inhibition of mRNA synthesis alone and may represent a post-transcriptional effect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oron, Y -- Straub, R E -- Traktman, P -- Gershengorn, M C -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1406-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Gene Expression Regulation/drug effects ; Membrane Potentials ; Neoplasm Proteins/metabolism ; Oocytes/drug effects/*metabolism ; Pituitary Neoplasms/pathology ; RNA, Messenger/*biosynthesis ; RNA, Neoplasm/biosynthesis ; Rats ; Receptors, Neurotransmitter/genetics/*metabolism ; Receptors, Thyrotropin-Releasing Hormone ; Thyrotropin-Releasing Hormone/metabolism/*pharmacology ; Tumor Cells, Cultured/metabolism ; Xenopus laevis
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  • 24
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    Coexistence of guanylate cyclase and atrial natriuretic factor receptor in a 180-kD protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: Atrial natriuretic factor (ANF) is a peptide hormone that is released from atria and regulates a number of physiological processes, including steroidogenesis in adrenal cortex and testes. The parallel stimulation of membrane guanylate cyclase and corticosterone production in isolated fasciculata cells of rat adrenal cortex has supported the hypothesis of a mediatory role for cyclic guanosine monophosphate (cyclic GMP) in signal transduction. A novel particulate guanylate cyclase tightly coupled with ANF receptor was purified approximately 273,000-fold by two-step affinity chromatography. The enzyme had a molecular size of 180 kilodaltons and was acidic in nature with a pI of 4.7. Its specific activity was 1800 nanomoles of cyclic GMP formed per minute per milligram of protein. The purified enzyme bound ANF with a specific binding activity of 4.01 nanomoles per milligram of protein, a value that is close to the theoretical binding activity of 5.55 nanomoles per milligram of protein for 1 mole of the ligand binding 1 mole of the receptor protein. These results indicate that the guanylate cyclase-coupled ANF receptor exists in a 180-kilodalton protein of rat adrenocortical carcinoma and represent a step toward the elucidation of the basic mechanism of cyclic GMP-mediated transmembrane signal transduction in response to a hormone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paul, A K -- Marala, R B -- Jaiswal, R K -- Sharma, R K -- NS23744/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1224-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2881352" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex ; Adrenal Gland Neoplasms/enzymology/metabolism/pathology ; Animals ; Carcinoma/enzymology/metabolism/pathology ; Cell Membrane/enzymology/metabolism ; Guanylate Cyclase/isolation & purification/*metabolism ; Membrane Proteins/*metabolism ; Rats ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*metabolism
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  • 25
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    Steroidogenesis-activator polypeptide isolated from a rat Leydig cell tumor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-10
    Description: A cycloheximide-sensitive protein responsive to adenosine 3',5'-monophosphate has been postulated to participate in the regulation of cholesterol side-chain cleavage activity in steroidogenic tissues. Such a steroidogenesis activator polypeptide (SAP) had been isolated from rat adrenocortical tissue and partially characterized. Now a polypeptide with comparable chromatographic behavior and biological activity has been purified from the rat H-540 Leydig cell tumor in quantities sufficient for amino acid sequencing. The activator contains 30 amino acid residues and has a molecular weight of 3215. The synthetic construct based on this sequence is virtually equipotent with native H-540 tumor SAP in an adrenal mitochondrial cholesterol side-chain cleavage assay. Hormonal regulation of the intracellular concentration of this activator may control the rate of cholesterol metabolism in steroidogenic organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedersen, R C -- Brownie, A C -- AM18141/AM/NIADDK NIH HHS/ -- HD00613/HD/NICHD NIH HHS/ -- HD19309/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):188-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563495" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/analysis ; Amino Acid Sequence ; Animals ; Cholesterol/metabolism ; Cholesterol Side-Chain Cleavage Enzyme/*metabolism ; Chromatography, High Pressure Liquid ; *Heat-Shock Proteins ; Leydig Cell Tumor/*analysis ; Male ; Mitochondria/enzymology ; *Molecular Chaperones ; Oxidoreductases/*metabolism ; Peptide Fragments/analysis ; Proteins/*analysis ; Rats ; Steroids/*biosynthesis
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  • 26
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    Evolutionary and somatic selection of the antibody repertoire in the mouse (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-20
    Description: The repertoire of antibody variable (V) regions has been subject to evolutionary selection, affecting both the diversity of V region genes in the germline and their expression in the B lymphocyte population and its subsets. In ontogeny, contact with an antigen leads to the expansion of B cells expressing antibodies complementary to it. In a defined phase of B cell differentiation, new sets of V regions are generated from the existing repertoire through somatic hypermutation. Cells carrying advantageous antibody mutants are selected into the memory compartment and produce a stable secondary response upon reexposure to the antigen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajewsky, K -- Forster, I -- Cumano, A -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1088-94.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Koln, FRG.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317826" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/*genetics ; *Antibody Diversity ; B-Lymphocytes/*physiology ; *Biological Evolution ; *Genes, Immunoglobulin ; Genes, Switch ; Immunity ; Immunoglobulin Isotypes/genetics ; Immunoglobulin Variable Region/genetics ; Mice ; Mutation ; Selection, Genetic
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  • 27
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    Cytochrome P-450--catalyzed formation of delta 4-VPA, a toxic metabolite of valproic acid (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-20
    Description: Liver damage induced by the antiepileptic drug valproic acid (VPA) is believed to be mediated by an unsaturated metabolite of the drug, delta 4-VPA. In studies of the biological origin of this hepatotoxic compound, it was found that liver microsomes from phenobarbital-treated rats catalyzed the desaturation of VPA to delta 4-VPA. Indirect evidence suggested that cytochrome P-450 was the responsible enzyme, a conclusion that was verified by studies with a purified and reconstituted form of the hemoprotein, which catalyzed the oxidation of VPA to 4- and 5-hydroxyvalproic acid and to delta 4-VPA. Desaturation of a nonactivated alkyl substituent represents a novel metabolic function of cytochrome P-450 and probably proceeds via the conversion of substrate to a transient free radical intermediate, which partitions between recombination (alcohol formation) and elimination (olefin production) pathways. These findings have broad implications with respect to the metabolic generation of olefins and may explain the increased hepatotoxic potential of VPA when it is administered in combination with potent enzyme-inducing anticonvulsants such as phenobarbital.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rettie, A E -- Rettenmeier, A W -- Howald, W N -- Baillie, T A -- DK 30699/DK/NIDDK NIH HHS/ -- GM 32165/GM/NIGMS NIH HHS/ -- NS 17111/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):890-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3101178" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytochrome P-450 Enzyme System/*metabolism ; Drug-Induced Liver Injury ; *Fatty Acids, Monounsaturated ; Fatty Acids, Unsaturated/*metabolism ; Microsomes, Liver/*metabolism ; Mixed Function Oxygenases/*metabolism ; Rats ; Valproic Acid/adverse effects/*metabolism
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  • 28
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    A chimeric, ligand-binding v-erbB/EGF receptor retains transforming potential (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-10
    Description: Comparison of amino acid sequences from human epidermal growth factor (EGF) receptor and avian erythroblastosis virus erbB oncogene product suggests that v-erbB represents a truncated avian EGF receptor gene product. Although both proteins are transmembrane tyrosine kinases, the v-erbB protein lacks most of the extracellular ligand-binding domain and a 32-amino acid cytoplasmic sequence present in the human EGF receptor. To test the validity of the proposed origin of v-erbB and to investigate the functional significance of the deleted extracellular sequences, a chimeric gene encoding the extracellular and the transmembrane domain of the human EGF receptor joined to sequences coding for the cytoplasmic domain of the avian erbB oncogene product was constructed. When expressed in Rat1 fibroblasts, this reconstituted gene product (HER-erbB) was transported to the cell surface and bound EGF. Its autophosphorylation activity was stimulated by interaction with the ligand. Expression of the HER-erbB chimera led to anchorage-independent cell growth in soft agar and EGF-induced focus formation in Rat1 monolayers. Thus, it appears that v-erbB protein sequences in the chimeric receptor retain their transforming activity under the influence of the human extracellular EGF-binding domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riedel, H -- Schlessinger, J -- Ullrich, A -- New York, N.Y. -- Science. 1987 Apr 10;236(4798):197-200.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3494307" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Line ; *Cell Transformation, Neoplastic ; DNA, Recombinant ; Epidermal Growth Factor/*physiology ; Humans ; *Oncogenes ; Phosphorylation ; Protein-Tyrosine Kinases/*genetics ; Rats ; Receptor, Epidermal Growth Factor/*genetics
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  • 29
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    Cocaine receptors on dopamine transporters are related to self-administration of cocaine (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-04
    Description: Although cocaine binds to several sites in the brain, the biochemical receptor mechanism or mechanisms associated with its dependence producing properties are unknown. It is shown here that the potencies of cocaine-like drugs in self-administration studies correlate with their potencies in inhibiting [3H]mazindol binding to the dopamine transporters in the rat striatum, but not with their potencies in binding to a large number of other presynaptic and postsynaptic binding sites. Thus, the cocaine receptor related to substance abuse is proposed to be the one associated with dopamine uptake inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ritz, M C -- Lamb, R J -- Goldberg, S R -- Kuhar, M J -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1219-23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2820058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/drug effects/*metabolism ; Cattle ; Cocaine/administration & dosage/*pharmacology ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Haplorhini ; Male ; Mazindol/metabolism ; Norepinephrine/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic/drug effects/metabolism ; Receptors, Dopamine/drug effects/*metabolism ; Receptors, Serotonin/drug effects/metabolism ; Self Administration ; Serotonin/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Identification of a novel thyroid hormone receptor expressed in the mammalian central nervous system (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-09-25
    Description: A complementary DNA clone derived from rat brain messenger RNA has been isolated on the basis of homology to the human thyroid hormone receptor gene. Expression of this complementary DNA produces a high-affinity binding protein for thyroid hormones. Sequence analysis and the mapping of this gene to a distinct human genetic locus indicate the existence of multiple human thyroid hormone receptors. Messenger RNA from this gene is expressed in a tissue-specific fashion with highest levels in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, C C -- Weinberger, C -- Lebo, R -- Evans, R M -- GM-266444-09/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1610-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629259" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/*physiology ; DNA/genetics ; DNA-Binding Proteins/*genetics ; Gene Expression Regulation ; Genes ; Humans ; RNA, Messenger/genetics ; Rats ; Receptors, Thyroid Hormone/*genetics/metabolism ; Tissue Distribution ; Triiodothyronine/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Thrombospondin promotes cell-substratum adhesion (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-19
    Description: The physiological role of the platelet-secreted protein thrombospondin (TSP) is poorly understood, although it has been postulated to be involved in platelet aggregation and cellular adhesion. In this report, TSP isolated from human platelets was found to promote, in vitro, the cell-substratum adhesion of a variety of cells, including platelets, melanoma cells, muscle cells, endothelial cells, fibroblasts, and epithelial cells. The adhesion-promoting activity of TSP was species independent, specific, and not due to contamination by fibronectin, vitronectin, laminin, or platelet factor 4. The cell surface receptor for TSP is protein in nature and appears distinct from that for fibronectin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuszynski, G P -- Rothman, V -- Murphy, A -- Siegler, K -- Smith, L -- Smith, S -- Karczewski, J -- Knudsen, K A -- New York, N.Y. -- Science. 1987 Jun 19;236(4808):1570-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2438772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD36 ; Cattle ; Cell Adhesion/*drug effects ; Fibroblasts/drug effects ; Fibronectins/pharmacology ; Glycoproteins/*pharmacology ; Humans ; Melanoma/metabolism ; Mice ; Platelet Aggregation/drug effects ; Rabbits ; Rats ; Receptors, Mitogen/metabolism ; Swine ; Thrombospondins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Carbon tetrachloride at hepatotoxic levels blocks reversibly gap junctions between rat hepatocytes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: Electrical coupling and dye coupling between pairs of rat hepatocytes were reversibly reduced by brief exposure to halogenated methanes (CBrCl3, CCl4, and CHCl3). The potency of different halomethanes in uncoupling hepatocytes was comparable to their hepatotoxicity in vivo, and the rank order was the same as that of their tendency to form free radicals. The effect of carbon tetrachloride (CCl4) on hepatocytes was substantially reduced by prior treatment with SKF 525A, an inhibitor of cytochrome P-450, and by exposure to the reducing reagent beta-mercaptoethanol. Halomethane uncoupling occurred with or without extracellular calcium and did not change intracellular concentrations of calcium and hydrogen ions or the phosphorylation state of the main gap-junctional protein. Thus the uncoupling appears to depend on cytochrome P-450 oxidative metabolism in which free radicals are generated and may result from oxidation of the gap-junctional protein or of a regulatory molecule that leads to closure of gap-junctional channels. Decreases in junctional conductance may be a rapid cellular response to injury that protects healthy cells by uncoupling them from unhealthy ones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saez, J C -- Bennett, M V -- Spray, D C -- GM 30667/GM/NIGMS NIH HHS/ -- NS 07512/NS/NINDS NIH HHS/ -- NS 16424/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):967-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bromotrichloromethane/toxicity ; Carbon Tetrachloride/*toxicity ; Carbon Tetrachloride Poisoning/*physiopathology ; Chloroform/toxicity ; Electric Conductivity ; Intercellular Junctions/drug effects/*physiology ; Liver/drug effects/pathology/*physiopathology ; Rats
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    The evolution of catalytic function (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharp, P A -- Eisenberg, D -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):729-30, 807.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2445035" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Catalysis ; Escherichia coli/genetics ; Proteins/genetics ; RNA/*genetics ; Viruses/genetics
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    Synthesis of a sequence-specific DNA-cleaving peptide (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: A synthetic 52-residue peptide based on the sequence-specific DNA-binding domain of Hin recombinase (139-190) has been equipped with ethylenediaminetetraacetic acid (EDTA) at the amino terminus. In the presence of Fe(II), this synthetic EDTA-peptide cleaves DNA at Hin recombination sites. The cleavage data reveal that the amino terminus of Hin(139-190) is bound in the minor groove of DNA near the symmetry axis of Hin recombination sites. This work demonstrates the construction of a hybrid peptide combining two functional domains: sequence-specific DNA binding and DNA cleavage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sluka, J P -- Horvath, S J -- Bruist, M F -- Simon, M I -- Dervan, P B -- GM-09534-02/GM/NIGMS NIH HHS/ -- T32GM07616/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1129-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3120311" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*metabolism ; DNA/*metabolism ; DNA Nucleotidyltransferases/*metabolism ; DNA-Binding Proteins/*chemical synthesis ; Edetic Acid ; Ferrous Compounds ; Models, Molecular ; Nucleic Acid Conformation ; Oxidation-Reduction ; Peptide Fragments ; Protein Binding ; Structure-Activity Relationship
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    Decreased hippocampal inhibition and a selective loss of interneurons in experimental epilepsy (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: The occurrence of seizure activity in human temporal lobe epilepsy or status epilepticus is often associated with a characteristic pattern of cell loss in the hippocampus. An experimental model that replicates this pattern of damage in normal animals by electrical stimulation of the afferent pathway to the hippocampus was developed to study changes in structure and function that occur as a result of repetitive seizures. Hippocampal granule cell seizure activity caused a persistent loss of recurrent inhibition and irreversibly damaged adjacent interneurons. Immunocytochemical staining revealed unexpectedly that gamma-aminobutyric acid (GABA)-containing neurons, thought to mediate inhibition in this region and predicted to be damaged by seizures, had survived. In contrast, there was a nearly complete loss of adjacent somatostatin-containing interneurons and mossy cells that may normally activate inhibitory neurons. These results suggest that the seizure-induced loss of a basket cell-activating system, rather than a loss of inhibitory basket cells themselves, may cause disinhibition and thereby play a role in the pathophysiology and pathology of the epileptic state.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sloviter, R S -- NS 18201/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):73-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2879352" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholecystokinin/physiology ; Disease Models, Animal ; Electric Stimulation ; Epilepsy/pathology/*physiopathology ; Hippocampus/*physiopathology ; Immunologic Techniques ; Interneurons/*pathology/physiopathology ; Male ; Neural Inhibition ; Rats ; Somatostatin/*physiology ; Time Factors ; Vasoactive Intestinal Peptide/metabolism ; gamma-Aminobutyric Acid/*physiology
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    Brain barrier tissues: end organs for atriopeptins (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Little is known about the pathophysiology of cerebral edema and other disturbances of water balance that involve the barrier tissues at the interface of blood and brain. The present experiments show that these barrier tissues contain receptors and second messenger systems for atriopeptins, recently identified cardiac peptides involved in peripheral water regulation. They also show that atriopeptins can alter the rate of cerebrospinal fluid production. Because the blood-brain and blood-cerebrospinal fluid barriers are involved in normal water movements in the central nervous system, these studies suggest that brain barrier tissues may be important end organs for the atriopeptins and that atriopeptins could have therapeutic application to disorders of water balance in the central nervous system. An isolated, purified population of atriopeptin receptor cells, obtained from choroid epithelium, was used in these experiments. This cell population may provide a valuable model system for investigating the intracellular biochemical mechanisms through which atriopeptins exert their actions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steardo, L -- Nathanson, J A -- AM/NS 26252/AM/NIADDK NIH HHS/ -- EY-5077/EY/NEI NIH HHS/ -- NS-16356/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):470-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2879355" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Atrial Natriuretic Factor/*metabolism ; *Blood-Brain Barrier ; Brain/*physiology ; Brain Edema/physiopathology ; Brain Mapping ; Choroid Plexus/metabolism ; Epithelium/metabolism ; Guanylate Cyclase/metabolism ; Rabbits ; Rats ; Receptors, Atrial Natriuretic Factor ; Receptors, Cell Surface/*physiology ; Water-Electrolyte Balance
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    Two mammalian genes transcribed from opposite strands of the same DNA locus (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-20
    Description: This report describes the characterization of a genomic locus in the rat that encodes overlapping genes occupying both strands of the same piece of DNA. One gene (strand) encodes gonadotropin-releasing hormone (GnRH). A second gene, SH, is transcribed from the other DNA strand to produce RNA of undefined function. The RNAs transcribed from each DNA strand are spliced and polyadenylated, and share significant exon domains. GnRH is expressed in the central nervous system while SH transcripts are present in the heart. Thus, the genome of a mammalian organism encodes two distinct genes by using both strands of the same DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adelman, J P -- Bond, C T -- Douglass, J -- Herbert, E -- AM-16879/AM/NIADDK NIH HHS/ -- AM-30155/AM/NIADDK NIH HHS/ -- DA-02736/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1514-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3547652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/*genetics ; Exons ; *Genes ; Gonadotropin-Releasing Hormone/*genetics ; Heart/physiology ; Hypothalamus/physiology ; Introns ; RNA Splicing ; RNA, Messenger/*genetics ; Rats ; Templates, Genetic ; Transcription, Genetic
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    Identification of a family of muscarinic acetylcholine receptor genes (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-31
    Description: Complementary DNAs for three different muscarinic acetylcholine receptors were isolated from a rat cerebral cortex library, and the cloned receptors were expressed in mammalian cells. Analysis of human and rat genomic clones indicates that there are at least four functional muscarinic receptor genes and that these genes lack introns in the coding sequence. This gene family provides a new basis for evaluating the diversity of muscarinic mechanisms in the nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonner, T I -- Buckley, N J -- Young, A C -- Brann, M R -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):527-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037705" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/metabolism ; Cloning, Molecular ; Codon ; Dna ; DNA Restriction Enzymes ; *Genes ; Genetic Code ; Humans ; Models, Molecular ; Nucleic Acid Hybridization ; Rats ; Receptors, Muscarinic/classification/*genetics ; Swine ; Transfection
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    Three-dimensional structure of interleukin-2 (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: Interleukin-2 is an effector protein that participates in modulating the immune response; it has become a focal point for the study of lymphokine structure and function. The three-dimensional structure of the interleukin molecule has been solved to 3.0 angstrom resolution. Interleukin-2 has a novel alpha-helical tertiary structure that suggests one portion of the molecule forms a structural scaffold, which underlies the receptor binding facets of the molecule.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brandhuber, B J -- Boone, T -- Kenney, W C -- McKay, D B -- A1-00631/PHS HHS/ -- A1-19762/PHS HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1707-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Interleukin-2/isolation & purification ; Mice ; Models, Molecular ; Protein Conformation ; Solvents ; X-Ray Diffraction
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  • 40
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    Diurnal expression of transducin mRNA and translocation of transducin in rods of rat retina (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-30
    Description: The messenger RNA (mRNA) that encodes alpha subunit of the guanosine triphosphate-binding protein transducin (T alpha) and T alpha immunoreactivity were localized and measured in the rat retina during the light-dark cycle with in situ hybridization and immunohistochemistry. Both T alpha mRNA and T alpha immunoreactivity were observed only in photoreceptors. Within the photoreceptor T alpha mRNA was present primarily in the inner segments and to a lesser extent in the outer nuclear layer at all times during the day and night. However, the distribution of T alpha immunoreactivity varied profoundly with the light-dark cycle; during the day, T alpha immunoreactivity was highest in the inner segments, and at night the outer segments were more immunoreactive. The amounts of T alpha mRNA and T alpha immunoreactivity also depended on the light-dark cycle. Levels of T alpha mRNA were high immediately before and after lights on; levels were low for the rest of the light-dark cycle. During the day, T alpha immunoreactivity increased in the inner segments following the increase in T alpha mRNA. After the lights were turned off, T alpha immunoreactivity decreased in the inner segments and increased in the outer segments. Thus, it appears that T alpha is synthesized in the inner segments after a morning increase in T alpha mRNA. Newly synthesized T alpha remains in the inner segments until it is transported to the outer segments at night, where it may be involved in the increase in the sensitivity of photoreceptor rods at night.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brann, M R -- Cohen, L V -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):585-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3101175" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; Circadian Rhythm ; GTP-Binding Proteins/*genetics/immunology/metabolism ; Gene Expression Regulation ; Immunoenzyme Techniques ; Male ; Membrane Proteins/*genetics/immunology/metabolism ; Photoreceptor Cells/*physiology/ultrastructure ; RNA, Messenger/genetics ; Rats ; Transducin
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    Effect of membrane potential changes on the calcium transient in single rat cardiac muscle cells (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: The mechanism that links membrane potential changes to the release of calcium from internal stores to cause contraction of cardiac cells is unclear. By using the calcium indicator fura-2 under voltage-clamp conditions, changes in intracellular calcium could be monitored in single rat ventricular cells while controlling membrane potential. The voltage dependence of the depolarization-induced increase in intracellular calcium was not the same as that of the calcium current (Isi), which suggests that only a small fraction of Isi is required to trigger calcium release from the sarcoplasmic reticulum. In addition, sarcoplasmic reticulum calcium release may be partly regulated by membrane potential, since repolarization could terminate the rise in intracellular calcium. Thus, changes in the action potential will have immediate effects on the time course of the calcium transient beyond those associated with its effects on Isi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannell, M B -- Berlin, J R -- Lederer, W J -- HL25675/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1419-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Miami School of Medicine, FL 33136.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2446391" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Heart/*physiology ; Ion Channels/metabolism ; *Membrane Potentials ; Myocardium/*cytology/metabolism ; Rats
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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)
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    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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    Expression of functional cell-cell channels from cloned rat liver gap junction complementary DNA (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-06-05
    Description: An oocyte expression system was used to test the relation between a complementary DNA (cDNA) clone encoding the liver gap junction protein and cell-cell channels. Total liver polyadenylated messenger RNA injected into oocytes induced cell-cell channels between paired oocytes. This induction was blocked by simultaneous injection of antisense RNA transcribed from the gap junction cDNA. Messenger RNA selected by hybridization to the cDNA clone and translated in oocyte pairs yielded a higher junctional conductance than unselected liver messenger RNA. Cell-cell channels between oocytes were also formed when the cloned cDNA was expressed under the control of a heat-shock promoter. A concentration-dependent induction of channels was observed in response to injection with in vitro transcribed gap junction messenger RNA. Thus, the liver gap junction cDNA encodes a protein that is essential for the formation of functional cell-cell channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dahl, G -- Miller, T -- Paul, D -- Voellmy, R -- Werner, R -- GM 31125/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 5;236(4806):1290-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3035715" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; Connexins ; DNA/metabolism ; Heat-Shock Proteins/genetics ; Intercellular Junctions/*metabolism ; Liver/*metabolism ; Membrane Proteins/biosynthesis/*genetics ; Nucleic Acid Hybridization ; Oocytes/metabolism ; Promoter Regions, Genetic ; RNA, Messenger/biosynthesis ; Rats ; Transcription, Genetic ; Xenopus
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    Elevated levels of glucose transport and transporter messenger RNA are induced by ras or src oncogenes (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-20
    Description: An accelerated rate of glucose transport is among the most characteristic biochemical markers of cellular transformation. To study the molecular mechanism by which transporter activity is altered, cultured rodent fibroblasts transfected with activated myc, ras, or src oncogenes were used. In myc-transfected cells, the rate of 2-deoxy-D-glucose uptake was unchanged. However, in cells transfected with activated ras and src oncogenes, the rate of glucose uptake was markedly increased. The increased transport rate in ras- and src-transfected cells was paralleled by a marked increase in the amount of glucose transporter protein, as assessed by immunoblots, as well as by a markedly increased abundance of glucose transporter messenger RNA. Exposure of control cells to the tumor-promoting phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) for 18 hours had a similar effect of increasing the rate of glucose transport and the abundance of transporter messenger RNA. For ras, src, and TPA, the predominant mechanism responsible for activation of the transport system is increased expression of the structural gene encoding the glucose transport protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, J S -- Mueckler, M M -- Usher, P -- Lodish, H F -- AM00856/AM/NIADDK NIH HHS/ -- AM28082/AM/NIADDK NIH HHS/ -- GM35012/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1492-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Membrane/physiology ; Cell Transformation, Neoplastic/*physiopathology ; Deoxyglucose/metabolism ; GTP-Binding Proteins/physiology ; Gene Expression Regulation ; Glucose/*metabolism ; Monosaccharide Transport Proteins/*genetics ; *Oncogenes ; Protein-Tyrosine Kinases/physiology ; RNA, Messenger/genetics ; Rats ; Tetradecanoylphorbol Acetate/pharmacology ; Transfection
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    Bacterial resistance to beta-lactam antibiotics: crystal structure of beta-lactamase from Staphylococcus aureus PC1 at 2.5 A resolution (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: beta-lactamases are enzymes that protect bacteria from the lethal effects of beta-lactam antibiotics, and are therefore of considerable clinical importance. The crystal structure of beta-lactamase from the Gram-positive bacterium Staphylococcus aureus PC1 has been determined at 2.5 angstrom resolution. It reveals a molecule of novel topology, made up of two closely associated domains. The active site is located at the interface between the domains, with the key catalytic residue Ser70 at the amino terminus of a buried helix. Examination of the disposition of the functionally important residues within the active site depression leads to a model for the binding of a substrate and a functional analogy to the serine proteases. The unusual topology of the secondary structure units is relevant to questions concerning the evolutionary relation to the beta-lactam target enzymes of the bacterial cell wall.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herzberg, O -- Moult, J -- New York, N.Y. -- Science. 1987 May 8;236(4802):694-701.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107125" target="_blank"〉PubMed〈/a〉
    Keywords: *Anti-Bacterial Agents/metabolism ; Binding Sites ; Biological Evolution ; Catalysis ; Crystallization ; Drug Resistance, Microbial ; Endopeptidases ; Models, Molecular ; Polyethylene Glycols ; Protein Conformation ; Serine ; Serine Endopeptidases ; Solvents ; Staphylococcus aureus/*enzymology ; *beta-Lactamases/metabolism ; beta-Lactams
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    Cloning of complementary DNA for GAP-43, a neuronal growth-related protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-01
    Description: GAP-43 is one of a small subset of cellular proteins selectively transported by a neuron to its terminals. Its enrichment in growth cones and its increased levels in developing or regenerating neurons suggest that it has an important role in neurite growth. A complementary DNA (cDNA) that encodes rat GAP-43 has been isolated to study its structural characteristics and regulation. The predicted molecular size is 24 kilodaltons, although its migration in SDS-polyacrylamide gels is anomalously retarded. Expression of GAP-43 is limited to the nervous system, where its levels are highest during periods of neurite outgrowth. Nerve growth factor or adenosine 3',5'-monophosphate induction of neurites from PC12 cells is accompanied by increased GAP-43 expression. GAP-43 RNA is easily detectable, although at diminished levels, in the adult rat nervous system. This regulation of GAP-43 is concordant with a role in growth-related processes of the neuron, processes that may continue in the mature animal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karns, L R -- Ng, S C -- Freeman, J A -- Fishman, M C -- New York, N.Y. -- Science. 1987 May 1;236(4801):597-600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437653" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Axons/physiology ; Bacteriophage lambda/genetics ; Base Sequence ; *Cloning, Molecular ; DNA/*genetics ; Electrophoresis, Polyacrylamide Gel ; GAP-43 Protein ; Ganglia, Spinal/analysis/embryology ; Gene Expression Regulation ; Growth Substances/genetics ; Immunosorbent Techniques ; Membrane Proteins/*genetics ; Nerve Tissue Proteins/*genetics ; Protein Biosynthesis ; RNA/genetics ; RNA, Messenger/genetics ; Rats
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    What babies know, and noises parents make (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):726.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616605" target="_blank"〉PubMed〈/a〉
    Keywords: *Acoustic Stimulation ; Animals ; Behavior/*physiology ; Conditioning (Psychology)/physiology ; Humans ; Infant, Newborn/*physiology ; *Noise ; Parents ; Rats
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    Similarity of synthetic peptide from human tumor to parathyroid hormone in vivo and in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-11
    Description: One mechanism considered responsible for the hypercalcemia that frequently accompanies malignancy is secretion by the tumor of a circulating factor that alters calcium metabolism. The structure of a tumor-secreted peptide was recently determined and found to be partially homologous to parathyroid hormone (PTH). The amino-terminal 1-34 region of the factor was synthesized and evaluated biologically. In vivo it produced hypercalcemia, acted on bone and kidney, and stimulated 1,25-dihydroxy-vitamin D3 formation. In vitro it interacted with PTH receptors and, in some systems, was more potent than PTH. These studies support a long-standing hypothesis regarding pathogenesis of malignancy-associated hypercalcemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horiuchi, N -- Caulfield, M P -- Fisher, J E -- Goldman, M E -- McKee, R L -- Reagan, J E -- Levy, J J -- Nutt, R F -- Rodan, S B -- Schofield, T L -- AR 36446/AR/NIAMS NIH HHS/ -- AR 39191/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regional Bone Center, Helen Hayes Hospital (New York State Department of Health), West Haverstraw 10993.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/blood ; Humans ; Hypercalcemia/etiology ; Neoplasms/*physiopathology ; Parathyroid Glands/physiology ; Parathyroid Hormone/pharmacology/*physiology ; Peptides/*physiology ; Rats ; Rats, Inbred Strains ; Thyroidectomy
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    Neurosteroids: cytochrome P-450scc in rat brain (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-04
    Description: The steroid hormones corticosterone and testosterone are supplied to the central nervous system by endocrine glands, the adrenals and gonads. In contrast, the 3 beta-hydroxy-delta 5-derivatives of cholesterol, pregnenolone and dehydroepiandrosterone, accumulate in the rat brain through mechanisms independent of peripheral sources. Immunohistochemical studies have been performed with specific antibodies to bovine adrenal cytochrome P-450scc, which is involved in cholesterol side-chain cleavage and pregnenolone formation. The enzyme was localized in the white matter throughout the brain. Scarce clusters of cell bodies were also stained in the entorhinal and cingulate cortex and in the olfactory bulb. These observations strongly support the existence of "neurosteroids," which have been posited on the basis of biochemical, physiological, and behavioral studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Le Goascogne, C -- Robel, P -- Gouezou, M -- Sananes, N -- Baulieu, E E -- Waterman, M -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1212-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306919" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/metabolism ; Animals ; Brain/cytology/*metabolism ; Cholesterol Side-Chain Cleavage Enzyme/*metabolism ; Female ; Histocytochemistry ; Hormones/*biosynthesis ; Immunoenzyme Techniques ; Oxidoreductases/*metabolism ; Rats ; Steroids/*biosynthesis ; Tissue Distribution
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    Glucocorticoid receptor mutants that define a small region sufficient for enhancer activation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-24
    Description: Transcriptional enhancement is a general mechanism for regulation of gene expression in which particular proteins bound to specific DNA sequences stimulate the efficiency of initiation from linked promoters. One such protein, the glucocorticoid receptor, mediates enhancement in a glucocorticoid hormone-dependent manner. In this study, a region of the 795-amino acid rat glucocorticoid receptor that is active in transcriptional enhancement was identified. The active region was defined by expressing various receptor deletion mutants in stably and transiently transfected cells and examining the regulated transcription of hormone-responsive genes. Mutant receptors lacking as many as 439 amino-terminal amino acids retained activity, as did those with as many as 270 carboxyl-terminal amino acids deleted. This suggests that the 86-amino acid segment between the most extensive terminal deletions, which also includes sequences required for specific DNA binding in vitro, is sufficient for enhancer activation. In fact, a 150-amino acid receptor fragment that encompasses this segment mediates constitutive enhancement.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miesfeld, R -- Godowski, P J -- Maler, B A -- Yamamoto, K R -- New York, N.Y. -- Science. 1987 Apr 24;236(4800):423-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563519" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA-Binding Proteins/*genetics ; *Enhancer Elements, Genetic ; *Genes, Regulator ; Mutation ; Rats ; Receptors, Glucocorticoid/*genetics ; Structure-Activity Relationship ; Transfection
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    Asymmetry of neural feedback in the organization of behavioral states (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mesulam, M M -- New York, N.Y. -- Science. 1987 Jul 31;237(4814):537-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3110953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/physiology ; Brain Stem/*physiology ; Cerebral Cortex/*physiology ; Feedback ; Haplorhini ; Neural Pathways/physiology ; Rats
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    D1 dopamine receptor activation required for postsynaptic expression of D2 agonist effects (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-08
    Description: D1 and D2 dopamine receptors exert synergistic effects on the firing rates of basal ganglia neurons and on the expression of stereotyped behavior in rats. Moreover, the ability of D2 agonists to induce changes in basal ganglia single unit activity and spontaneous motor activity is dependent upon the presence of endogenous dopamine to stimulate D1 receptors; in rats treated with alpha-methyl-rho-tyrosine to reduce endogenous dopamine levels, the neurophysiological and behavioral effects of the D2 agonist quinpirole are significantly attenuated, while the effects of nonselective agonists like apomorphine, which stimulate both D1 and D2 receptors, or combinations of a D2 agonist and a D1 agonist are not attenuated. Thus, the previously held view that D2 receptors alone are responsible for evoking the changes in behavior and basal ganglia output induced by nonselective dopamine agonists and endogenous dopamine is not supported by these results, which indicate that these phenomena require concurrent stimulation of both dopamine receptor subtypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walters, J R -- Bergstrom, D A -- Carlson, J H -- Chase, T N -- Braun, A R -- New York, N.Y. -- Science. 1987 May 8;236(4802):719-22.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2953072" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine ; Animals ; Apomorphine/pharmacology ; Basal Ganglia/*physiology ; Benzazepines/pharmacology ; Dopamine/physiology ; Ergolines/pharmacology ; Methyltyrosines/pharmacology ; Neurons/physiology ; Phenethylamines/pharmacology ; Quinpirole ; Rats ; Receptors, Dopamine/drug effects/*physiology ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Stereotyped Behavior/*physiology ; alpha-Methyltyrosine
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    Cellular and subcellular heterogeneity of [Ca2+]i in single heart cells revealed by fura-2 (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-16
    Description: Digital imaging of calcium indicator signals (fura-2 fluorescence) from single cardiac cells has revealed different subcellular patterns of cytoplasmic calcium ion concentration ([Ca2+]i) that are associated with different types of cellular appearance and behavior. In any population of enzymatically isolated rat heart cells, there are mechanically quiescent cells in which [Ca2+]i is spatially uniform, constant over time, and relatively low; spontaneously contracting cells, which have an increased [Ca2+]i, but in which the spatial uniformity of [Ca2+]i is interrupted periodically by spontaneous propagating waves of high [Ca2+]i; and cells that are hypercontracted (rounded up) and that have higher levels of [Ca2+]i than the other two types. The observed cellular and subcellular heterogeneity of [Ca2+]i in isolated cells indicates that experiments performed on suspensions of cells should be interpreted with caution. The spontaneous [Ca2+]i fluctuations previously observed without spatial resolution in multicellular preparations may actually be inhomogeneous at the subcellular level.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wier, W G -- Cannell, M B -- Berlin, J R -- Marban, E -- Lederer, W J -- HL25675/HL/NHLBI NIH HHS/ -- HL29473/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):325-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Benzofurans ; Calcium/*metabolism ; Cell Compartmentation ; Fura-2 ; In Vitro Techniques ; Myocardial Contraction ; Myocardium/*cytology/metabolism ; Rats ; Spectrometry, Fluorescence ; Time Factors
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    Interleukin-1 stimulates the secretion of hypothalamic corticotropin-releasing factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: There is now evidence that the immune system, during times of infectious challenge, can stimulate the secretion of glucocorticoids, the adrenal steroids that mediate important aspects of the response to stress. Specifically, secretion of interleukin-1 (IL-1), a monocyte lymphokine secreted after infection, appears at least in part responsible for this effect. Glucocorticoids are secreted in response to a neuroendocrine cascade involving, first, the brain, then the pituitary, and finally the adrenal gland. In this report, human IL-1 is shown to activate the adrenocortical axis at the level of the brain, stimulating the release of the controlling hormone corticotropin-releasing factor (CRF) from the hypothalamus. Infusion of IL-1 induced a significant secretion of CRF into the circulation exiting the hypothalamus, whereas immunoneutralization of CRF blocked the stimulatory effect of IL-1 on glucocorticoid secretion. IL-1 appeared to have no acute direct stimulatory effects on the pituitary or adrenal components of this system. Furthermore, IL-1 did not cause a nonspecific release of other hypothalamic hormones. Thus, the lymphokine acts in a specific manner to activate the adrenocortical axis at the level of the brain; this effect appears to be unrelated to the known pyrogenic effects of IL-1 within the hypothalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R -- Rivier, C -- Yamamoto, G -- Plotsky, P -- Vale, W -- AA06420/AA/NIAAA NIH HHS/ -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):522-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821621" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/physiology ; Adrenocorticotropic Hormone/secretion ; Animals ; Cell Line ; Corticosterone/secretion ; Corticotropin-Releasing Hormone/*secretion ; Hypothalamus/*secretion ; Immunologic Techniques ; Interleukin-1/*physiology ; Male ; Pituitary Gland, Anterior/secretion ; Pituitary Neoplasms/secretion ; Rats ; Rats, Inbred Strains
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    An in vitro neurite-promoting antigen functions in axonal regeneration in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-25
    Description: The function of the neurite growth-promoting antigen INO has been tested in an in vivo neurite regeneration system, the rat iris. The sympathetic innervation of the irides was removed by a single systemic injection of 6-hydroxydopamine. The subsequent regeneration of sympathetic axons into the iris of one eye bathed by the INO antibody, which inhibits neurite growth in vitro, was compared with the regrowth of sympathetic axons into the iris of the animal's other eye, which contained control antibody. Antibodies were released within the eye by implanted hybridoma cells. Neurite regeneration was measured by assaying [3H]norepinephrine uptake into freshly explained irides. The blockage of the function of the INO antigen by the antibody resulted in a decreased rate of axonal regeneration, thus suggesting the involvement of the INO antigen in the process of neurite regeneration in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandrock, A W Jr -- Matthew, W D -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- NS02253/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1605-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3306923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens/physiology ; Axons/physiology ; Fluorescent Antibody Technique ; Heparin/analogs & derivatives/immunology ; Hybridomas/transplantation ; Iris/innervation ; Laminin/physiology ; *Nerve Regeneration ; Norepinephrine/metabolism ; Proteoglycans/immunology ; Rats ; Sympathetic Nervous System/metabolism/*physiology
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    Environmental trends in extinction during the Paleozoic (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-02
    Description: Extinction intensities calculated from 505 Paleozoic marine assemblages divided among six environmental zones and 40 stratigraphic intervals indicate that whole communities exhibit increasing extinction offshore but that genera within individual taxonomic classes tend to have their highest extinction onshore. The offshore trend at the community level results from a concentration of genera in classes with low characteristic extinction rates in nearshore environments. This finding is consistent with the ecologic expectation that organisms inhabiting unpredictably fluctuating environments should suffer more extinction than counterparts living under more predictably equitable conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sepkoski, J J Jr -- DEB 81-08890/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 2;235:64-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of the Geophysical Sciences, University of Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11539724" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Classification ; Ecosystem ; *Environment ; *Fossils ; Invertebrates ; *Marine Biology ; Mollusca ; North America ; *Paleontology
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    A synaptic vesicle protein with a novel cytoplasmic domain and four transmembrane regions (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: Complementary DNA and genomic clones were isolated and sequenced corresponding to rat and human synaptophysin (p38), a major integral membrane protein of synaptic vesicles. The deduced amino acid sequences indicate an evolutionarily highly conserved protein that spans the membrane four times. Both amino and carboxyl termini face the cytoplasm, with the latter containing ten copies of a tyrosine-rich pentapeptide repeat. The structure of synaptophysin suggests that the protein may function as a channel in the synaptic vesicle membrane, with the carboxyl terminus serving as a binding site for cellular factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sudhof, T C -- Lottspeich, F -- Greengard, P -- Mehl, E -- Jahn, R -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1142-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Genetics, University of Texas Health Science Center, Dallas 75235.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3120313" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cloning, Molecular ; *Membrane Proteins/genetics ; Molecular Sequence Data ; Protein Conformation ; Rats ; Solubility ; Synaptic Vesicles/ultrastructure ; Synaptophysin
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    Fish oil prevents insulin resistance induced by high-fat feeding in rats (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-21
    Description: Non-insulin-dependent diabetes mellitus is an increasingly prevalent disease in Western and developing societies. A major metabolic abnormality of non-insulin-dependent diabetes is impaired insulin action (insulin resistance). Diets high in fat from vegetable and nonaquatic animal sources (rich in linoleic acid, an omega-6 fatty acid, and saturated fats) lead to insulin resistance. In rats fed high-fat diets, replacement of only 6 percent of the linoleic omega-6 fatty acids from safflower oil with long-chain polyunsaturated omega-3 fatty acids from fish oil prevented the development of insulin resistance. The effect was most pronounced in the liver and skeletal muscle, which have important roles in glucose supply and demand. The results may be important for therapy or prevention of non-insulin-dependent diabetes mellitus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Storlien, L H -- Kraegen, E W -- Chisholm, D J -- Ford, G L -- Bruce, D G -- Pascoe, W S -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):885-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3303333" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/physiology ; Adipose Tissue, Brown/metabolism ; Animals ; Diabetes Mellitus, Type 2/*prevention & control ; Dietary Fats/*adverse effects ; Fish Oils/*therapeutic use ; Glucose/metabolism ; Insulin/physiology ; *Insulin Resistance ; Liver/physiology ; Muscles/physiology ; Rats
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    Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: Low-stringency hybridization with human glucocorticoid receptor (hGR) complementary DNA was used to isolate a new gene encoding a predicted 107-kilodalton polypeptide. Expression studies demonstrate its ability to bind aldosterone with high affinity and to activate gene transcription in response to aldosterone, thus establishing its identity as the human mineralocorticoid receptor (hMR). This molecule also shows high affinity for glucocorticoids and stimulates a glucocorticoid-responsive promoter. Together the hMR and hGR provide unexpected functional diversity in which hormone-binding properties, target gene interactions, and patterns of tissue-specific expression may be used in a combinatorial fashion to achieve complex physiologic control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arriza, J L -- Weinberger, C -- Cerelli, G -- Glaser, T M -- Handelin, B L -- Housman, D E -- Evans, R M -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):268-75.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037703" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Chromosomes, Human, Pair 4 ; Cloning, Molecular ; DNA/genetics ; DNA-Binding Proteins/genetics ; Humans ; Rats ; Receptors, Glucocorticoid/*genetics ; Receptors, Mineralocorticoid ; Receptors, Steroid/*genetics ; Sequence Homology, Nucleic Acid ; Tissue Distribution ; Transcription Factors/*genetics ; Transcription, Genetic
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    Epitope mapping by chemical modification of free and antibody-bound protein antigen (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-13
    Description: A monoclonal antibody bound to a protein antigen slows the rate of chemical modification of amino acid residues located at the epitope. By comparing the degree of acetylation of 18 lysine and 7 threonine residues in free and antibody-bound horse cytochrome c, a discontiguous, conformational epitope was characterized on this protein antigen. The new approach is particularly suitable to probe discontiguous and conformational epitopes, which are difficult to analyze by other procedures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnens, A -- Demotz, S -- Corradin, G -- Binz, H -- Bosshard, H R -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):780-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433768" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/*immunology ; *Antigen-Antibody Complex ; Cytochrome c Group/*immunology ; Epitopes/*immunology ; Horses ; Humans ; Models, Molecular ; Protein Conformation ; Species Specificity
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    Paleolithic diet, evolution, and carcinogens (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, D L -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1633-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3120316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Carcinogens ; *Diet ; *Haplorhini ; Humans ; *Paleontology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Three-dimensional representation and analysis of brain energy metabolism (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-26
    Description: Quantitative autoradiography of brain glucose metabolism has been combined with digital image processing to represent the brain as a three-dimensional (3-D) reconstruction of brain energy use. Autoradiographs contain enormous amounts of potentially useful data, but conventional analyses, based on tedious manual methods, can sample and analyze only a small portion of this information. Computer 3-D reconstruction provides a mechanism for observing and analyzing all the data; therefore, a system of computer programs was developed for this purpose. The programs use digital imaging methods for image registration, superimpose whole brain data sets, and allow resampling of the 3-D data in arbitrary planes for pixel-by-pixel comparisons among multiple 3-D sets. These programs operate on the mathematical properties of the images alone, obviating the need for manual image alignment. Various statistical analyses can be applied to the data directly to study the patterns of metabolic changes in different experiments. The system is applied to data from experiments on the influence of injectable anesthetics on cerebral glucose metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hibbard, L S -- McGlone, J S -- Davis, D W -- Hawkins, R A -- AA06023/AA/NIAAA NIH HHS/ -- NS16389/NS/NINDS NIH HHS/ -- NS16737/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jun 26;236(4809):1641-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603004" target="_blank"〉PubMed〈/a〉
    Keywords: Anesthetics/pharmacology ; Animals ; Autoradiography ; Brain/drug effects/*metabolism ; *Energy Metabolism/drug effects ; Glucose/metabolism ; *Image Processing, Computer-Assisted ; Rats
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    Lipoprotein uptake by neuronal growth cones in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-22
    Description: Macrophages that rapidly enter injured peripheral nerve synthesize and secrete large quantities of apolipoprotein E. This protein may be involved in the redistribution of lipid, including cholesterol released during degeneration, to the regenerating axons. To test this postulate, apolipoprotein E-associated lipid particles released from segments of injured rat sciatic nerve and apolipoprotein E-containing lipoproteins from plasma were used to determine whether sprouting neurites, specifically their growth cones, possessed lipoprotein receptors. Pheochromocytoma (PC12) cells, which can be stimulated to produce neurites in vitro, were used as a model system. Apolipoprotein E-containing lipid particles and lipoproteins, which had been labeled with fluorescent dye, were internalized by the neurites and their growth cones; the unmetabolized dye appeared to be localized to the lysosomes. The rapid rate of accumulation in the growth cones precludes the possibility of orthograde transport of the fluorescent particles from the PC12 cell bodies. Thus, receptor-mediated lipoprotein uptake is performed by the apolipoprotein B,E(LDL) (low density lipoprotein) receptors, and in the regenerating peripheral nerve apolipoprotein E may deliver lipids to the neurites and their growth cones for membrane biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ignatius, M J -- Shooter, E M -- Pitas, R E -- Mahley, R W -- MH 17047/MH/NIMH NIH HHS/ -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):959-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576212" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Gland Neoplasms ; Animals ; Apolipoproteins E/*metabolism ; Axons/ultrastructure ; Cell Line ; Cells, Cultured ; Neurons/*cytology/metabolism ; Pheochromocytoma ; Rats ; Sciatic Nerve/*cytology/metabolism
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    Nerve growth factor treatment after brain injury prevents neuronal death (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-09
    Description: Cholinergic neuronal degeneration after axotomy has been proposed to be due to the loss of a retrogradely transported neurotrophic factor, possibly nerve growth factor (NGF). To test this hypothesis, NGF was continuously infused into the lateral ventricles of adult rats that had received bilateral lesions of all cholinergic axons projecting from the medial septum to the dorsal hippocampus. After 2 weeks of NGF treatment, identification of cholinergic neurons by the presence of the biosynthetic enzyme choline acetyltransferase revealed a dramatic increase (350%) in the survival of the axotomized septal cholinergic neurons. Thus, NGF or an NGF-like molecule can act as a neurotrophic factor for these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kromer, L F -- AG-06648/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 9;235(4785):214-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798108" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/*drug therapy/pathology ; Cell Survival ; Choline O-Acetyltransferase/metabolism ; Cholinergic Fibers/pathology ; Female ; Hippocampus/injuries ; Nerve Growth Factors/administration & dosage/*therapeutic use ; Neurons/enzymology/*pathology ; Rats ; Rats, Inbred Strains ; Septum Pellucidum/injuries
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    Clathrin light chains LCA and LCB are similar, polymorphic, and share repeated heptad motifs (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: The clathrin light chains fall into two major classes, LCA and LCB. In an intact clathrin triskelion, one light chain, of either class, is bound to the proximal segment of a heavy chain leg. Analysis of rat brain and liver complementary DNA clones for LCA and LCB shows that the two light chain classes are closely related. There appear to be several members of each class having deletions of varying length aligned at the same position. A set of ten heptad elements, characteristic of alpha-helical coiled coils, is a striking feature of the central part of each derived amino acid sequence. These observations suggest a model in which the alpha-helical segment mediates binding to clathrin heavy chains and the amino- and carboxyl-terminal segments mediate interactions with other proteins. They also suggest an explanation for the observed tissue-dependent size variation for members of each class.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirchhausen, T -- Scarmato, P -- Harrison, S C -- Monroe, J J -- Chow, E P -- Mattaliano, R J -- Ramachandran, K L -- Smart, J E -- Ahn, A H -- Brosius, J -- MH 38819/MH/NIMH NIH HHS/ -- R01 GM 36548-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):320-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563513" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/metabolism ; Clathrin/*genetics ; Cloning, Molecular ; DNA/analysis ; Liver/metabolism ; Macromolecular Substances ; *Polymorphism, Genetic ; Rats ; Repetitive Sequences, Nucleic Acid
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    New routes to early memories (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-06
    Description: Stimulation of one side of the olfactory system during training with odor-milk pairings in neonatal rats results in their ability to recall an odor memory by using the trained but not the untrained side of the brain. In 12-day-old rats, olfactory learning can be recalled by stimulation of either the trained or untrained side. The development of bilateral recall reflects the maturation of olfactory commissural pathways that provide access to the olfactory memory stored on the contralateral side. Furthermore, the commissural pathways need not be present at the time of memory formation but can establish new and specific access to already existing olfactory memories.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kucharski, D -- Hall, W G -- HD17458/HD/NICHD NIH HHS/ -- MH09436/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 6;238(4828):786-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Duke University, Durham, NC 27706.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3672125" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Brain/growth & development/physiology ; Central Nervous System/*growth & development ; Functional Laterality ; *Memory ; Milk ; *Odors ; Olfactory Pathways/*growth & development/physiology ; Rats
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    When does homology mean something else? (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 Sep 25;237(4822):1570.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629257" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Sequence ; *Biological Evolution ; *Sequence Homology, Nucleic Acid ; Terminology as Topic
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    Arginine vasopressin as a thyrotropin-releasing hormone (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-02-27
    Description: Although hypothyroidism (with concomitant increased levels of thyroid-stimulating hormone) has been associated with elevated plasma vasopressin, the role that vasopressin plays in controlling thyroid-stimulating hormone secretion from the adenohypophysis is not understood. In two in vitro pituitary cell systems, vasopressin caused a specific and dose-related release of thyroid-stimulating hormone from cells that was equal in potency to that elicited by thyrotropin-releasing hormone, the primary acknowledged regulator of thyroid-stimulating hormone release. When injected into the hypothalamus, however, vasopressin specifically inhibited the release of thyroid-stimulating hormone. Thus, vasopressin may exert differential regulatory effects on thyroid-stimulating hormone secretion in the hypothalamus and pituitary gland.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lumpkin, M D -- Samson, W K -- McCann, S M -- HD-09988/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1070-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2881350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*pharmacology/physiology ; Hypothalamus/drug effects/secretion ; Male ; Oxytocin/pharmacology ; Perfusion ; Pituitary Gland, Anterior/drug effects/*secretion ; Rats ; Rats, Inbred Strains ; Somatostatin/pharmacology ; Thyrotropin/*secretion ; Thyrotropin-Releasing Hormone/pharmacology
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    Isolation and structure of a covalent cross-link adduct between mitomycin C and DNA (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: A DNA cross-link adduct of the antitumor agent mitomycin C (MC) to DNA has been isolated and characterized; the results provide direct proof for bifunctional alkylation of DNA by MC. Exposure of MC to Micrococcus luteus DNA under reductive conditions and subsequent nuclease digestion yielded adducts formed between MC and deoxyguanosine residues. In addition to the two known monoadducts, a bisadduct was obtained. Reductive MC activation with Na2S2O4 (sodium dithionite) leads to exclusive bifunctional alkylation. The structure of the bisadduct was determined by spectroscopic methods that included proton magnetic resonance, differential Fourier transform infrared spectroscopy, and circular dichroism. Formation of the same bisadduct in vivo was demonstrated upon injection of rats with MC. Computer-generated models of the bisadduct that was incorporated into the center of the duplex B-DNA decamer d(CGTACGTACG)2 indicated that the bisadduct fit snugly into the minor groove with minimal distortion of DNA structure. A mechanistic analysis of the factors that govern monofunctional and bifunctional adduct formation is presented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomasz, M -- Lipman, R -- Chowdary, D -- Pawlak, J -- Verdine, G L -- Nakanishi, K -- CA 11572/CA/NCI NIH HHS/ -- CA 28681/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1204-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3103215" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Phenomena ; Chemistry ; Cross-Linking Reagents/*isolation & purification ; DNA/*metabolism ; Mass Spectrometry ; Mitomycin ; Mitomycins/*metabolism ; Models, Molecular
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    Structure of a psoralen cross-linked DNA in solution by nuclear magnetic resonance (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: One- and two-dimensional nuclear magnetic resonance (NMR) methods were used to determine a three-dimensional model of an eight-base-pair DNA fragment (d-GGGTACCC) cross-linked with psoralen in solution. Two-dimensional nuclear Overhauser effect experiments were used to assign the spectrum and estimate distances for 171 proton pairs in the cross-linked DNA. The NMR-derived model shows a 53 degree bend into the major groove that occurs primarily at the site of drug addition and a 56 degree unwinding that spans the eight-base-pair duplex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tomic, M T -- Wemmer, D E -- Kim, S H -- GM 31616/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3686011" target="_blank"〉PubMed〈/a〉
    Keywords: Base Composition ; *Cross-Linking Reagents ; *Dna ; Magnetic Resonance Spectroscopy/methods ; *Methoxsalen ; Models, Molecular ; Nucleic Acid Conformation ; *Oligodeoxyribonucleotides ; *Thymine
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    Expression of the multidrug-resistant gene in hepatocarcinogenesis and regenerating rat liver (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-29
    Description: Preneoplastic and neoplastic liver nodules and hepatocytes isolated from regenerating rat liver have been shown to be resistant to a broad range of carcinogenic agents. This phenomenon was studied by measuring the expression of the multidrug-resistant (mdr) gene in normal liver cells and in preneoplastic and neoplastic nodules and regenerating liver. Levels of messenger RNA for the mdr gene, which encodes P-glycoprotein, were elevated in both preneoplastic and neoplastic lesions. Expression of the mdr gene also reached high levels in regenerating rat liver 24 to 72 hours after partial hepatectomy. These results show that the expression of the mdr gene can be regulated in liver and is likely to be responsible for part of the multidrug-resistance phenotype of carcinogen-initiated hepatocytes and regenerating liver cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorgeirsson, S S -- Huber, B E -- Sorrell, S -- Fojo, A -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1987 May 29;236(4805):1120-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/*pharmacology ; Drug Resistance/*genetics ; *Genes ; Humans ; Liver/drug effects ; Liver Neoplasms, Experimental/chemically induced ; Liver Regeneration/*drug effects ; Male ; Precancerous Conditions/chemically induced ; RNA, Messenger/genetics ; Rats
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    Neocortical transplants in the mammalian brain lack a blood-brain barrier to macromolecules (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-13
    Description: In order to determine whether the blood-brain barrier was present in transplants of central nervous tissue, fetal neocortex, which already possesses blood-brain and blood-cerebrospinal fluid barriers to protein, was grafted into the undamaged fourth ventricle or directly into the neocortex of recipient rats. Horseradish peroxidase or a conjugated human immunoglobulin G-peroxidase molecule was systemically administered into the host. These proteins were detected within the cortical transplants within 2 minutes regardless of the age of the donor or postoperative time. At later times these compounds, which normally do not cross the blood-brain barrier, inundated the grafts and adjacent host brain and also entered the cerebrospinal fluid. Endogenous serum albumin detected immunocytochemically in untreated hosts had a comparable although less extensive distribution. Thus, transplants of fetal central nervous tissue have permanent barrier dysfunction, probably due to microvascular changes, and are not integrated physiologically within the host. Blood-borne compounds, either systemically administered or naturally occurring, which should never contact normal brain tissue, have direct access to these transplants and might affect neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenstein, J M -- NS-17468/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):772-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433767" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; *Blood-Brain Barrier ; Brain/*physiology ; Cerebral Cortex/physiology/*transplantation ; Cerebral Ventricles/physiology ; Female ; Fetus ; Gestational Age ; Horseradish Peroxidase/*metabolism ; Immunoglobulin G/metabolism ; Peroxidases/*metabolism ; Pregnancy ; Rats ; Rats, Inbred Strains
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    Tissue distribution and developmental expression of the messenger RNA encoding angiogenin (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-17
    Description: New blood vessel growth occurs during normal fetal development and in diseases such as cancer and diabetes. The polypeptide angiogenin induces new blood vessel growth in two biological assays and may play a role in the vascular development of the fetus and in the neovascularization that accompanies diseases and wound healing. A complementary DNA probe for human angiogenin was used to examine the tissue distribution of angiogenin messenger RNA (mRNA) in the developing rat and in selected transformed cell lines. Angiogenin mRNA was detected predominantly in adult liver but was also detectable at low levels in other tissues. The expression of the angiogenin gene in rat liver was found to be developmentally regulated; mRNA levels were low in the developing fetus, increased in the neonate, and maximal in the adult. The amount of angiogenin mRNA in human HT-29 colon carcinoma and SK-HEP hepatoma cells was not greater than that in normal rat liver. These results demonstrate that angiogenin is predominantly expressed in adult liver, that the pattern of angiogenin gene expression is not temporally related to vascular development in the rat, and that the transformed cells studied do not contain more angiogenin mRNA than does normal liver. If angiogenin activity is controlled at the transcriptional level, the results of this study suggest that the primary function of angiogenin in vivo may be in processes other than the regulation of vascular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Weiner, L H -- Swain, J L -- HL26831/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):280-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440105" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Line ; Gene Expression Regulation ; Humans ; Liver/physiology ; Neoplasm Proteins/*genetics ; Neovascularization, Pathologic ; RNA, Messenger/genetics ; Rats ; *Ribonuclease, Pancreatic ; Tissue Distribution
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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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    Thyroid hormone regulates TRH biosynthesis in the paraventricular nucleus of the rat hypothalamus (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-02
    Description: Thyroid hormone is important in the regulation of synthesis and secretion of thyroid-stimulating hormone (TSH) in the anterior pituitary, but its role in the control of hypothalamic thyrotropin-releasing hormone (TRH) is controversial. To determine whether thyroid hormone regulates the function of TRH in the hypothalamic tuberoinfundibular system, a study was made of the effect of hypothyroidism on thyrotropin-releasing hormone messenger RNA (proTRH mRNA) and TRH prohormone in the rat paraventricular nucleus. Extracts of rat hypothalamic paraventricular nucleus were examined by quantitative Northern blot analysis, and coronal sections of rat brain were examined by in situ hybridization histochemistry and immunocytochemistry. A nearly twofold increase in proTRH mRNA was observed in hypothyroid animals; this increase could be obliterated by levothyroxine treatment, suggesting an inverse relation between circulating thyroid hormone and proTRH mRNA. In situ hybridization showed that this response occurred exclusively in medial parvocellular neurons of the paraventricular nucleus. A simultaneous increase in proTRH mRNA and immunoreactive TRH prohormone in this region suggests that hypothyroidism induces both transcription and translation of the TRH prohormone in the paraventricular nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segerson, T P -- Kauer, J -- Wolfe, H C -- Mobtaker, H -- Wu, P -- Jackson, I M -- Lechan, R M -- DK 07900/DK/NIDDK NIH HHS/ -- DK 34540/DK/NIDDK NIH HHS/ -- DK 37021/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 2;238(4823):78-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, New England Medical Center Hospitals, Boston, MA 02111.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3116669" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Gene Expression Regulation ; Hypothyroidism/*physiopathology ; Immunoenzyme Techniques ; Paraventricular Hypothalamic Nucleus/*physiology ; RNA, Messenger/genetics ; Rats ; Thyroid Hormones/*physiology ; Thyrotropin-Releasing Hormone/*biosynthesis
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    The three-dimensional structure of Asn102 mutant of trypsin: role of Asp102 in serine protease catalysis (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: The structure of the Asn102 mutant of trypsin was determined in order to distinguish whether the reduced activity of the mutant at neutral pH results from an altered active site conformation or from an inability to stabilize a positive charge on the active site histidine. The active site structure of the Asn102 mutant of trypsin is identical to the native enzyme with respect to the specificity pocket, the oxyanion hole, and the orientation of the nucleophilic serine. The observed decrease in rate results from the loss of nucleophilicity of the active site serine. This decreased nucleophilicity may result from stabilization of a His57 tautomer that is unable to accept the serine hydroxyl proton.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprang, S -- Standing, T -- Fletterick, R J -- Stroud, R M -- Finer-Moore, J -- Xuong, N H -- Hamlin, R -- Rutter, W J -- Craik, C S -- AM26081/AM/NIADDK NIH HHS/ -- AM31507/AM/NIADDK NIH HHS/ -- GM24485/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):905-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3112942" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asparagine ; Aspartic Acid ; Binding Sites ; Cattle ; Computer Simulation ; Crystallography ; Histidine ; Hydrogen Bonding ; Hydrogen-Ion Concentration ; Protein Conformation ; Rats ; Serine ; Structure-Activity Relationship ; *Trypsin
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    Construction of a novel oncogene based on synthetic sequences encoding epidermal growth factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-16
    Description: The autocrine model postulates that constitutive release of a mitogenic growth factor can lead to uncontrolled proliferation and cell transformation. A synthetic polynucleotide encoding epidermal growth factor conferred a tumorigenic phenotype on cells. These cells were transformed through the action of an autocrine circuit having an extracellular component.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern, D F -- Hare, D L -- Cecchini, M A -- Weinberg, R A -- CA07285-03/CA/NCI NIH HHS/ -- R01CA39964/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):321-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3492043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Cell Division ; *Cell Transformation, Neoplastic/pathology ; DNA, Recombinant ; Epidermal Growth Factor/antagonists & inhibitors/*genetics/immunology ; Gene Expression Regulation ; Mice ; Neoplasms, Experimental/genetics/pathology ; *Oncogenes ; Rats ; Transfection
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    Xenopus oocytes injected with rat uterine RNA express very slowly activating potassium currents (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: Under the influence of estrogen, uterine smooth muscle becomes highly excitable, generating spontaneous and prolonged bursts of action potentials. In a study of the mechanisms by which this transition in excitability occurs, polyadenylated RNA from the uteri of estrogen-treated rats was injected into Xenopus oocytes. The injected oocytes expressed a novel voltage-dependent potassium current. This current was not observed in oocytes injected with RNA from several other excitable tissues, including rat brain and uterine smooth muscle from ovariectomized rats not treated with estrogen. The activation of this current on depolarization was exceptionally slow, particularly for depolarizations from relatively negative membrane potentials. Such a slowly activating channel may play an important role in the slow, repetitive bursts of action potentials in the myometrium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyle, M B -- Azhderian, E M -- MacLusky, N J -- Naftolin, F -- Kaczmarek, L K -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1221-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Egtazic Acid/pharmacology ; Female ; Injections ; Ion Channels/*metabolism ; Oocytes/*metabolism ; Potassium/*metabolism ; RNA/*pharmacology ; Rats ; Rats, Inbred Strains ; Time Factors ; Uterus/*metabolism ; Xenopus
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    Engineering enzyme specificity by "substrate-assisted catalysis" (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: A novel approach to engineering enzyme specificity is presented in which a catalytic group from an enzyme is first removed by site-directed mutagenesis causing inactivation. Activity is then partially restored by substrates containing the missing catalytic functional group. Replacement of the catalytic His with Ala in the Bacillus amyloliquefaciens subtilisin gene (the mutant is designated His64Ala) by site-directed mutagenesis reduces the catalytic efficiency (kcat/Km) by a factor of a million when assayed with N-succinyl-L-Phe-L-Ala-L-Ala-L-Phe-p-nitroanilide (sFAAF-pNA). Model building studies showed that a His side chain at the P2 position of a substrate bound at the active site of subtilisin could be virtually superimposed on the catalytic His side chain of this serine protease. Accordingly, the His64Ala mutant hydrolyzes a His P2 substrate (sFAHF-pNA) up to 400 times faster than a homologous Ala P2 or Gln P2 substrate (sFAAF-pNA or sFAQF-pNA) at pH 8.0. In contrast, the wild-type enzyme hydrolyzes these three substrates with similar catalytic efficiencies. Additional data from substrate-dependent pH profiles and hydrolysis of large polypeptides indicate that the His64Ala mutant enzyme can recover partially the function of the lost catalytic histidine from a His P2 side chain on the substrate. Such "substrate-assisted catalysis" provides a new basis for engineering enzymes with very narrow and potentially useful substrate specificities. These studies also suggest a possible functional intermediate in the evolution of the catalytic triad of serine proteases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carter, P -- Wells, J A -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):394-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299704" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Enzymes/*metabolism ; Models, Molecular ; Molecular Conformation ; Mutation ; Protein Binding ; Protein Conformation ; Substrate Specificity ; Subtilisins/genetics/*metabolism
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    Organ-resident, nonlymphoid cells suppress proliferation of autoimmune T-helper lymphocytes (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-28
    Description: Local presentation of autoantigen by organ-resident cells inappropriately expressing Ia determinants has been implicated in organ-specific autoimmunity. Experimental autoimmune uveoretinitis, induced in rats by immunization with retinal soluble antigen, is used as a model of organ-specific autoimmunity. In an in vitro system derived from this model, uveitogenic rat T-helper lymphocytes specific to the retinal soluble antigen, or control T-helper lymphocytes reactive to the purified protein derivative of tuberculin, were cocultured with Ia-expressing syngeneic retinal glial cells (Muller cells) in the presence of specific antigen. Antigen presentation was not apparent under ordinary culture conditions, and the Muller cells profoundly suppressed the proliferative response of primed T-helper lymphocytes to antigen presented on conventional antigen-presenting cells, as well as their subsequent interleukin-2 (IL-2)-dependent expansion. Suppression of proliferation was accompanied by inhibition of IL-2 production in response to antigen, as well as by reduction in high-affinity IL-2 receptor expression, and proceeded via a contact-dependent mechanism. These results suggest a role for locally acting suppression mechanisms in immune regulation and maintenance of tissue homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caspi, R R -- Roberge, F G -- Nussenblatt, R B -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1029-32.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2956685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; Interleukin-2/biosynthesis ; *Lymphocyte Activation ; Rats ; Retinitis/immunology ; T-Lymphocytes, Helper-Inducer/*physiology ; T-Lymphocytes, Regulatory/physiology ; Uveitis/immunology
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    Human amnion membrane serves as a substratum for growing axons in vitro and in vivo (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-29
    Description: The epithelial cell layer of human amnion membrane can be removed while the basement membrane and stromal surfaces remain morphologically intact. Such a preparation has been used as a substratum for the in vitro culture of dissociated neurons. Embryonic motor neurons from chick ciliary ganglion attached to both surfaces but grew extensive neurites only on the basement membrane. On cross sections of rolled amnion membranes, regenerating axons of cultured neurons were guided along pathways of basement membrane that were immunoreactive with an antibody to laminin. In addition, when rolled amnion membranes were implanted into a lesion cavity between the rat septum and hippocampus, cholinergic neurons extended axons through the longitudinally oriented implant into the hippocampus. Thus, this amnion preparation can serve as a bridge to promote axonal regeneration in vivo in damaged adult brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, G E -- Blaker, S N -- Engvall, E -- Varon, S -- Manthorpe, M -- Gage, F H -- AM30051/AM/NIADDK NIH HHS/ -- CA28896/CA/NCI NIH HHS/ -- NS16349/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 29;236(4805):1106-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576223" target="_blank"〉PubMed〈/a〉
    Keywords: *Amnion ; Animals ; Axons/*growth & development ; Basement Membrane ; Chick Embryo ; Humans ; In Vitro Techniques ; Motor Neurons/growth & development ; Rats
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    Neuronal circuits and evolution (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, B R -- Leise, E M -- New York, N.Y. -- Science. 1987 Jun 26;236(4809):1681-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603007" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Biological ; Animals ; *Biological Evolution ; Humans ; Nervous System/*anatomy & histology
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    Tumor cell rejection through terminal cell differentiation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: Leukemic cells cultured in the presence of various conditioned media differentiate into macrophages. This finding suggested that the maintenance of undifferentiated state and self-renewal in vivo may be related to the inability of the host to generate an appropriate level of differentiation factor (DF). Evidence for this hypothesis was derived from experiments in vitro and in vivo with myeloid leukemia of rat. The following results were obtained: (i) in vitro, the percentage of cell differentiation at a fixed concentration of DF was inversely related to the concentration of cells; (ii) leukemic cell inoculates that were lethal to 7-day-old rats were rejected by 21-day-old rats; (iii) leukemic cells in diffusion chambers underwent differentiation in 21-day-old rats but not in 7-day-old rats; (iv) organs from 21-day-old rats contained more DF activity than those of 7-day-old rats; (v) treatment of rats with DF in diffusion chambers resulted in leukemic cell differentiation inside the chamber; and (vi) the development of leukemia in 7-day-old rats was aborted by treatment with DF. These results show that the differentiation of rat leukemia cells requires the appropriate level of DF. The proliferation of transplanted leukemia cells in 7-day-old rats goes unchecked because of inadequate generation of DF. Conversely, in the 21-day-old rats, rejection is accomplished by differentiation of the transplanted cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jimenez, J J -- Yunis, A A -- AM 07114/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1278-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Miami School of Medicine, FL 33101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Differentiation ; Cell Division ; Cell Line ; Cell Survival ; *Graft Rejection ; Leukemia, Experimental/*pathology ; Neoplasm Transplantation ; Phagocytosis ; Rats
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    Atomic structure of thymidylate synthase: target for rational drug design (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-23
    Description: The atomic structure of thymidylate synthase from Lactobacillus casei was determined at 3 angstrom resolution. The native enzyme is a dimer of identical subunits. The dimer interface is formed by an unusual association between five-stranded beta sheets present in each monomer. Comparison of known sequences with the Lactobacillus casei structure suggests that they all have a common core structure around which loops are inserted or deleted in different sequences. Residues from both subunits contribute to each active site. Two arginine side chains can contribute to binding phosphate on the substrate. The side chains of several conserved amino acids can account for other determinants of substrate binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardy, L W -- Finer-Moore, J S -- Montfort, W R -- Jones, M O -- Santi, D V -- Stroud, R M -- AI 19358/AI/NIAID NIH HHS/ -- CA41323/CA/NCI NIH HHS/ -- GM 24485/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):448-55.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3099389" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Crystallography ; Deoxyuracil Nucleotides/metabolism ; Lactobacillus casei/enzymology ; Models, Molecular ; Protein Conformation ; Structure-Activity Relationship ; *Thymidylate Synthase/antagonists & inhibitors
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    The origin of the modern human mind (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1987 May 8;236(4802):668-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576191" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Brain/*physiology ; Esthetics ; Humans ; Language ; Thinking
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    Astrocytes block axonal regeneration in mammals by activating the physiological stop pathway (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-07
    Description: Regenerating sensory axons in the dorsal roots of adult mammals are stopped at the junction between the root and spinal cord by reactive astrocytes. Do these cells stop axonal elongation by activating the physiological mechanisms that normally operate to stop axons during development, or do they physically obstruct the elongating axons? In order to distinguish these possibilities, the cytology of the axon tips of regenerating axons that were stopped by astrocytes was compared with the axon tips that were physically obstructed at a cul-de-sac produced by ligating a peripheral nerve. The terminals of the physically obstructed axon tips were distended with neurofilaments and other axonally transported structures that had accumulated when the axons stopped elongating. By contrast, neurofilaments did not accumulate in the tips of regenerating axons that were stopped by spinal cord astrocytes at the dorsal root transitional zone. These axo-glial terminals resembled the terminals that axons make on target neurons during normal development. On the basis of these observations, astrocytes appear to stop axons from regenerating in the mammalian spinal cord by activating the physiological stop pathway that is built into the axon and that normally operates when axons form stable terminals on target cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liuzzi, F J -- Lasek, R J -- NS14900-09/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):642-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603044" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*physiology/ultrastructure ; Axons/*physiology ; Humans ; Intermediate Filaments/ultrastructure ; Ligation ; *Nerve Regeneration ; Neurons, Afferent/physiology ; Rats
    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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  • 87
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    Identification by cell fusion of gene sequences that interact with positive trans-acting factors (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: Cell fusion experiments have implicated positive or negative regulatory factors in the cell type--specific expression of specialized endogenous genes. The inability to readily manipulate such genes has prevented characterization of the cis-acting DNA sequences that interact with these factors. A transfection-fusion technique, which combined stable gene transfer and formation of transient heterokaryons, was used to study this class of factors and their DNA binding sites. Messenger RNA directed by a quiescent, rat prolactin promoter region stably transferred into mouse fibroblasts was detected only after fusion to rat pituitary cells, implying that pituitary cells contain a positive cell type--specific factor or factors. Nuclear run-on assays showed that fusion activation is transcriptional. Fusion did not activate either a stably transferred rat growth hormone gene promoter or expression of the endogenous silent fibroblast prolactin or growth hormone genes. Analysis by 5'-deletion mutation identified a 30-base pair DNA sequence required for cell fusion activation of the rat prolactin promoter region. Comparison with previous results from direct cellular transfer of this region implies that transfection-fusion identifies novel regulatory DNA sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lufkin, T -- Bancroft, C -- GM36847/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):283-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3474782" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Cell Fusion ; Chloramphenicol O-Acetyltransferase ; Gene Expression Regulation ; Growth Hormone/genetics ; Pituitary Gland/*physiology ; Prolactin/*genetics ; *Promoter Regions, Genetic ; Rats ; Transcription Factors/*genetics ; Transcription, Genetic ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 88
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    Seizures in drug-treated animals (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miczek, K A -- Weerts, E M -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1127-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3823870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azides/*adverse effects ; Benzodiazepines/*adverse effects ; Male ; Rats ; Rats, Inbred Strains ; Saimiri ; Seizures/*chemically induced
    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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  • 89
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    Delayed transneuronal death of substantia nigra neurons prevented by gamma-aminobutyric acid agonist (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: In an investigation of the mechanism by which brain lesions result in delayed degeneration of neurons remote from the site of injury, neurons within the caudate nucleus of rats were destroyed by local injection of the excitotoxin ibotenic acid. Treatment resulted in the rapid degeneration of the striatonigral pathway including projections containing the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and delayed transneuronal death of neurons in the substantia nigra pars reticulata. The distribution of nigral cell loss corresponded to the loss of GABAergic terminals. Neuronal death was prevented by long-term intraventricular infusion of the GABA agonist muscimol. Delayed transneuronal degeneration may be produced by neuronal disinhibition consequent to loss of inhibitory inputs. Replacement of inhibitory transmitters by suitable drugs may prevent some forms of delayed neuronal death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saji, M -- Reis, D J -- HL18974/HL/NHLBI NIH HHS/ -- NS03346/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):66-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798095" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/drug effects ; Ibotenic Acid/antagonists & inhibitors/pharmacology ; Male ; Muscimol/*pharmacology ; Nerve Degeneration/*drug effects ; Neural Inhibition ; Rats ; Substantia Nigra/*cytology/physiology ; gamma-Aminobutyric Acid/*physiology
    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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  • 90
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    A tunnel in the large ribosomal subunit revealed by three-dimensional image reconstruction (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: A better understanding of the molecular mechanism of protein biosynthesis depends on the availability of a reliable model for the ribosome particle. The application of a diffraction technique, namely, three-dimensional image reconstruction from two-dimensional sheets of the large ribosomal subunits of Bacillus stearothermophilus at a resolution of 30 angstroms is described. The resulting three-dimensional model shows at least four projecting arms, arranged radially near the presumed interface with the 30S subunit. The projecting arms are positioned around a cleft, which turns into a tunnel with a length of 100 to 120 angstroms and a diameter of up to 25 angstroms. This tunnel spans the particle and may provide the path taken by the nascent polypeptide chain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonath, A -- Leonard, K R -- Wittmann, H G -- GM34360/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 15;236(4803):813-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576200" target="_blank"〉PubMed〈/a〉
    Keywords: Geobacillus stearothermophilus/*ultrastructure ; Microscopy, Electron ; Models, Molecular ; Ribosomes/*ultrastructure
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    Development of two types of calcium channels in cultured mammalian hippocampal neurons (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-06
    Description: Calcium influx through voltage-gated membrane channels plays a crucial role in a variety of neuronal processes, including long-term potentiation and epileptogenesis in the mammalian cortex. Recent studies indicate that calcium channels in some cell types are heterogeneous. This heterogeneity has now been shown for calcium channels in mammalian cortical neurons. When dissociated embryonic hippocampal neurons from rat were grown in culture they first had only low voltage-activated, fully inactivating somatic calcium channels. These channels were metabolically stable and conducted calcium better than barium. Appearing later in conjunction with neurite outgrowth and eventually predominating in the dendrites, were high voltage-activated, slowly inactivating calcium channels. These were metabolically labile and more selective to barium than to calcium. Both types of calcium currents were reduced by classical calcium channel antagonists, but the low voltage-activated channels were more strongly blocked by the anticonvulsant drug phenytoin. These findings demonstrate the development and coexistence of two distinct types of calcium channels in mammalian cortical neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yaari, Y -- Hamon, B -- Lux, H D -- New York, N.Y. -- Science. 1987 Feb 6;235(4789):680-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barium/pharmacology ; Cadmium/pharmacology ; Calcium/*physiology ; Cell Differentiation ; Cells, Cultured ; Hippocampus/cytology/*physiology ; Ion Channels/classification/drug effects/*physiology ; Membrane Potentials ; Rats
    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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