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  • Articles  (131)
  • Rats  (68)
  • RNA, Messenger/genetics  (38)
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  • LUNAR AND PLANETARY EXPLORATION
  • Life and Medical Sciences
  • American Association for the Advancement of Science (AAAS)  (131)
  • 2015-2019
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  • 1985-1989  (131)
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  • 1987  (131)
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  • Articles  (131)
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  • 2005-2009
  • 1985-1989  (131)
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  • 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
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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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    Relationship between the c-myb locus and the 6q-chromosomal aberration in leukemias and lymphomas (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: Deletions of the long arm of chromosome 6 (6q-) are frequently found in hematopoietic neoplasms, including acute lymphoblastic leukemias, non-Hodgkin lymphomas and (less frequently) myeloid leukemias. The c-myb proto-oncogene has been mapped to region 6q21-24, which suggests that it could be involved in the 6q- aberrations. By means of in situ chromosomal hybridization on cells from six hematopoietic malignancies, it was demonstrated that the c-myb locus is not deleted, but is retained on band q22, which is consistently bordered by the chromosomal breakpoints in both interstitial and terminal 6q- deletions. The deletion breakpoints were located at some distance from the myb locus since no rearrangement of c-myb sequences was found. In one case, however, amplification of the entire c-myb locus was detectable. Furthermore, in all cases tested that carry 6q- deletions, myb messenger RNA levels were significantly higher than in normal cells or in malignant cells matched for lineage and stage of differentiation but lacking the 6q- marker. These results indicate that 6q- deletions are accompanied by structural and functional alterations of the c-myb locus and that these alterations may be involved in the pathogenesis of leukemias and lymphomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barletta, C -- Pelicci, P G -- Kenyon, L C -- Smith, S D -- Dalla-Favera, R -- CA16239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1064-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3469751" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Deletion ; *Chromosomes, Human, Pair 6 ; DNA/genetics ; Gene Amplification ; Humans ; Leukemia/*genetics ; Leukemia, Lymphoid/genetics ; Leukemia, Myeloid/genetics ; Lymphoma, Non-Hodgkin/*genetics ; Nucleic Acid Hybridization ; RNA, Messenger/genetics
    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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    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
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  • 5
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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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  • 6
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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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  • 7
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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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  • 8
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    A mammalian mitochondrial RNA processing activity contains nucleus-encoded RNA (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-03-06
    Description: Ribonuclease mitochondrial RNA processing, a site-specific endoribonuclease involved in primer RNA metabolism in mammalian mitochondria, requires an RNA component for its activity. On the basis of copurification and selective inactivation with complementary oligonucleotides, a 135-nucleotide RNA species, not encoded in the mitochondrial genome, is identified as the RNA moiety of the endoribonuclease. This finding implies transport of a nucleus-encoded RNA, essential for organelle DNA replication, to the mitochondrial matrix.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, D D -- Clayton, D A -- GM-33088-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1178-84.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/*physiology ; Chemical Phenomena ; Chemistry ; Drug Resistance ; Endonucleases/isolation & purification/metabolism ; Enzyme Activation/drug effects ; *Genetic Code ; Humans ; Mammals/*genetics/metabolism ; Micrococcal Nuclease/pharmacology ; Mitochondria/*metabolism ; Oligonucleotides/pharmacology ; Organoids/physiology ; RNA/*biosynthesis/genetics/isolation & purification/physiology ; Ribonucleases/metabolism ; Subcellular Fractions/metabolism
    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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  • 9
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    Oncogenes in radioresistant, noncancerous skin fibroblasts from a cancer-prone family (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
    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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  • 10
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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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  • 11
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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
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  • 12
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    Transformation by oncogenes encoding protein kinases induces the metastatic phenotype (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-09
    Description: Oncogenes encoding serine/threonine or tyrosine kinases were introduced into the established rodent fibroblast cell line NIH 3T3 and tested for tumorigenic and metastatic behavior in T cell-deficient nude mice. Transforming oncogenes of the ras family were capable of converting fibroblast cell lines to fully metastatic tumors. Cell lines transformed by the kinase oncogenes mos, raf, src, fes, and fms formed experimental metastases and (in some cases) these genes were more efficient at metastatic conversion than a mutant ras gene. In contrast, cells transformed by either of two nuclear oncogenes, myc or p53, were tumorigenic when injected subcutaneously but were virtually nonmetastatic after intravenous injection. These data demonstrate that, in addition to ras, a structurally divergent group of kinase oncogenes can induce the metastatic phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, S E -- Wright, J A -- Jarolim, L -- Yanagihara, K -- Bassin, R H -- Greenberg, A H -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):202-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Cells, Cultured ; *Genes ; Mice ; *Neoplasm Metastasis ; *Oncogenes ; Phenotype ; Protein Kinases/*genetics
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  • 13
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    Identification and localization of mutations at the Lesch-Nyhan locus by ribonuclease A cleavage (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: Many mutations leading to human disease are the result of single DNA base pair changes that cannot be identified by Southern analysis. This has prompted the development of alternative assays for point mutation detection. The recently described ribonuclease A cleavage procedure, with a polyuridylic acid-paper affinity chromatography step, has been used to identify the mutational lesions in the hypoxanthine phosphoribosyltransferase (HPRT) messenger RNAs of patients with Lesch-Nyhan syndrome. Distinctive ribonuclease A cleavage patterns were identified in messenger RNA from 5 of 14 Lesch-Nyhan patients who were chosen because no HPRT Southern or Northern blotting pattern changes had been found. This approach now allows HPRT mutation detection in 50 percent of the cases of Lesch-Nyhan syndrome. The polyuridylic acid-paper affinity procedure provides a general method for analysis of low abundance messenger RNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbs, R A -- Caskey, C T -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):303-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563511" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Chromosome Deletion ; HeLa Cells/enzymology ; Humans ; Hypoxanthine Phosphoribosyltransferase/*genetics ; Lesch-Nyhan Syndrome/*genetics ; *Mutation ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Ribonuclease, Pancreatic
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  • 14
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    Characterization and chromosomal localization of a cDNA encoding brain amyloid of Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: Four clones were isolated from an adult human brain complementary DNA library with an oligonucleotide probe corresponding to the first 20 amino acids of the beta peptide of brain amyloid from Alzheimer's disease. The open reading frame of the sequenced clone coded for 97 amino acids, including the known amino acid sequence of this polypeptide. The 3.5-kilobase messenger RNA was detected in mammalian brains and human thymus. The gene is highly conserved in evolution and has been mapped to human chromosome 21.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldgaber, D -- Lerman, M I -- McBride, O W -- Saffiotti, U -- Gajdusek, D C -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):877-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3810169" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amino Acid Sequence ; Amyloid/*genetics ; *Chromosomes, Human, Pair 21 ; Cloning, Molecular ; DNA/genetics ; Humans ; Protein Conformation ; RNA, Messenger/genetics ; Solubility ; Transcription, Genetic
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  • 15
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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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  • 16
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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)
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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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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)
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    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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  • 18
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    Conservation of the Duchenne muscular dystrophy gene in mice and humans (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-16
    Description: A portion of the Duchenne muscular dystrophy (DMD) gene transcript from human fetal skeletal muscle and mouse adult heart was sequenced, representing approximately 25 percent of the total, 14-kb DMD transcript. The nucleic acid and predicted amino acid sequences from the two species are nearly 90 percent homologous. The amino acid sequence that is predicted from this portion of the DMD gene indicates that the protein product might serve a structural role in muscle, but the abundance and tissue distribution of the messenger RNA suggests that the DMD protein is not nebulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffman, E P -- Monaco, A P -- Feener, C C -- Kunkel, L M -- 2T 32 GM07753-07/GM/NIGMS NIH HHS/ -- HD18658/HD/NICHD NIH HHS/ -- R01 NS23740/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):347-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Children's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659917" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/*genetics ; DNA, Recombinant ; Exons ; Humans ; Male ; Mice ; Molecular Sequence Data ; Muscle Proteins/genetics ; Muscles/analysis/embryology ; Muscular Dystrophies/*genetics ; Muscular Dystrophy, Animal/*genetics ; Myocardium/analysis ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; X Chromosome
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  • 19
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    Identification of an amplified, highly expressed gene in a human glioma (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-03
    Description: A gene, termed gli, was identified that is amplified more than 50-fold in a malignant glioma. The gene is expressed at high levels in the original tumor and its derived cell line and is located at chromosome 12 position (q13 to q14.3). The gli gene is a member of a select group of cellular genes that are genetically altered in primary human tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Bigner, S H -- Bigner, D D -- Trent, J M -- Law, M L -- O'Brien, S J -- Wong, A J -- Vogelstein, B -- CA-09243/CA/NCI NIH HHS/ -- CA-43722/CA/NCI NIH HHS/ -- NS-20023/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):70-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3563490" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; *Chromosomes, Human, Pair 12 ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; *Gene Amplification ; Gene Expression Regulation ; Glioma/*genetics ; Humans ; RNA, Messenger/genetics ; RNA, Neoplasm/genetics
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  • 20
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    Model studies of polychlorinated dibenzo-p-dioxin formation during municipal refuse incineration (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-14
    Description: Toxic chlorinated dibenzo-p-dioxins are known to be formed in incinerators that burn municipal refuse. These compounds were synthesized by surface-catalyzed reactions on fly ash particulates taken from incinerators. Dioxins were produced catalytically from chlorinated phenol precursors, from non-chlorinated compounds that were chemically dissimilar to dioxins, and from reaction of phenol with inorganic chlorides. The relative amounts of dioxins formed from [13C6]pentachlorophenol with different fly ashes that had been cleaned of all organic compounds corresponded well with those amounts originally found on the samples as received from the incinerators. The optimum temperature range for the formation of dioxins from pentachlorophenol was 250 degrees to 350 degrees C.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karasek, F W -- Dickson, L C -- New York, N.Y. -- Science. 1987 Aug 14;237(4816):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616606" target="_blank"〉PubMed〈/a〉
    Keywords: Chemical Phenomena ; Chemistry ; Dioxins/*chemical synthesis ; Gas Chromatography-Mass Spectrometry ; *Hot Temperature ; Pentachlorophenol ; Polyvinyl Chloride ; *Refuse Disposal ; Tetrachlorodibenzodioxin/analogs & derivatives/*chemical synthesis
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  • 21
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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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  • 22
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    Ouabain resistance conferred by expression of the cDNA for a murine Na+, K+-ATPase alpha subunit (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: The molecular basis for the marked difference between primate and rodent cells in sensitivity to the cardiac glycoside ouabain has been established by genetic techniques. A complementary DNA encoding the entire alpha 1 subunit of the mouse Na+- and K+-dependent adenosine triphosphatase (ATPase) was inserted into the expression vector pSV2. This engineered DNA molecule confers resistance against 10(-4) M ouabain to monkey CV-1 cells. Deletion of sequences encoding the carboxyl terminus of the alpha 1 subunit abolish the activity of the complementary DNA. The ability to assay the biological activity of this ATPase in a transfection protocol permits the application of molecular genetic techniques to the analysis of structure-function relationships for the enzyme that establishes the internal Na+/K+ environment of most animal cells. The full-length alpha 1 subunit complementary DNA will also be useful as a dominant selectable marker for somatic cell genetic studies utilizing ouabain-sensitive cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kent, R B -- Emanuel, J R -- Ben Neriah, Y -- Levenson, R -- Housman, D E -- CA-07919/CA/NCI NIH HHS/ -- CA-26712/CA/NCI NIH HHS/ -- CA-38992/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):901-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3039660" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cercopithecus aethiops ; DNA/genetics ; Drug Resistance ; Gene Expression Regulation ; Macromolecular Substances ; Mice ; Ouabain/*pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors/*genetics ; Species Specificity ; Structure-Activity Relationship ; Transfection
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  • 23
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    Chemical identification of a tumor-derived angiogenic factor (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Neoplasms produce substances that induce blood vessel formation (angiogenesis). Fractions from ethanol extracts of the Walker 256 carcinoma were isolated by silica column chromatography and C18 reversed-phase high-performance liquid chromatography. Two of the isolated fractions induced neovascularization when tested in the rabbit corneal micropocket assay. One of the fractions was identified as nicotinamide by desorption-electron impact mass spectrometry, nuclear magnetic resonance spectroscopy, and gas chromatography-mass spectrometry. The second active fraction contained nicotinamide as part of a more complex, as yet unidentified, molecular arrangement. Microgram quantities of commercial nicotinamide induced neovascularization in the corneal micropocket assay and in the chick chorioallantoic membrane assay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kull, F C Jr -- Brent, D A -- Parikh, I -- Cuatrecasas, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):843-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2437656" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents/*isolation & purification/pharmacology ; Animals ; Carcinoma 256, Walker/*physiopathology ; Cells, Cultured ; Chick Embryo ; Cornea/blood supply ; Endothelium/cytology/drug effects ; Gas Chromatography-Mass Spectrometry ; Growth Substances/*isolation & purification ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Mice ; Neovascularization, Pathologic ; Niacinamide/isolation & purification/pharmacology
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  • 24
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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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  • 25
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    Smooth muscle-mediated connective tissue remodeling in pulmonary hypertension (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: Abnormal accumulation of connective tissue in blood vessels contributes to alterations in vascular physiology associated with disease states such as hypertension and atherosclerosis. Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production. A two- to fourfold increase in elastin production was observed in pulmonary artery tissue and medial smooth muscle cells from hypertensive calves. This stimulation of elastin production was accompanied by a corresponding increase in elastin messenger RNA consistent with regulation at the transcriptional level. Conditioned serum harvested from cultures of pulmonary artery smooth muscle cells isolated from hypertensive animals contained one or more low molecular weight elastogenic factors that stimulated the production of elastin in both fibroblasts and smooth muscle cells and altered the chemotactic responsiveness of fibroblasts to elastin peptides. These results suggest that connective tissue changes in the pulmonary vasculature in response to pulmonary hypertension are orchestrated by the medial smooth muscle cell through the generation of specific differentiation factors that alter both the secretory phenotype and responsive properties of surrounding cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mecham, R P -- Whitehouse, L A -- Wrenn, D S -- Parks, W C -- Griffin, G L -- Senior, R M -- Crouch, E C -- Stenmark, K R -- Voelkel, N F -- CA31777/CA/NCI NIH HHS/ -- HD20521/HD/NICHD NIH HHS/ -- HL14985/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):423-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoxia ; Cattle ; Connective Tissue/pathology/*physiopathology ; Disease Models, Animal ; Elastin/genetics/physiology ; Humans ; Hypertension, Pulmonary/pathology/*physiopathology ; Muscle, Smooth, Vascular/pathology/*physiopathology ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 26
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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)
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    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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  • 27
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    A stereospecific cyclization catalyzed by an antibody (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-28
    Description: A monoclonal antibody elicited by a transition-state analog that is representative of an intramolecular six-membered ring cyclization reaction acted as a stereospecific, enzyme-like catalyst for the appropriate substrate. Formation of a single enantiomer of a delta-lactone from the corresponding racemic delta-hydroxyester was accelerated by the antibody by about a factor of 170, which permitted isolation of the lactone in an enantiomeric excess of about 94 percent. This finding demonstrates the feasibility of catalytic-antibody generation for chemical transformations that require stereochemical control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Napper, A D -- Benkovic, S J -- Tramontano, A -- Lerner, R A -- GM 13306/GM/NIGMS NIH HHS/ -- GM 35318/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1041-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616626" target="_blank"〉PubMed〈/a〉
    Keywords: *Antibodies, Monoclonal ; Catalysis ; Chemical Phenomena ; Chemistry ; Cyclization ; *Stereoisomerism
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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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    Allelic exclusion in transgenic mice that express the membrane form of immunoglobulin mu (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-05-15
    Description: Antibody-producing cells display a special form of regulation whereby each cell produces immunoglobulin from only one of its two sets of antibody genes. This phenomenon, called allelic exclusion, is thought to be mediated by the product of one heavy chain allele restricting the expression of the other. Heavy chains are synthesized in two molecular forms, secreted and membrane bound. In order to determine whether it is specifically the membrane-bound form of the immunoglobulin M (IgM) heavy chain (mu) that mediates this regulation, transgenic mice were created that carry a human mu chain gene altered so that it can only direct the synthesis of the membrane-bound protein. The membrane-bound form of the human mu chain was made by most of the B cells in these animals as measured by assays of messenger RNA and surface immunoglobulins. Further, the many B cells that express the human gene do not express endogenous mouse IgM, and the few B cells that express endogenous mouse mu do not express the transgene. Thus, the membrane-bound form of the mu chain is sufficient to mediate allelic exclusion. In addition, the molecular structures recognized for this purpose are conserved between human and mouse systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussenzweig, M C -- Shaw, A C -- Sinn, E -- Danner, D B -- Holmes, K L -- Morse, H C 3rd -- Leder, P -- New York, N.Y. -- Science. 1987 May 15;236(4803):816-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107126" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Antibody-Producing Cells/*immunology ; Gene Expression Regulation ; *Genes ; Humans ; Immunoglobulin M/genetics ; Immunoglobulin mu-Chains/*genetics ; Mice ; Mice, Inbred Strains ; RNA, Messenger/genetics ; Transcription, Genetic
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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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    The mitochondrial genotype can influence nuclear gene expression in yeast (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-30
    Description: Isochromosomal, respiratory-deficient yeast strains, such as a mit-, a hypersuppressive petite, and a petite lacking mitochondrial DNA, are phenotypically identical in spite of differences in their mitochondrial genomes. Subtractive hybridizations of complementary DNA's to polyadenylated RNA isolated from derepressed cultures of these strains reveal the presence of nuclear-encoded transcripts whose abundance varies not only between them and their respiratory-competent parent, but among the respiratory-deficient strains themselves. Transcripts of some nuclear-encoded mitochondrial proteins, like cytochrome c and the alpha and beta subunits of the mitochondrial adenosine triphosphatase, whose abundance is affected by glucose or heme, do not vary. In the absence of major metabolic variables, yeast cells seem to respond to the quality and quantity of mitochondrial DNA and modulate the levels of nuclear-encoded RNA's, perhaps as a means of intergenomic regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parikh, V S -- Morgan, M M -- Scott, R -- Clements, L S -- Butow, R A -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):576-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3027892" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Nucleus/physiology ; Cytochrome c Group/genetics ; DNA, Fungal/genetics ; DNA, Mitochondrial/genetics ; Electron Transport Complex IV/genetics ; Gene Expression Regulation ; Genes, Fungal ; Genotype ; Mitochondria/*physiology ; Mutation ; RNA, Fungal/genetics ; RNA, Messenger/genetics ; RNA, Ribosomal/genetics ; Saccharomyces cerevisiae/*genetics
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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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    Pancreatic neoplasia induced by SV40 T-antigen expression in acinar cells of transgenic mice (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-09
    Description: Three lines of transgenic mice were produced that develop pancreatic neoplasms as a consequence of expression of an elastase I-SV40 T-antigen fusion gene in the acinar cells. A developmental analysis suggests at least a two-stage process in the ontogeny of this disease. The first stage is a T antigen-induced, preneoplastic state characterized by a progression from hyperplasia to dysplasia of the exocrine pancreas, by an increased percentage of tetraploid cells, and by an arrest in acinar cell differentiation. The second stage is characterized by the formation of tumor nodules that appear to be monoclonal, because they have discrete aneuploid DNA contents. The cells within the nodules as compared to normal pancreatic tissue have less total RNA by a factor of 5, less pancreas-specific messenger RNA by a factor of about 50, and increased levels of T-antigen messenger RNA. A tumor cell line has been derived that retains both pancreatic and neoplastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ornitz, D M -- Hammer, R E -- Messing, A -- Palmiter, R D -- Brinster, R L -- GM-07266/GM/NIGMS NIH HHS/ -- HD-09172/HD/NICHD NIH HHS/ -- NS-00956/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):188-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Laboratory, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821617" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/*genetics ; *Cell Transformation, Neoplastic ; DNA Restriction Enzymes ; Genes ; Genes, Viral ; Mice ; Mice, Transgenic ; Pancreatic Elastase/genetics ; Pancreatic Neoplasms/genetics/*microbiology/pathology ; Protein Kinases/*genetics ; RNA, Messenger/genetics ; Simian virus 40/*genetics
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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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    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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    Variable occurrence of the nrdB intron in the T-even phages suggests intron mobility (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-10
    Description: The bacteriophage T4 nrdB gene, encoding nucleoside diphosphate reductase subunit B, contains a self-splicing group I intervening sequence. The nrdB intron was shown to be absent from the genomes of the closely related T-even phages T2 and T6. Evidence for variable intron distribution was provided by autocatalytic 32P-guanosine 5'-triphosphate labeling of T-even RNAs, DNA and RNA hybridization analyses, and DNA sequencing studies. The results indicate the nonessential nature of the intron in nrdB expression and phage viability. Furthermore, they suggest that either precise intron loss from T2 and T6 or lateral intron acquisition by T4 occurred since the evolution of these phages from a common ancestor. Intron movement in the course of T-even phage divergence raises provocative questions about the origin of these self-splicing elements in prokaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedersen-Lane, J -- Belfort, M -- GM 33314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3037701" target="_blank"〉PubMed〈/a〉
    Keywords: *DNA Transposable Elements ; Genes ; *Genes, Viral ; *Introns ; Phylogeny ; RNA Splicing ; RNA, Messenger/genetics ; RNA, Viral/genetics ; Ribonucleoside Diphosphate Reductase/*genetics ; Ribonucleotide Reductases/*genetics ; T-Phages/*genetics ; Viral Proteins/*genetics
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    Localization, secretion, and action of inhibin in human placenta (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-10
    Description: Inhibin is a gonadal glycoprotein hormone that regulates the production of follicle-stimulating hormone (FSH) by the anterior pituitary gland and exhibits intragonadal actions as well. The present study shows that inhibin-like immunoreactivity (inhibin-LI) is present in cells of the cytotrophoblast layer of human placenta at term and in primary cultures of human trophoblasts. Human chorionic gonadotropin (hCG) stimulated secretion of inhibin-LI from these cultured placental cells. This effect was mimicked by 8-bromo-cyclic adenosine monophosphate (8-bromo-cAMP), forskolin, and cholera toxin, suggesting that the mechanism of hCG induction of placental inhibin-LI secretion is cAMP-dependent. Incubation with an antiserum that binds the alpha-subunit of human inhibin increased the secretion of hCG and gonadotropin-releasing hormone-like immunoreactivity (GnRH-LI) from trophoblast cells in culture, suggesting a local tonic inhibitory action of endogenous inhibin on hCG and GnRH-LI release. The action of inhibin on hCG secretion may partially require the presence of placental GnRH, as suggested by evidence that a synthetic GnRH antagonist partially reverses the hCG increase induced by inhibin immunoneutralization. Results suggest paracrine roles for both inhibin and GnRH in the regulation of placental hCG production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petraglia, F -- Sawchenko, P -- Lim, A T -- Rivier, J -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- HD13527/HD/NICHD NIH HHS/ -- NS21182/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):187-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299703" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Cells, Cultured ; Cholera Toxin/pharmacology ; Chorionic Gonadotropin/pharmacology/*secretion ; Chorionic Villi/analysis ; Colforsin/pharmacology ; Feedback ; Female ; Gonadotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/secretion ; Humans ; Infant, Newborn ; Inhibins/analysis/*physiology ; Male ; Pregnancy ; Secretory Rate/drug effects ; Trophoblasts/analysis/drug effects/*secretion
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    Identification of human uromodulin as the Tamm-Horsfall urinary glycoprotein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-04-03
    Description: The primary structure of human uromodulin, a 616-amino acid, 85-kilodalton glycoprotein with in vitro immunosuppressive properties, was determined through isolation and characterization of complementary DNA and genomic clones. The amino acid sequence encoded by one of the exons of the uromodulin gene has homology to the low-density-lipoprotein receptor and the epidermal growth factor precursor. Northern hybridization analyses demonstrate that uromodulin is synthesized by the kidney. Evidence is provided that uromodulin is identical to the previously characterized Tamm-Horsfall glycoprotein, the most abundant protein in normal human urine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennica, D -- Kohr, W J -- Kuang, W J -- Glaister, D -- Aggarwal, B B -- Chen, E Y -- Goeddel, D V -- New York, N.Y. -- Science. 1987 Apr 3;236(4797):83-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3453112" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/analysis ; Base Sequence ; Chemistry, Physical ; Cloning, Molecular ; Cysteine ; DNA/genetics ; Gene Expression Regulation ; Genes ; Glycoproteins/*genetics ; Humans ; Mucoproteins/*analysis/*genetics ; Peptide Fragments/analysis ; Physicochemical Phenomena ; RNA, Messenger/genetics ; Uromodulin
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  • 39
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    Chemistry of pheromone and hormone metabolism in insects (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-28
    Description: Chemical evidence is needed in both insect endocrinology and sensory physiology to understand hormone and pheromone action at the molecular level. Radiolabeled pheromones and hormones have been synthesized and used to identify binding and catabolic proteins from insect tissues. Chemically modified analogs, including photoaffinity labels and enzyme inhibitors, are among the tools used to covalently modify the specific acceptor or catalytic sites. Such targeted agents can also provide leads for the design of growth and mating disruptants by allowing manipulation of the physiologically important interactions of the chemical signals with macromolecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prestwich, G D -- GM-30899/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):999-1006.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bees/metabolism ; Chemical Phenomena ; Chemistry ; Cockroaches/metabolism ; Female ; Insect Hormones/*metabolism ; Insects/metabolism ; Juvenile Hormones/metabolism ; Male ; Methoprene/metabolism ; Moths/metabolism ; Pheromones/*metabolism
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    The role of protein structure in chromatographic behavior (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-16
    Description: Chromatographic retention is determined by a relatively small number of amino acids located in a chromatographic contact region on the surface of a polypeptide. This region is determined by the mode of separation and the amino acid distribution within the polypeptide. The contact area may be as small as a few hundred square angstroms in bioaffinity chromatography. In contrast, the contact region in ion exchange, reversed phase, hydrophobic interaction and the other nonbioaffinity separation modes is much broader, ranging from one side to the whole external surface of a polypeptide. Furthermore, structural changes that alter the chromatographic contact region will alter chromatographic properties. Thus, although immunosorbents can be very useful in purifying proteins of similar primary structure, they will be ineffective in discriminating between small, random variations within a structure. Nonbioaffinity columns complement affinity columns in probing a much larger portion of solute surface and being able to discriminate between protein variants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Regnier, F E -- GM25431/GM/NIGMS NIH HHS/ -- GM33644/GM/NIGMS NIH HHS/ -- GM34759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 16;238(4825):319-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Purdue University, West Lafayette, IN 47907.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3310233" target="_blank"〉PubMed〈/a〉
    Keywords: Adsorption ; Amino Acids ; Chemical Phenomena ; Chemistry ; *Chromatography ; Chromatography, Affinity ; Chromatography, High Pressure Liquid ; Chromatography, Ion Exchange ; Protein Conformation ; Protein Denaturation ; *Proteins ; Recombinant Proteins ; Surface Properties
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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)
    Details
    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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  • 42
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    D-alanine in the frog skin peptide dermorphin is derived from L-alanine in the precursor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-09
    Description: A D-alanine-containing peptide termed dermorphin, with potent opiate-like activity, has been isolated from skin of the frog Phyllomedusa sauvagei. Complementary DNA (cDNA) libraries were constructed from frog skin messenger RNA and screened with a mixture of oligonucleotides that contained the codons complementary to five amino acids of dermorphin. Clones were detected with inserts coding for different dermorphin precursors. The predicted amino acid sequences of these precursors contained homologous repeats of 35 amino acids that included one copy of the heptapeptide dermorphin. In these cloned cDNAs, the alanine codon GCG occurred at the position where D-alanine is present in the end product. This suggests the existence of a novel post-translational reaction for the conversion of an L-amino acid to its D-isomer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Richter, K -- Egger, R -- Kreil, G -- New York, N.Y. -- Science. 1987 Oct 9;238(4824):200-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, Austrian Academy of Sciences, Salzburg.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659910" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine/*metabolism ; Amino Acid Sequence ; Animals ; Anura ; Base Sequence ; Cloning, Molecular ; DNA/analysis ; Molecular Sequence Data ; Oligopeptides/*genetics ; Opioid Peptides ; RNA, Messenger/genetics ; Skin/*metabolism ; Stereoisomerism
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  • 43
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    Activated oncogenes in B6C3F1 mouse liver tumors: implications for risk assessment (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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  • 44
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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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  • 45
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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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  • 46
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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)
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    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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  • 47
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    Thrombospondin promotes cell-substratum adhesion (1987)
    American Association for the Advancement of Science (AAAS)
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    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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  • 48
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    A cell-cycle constraint on the regulation of gene expression by platelet-derived growth factor (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-11-27
    Description: In density-arrested monolayer cultures of Balb/c 3T3 cells, platelet-derived growth factor (PDGF) stimulates expression of the c-myc and c-fos proto-oncogenes, as well as the functionally uncharacterized genes, JE, KC, and JB. These genes are not coordinately regulated. Under ordinary conditions, c-fos, JE, KC, and JB respond to PDGF only when the cells are in a state of G0 growth arrest at the time of PDGF addition. The c-myc gene is regulated in opposition to the other genes, responding best to PDGF in cycling cultures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rollins, B J -- Morrison, E D -- Stiles, C D -- CA 20042-09/CA/NCI NIH HHS/ -- GM 31489-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 27;238(4831):1269-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Division/drug effects ; Cells, Cultured ; Gene Expression Regulation/*drug effects ; Interphase ; Mice ; Mice, Inbred BALB C ; Platelet-Derived Growth Factor/*pharmacology ; Proto-Oncogenes/*drug effects ; Transcription, Genetic/*drug effects
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  • 49
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    The molecular basis of the sparse fur mouse mutation (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: The ornithine transcarbamylase-deficient sparse fur mouse is an excellent model to study the most common human urea cycle disorder. The mutation has been well characterized by both biochemical and enzymological methods, but its exact nature has not been revealed. A single base substitution in the complementary DNA for ornithine transcarbamylase from the sparse fur mouse has been identified by means of a combination of two recently described techniques for rapid mutational analysis. This strategy is simpler than conventional complementary DNA library construction, screening, and sequencing, which has often been used to find a new mutation. The ornithine transcarbamylase gene in the sparse fur mouse contains a C to A transversion that alters a histidine residue to an asparagine residue at amino acid 117.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Veres, G -- Gibbs, R A -- Scherer, S E -- Caskey, C T -- HD21452/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):415-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603027" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA/analysis ; Disease Models, Animal ; *Genes ; Mice ; Mice, Mutant Strains ; *Mutation ; Ornithine Decarboxylase/deficiency/*genetics ; RNA, Messenger/genetics
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  • 50
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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)
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    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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  • 51
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    Human CSF-1: molecular cloning and expression of 4-kb cDNA encoding the human urinary protein (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-20
    Description: A 4-kilobase complementary DNA (cDNA) encoding human macrophage-specific colony-stimulating factor (CSF-1) was isolated. When introduced into mammalian cells, this cDNA directs the expression of CSF-1 that is structurally and functionally indistinguishable from the natural human urinary CSF-1. Direct structural analysis of both the recombinant CSF-1 and the purified human urinary protein revealed that these species contain a sequence of at least 40 amino acids at their carboxyl termini which are not found in the coding region of a 1.6-kilobase CSF-1 cDNA that was previously described. These results demonstrate that the human CSF-1 gene can be expressed to yield at least two different messenger RNA species that encode distinct but related forms of CSF-1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G G -- Temple, P A -- Leary, A C -- Witek-Giannotti, J S -- Yang, Y C -- Ciarletta, A B -- Chung, M -- Murtha, P -- Kriz, R -- Kaufman, R J -- New York, N.Y. -- Science. 1987 Mar 20;235(4795):1504-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3493529" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; Colony-Stimulating Factors/*genetics/urine ; DNA/genetics ; Gene Expression Regulation ; Humans ; Macrophages/physiology ; Molecular Weight ; Peptide Fragments ; Protein Processing, Post-Translational ; RNA, Messenger/genetics
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  • 52
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    Quantal release of transmitter is not associated with channel opening on the neuronal membrane (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-18
    Description: The traditional view that quantal release of neurotransmitter results from the fusion of transmitter-containing vesicles with the neuronal membrane has been recently challenged. Although various alternative mechanisms have been proposed, a common element among them is the release of cytoplasmic transmitter, which, in one view, could occur through large conductance channels on the presynaptic membrane. Six nerve-muscle cell pairs were examined with a whole-cell patch clamp for the presence of such channels that are associated with the production of miniature end-plate potentials. Examination of the neuronal membrane current during the occurrence of 822 miniature end-plate potentials produced no evidence of large channels. Thus it is unlikely that quantal release is mediated by such channels in the neuromuscular junction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, S H -- Chow, I -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1712-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, UCLA School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2891190" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/*physiology ; Cells, Cultured ; Membrane Potentials ; Motor Endplate/cytology/*physiology ; Neuromuscular Junction/*physiology ; Neurons/cytology/*physiology ; Neurotransmitter Agents/*secretion ; Xenopus
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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)
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    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)
    Details
    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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    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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    Reading frame selection and transfer RNA anticodon loop stacking (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-11
    Description: Messenger RNA's are translated in successive three-nucleotide steps (a reading frame), therefore decoding must proceed in only one of three possible frames. A molecular model for correct propagation of the frame is presented based on (i) the measured translational properties of transfer RNA's (tRNA's) that contain an extra nucleotide in the anticodon loop and (ii) a straightforward concept about anticodon loop structure. The model explains the high accuracy of reading frame maintenance by normal tRNA's, as well as activities of all characterized frameshift suppressor tRNA's that have altered anticodon loops.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curran, J F -- Yarus, M -- GM30881/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1545-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder 80309.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685992" target="_blank"〉PubMed〈/a〉
    Keywords: Anticodon/*genetics ; Base Sequence ; Codon ; Mutation ; Nucleic Acid Conformation ; Protein Biosynthesis ; RNA, Messenger/genetics ; RNA, Transfer/*genetics
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    The sor gene of HIV-1 is required for efficient virus transmission in vitro (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-21
    Description: The genome of the human immunodeficiency virus HIV-1 contains at least eight genes, of which three (sor, R, and 3' orf) have no known function. In this study, the role of the sor gene was examined by constructing a series of proviral genomes of HIV-1 that either lacked the coding sequences for sor or contained point mutations in sor. Analysis of four such mutants revealed that although each clone could generate morphologically normal virus particles upon transfection, the mutant viruses were limited in their capacity to establish stable infection. Virus derived from transfection of Cos-1 cells (OKT4-) with sor mutant proviral DNA's was resistant to transmission to OKT4+ "susceptible" cells under cell-free conditions, and was transmitted poorly by coculture. In contrast, virus derived from clones with an intact sor frame was readily propagated by either approach. Normal amounts of gag-, env-, and pol-derived proteins were produced by all four mutants and assays in both lymphoid and nonlymphoid cells indicated that their trans-activating capacity was intact and comparable with wild type. Thus the sor gene, although not absolutely required in HIV virion formation, influences virus transmission in vitro and is crucial in the efficient generation of infectious virus. The data also suggest that sor influences virus replication at a novel, post-translational stage and that its action is independent of the regulatory genes tat and trs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fisher, A G -- Ensoli, B -- Ivanoff, L -- Chamberlain, M -- Petteway, S -- Ratner, L -- Gallo, R C -- Wong-Staal, F -- New York, N.Y. -- Science. 1987 Aug 21;237(4817):888-93.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3497453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cells, Cultured ; Cercopithecus aethiops ; Cytopathogenic Effect, Viral ; Genes, Viral ; HIV/*genetics ; T-Lymphocytes/microbiology ; Viral Proteins/*physiology ; *Virus Replication
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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)
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    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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    Severely impaired adipsin expression in genetic and acquired obesity (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-07-24
    Description: Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (greater than 100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flier, J S -- Cook, K S -- Usher, P -- Spiegelman, B M -- AM28082/AM/NIADDK NIH HHS/ -- AM31405/AM/NIADDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):405-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299706" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/enzymology ; Animals ; Antigen-Antibody Complex ; Complement Factor D ; Endopeptidases/*genetics/metabolism ; Immune Sera ; Mice ; Mice, Obese ; Obesity/*enzymology/genetics ; RNA, Messenger/genetics ; Reference Values ; *Serine Endopeptidases ; *Transcription, Genetic
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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)
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    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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    Recombinant fragment of protein kinase inhibitor blocks cyclic AMP-dependent gene transcription (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-10-23
    Description: Transcriptional regulation by cyclic adenosine monophosphate (cAMP) in mammalian cells could be mediated by a phosphoprotein substrate of the cAMP-dependent protein kinase or, as in prokaryotes, by a cAMP-binding protein. Two synthetic genes that code for an active fragment of the protein inhibitor of this kinase and a mutant inactive fragment were constructed and used to distinguish these alternatives. Transient expression of the active peptide product specifically inhibited the cAMP-stimulated expression of a cotransfected reporter gene by more than 90 percent, whereas the expression of the inactive peptide did not alter cAMP-stimulated gene expression. The results indicate that an active kinase catalytic subunit is a necessary intermediate in the cAMP stimulation of gene transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grove, J R -- Price, D J -- Goodman, H M -- Avruch, J -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):530-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821622" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Carrier Proteins/*pharmacology ; Chloramphenicol O-Acetyltransferase ; Cyanogen Bromide ; Cyclic AMP/*pharmacology ; DNA, Recombinant ; Escherichia coli/genetics ; *Intracellular Signaling Peptides and Proteins ; Nucleic Acid Hybridization ; Peptide Fragments/*pharmacology ; Phosphorylation ; Plasmids ; Protein Kinase Inhibitors ; Protein Kinases/metabolism ; RNA, Messenger/genetics ; Recombinant Proteins/*pharmacology ; Transcription, Genetic/*drug effects ; Transfection
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    Forskolin and phorbol esters reduce the same potassium conductance of mouse neurons in culture (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-01-16
    Description: Second messenger systems may modulate neuronal activity through protein phosphorylation. However, interactions between two major second messenger pathways, the cyclic AMP and phosphatidylinositol systems, are not well understood. The effects of activators of cyclic AMP-dependent protein kinase and protein kinase C on resting membrane properties, action potentials, and currents recorded from mouse dorsal root ganglion neurons and cerebral hemisphere neurons grown in primary dissociated cell culture were investigated. Neither forskolin (FOR) nor phorbol 12,13-dibutyrate (PDBu) altered resting membrane properties but both increased the duration of calcium-dependent action potentials in both central and peripheral neurons. By means of the single-electrode voltage clamp technique, FOR and PDBu were shown to decrease the same voltage-dependent potassium conductance. This suggests that two independent second messenger systems may affect the same potassium conductance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grega, D S -- Werz, M A -- Macdonald, R L -- NS 07231/NS/NINDS NIH HHS/ -- NS 19613/NS/NINDS NIH HHS/ -- NS 19692/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):345-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432663" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/*drug effects ; Animals ; Brain/cytology ; Calcium/physiology ; Cells, Cultured ; Colforsin/*pharmacology ; Electric Conductivity ; Ganglia, Spinal/cytology ; Ion Channels/physiology ; Membrane Potentials ; Mice ; Neurons/drug effects/*physiology ; Phorbol Esters/*pharmacology ; Potassium/*physiology
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    Diversity of alpha-fetoprotein gene expression in mice is generated by a combination of separate enhancer elements (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-02
    Description: The 5' flanking region of the mouse alpha-fetoprotein (AFP) gene contains a tissue-specific promoter and three upstream regulatory elements that behave as classical enhancers. At least one of these enhancers is now shown to be required for the tissue-specific expression of the AFP gene when it is introduced into the mouse genome by microinjection of cloned DNA fragments into fertilized eggs. Each enhancer can direct expression in the appropriate tissues, the visceral endoderm of the yolk sac, the fetal liver, and the gastrointestinal tract, but each exerts different influence in these three tissues. These differences may explain the tissue-specific diversity in the levels of expression characteristic of the AFP gene. The postnatal repression of transcription of the AFP gene in both liver and gut, as well as the reinitiation of its transcription during liver regeneration, is mimicked by the introduced gene when it is linked to the enhancer domains together or singly. Thus, the DNA sequence elements responsible for directing the activation of AFP transcription, its repression, and reinduction are contained in a limited segment of DNA within or 5' to the gene (or both) and are operative in the absence of the closely linked albumin gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hammer, R E -- Krumlauf, R -- Camper, S A -- Brinster, R L -- Tilghman, S M -- CA06927/CA/NCI NIH HHS/ -- CA28050/CA/NCI NIH HHS/ -- HD17321/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jan 2;235(4784):53-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cloning, Molecular ; *Enhancer Elements, Genetic ; Gene Expression Regulation ; Genes ; *Genes, Regulator ; Intestines/physiology ; Liver/physiology ; Mice ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; Tissue Distribution ; Transcription, Genetic ; Transfection ; Yolk Sac/physiology ; alpha-Fetoproteins/*genetics
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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)
    Details
    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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    Eosinophils cocultured with endothelial cells have increased survival and functional properties (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-08-07
    Description: Human peripheral blood eosinophils, cells often associated with allergic and parasitic diseases, were maintained in vitro for at least 14 days when they were cocultured with bovine endothelial cells and for at least 7 days when cultured with either bovine or human endothelial cell-derived conditioned medium. The cocultured eosinophils became hypodense and generated about three times as much leukotriene C4 upon activation with calcium ionophore and killed about three times as many antibody-coated larvae of Schistosoma mansoni as freshly isolated normodense eosinophils. That these cells can be maintained in vitro by coculture with endothelial cells, and the surprising finding that the cocultured eosinophils have biochemical, cytotoxic, and density properties similar to those of eosinophils in patients with allergic and other disorders, will facilitate investigation of the regulation and role of these cells in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothenberg, M E -- Owen, W F Jr -- Silberstein, D S -- Soberman, R J -- Austen, K F -- Stevens, R L -- AI-22531/AI/NIAID NIH HHS/ -- AI-23483/AI/NIAID NIH HHS/ -- AM-01401/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):645-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3110954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Dependent Cell Cytotoxicity ; Calcimycin/pharmacology ; Cattle ; *Cell Communication ; Cell Survival ; Cells, Cultured ; Endothelium/*cytology ; Eosinophils/*cytology ; Humans ; SRS-A/biosynthesis ; Schistosoma mansoni/immunology ; Time Factors
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    The molecular control of blood cell development (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-04
    Description: The establishment of a cell culture system for the clonal development of blood cells has made it possible to identify the proteins that regulate the growth and differentiation of different blood cell lineages and to discover the molecular basis of normal and abnormal cell development in blood forming tissues. A model system with myeloid blood cells has shown that (i) normal blood cells require different proteins to induce cell multiplication (growth inducers) and cell differentiation (differentiation inducers), (ii) there is a hierarchy of growth inducers as cells become more restricted in their developmental program, and (iii) a cascade of interactions between proteins determines the correct balance between immature and mature cells in normal blood cell development. Gene cloning has shown that there is a family of different genes for these proteins. Normal protein regulators of blood cell development can control the abnormal growth of certain types of leukemic cells and suppress malignancy by inducing differentiation to mature nondividing cells. Chromosome abnormalities that give rise to malignancy in these leukemic cells can be bypassed and their effects nullified by inducing differentiation, which stops cells from multiplying. These blood cell regulatory proteins are active in culture and in the body, and they can be used clinically to correct defects in blood cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sachs, L -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1374-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Weizmann Institute of Science, Rehovot, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3317831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells ; Cell Differentiation/drug effects ; Cells, Cultured ; Clone Cells/cytology ; Colony-Stimulating Factors/physiology/therapeutic use ; *Hematopoiesis/drug effects ; Hematopoietic Stem Cells/cytology ; Humans ; Interleukin-3/physiology/therapeutic use ; Leukemia, Myeloid/drug therapy/physiopathology ; Mice ; Neoplastic Stem Cells/drug effects/pathology
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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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    Why nature chose phosphates (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: Phosphate esters and anhydrides dominate the living world but are seldom used as intermediates by organic chemists. Phosphoric acid is specially adapted for its role in nucleic acids because it can link two nucleotides and still ionize; the resulting negative charge serves both to stabilize the diesters against hydrolysis and to retain the molecules within a lipid membrane. A similar explanation for stability and retention also holds for phosphates that are intermediary metabolites and for phosphates that serve as energy sources. Phosphates with multiple negative charges can react by way of the monomeric metaphosphate ion PO3- as an intermediate. No other residue appears to fulfill the multiple roles of phosphate in biochemistry. Stable, negatively charged phosphates react under catalysis by enzymes; organic chemists, who can only rarely use enzymatic catalysis for their reactions, need more highly reactive intermediates than phosphates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westheimer, F H -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1173-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434996" target="_blank"〉PubMed〈/a〉
    Keywords: Amides ; Animals ; Arsenates ; Chemical Phenomena ; Chemistry ; Citrates ; Citric Acid ; Electrochemistry ; Humans ; Hydrolysis ; Ions ; Nucleic Acids/metabolism ; Phosphates/metabolism/*physiology ; RNA/metabolism ; Silicic Acid
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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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    Aromatic cross-links in insect cuticle: detection by solid-state 13C and 15N NMR (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-03-06
    Description: Cross-polarization magic-angle-spinning nuclear magnetic resonance spectroscopy has been used to determine insect cuticle composition and cross-link structure during sclerotization or tanning. Unsclerotized cuticle from newly ecdysed pupae of the tobacco hornworm, Manduca sexta L., had a high protein content with lesser amounts of lipid and chitin. Concentrations of chitin, protein, and catechol increased substantially as dehydration and sclerotization progressed. Analysis of intact cuticle specifically labeled with carbon-13 and nitrogen-15 revealed direct covalent linkages between ring nitrogens of protein histidyl residues and ring carbons derived from the catecholamine dopamine. This carbon-nitrogen adduct was present in chitin isolated from cuticle by alkaline extraction and is probably bound covalently to chitin. These data support the hypothesis that the stiffening of insect cuticle during sclerotization results primarily from the deposition of protein and chitin polymers and their crosslinking by quinonoid derivatives of catecholamines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaefer, J -- Kramer, K J -- Garbow, J R -- Jacob, G S -- Stejskal, E O -- Hopkins, T L -- Speirs, R D -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1200-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3823880" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Isotopes ; Chemical Phenomena ; Chemistry ; Cross-Linking Reagents/*metabolism ; Insects/*metabolism ; Magnetic Resonance Spectroscopy ; Nitrogen Isotopes ; Skin/*metabolism
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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)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 82
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    Implantation of genetically engineered fibroblasts into mice: implications for gene therapy (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-08
    Description: In a variety of human genetic diseases, replacement of the absent or defective protein provides significant therapeutic benefits. As a model for a somatic cell gene therapy system, cultured murine fibroblasts were transfected with a human growth hormone (hGH) fusion gene and cells from one of the resulting clonal lines were subsequently implanted into various locations in mice. Such implants synthesized and secreted hGH, which was detectable in the serum. The function of the implants depended on their location and size, and on the histocompatibility of the donor cells with their recipients. The expression of hGH could be modified by addition of regulatory effectors, and, with appropriate immunosuppression, the implants survived for more than 3 months. This approach to gene therapy, here termed "transkaryotic implantation," is potentially applicable to many genetic diseases in that the transfected cell line can be extensively characterized prior to implantation, several anatomical sites are suitable for implantation, and regulated expression of the gene of therapeutic interest can be obtained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selden, R F -- Skoskiewicz, M J -- Howie, K B -- Russell, P S -- Goodman, H M -- AM-07055/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 May 8;236(4802):714-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3472348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA, Recombinant ; Fibroblasts/immunology/*transplantation ; *Genetic Engineering ; Graft Survival ; Growth Hormone/biosynthesis/*genetics ; Humans ; Immunosuppression ; Kidney ; Kinetics ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Plasmids ; Therapeutics ; Transfection
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  • 83
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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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  • 84
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 85
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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)
    Details
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
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    Localization of amyloid beta protein messenger RNA in brains from patients with Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-03
    Description: The distribution of cells containing messenger RNA that encodes amyloid beta protein was determined in hippocampi and in various cortical regions from cynomolgus monkeys, normal humans, and patients with Alzheimer's disease by in situ hybridization. Both 35S-labeled RNA antisense and sense probes to amyloid beta protein messenger RNA were used to ensure specific hybridization. Messenger RNA for amyloid beta protein was expressed in a subset of neurons in the prefrontal cortex from monkeys, normal humans, and patients with Alzheimer's disease. This messenger RNA was also present in the neurons of all the hippocampal fields from monkeys, normal humans and, although to a lesser extent in cornu ammonis 1, patients with Alzheimer's disease. The distribution of amyloid beta protein messenger RNA was similar to that of the neurofibrillary tangles of Alzheimer's disease in some regions, but the messenger RNA was also expressed in other neurons that are not usually involved in the pathology of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bahmanyar, S -- Higgins, G A -- Goldgaber, D -- Lewis, D A -- Morrison, J H -- Wilson, M C -- Shankar, S K -- Gajdusek, D C -- AG05131/AG/NIA NIH HHS/ -- MH00519/MH/NIMH NIH HHS/ -- NS23038/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 3;237(4810):77-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299701" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid/*genetics ; Amyloid beta-Peptides ; Animals ; Brain/*physiopathology ; Cerebral Cortex/physiology ; Gene Expression Regulation ; Hippocampus/physiology ; Humans ; Macaca fascicularis ; Nucleic Acid Hybridization ; RNA, Messenger/genetics
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  • 87
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    Tissue-specific expression of functionally rearranged lambda 1 Ig gene through a retrovirus vector (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: To explore the potential use of retrovirus vectors for the transfer of genomic DNA sequences into mammalian cells, recombinant retroviral genomes were constructed that encode a functionally rearranged murine lambda 1 immunoglobulin gene. Several of these genomes could be transmitted intact to recipient cells by viral infection, although successful transmission depended both on the orientation of the lambda 1 sequences and on their specific placement within vector sequences. The lambda 1 gene transduced by viral infection was expressed in a cell lineage-specific manner, albeit at lower levels than endogenous lambda 1 gene expression in cells from the B-lymphocyte lineage. Vectors yielding integrated proviruses that lacked viral transcriptional enhancer sequences were used to show that neither viral transcription nor the viral transcriptional sequences themselves had any effect on the tissue specificity of lambda 1 gene expression or the absolute amount of lambda 1 transcription. Vector transcription did, however, dramatically decrease the amount of lambda 1 protein that could be detected in tranduced cells. These results suggest that retrovirus vectors may be useful reagents not only for the expression of complementary DNA sequences but also for studies of tissue-specific transcription in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cone, R D -- Reilly, E B -- Eisen, H N -- Mulligan, R C -- CA26712/CA/NCI NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):954-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Enhancer Elements, Genetic ; *Genes ; *Genes, Viral ; Genetic Vectors ; Immunoglobulin lambda-Chains/*genetics ; Retroviridae/*genetics ; *Transcription, Genetic
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  • 88
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    Mutations in diphtheria toxin separate binding from entry and amplify immunotoxin selectivity (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-23
    Description: Monoclonal antibodies linked to toxic proteins (immunotoxins) can selectively kill some tumor cells in vitro and in vivo. However, reagents that combine the full potency of the native toxins with the high degree of cell type selectivity of monoclonal antibodies have not previously been designed. Two heretofore inseparable activities on one polypeptide chain of diphtheria toxin and ricin account for the failure to construct optimal reagents. The B chains (i) facilitate entry of the A chain to the cytosol, which allows immunotoxins to efficiently kill target cells, and (ii) bind to receptors present on most cells, which imparts to immunotoxins a large degree of non-target cell toxicity. This report identifies point mutations in the B polypeptide chain of diphtheria toxin that block binding but allow cytosol entry. Three mutants of diphtheria toxin have 1/1,000 to 1/10,000 the toxicity and 1/100 to 1/8,000 the binding activity of diphtheria toxin. Linking of either of two of the inactivated mutant toxins (CRM103, Phe508; CRM107, Phe390, Phe525) to a monoclonal antibody specific for human T cells reconstitutes full target-cell toxicity--indistinguishable from that of the native toxin linked to the same antibody--without restoring non-target cell toxicity. This separation of the entry function from the binding function generates a uniquely potent and cell type-specific immunotoxin that retains full diphtheria toxin toxicity, yet is four to five orders of magnitude less toxic than the native toxin is to nontarget cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenfield, L -- Johnson, V G -- Youle, R J -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):536-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbial Genetics, Cetus Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3498987" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Differentiation, T-Lymphocyte/immunology ; Antigens, Surface/immunology ; Cell Line ; Cell Survival/drug effects ; Chemical Phenomena ; Chemistry ; Diphtheria Toxin/genetics/*metabolism/pharmacology ; Heparin-binding EGF-like Growth Factor ; Immunotoxins/*pharmacology ; Intercellular Signaling Peptides and Proteins ; *Mutation ; *Receptors, Cell Surface ; Receptors, Cholinergic/metabolism ; Ricin/metabolism ; Structure-Activity Relationship ; T-Lymphocytes/immunology ; Vero Cells
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  • 89
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    Identification of putative human T cell receptor delta complementary DNA clones (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: A novel T cell receptor (TCR) subunit termed TCR delta, associated with TCR gamma and CD3 polypeptides, was recently found on a subpopulation of human T lymphocytes. T cell-specific complementary DNA clones present in a human TCR gamma delta T cell complementary DNA library were obtained and characterized in order to identify candidate clones encoding TCR delta. One cross-hybridizing group of clones detected transcripts that are expressed in lymphocytes bearing TCR gamma delta but not in other T lymphocytes and are encoded by genes that are rearranged in TCR gamma delta lymphocytes but deleted in other T lymphocytes. Their sequences indicate homology to the variable, joining, and constant elements of other TCR and immunoglobulin genes. These characteristics, as well as the immunochemical data presented in a companion paper, are strong evidence that the complementary DNA clones encode TCR delta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hata, S -- Brenner, M B -- Krangel, M S -- 1-K01-AM01598/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):678-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Tumor Virology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3499667" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Genes ; Humans ; Membrane Proteins/genetics ; Molecular Sequence Data ; RNA, Messenger/genetics ; Receptors, Antigen, T-Cell/*genetics ; T-Lymphocytes/*physiology
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  • 90
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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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  • 91
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    Macrophage cytotoxicity: role for L-arginine deiminase and imino nitrogen oxidation to nitrite (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-23
    Description: Previous studies have shown that cytotoxic activated macrophages cause inhibition of DNA synthesis, of mitochondrial respiration, and of aconitase activity in tumor target cells. An L-arginine-dependent biochemical pathway synthesizing L-citrulline and nitrite, coupled to an effector mechanism, is now shown to cause this pattern of metabolic inhibition. Murine cytotoxic activated macrophages synthesize L-citrulline and nitrite in the presence of L-arginine but not D-arginine. L-Citrulline and nitrite biosynthesis by cytotoxic activated macrophages is inhibited by NG-monomethyl-L-arginine, which also inhibits this cytotoxic effector mechanism. This activated macrophage cytotoxic effector system is associated with L-arginine deiminase activity, and the imino nitrogen removed from the guanido group of L-arginine by the deiminase reaction subsequently undergoes oxidation to nitrite. L-Homoarginine, an alternative substrate for this deiminase, is converted to L-homocitrulline with concurrent nitrite synthesis and similar biologic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hibbs, J B Jr -- Taintor, R R -- Vavrin, Z -- New York, N.Y. -- Science. 1987 Jan 23;235(4787):473-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2432665" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonia/biosynthesis ; Animals ; Cells, Cultured ; Citrulline/biosynthesis ; Cytotoxicity, Immunologic ; Homoarginine/metabolism ; Hydrolases/metabolism ; *Macrophage Activation ; Macrophages/*physiology ; Mice ; Nitrates/metabolism ; Nitrites/metabolism
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  • 92
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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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  • 93
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    Parathyroid hormone-related protein of malignancy: active synthetic fragments (1987)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1987-12-11
    Description: Peptides corresponding to the amino-terminal region of the parathyroid hormone-related protein (PTHrP) of humoral hypercalcemia of malignancy were synthesized. A 34-amino acid peptide, PTHrP(1-34), was two to four times more potent than bovine or human PTH(1-34) in bioassays promoting the formation of adenosine 3',5'-monophosphate (cAMP) and plasminogen activator activity in osteogenic sarcoma cells and adenylate cyclase activity in chick kidney membranes. Like parathyroid hormone itself, in which the activity resides in the first 34 residues, PTHrP peptides of less than 30 residues from the amino terminus showed substantially reduced activity. PTHrP(1-34) had only 6% of the potency of bovine PTH(1-34) in promoting bone resorption in vitro. PTHrP(1-34) strongly promoted the excretion of cAMP and phosphorus and reduced the excretion of calcium in the isolated, perfused rat kidney consistent with the symptoms seen in malignant hypercalcemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kemp, B E -- Moseley, J M -- Rodda, C P -- Ebeling, P R -- Wettenhall, R E -- Stapleton, D -- Diefenbach-Jagger, H -- Ure, F -- Michelangeli, V P -- Simmons, H A -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1568-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Melbourne, Department of Medicine, Repatriation General Hospital, Heidelberg, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685995" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Resorption/*drug effects ; Bone and Bones/metabolism ; Calcium/metabolism ; Cattle ; Cells, Cultured ; Humans ; Hypercalcemia/etiology ; Neoplasms/*physiopathology ; Parathyroid Hormone/*pharmacology/physiology ; Peptide Fragments/*pharmacology/physiology ; Structure-Activity Relationship ; Teriparatide
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  • 94
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    Lymphotoxin is an important T cell-derived growth factor for human B cells (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-20
    Description: Two different assays for B cell growth factors (BCGF) and an antibody against lymphotoxin were used to show that the presence of lymphotoxin in conditioned media derived from normal activated T cells and in a partially purified BCGF accounts for a substantial portion of their B cell growth-promoting activity. A competitive binding assay confirmed the presence of significant amounts of lymphotoxin in the partially purified BCGF. Recombinant lymphotoxin enhanced the proliferation of activated B cells and augmented B cell proliferation and immunoglobulin secretion induced by interleukin-2.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kehrl, J H -- Alvarez-Mon, M -- Delsing, G A -- Fauci, A S -- New York, N.Y. -- Science. 1987 Nov 20;238(4830):1144-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3500512" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody Formation/drug effects ; B-Lymphocytes/*cytology ; Cell Differentiation/drug effects ; Cells, Cultured ; DNA/biosynthesis ; Growth Substances/*physiology ; Humans ; In Vitro Techniques ; Interleukin-4 ; *Interleukins ; Lymphocyte Activation ; Lymphotoxin-alpha/*physiology ; Recombinant Proteins/pharmacology ; T-Lymphocytes/*physiology
    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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  • 95
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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
    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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  • 96
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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
    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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  • 97
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    Expression of the art/trs protein of HIV and study of its role in viral envelope synthesis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: The art/trs transactivator protein of human immunodeficiency virus (HIV) was expressed in mammalian cells as a 19-kilodalton protein that was immunoreactive with sera from HIV-infected patients. Separate plasmids encoding the art/trs protein, the tat protein, or the envelope glycoprotein gp120 were used to demonstrate that both art/trs and tat are absolutely required for the synthesis of gp120 from its cognate messenger RNA. In addition, both the tat and art/trs proteins influence the level of envelope RNA. The results suggest that art/trs and tat may be ideal targets for potential anti-HIV agents in AIDS therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knight, D M -- Flomerfelt, F A -- Ghrayeb, J -- New York, N.Y. -- Science. 1987 May 15;236(4803):837-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3033827" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/immunology ; DNA Restriction Enzymes ; Gene Products, rev ; *Genes ; *Genes, Viral ; HIV/*genetics/metabolism ; Humans ; Plasmids ; RNA, Messenger/genetics ; Viral Envelope Proteins/*biosynthesis ; Viral Proteins/biosynthesis/*genetics ; rev Gene Products, Human Immunodeficiency Virus
    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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  • 98
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    Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-15
    Description: Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koyanagi, Y -- Miles, S -- Mitsuyasu, R T -- Merrill, J E -- Vinters, H V -- Chen, I S -- New York, N.Y. -- Science. 1987 May 15;236(4803):819-22.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3646751" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*microbiology/pathology ; Brain/*microbiology/pathology ; Cells, Cultured ; HIV/isolation & purification ; Humans ; Lymphocyte Activation ; Lymphocytes/immunology/microbiology ; Macrophages/microbiology ; Monocytes/microbiology ; Species Specificity ; Virus Replication
    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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  • 99
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    New routes to early memories (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 100
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    Concanavalin A alters synaptic specificity between cultured Aplysia neurons (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-08-07
    Description: Factors that regulate synaptic specificity were investigated with Aplysia buccal and bag cell neurons in primary cell culture. In the presence of fetal calf serum electrical synapses are formed between buccal-buccal or bag-bag cell pairs, but not between buccal-bag cell pairs. Instead, buccal neurons make inhibitory chemical synapses on bag cells. However, in the presence of nanomolar concentrations of the lectin concanavalin A this pattern changes, such that more than 75 percent of buccal-bag pairs exhibit electrical synapses and the frequency of occurrence of buccal-bag chemical synapses is reduced. Such changes in synaptic specificity may be important in determining the types of synapses formed during neuronal development and neurite regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, S S -- Levitan, I B -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):648-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603045" target="_blank"〉PubMed〈/a〉
    Keywords: Aplysia ; Cell Communication ; Cells, Cultured ; Concanavalin A/*pharmacology ; Microelectrodes ; Neurons/*drug effects ; Organ Specificity ; Synapses/*drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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