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  • 1
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    Structure and functional expression of an omega-conotoxin-sensitive human N-type calcium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: N-type calcium channels are omega-conotoxin (omega-CgTx)-sensitive, voltage-dependent ion channels involved in the control of neurotransmitter release from neurons. Multiple subtypes of voltage-dependent calcium channel complexes exist, and it is the alpha 1 subunit of the complex that forms the pore through which calcium enters the cell. The primary structures of human neuronal calcium channel alpha 1B subunits were deduced by the characterization of overlapping complementary DNAs. Two forms (alpha 1B-1 and alpha 1B-2) were identified in human neuroblastoma (IMR32) cells and in the central nervous system, but not in skeletal muscle or aorta tissues. The alpha 1B-1 subunit directs the recombinant expression of N-type calcium channel activity when it is transiently co-expressed with human neuronal beta 2 and alpha 2b subunits in mammalian HEK293 cells. The recombinant channel was irreversibly blocked by omega-CgTx but was insensitive to dihydropyridines. The alpha 1B-1 alpha 2b beta 2-transfected cells displayed a single class of saturable, high-affinity (dissociation constant = 55 pM) omega-CgTx binding sites. Co-expression of the beta 2 subunit was necessary for N-type channel activity, whereas the alpha 2b subunit appeared to modulate the expression of the channel. The heterogeneity of alpha 1B subunits, along with the heterogeneity of alpha 2 and beta subunits, is consistent with multiple, biophysically distinct N-type calcium channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, M E -- Brust, P F -- Feldman, D H -- Patthi, S -- Simerson, S -- Maroufi, A -- McCue, A F -- Velicelebi, G -- Ellis, S B -- Harpold, M M -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):389-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SIBIA, Inc., La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321501" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Calcium/metabolism ; Calcium Channels/*drug effects/*genetics/*metabolism ; Cell Line ; Female ; Humans ; Male ; Membrane Potentials ; Molecular Sequence Data ; Neuroblastoma/metabolism ; Peptides, Cyclic/*pharmacology ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Transfection ; omega-Conotoxin GVIA
    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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    Nitric oxide: a physiologic mediator of penile erection (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-17
    Description: Nitric oxide (NO) is a cytotoxic agent of macrophages, a messenger molecule of neurons, and a vasodilator produced by endothelial cells. NO synthase, the synthetic enzyme for NO, was localized to rat penile neurons innervating the corpora cavernosa and to neuronal plexuses in the adventitial layer of penile arteries. Small doses of NO synthase inhibitors abolished electrophysiologically induced penile erections. These results establish NO as a physiologic mediator of erectile function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnett, A L -- Lowenstein, C J -- Bredt, D S -- Chang, T S -- Snyder, S H -- DA-00266/DA/NIDA NIH HHS/ -- DK-19300/DK/NIDDK NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Jul 17;257(5068):401-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1378650" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/biosynthesis ; Animals ; Arginine/analogs & derivatives/pharmacology ; Dose-Response Relationship, Drug ; Male ; Nerve Fibers/metabolism ; *Nitric Oxide ; Nitric Oxide Synthase ; Nitroarginine ; Penile Erection/drug effects/*physiology ; Penis/metabolism ; Rats ; Urethra/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Block of Ca2+ wave and Ca2+ oscillation by antibody to the inositol 1,4,5-trisphosphate receptor in fertilized hamster eggs (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-07-10
    Description: The concentration of cytoplasmic free calcium (Ca2+) increases in various stimulated cells in a wave (Ca2+ wave) and in periodic transients (Ca2+ oscillations). These phenomena are explained by inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release (IICR) and Ca(2+)-induced Ca2+ release (CICR) from separate intracellular stores, but decisive evidence is lacking. A monoclonal antibody to the IP3 receptor inhibited both IICR and CICR upon injection of IP3 and Ca2+ into hamster eggs, respectively. The antibody completely blocked sperm-induced Ca2+ waves and Ca2+ oscillations. The results indicate that Ca2+ release in fertilized hamster eggs is mediated solely by the IP3 receptor, and Ca(2+)-sensitized IICR, but not CICR, generates Ca2+ waves and Ca2+ oscillations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, S -- Yuzaki, M -- Nakada, K -- Shirakawa, H -- Nakanishi, S -- Nakade, S -- Mikoshiba, K -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):251-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Tokyo Women's Medical College, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1321497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Caffeine/pharmacology ; Calcium/*metabolism ; *Calcium Channels ; Cricetinae ; Dose-Response Relationship, Drug ; Fertilization/*physiology ; Immunoblotting ; Inositol 1,4,5-Trisphosphate Receptors ; Male ; Ovum/*metabolism ; Receptors, Cell Surface/drug effects/*physiology ; *Receptors, Cytoplasmic and Nuclear ; Ryanodine/pharmacology ; Spermatozoa/physiology ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Structure and function of lipopolysaccharide binding protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: The primary structure of lipopolysaccharide binding protein (LBP), a trace plasma protein that binds to the lipid A moiety of bacterial lipopolysaccharides (LPSs), was deduced by sequencing cloned complementary DNA. LBP shares sequence identity with another LPS binding protein found in granulocytes, bactericidal/permeability-increasing protein, and with cholesterol ester transport protein of the plasma. LBP may control the response to LPS under physiologic conditions by forming high-affinity complexes with LPS that bind to monocytes and macrophages, which then secrete tumor necrosis factor. The identification of this pathway for LPS-induced monocyte stimulation may aid in the development of treatments for diseases in which Gram-negative sepsis or endotoxemia are involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumann, R R -- Leong, S R -- Flaggs, G W -- Gray, P W -- Wright, S D -- Mathison, J C -- Tobias, P S -- Ulevitch, R J -- AI 15136/AI/NIAID NIH HHS/ -- AI 25563/AI/NIAID NIH HHS/ -- GM 28485/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1429-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402637" target="_blank"〉PubMed〈/a〉
    Keywords: *Acute-Phase Proteins ; Amino Acid Sequence ; Animals ; Base Sequence ; Blood Proteins/*genetics ; Carrier Proteins/*genetics/metabolism ; Gene Library ; Humans ; Kinetics ; Lipid A/metabolism ; Lipopolysaccharides/*metabolism/pharmacology ; Male ; *Membrane Glycoproteins ; Molecular Sequence Data ; Oligonucleotide Probes ; Rabbits ; Sequence Homology, Nucleic Acid ; Sheep ; Staphylococcus aureus ; Tumor Necrosis Factor-alpha/biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Clues to the pathogenesis of familial colorectal cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: A predisposition to colorectal cancer is shown to be linked to markers on chromosome 2 in some families. Molecular features of "familial" cancers were compared with those of sporadic colon cancers. Neither the familial nor sporadic cancers showed loss of heterozygosity for chromosome 2 markers, and the incidence of mutations in KRAS, P53, and APC was similar in the two groups of tumors. Most of the familial cancers, however, had widespread alterations in short repeated DNA sequences, suggesting that numerous replication errors had occurred during tumor development. Thirteen percent of sporadic cancers had identical abnormalities and these cancers shared biologic properties with the familial cases. These data suggest a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aaltonen, L A -- Peltomaki, P -- Leach, F S -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Powell, S M -- Jen, J -- Hamilton, S R -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):812-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484121" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Female ; Genetic Markers ; Humans ; Lod Score ; Male ; Mutation ; Pedigree ; Polymorphism, Genetic ; Rectal Neoplasms/genetics ; 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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  • 6
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    A genetic linkage map for the zebrafish (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: To facilitate molecular genetic analysis of vertebrate development, haploid genetics was used to construct a recombination map for the zebrafish Danio (Brachydanio) rerio. The map consists of 401 random amplified polymorphic DNAs (RAPDs) and 13 simple sequence repeats spaced at an average interval of 5.8 centimorgans. Strategies that exploit the advantages of haploid genetics and RAPD markers were developed that quickly mapped lethal and visible mutations and that placed cloned genes on the map. This map is useful for the position-based cloning of mutant genes, the characterization of chromosome rearrangements, and the investigation of evolution in vertebrate genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Postlethwait, J H -- Johnson, S L -- Midson, C N -- Talbot, W S -- Gates, M -- Ballinger, E W -- Africa, D -- Andrews, R -- Carl, T -- Eisen, J S -- 1RO1AI26734/AI/NIAID NIH HHS/ -- HD07470/HD/NICHD NIH HHS/ -- NS23915/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):699-703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurosciences, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Cloning, Molecular ; Female ; Genetic Markers ; Genotype ; Male ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Software ; Zebrafish/*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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  • 7
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    Connexin mutations in X-linked Charcot-Marie-Tooth disease (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-12-24
    Description: X-linked Charcot-Marie-Tooth disease (CMTX) is a form of hereditary neuropathy with demyelination. Recently, this disorder was mapped to chromosome Xq13.1. The gene for the gap junction protein connexin32 is located in the same chromosomal segment, which led to its consideration as a candidate gene for CMTX. With the use of Northern (RNA) blot and immunohistochemistry technique, it was found that connexin32 is normally expressed in myelinated peripheral nerve. Direct sequencing of the connexin32 gene showed seven different mutations in affected persons from eight CMTX families. These findings, a demonstration of inherited defects in a gap junction protein, suggest that connexin32 plays an important role in peripheral nerve.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bergoffen, J -- Scherer, S S -- Wang, S -- Scott, M O -- Bone, L J -- Paul, D L -- Chen, K -- Lensch, M W -- Chance, P F -- Fischbeck, K H -- GM37751/GM/NIGMS NIH HHS/ -- NS01565/NS/NINDS NIH HHS/ -- NS08075/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1993 Dec 24;262(5142):2039-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Pennsylvania Medical School, Children's Hospital of Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8266101" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Charcot-Marie-Tooth Disease/*genetics ; Chromosome Mapping ; Connexins/analysis/*genetics ; Female ; Genetic Linkage ; Humans ; Male ; Molecular Sequence Data ; *Mutation ; Nerve Fibers, Myelinated/chemistry ; Nerve Tissue Proteins/analysis ; Peripheral Nerves/chemistry ; Rats ; X Chromosome
    Print ISSN: 0036-8075
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  • 8
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    Identification of mutations in the COL4A5 collagen gene in Alport syndrome (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-08
    Description: X-linked Alport syndrome is a hereditary glomerulonephritis in which progressive loss of kidney function is often accompanied by progressive loss of hearing. Ultrastructural defects in glomerular basement membranes (GBM) of Alport syndrome patients implicate an altered structural protein as the cause of nephritis. The product of COL4A5, the alpha 5(IV) collagen chain, is a specific component of GBM within the kidney, and the gene maps to the same X chromosomal region as does Alport syndrome. Three structural aberrations were found in COL4A5, in intragenic deletion, a Pst I site variant, and an uncharacterized abnormality, which appear to cause nephritis and deafness, with allele-specific severity, in three Alport syndrome kindreds in Utah.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, D F -- Hostikka, S L -- Zhou, J -- Chow, L T -- Oliphant, A R -- Gerken, S C -- Gregory, M C -- Skolnick, M H -- Atkin, C L -- Tryggvason, K -- DK 36200/DK/NIDDK NIH HHS/ -- DK 39497/DK/NIDDK NIH HHS/ -- M01 RR 00064/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 8;248(4960):1224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Informatics, University of Utah School of Medicine, Salt Lake City 84132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2349482" target="_blank"〉PubMed〈/a〉
    Keywords: Blotting, Southern ; Cloning, Molecular ; Collagen/*genetics ; DNA/genetics/isolation & purification ; Exons ; Female ; *Genes ; Humans ; Male ; Molecular Weight ; *Mutation ; Nephritis, Hereditary/*genetics ; Pedigree ; Restriction Mapping ; X Chromosome
    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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  • 9
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    Activity and distribution of binding sites in brain of a nonpeptide substance P (NK1) receptor antagonist (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-01-25
    Description: CP-96,345, a nonpeptide substance P antagonist, is selective for the tachykinin NK1 receptor. The compound binds to a single population of sites in guinea pig brain and potently inhibits substance P-induced excitation of locus ceruleus neurons. CP-96,345 should be a useful tool for studying the action of substance P in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLean, S -- Ganong, A H -- Seeger, T F -- Bryce, D K -- Pratt, K G -- Reynolds, L S -- Siok, C J -- Lowe, J A 3rd -- Heym, J -- New York, N.Y. -- Science. 1991 Jan 25;251(4992):437-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Central Research Division, Pfizer Inc., Groton, CT 06340.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1703324" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Autoradiography ; Binding Sites ; Binding, Competitive ; Biphenyl Compounds/*metabolism/pharmacology ; Brain/*metabolism/radionuclide imaging ; Corpus Striatum/*metabolism/radionuclide imaging ; Guinea Pigs ; Hydrogen-Ion Concentration ; Male ; Receptors, Neurokinin-1 ; Receptors, Neurotransmitter/*antagonists & inhibitors/*metabolism ; Receptors, Tachykinin ; Spectrophotometry ; Substance P/metabolism ; Tachykinins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Lymphoid development in mice congenitally lacking T cell receptor alpha beta-expressing cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-06-05
    Description: Vertebrate T cells express either an alpha beta or gamma delta T cell receptor (TCR). The developmental relatedness of the two cell types is unresolved. alpha beta + T cells respond to specific pathogens by collaborating with immunoglobulin-producing B cells in distinct lymphoid organs such as the spleen and Peyer's patches. The precise influence of alpha beta + T cells on B cell development is poorly understood. To investigate the developmental effects of alpha beta + T cells on B cells and gamma delta + T cells, mice homozygous for a disrupted TCR alpha gene were generated. The homozygotes showed elimination of alpha beta + T cells and the loss of thymic medullae. Despite this, gamma delta + T cells developed in normal numbers, and there was an increase in splenic B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Philpott, K L -- Viney, J L -- Kay, G -- Rastan, S -- Gardiner, E M -- Chae, S -- Hayday, A C -- Owen, M J -- GM37759/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jun 5;256(5062):1448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1604321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Blastocyst ; Blotting, Southern ; Chimera ; Clone Cells ; DNA/genetics/isolation & purification ; Female ; Lymphoid Tissue/growth & development/*immunology ; Macromolecular Substances ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Peyer's Patches/immunology ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/*genetics ; Spleen/immunology ; T-Lymphocytes/*immunology ; Thymus Gland/immunology
    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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