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  • Articles  (302)
  • Male  (302)
  • Cell & Developmental Biology
  • American Association for the Advancement of Science (AAAS)  (302)
  • 1990-1994  (117)
  • 1980-1984  (185)
  • Natural Sciences in General  (302)
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  • Articles  (302)
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  • American Association for the Advancement of Science (AAAS)  (302)
  • Wiley-Blackwell  (59)
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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
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    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
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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Multiple daily amphetamine administration: behavioral and neurochemical alterations (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-02-15
    Description: In rats, multiple daily amphetamine injections (2.5 milligrams per kilogram of body weight, injected subcutaneously every 4 hours for 5 days) resulted in a progressive augmentation in response, characterized by a more rapid onset and an increased magnitude of stereotypy. By contrast, offset times of both the stereotypy and the poststereotypy hyperactivity periods were markedly shortened. When the animals were retested with the same dose of amphetamine 8 days after the long-term treatment was discontinued, the time of offset of the stereotypy and hyperactivity phases had recovered to values found with short-term amphetamine treatment, whereas the more rapid onset of stereotypy persisted. Brain monoamine and amphetamine concentrations and tyrosine hydroxylase activity were determined in comparably treated rats at times corresponding to the behavioral observations. The behavioral data indicate that enhanced responsiveness to amphetamine following its repeated administration may contribute to the development of amphetamine psychosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segal, D S -- Weinberger, S B -- Cahill, J -- McCunney, S J -- New York, N.Y. -- Science. 1980 Feb 15;207(4433):905-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7188815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior/*drug effects ; Behavior, Animal/*drug effects ; Brain/metabolism ; Brain Chemistry/drug effects ; Dextroamphetamine/administration & dosage/*pharmacology ; Dopamine/metabolism ; Dose-Response Relationship, Drug ; Humans ; Male ; Motor Activity/drug effects ; Norepinephrine/metabolism ; Rats ; Serotonin/metabolism ; Stereotyped Behavior/*drug effects ; Time Factors
    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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    Separation of morphine analgesia from physical dependence (1984)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1984-10-26
    Description: Intravenous infusion of morphine sulfate in rats for 24 hours produced marked opioid dependence, manifested by a series of well-documented signs appearing after injection of the opiate antagonist naloxone. Treatment of rats with naloxonazine significantly reduced the analgesia associated with the morphine infusions for more than 24 hours. Furthermore, 14 of 16 withdrawal signs observed in naloxonazine-treated rats were virtually identical to those in rats that received morphine alone. These results raise the possibility that different receptor mechanisms mediate morphine analgesia and many of the withdrawal signs associated with morphine dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ling, G S -- MacLeod, J M -- Lee, S -- Lockhart, S H -- Pasternak, G W -- DA 002615/DA/NIDA NIH HHS/ -- NS 00415/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1984 Oct 26;226(4673):462-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6541807" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Humans ; Male ; Morphine/*pharmacology ; Naloxone/*analogs & derivatives/pharmacology ; Rats ; Rats, Inbred Strains ; Substance Withdrawal Syndrome ; *Substance-Related Disorders
    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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    Sparing of the brain in neonatal undernutrition: amino acid transport and incorporation into brain and muscle (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-02-22
    Description: Rates of tyrosine and lysine transport and incorporation into protein were measured in control and undernourished weanling rats. Undernutrition was induced by feeding lactating dams a low protein diet (12 percent casein) from birth to day 21. At weaning, body and brain weights of undernourished rats were 50 percent and 88 percent, respectively, of control values. Lysine and tyrosine transport rates into skeletal muscle were reduced by over 75 percent, more than twice the reduction seen in brain. Rates of amino acid incorporation into muscle protein were reduced by approximately 50 percent; the change in rate of incorporation into brain protein was not statistically significant. These data indicate that, in spite of marked retardation of amino acid transport into brain, the brain seems fully capable of maintaining normal rates of protein synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freedman, L S -- Samuels, S -- Fish, I -- Schwartz, S A -- Lange, B -- Katz, M -- Morgano, L -- New York, N.Y. -- Science. 1980 Feb 22;207(4433):902-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6766565" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/*metabolism ; Animals ; Animals, Newborn/metabolism ; Biological Transport ; Body Weight ; Brain/growth & development/*metabolism ; Disease Models, Animal ; Female ; Lactation ; Male ; Muscles/*metabolism ; Pregnancy ; Protein-Energy Malnutrition/*metabolism ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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