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  • Animals  (51)
  • Aerospace Medicine
  • American Association for the Advancement of Science (AAAS)  (51)
  • 1990-1994  (51)
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  • American Association for the Advancement of Science (AAAS)  (51)
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  • 1
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    Multiple representations of pain in human cerebral cortex (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: The representation of pain in the cerebral cortex is less well understood than that of any other sensory system. However, with the use of magnetic resonance imaging and positron emission tomography in humans, it has now been demonstrated that painful heat causes significant activation of the contralateral anterior cingulate, secondary somatosensory, and primary somatosensory cortices. This contrasts with the predominant activation of primary somatosensory cortex caused by vibrotactile stimuli in similar experiments. Furthermore, the unilateral cingulate activation indicates that this forebrain area, thought to regulate emotions, contains an unexpectedly specific representation of pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Talbot, J D -- Marrett, S -- Evans, A C -- Meyer, E -- Bushnell, M C -- Duncan, G H -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1355-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de neurophysiologie comportementale, Faculte de medecine dentaire, Universite de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2003220" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Anxiety/physiopathology ; Brain Mapping ; Cerebral Cortex/*physiology ; Functional Laterality ; Hot Temperature ; Humans ; Magnetic Resonance Imaging ; Male ; Pain/*physiopathology ; Tomography, Emission-Computed
    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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    A multifunctional aqueous channel formed by CFTR (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-27
    Description: The cystic fibrosis gene product (CFTR) is a complex protein that functions as an adenosine 3,5-monophosphate (cAMP)-stimulated ion channel and possibly as a regulator of intracellular processes. In order to determine whether the CFTR molecule contains a functional aqueous pathway, anion, water, and urea transport were measured in Xenopus oocytes expressing CFTR. Cyclic AMP agonists induced a Cl- conductance of 94 microsiemens and an increase in water permeability of 4 x 10(-4) centimeter per second that was inhibited by a Cl- channel blocker and was dependent on anion composition. CFTR has a calculated single channel water conductance of 9 x 10(-13) cubic centimeter per second, suggesting a pore-like aqueous pathway. Oocytes expressing CFTR also showed cAMP-stimulated transport of urea but not the larger solute sucrose. Thus CFTR contains a cAMP-stimulated aqueous pore that can transport anions, water, and small solutes. The results also provide functional evidence for water movement through an ion channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasegawa, H -- Skach, W -- Baker, O -- Calayag, M C -- Lingappa, V -- Verkman, A S -- DK35124/DK/NIDDK NIH HHS/ -- DK43840/DK/NIDDK NIH HHS/ -- HL42368/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1992 Nov 27;258(5087):1477-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0532.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1279809" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Biological Transport/physiology ; Chlorides/metabolism ; Cyclic AMP/physiology ; Cystic Fibrosis Transmembrane Conductance Regulator ; Female ; Humans ; In Vitro Techniques ; Ion Channels/*physiology ; Membrane Proteins/*physiology ; Molecular Sequence Data ; Oocytes ; Urea/metabolism ; Water/metabolism ; Xenopus
    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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    Flow-dependent cytosolic acidification of vascular endothelial cells (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-23
    Description: Hemodynamic shear stress affects endothelial cell structure and function, but little is known about the signal transduction mechanisms involved in these processes. The effect of laminar shear stress on cytosolic pH (pHi) was examined in rat aortic endothelial cells cultured in glass capillary tubes. Shear stress forces led to a rapid decrease in pHi (maximal effect 0.09 pH unit at 13.4 dynes per square centimeter). Removal of specific ions or addition of exchange inhibitors suggests that in vascular endothelial cells shear stress forces activate both an alkali extruder, sodium ion-independent chloride-bicarbonate ion exchange, and an acid extruder, sodium-hydrogen ion exchange; the net effect in physiologic buffer with the bicarbonate ion is a decrease in pHi.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ziegelstein, R C -- Cheng, L -- Capogrossi, M C -- New York, N.Y. -- Science. 1992 Oct 23;258(5082):656-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1329207" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicarbonates/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Chloride-Bicarbonate Antiporters ; Cytosol/*physiology ; Endothelium, Vascular/*physiology ; Hydrogen-Ion Concentration ; Membrane Proteins/physiology ; Rats ; Signal Transduction/physiology ; Sodium-Hydrogen Antiporter ; Stress, Mechanical
    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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    Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-04-20
    Description: The mechanism by which erythropoietin controls mammalian erythrocyte production is unknown. Labeling experiments in vitro with [3H]thymidine demonstrated DNA cleavage in erythroid progenitor cells that was accompanied by DNA repair and synthesis. Erythropoietin reduced DNA cleavage by a factor of 2.6. In the absence of erythropoietin, erythroid progenitor cells accumulated DNA cleavage fragments characteristic of those found in programmed cell death (apoptosis) by 2 to 4 hours and began dying by 16 hours. In the presence of erythropoietin, the progenitor cells survived and differentiated into reticulocytes. Thus, apoptosis is a major component of normal erythropoiesis, and erythropoietin controls erythrocyte production by retarding DNA breakdown and preventing apoptosis in erythroid progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koury, M J -- Bondurant, M C -- DK 31513/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):378-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Vanderbilt University Medical Center, Nashville, TN.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2326648" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; DNA/biosynthesis/*drug effects/metabolism ; DNA Repair ; Erythrocyte Aging/drug effects ; Erythroid Precursor Cells/cytology/drug effects/*metabolism ; Erythropoietin/*pharmacology ; Friend murine leukemia virus ; Leukemia, Erythroblastic, Acute ; Mice ; Molecular Weight
    Print ISSN: 0036-8075
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  • 5
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    Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-15
    Description: Recent studies have suggested the existence of a tumor suppressor gene located at chromosome region 5q21. DNA probes from this region were used to study a panel of sporadic colorectal carcinomas. One of these probes, cosmid 5.71, detected a somatically rearranged restriction fragment in the DNA from a single tumor. Further analysis of the 5.71 cosmid revealed two regions that were highly conserved in rodent DNA. These sequences were used to identify a gene, MCC (mutated in colorectal cancer), which encodes an 829-amino acid protein with a short region of similarity to the G protein-coupled m3 muscarinic acetylcholine receptor. The rearrangement in the tumor disrupted the coding region of the MCC gene. Moreover, two colorectal tumors were found with somatically acquired point mutations in MCC that resulted in amino acid substitutions. MCC is thus a candidate for the putative colorectal tumor suppressor gene located at 5q21. Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinzler, K W -- Nilbert, M C -- Vogelstein, B -- Bryan, T M -- Levy, D B -- Smith, K J -- Preisinger, A C -- Hamilton, S R -- Hedge, P -- Markham, A -- 6M 07184/PHS HHS/ -- CA 06973/CA/NCI NIH HHS/ -- CA 09243/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Mar 15;251(4999):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1848370" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Amino Acid Sequence ; Animals ; Base Sequence ; *Chromosomes, Human, Pair 5 ; Colorectal Neoplasms/*genetics ; Exons ; GTP-Binding Proteins/metabolism ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Mutation ; Oligonucleotides/chemistry ; Polymerase Chain Reaction ; Proteins/*genetics/metabolism ; Rats ; Sequence Homology, Nucleic Acid ; *Tumor Suppressor Proteins
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  • 6
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    Slow mortality rate accelerations during aging in some animals approximate that of humans (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-08-24
    Description: A general measure of the rate of senescence is the acceleration of mortality rate, represented here by the time required for the mortality rate to double (MRD). Rhesus monkeys have an MRD close to that of humans, about 8 years; their shorter life-span results mainly from higher mortality at all ages. In contrast, some groups with short life-spans (rodents and galliform birds) have shorter MRDs and faster senescence. On the basis of the Gompertz mortality rate model, one may estimate the MRD from the maximum life-span (tmax) and the overall population mortality rate. Such calculations show that certain birds have MRDs that are as long as that of humans. These results show that high overall mortality rates or small body sizes do not preclude slow rates of senescence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finch, C E -- Pike, M C -- Witten, M -- New York, N.Y. -- Science. 1990 Aug 24;249(4971):902-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, University of Southern California, University Park 90089.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2392680" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; *Aging ; *Animal Population Groups ; Animals ; Birds ; *Hominidae ; Humans ; Mammals ; Mathematics ; Models, Statistical ; *Mortality
    Print ISSN: 0036-8075
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  • 7
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    A borna virus cDNA encoding a protein recognized by antibodies in humans with behavioral diseases (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-30
    Description: Borna disease virus (BDV) causes a rare neurological disease in horses and sheep. The virus has not been classified because neither an infectious particle nor a specific nucleic acid had been identified. To identify the genome of BDV, a subtractive complementary DNA expression library was constructed with polyadenylate-selected RNA from a BDV-infected MDCK cell line. A clone (B8) was isolated that specifically hybridized to RNA isolated from BDV-infected brain tissue and BDV-infected cell lines. This clone hybridized to four BDV-specific positive strand RNAs (10.5, 3.6, 2.1, and 0.85 kilobases) and one negative strand RNA (10.5 kilobases) in BDV-infected rat brain. Nucleotide sequence analysis of the clone suggested that it represented a full-length messenger RNA which contained several open reading frames. In vitro transcription and translation of the clone resulted in the synthesis of the 14- and 24-kilodalton BDV-specific proteins. The 24-kilodalton protein, when translated in vitro from the clone, was recognized by antibodies in the sera of patients (three of seven) with behavioral disorders. This BDV-specific clone will provide the means to isolate the other BDV-specific nucleic acids and to identify the virus responsible for Borna disease. In addition, the significance of BDV or a BDV-related virus as a human pathogen can now be more directly examined.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉VandeWoude, S -- Richt, J A -- Zink, M C -- Rott, R -- Narayan, O -- Clements, J E -- RR00130/RR/NCRR NIH HHS/ -- RR07002/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 30;250(4985):1278-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Colorado State University, Lab Animal Resources, Fort Collins 80532.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2244211" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Viral/*blood ; Borna Disease/*microbiology ; Borna disease virus/*genetics/immunology ; Brain/microbiology ; Cloning, Molecular ; DNA/*genetics ; Fluorescent Antibody Technique ; Humans ; Immunoblotting ; Mental Disorders/*microbiology ; Molecular Sequence Data ; Molecular Weight ; Nucleic Acid Hybridization ; RNA, Messenger/analysis/genetics ; RNA, Viral/analysis/genetics ; Rats ; Transcription, Genetic ; Viral Proteins/*genetics/immunology
    Print ISSN: 0036-8075
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  • 8
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    Implication of GAP in Ras-dependent transactivation of a polyoma enhancer sequence (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Controversy exists as to whether the interaction of a guanosine triphosphatase activating protein (GAP) with Ras proteins functions both to initiate and to terminate Ras-dependent signaling events or only to terminate them. GAP-C, a carboxyl-terminal fragment of GAP that is sufficient to stimulate GTPase activity, inhibited the stimulation of transcription produced by some oncoproteins (v-Src, polyoma middle T, wild-type Ras, and oncogenic Ras) but not that produced by v-Mos. Wild-type GAP did not affect transcription induced by oncogenic Ras but reversed the inhibitory effect of GAP-C on transcription induced by oncogenic Ras. These results indicate that GAP is a negative regulator of wild-type Ras and elicits a downstream signal by interacting with Ras-GTP (guanosine triphosphate).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schweighoffer, F -- Barlat, I -- Chevallier-Multon, M C -- Tocque, B -- New York, N.Y. -- Science. 1992 May 8;256(5058):825-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rhone-Poulenc Rorer, Centre de Recherche de Vitry-Alfortville, Vitry Sur Seine.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1317056" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antigens, Polyomavirus Transforming/genetics ; CHO Cells ; *Cell Cycle Proteins ; *Cell Transformation, Neoplastic ; Chloramphenicol O-Acetyltransferase/genetics/metabolism ; Cricetinae ; *Enhancer Elements, Genetic ; Fungal Proteins/genetics/metabolism ; GTPase-Activating Proteins ; *Genes, ras ; Humans ; Mice ; Oncogene Proteins v-mos ; Oncogenes ; Polyomavirus/*genetics ; Promoter Regions, Genetic ; Protein-Tyrosine Kinases/genetics ; Proteins/*metabolism ; Retroviridae Proteins, Oncogenic/genetics ; Signal Transduction ; Simian virus 40/genetics ; Transcription, Genetic ; *Transcriptional Activation ; Transfection ; ras GTPase-Activating Proteins ; *ras-GRF1
    Print ISSN: 0036-8075
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  • 9
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    The skeletal muscle chloride channel in dominant and recessive human myotonia (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: Autosomal recessive generalized myotonia (Becker's disease) (GM) and autosomal dominant myotonia congenita (Thomsen's disease) (MC) are characterized by skeletal muscle stiffness that is a result of muscle membrane hyperexcitability. For both diseases, alterations in muscle chloride or sodium currents or both have been observed. A complementary DNA for a human skeletal muscle chloride channel (CLC-1) was cloned, physically localized on chromosome 7, and linked to the T cell receptor beta (TCRB) locus. Tight linkage of these two loci to GM and MC was found in German families. An unusual restriction site in the CLC-1 locus in two GM families identified a mutation associated with that disease, a phenylalanine-to-cysteine substitution in putative transmembrane domain D8. This suggests that different mutations in CLC-1 may cause dominant or recessive myotonia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koch, M C -- Steinmeyer, K -- Lorenz, C -- Ricker, K -- Wolf, F -- Otto, M -- Zoll, B -- Lehmann-Horn, F -- Grzeschik, K H -- Jentsch, T J -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Center for Human Genetics, Marburg University, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1379744" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Southern ; Chloride Channels ; *Chromosomes, Human, Pair 7 ; Cloning, Molecular ; DNA/genetics ; Female ; *Genes, Dominant ; *Genes, Recessive ; Genetic Linkage ; Humans ; Ion Channels/*genetics ; Lod Score ; Male ; Membrane Proteins/*genetics ; Molecular Sequence Data ; Muscular Dystrophies/*genetics ; Myotonia Congenita/*genetics ; Pedigree ; Polymorphism, Restriction Fragment Length ; Receptors, Antigen, T-Cell/genetics ; Recombination, Genetic ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
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  • 10
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    Cloning and expression of a rat brain GABA transporter (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-14
    Description: A complementary DNA clone (designated GAT-1) encoding a transporter for the neurotransmitter gamma-aminobutyric acid (GABA) has been isolated from rat brain, and its functional properties have been examined in Xenopus oocytes. Oocytes injected with GAT-1 synthetic messenger RNA accumulated [3H]GABA to levels above control values. The transporter encoded by GAT-1 has a high affinity for GABA, is sodium-and chloride-dependent, and is pharmacologically similar to neuronal GABA transporters. The GAT-1 protein shares antigenic determinants with a native rat brain GABA transporter. The nucleotide sequence of GAT-1 predicts a protein of 599 amino acids with a molecular weight of 67 kilodaltons. Hydropathy analysis of the deduced protein suggests multiple transmembrane regions, a feature shared by several cloned transporters; however, database searches indicate that GAT-1 is not homologous to any previously identified proteins. Therefore, GAT-1 appears to be a member of a previously uncharacterized family of transport molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guastella, J -- Nelson, N -- Nelson, H -- Czyzyk, L -- Keynan, S -- Miedel, M C -- Davidson, N -- Lester, H A -- Kanner, B I -- GM 10991/GM/NIGMS NIH HHS/ -- GM 29836/GM/NIGMS NIH HHS/ -- NS 16708/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 14;249(4974):1303-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1975955" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Brain/metabolism ; Carrier Proteins/antagonists & inhibitors/*genetics/metabolism ; Chlorine/physiology ; Cloning, Molecular ; GABA Plasma Membrane Transport Proteins ; Gene Expression ; Membrane Proteins/antagonists & inhibitors/*genetics/metabolism ; *Membrane Transport Proteins ; Microinjections ; Molecular Sequence Data ; Nerve Tissue Proteins/antagonists & inhibitors/*genetics/metabolism ; Oocytes/metabolism ; *Organic Anion Transporters ; Poly A/analysis ; RNA, Messenger/analysis ; Rats ; Sodium/physiology ; Structure-Activity Relationship ; Xenopus ; gamma-Aminobutyric Acid/*metabolism
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