ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • Artikel  (355)
  • Rats  (355)
  • American Association for the Advancement of Science (AAAS)  (355)
  • 1990-1994  (355)
Sammlung
  • Artikel  (355)
Datenquelle
Schlagwörter
Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (355)
Erscheinungszeitraum
Jahr
Zeitschrift
Thema
  • 1
    facet.materialart.
    Unbekannt
    An all D-amino acid opioid peptide with central analgesic activity from a combinatorial library (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-23
    Beschreibung: A synthetic combinatorial library containing 52,128,400 D-amino acid hexapeptides was used to identify a ligand for the mu opioid receptor. The peptide, Ac-rfwink-NH2, bears no resemblance to any known opioid peptide. Simulations using molecular dynamics, however, showed that three amino acid moieties have the same spatial orientation as the corresponding pharmacophoric groups of the opioid peptide PLO17. Ac-rfwink-NH2 was shown to be a potent agonist at the mu receptor and induced long-lasting analgesia in mice. Analgesia produced by intraperitoneally administered Ac-rfwink-NH2 was blocked by intracerebroventricular administration of naloxone, demonstrating that this peptide may cross the blood-brain barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dooley, C T -- Chung, N N -- Wilkes, B C -- Schiller, P W -- Bidlack, J M -- Pasternak, G W -- Houghten, R A -- DA-000138/DA/NIDA NIH HHS/ -- DA-02615/DA/NIDA NIH HHS/ -- DA-03742/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):2019-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Torrey Pines Institute for Molecular Studies, San Diego, CA 92121.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801131" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Analgesics/chemistry/metabolism/*pharmacology ; Animals ; Brain/metabolism ; Dose-Response Relationship, Drug ; Endorphins/pharmacology ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- ; Enkephalin, D-Penicillamine (2,5)- ; Enkephalins/metabolism ; Guinea Pigs ; Injections, Intraventricular ; Male ; Mice ; Models, Molecular ; Molecular Sequence Data ; Naloxone/administration & dosage/pharmacology ; Opioid Peptides/chemistry/metabolism/*pharmacology ; Pain Measurement ; Protein Conformation ; Rats ; Receptors, Opioid, mu/agonists/metabolism ; Stereoisomerism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 2
    facet.materialart.
    Unbekannt
    Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-16
    Beschreibung: Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettit, D L -- Perlman, S -- Malinow, R -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1881-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997883" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Genetic Vectors ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/enzymology/*physiology ; Rats ; Recombinant Proteins/metabolism ; Synaptic Transmission/drug effects/*physiology ; Transfection ; Vaccinia virus/genetics/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 3
    facet.materialart.
    Unbekannt
    Correction of lethal intestinal defect in a mouse model of cystic fibrosis by human CFTR (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-09
    Beschreibung: Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). A potential animal model of CF, the CFTR-/- mouse, has had limited utility because most mice die from intestinal obstruction during the first month of life. Human CFTR (hCFTR) was expressed in CFTR-/- mice under the control of the rat intestinal fatty acid-binding protein gene promoter. The mice survived and showed functional correction of ileal goblet cell and crypt cell hyperplasia and cyclic adenosine monophosphate-stimulated chloride secretion. These results support the concept that transfer of the hCFTR gene may be a useful strategy for correcting physiologic defects in patients with CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, L -- Dey, C R -- Wert, S E -- DuVall, M D -- Frizzell, R A -- Whitsett, J A -- DK38518/DK/NIDDK NIH HHS/ -- HL49004/HL/NHLBI NIH HHS/ -- HL51832/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, OH 45229-3039.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527588" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Carrier Proteins/genetics ; Chlorides/metabolism ; Colforsin/pharmacology ; Colon/chemistry/pathology ; Cystic Fibrosis/genetics/metabolism/pathology/*therapy ; Cystic Fibrosis Transmembrane Conductance Regulator ; Disease Models, Animal ; Fatty Acid-Binding Proteins ; Gene Expression ; *Genetic Therapy ; Humans ; Intestinal Mucosa/chemistry/*pathology/secretion ; Intestine, Small/chemistry/pathology ; Membrane Proteins/analysis/*genetics/physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Promoter Regions, Genetic ; RNA, Messenger/analysis/genetics ; Rats ; Recombinant Proteins/biosynthesis ; *Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 4
    facet.materialart.
    Unbekannt
    Control of kinetic properties of AMPA receptor channels by nuclear RNA editing (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-09
    Beschreibung: AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor channels mediate the fast component of excitatory postsynaptic currents in the central nervous system. Site-selective nuclear RNA editing controls the calcium permeability of these channels, and RNA editing at a second site is shown here to affect the kinetic aspects of these channels in rat brain. In three of the four AMPA receptor subunits (GluR-B, -C, and -D), intronic elements determine a codon switch (AGA, arginine, to GGA, glycine) in the primary transcripts in a position termed the R/G site, which immediately precedes the alternatively spliced modules "flip" and "flop." The extent of editing at this site progresses with brain development in a manner specific for subunit and splice form, and edited channels possess faster recovery rates from desensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lomeli, H -- Mosbacher, J -- Melcher, T -- Hoger, T -- Geiger, J R -- Kuner, T -- Monyer, H -- Higuchi, M -- Bach, A -- Seeburg, P H -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1709-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992055" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Brain/embryology/*metabolism ; Cell Nucleus/metabolism ; Exons ; Glutamic Acid/pharmacology ; Glycine/genetics ; Introns ; Kinetics ; Membrane Potentials ; Molecular Sequence Data ; Oocytes ; PC12 Cells ; Patch-Clamp Techniques ; *RNA Editing ; Rats ; Rats, Wistar ; Receptors, AMPA/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Xenopus
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 5
    facet.materialart.
    Unbekannt
    Resetting the biological clock: mediation of nocturnal circadian shifts by glutamate and NO (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-09
    Beschreibung: Circadian rhythms of mammals are timed by an endogenous clock with a period of about 24 hours located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Light synchronizes this clock to the external environment by daily adjustments in the phase of the circadian oscillation. The mechanism has been thought to involve the release of excitatory amino acids from retinal afferents to the SCN. Brief treatment of rat SCN in vitro with glutamate (Glu), N-methyl-D-aspartate (NMDA), or nitric oxide (NO) generators produced lightlike phase shifts of circadian rhythms. The SCN exhibited calcium-dependent nitric oxide synthase (NOS) activity. Antagonists of NMDA or NOS pathways blocked Glu effects in vitro, and intracerebroventricular injection of a NOS inhibitor in vivo blocked the light-induced resetting of behavioral rhythms. Together, these data indicate that Glu release, NMDA receptor activation, NOS stimulation, and NO production link light activation of the retina to cellular changes within the SCN mediating the phase resetting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, J M -- Chen, D -- Weber, E T -- Faiman, L E -- Rea, M A -- Gillette, M U -- NS22155/NS/NINDS NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1713-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527589" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Oxidoreductases/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Biological Clocks/drug effects/*physiology ; Circadian Rhythm/drug effects/*physiology ; Glutamic Acid/*metabolism/pharmacology ; In Vitro Techniques ; Light ; N-Methylaspartate/pharmacology ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent/physiology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Retina/physiology ; Signal Transduction ; Suprachiasmatic Nucleus/drug effects/metabolism/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 6
    facet.materialart.
    Unbekannt
    Differential activation of ERK and JNK mitogen-activated protein kinases by Raf-1 and MEKK (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-09
    Beschreibung: Growth factors activate mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs) and Jun kinases (JNKs). Although the signaling cascade from growth factor receptors to ERKs is relatively well understood, the pathway leading to JNK activation is more obscure. Activation of JNK by epidermal growth factor (EGF) or nerve growth factor (NGF) was dependent on H-Ras activation, whereas JNK activation by tumor necrosis factor alpha (TNF-alpha) was Ras-independent. Ras activates two protein kinases, Raf-1 and MEK (MAPK, or ERK, kinase) kinase (MEKK). Raf-1 contributes directly to ERK activation but not to JNK activation, whereas MEKK participated in JNK activation but caused ERK activation only after overexpression. These results demonstrate the existence of two distinct Ras-dependent MAPK cascades--one initiated by Raf-1 leading to ERK activation, and the other initiated by MEKK leading to JNK activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minden, A -- Lin, A -- McMahon, M -- Lange-Carter, C -- Derijard, B -- Davis, R J -- Johnson, G L -- Karin, M -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1719-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California at San Diego, La Jolla 92093-0636.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992057" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 3T3 Cells ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Enzyme Activation/drug effects ; Epidermal Growth Factor/pharmacology ; Genes, ras ; HeLa Cells ; Humans ; JNK Mitogen-Activated Protein Kinases ; *MAP Kinase Kinase Kinase 1 ; Mice ; Mitogen-Activated Protein Kinase 1 ; *Mitogen-Activated Protein Kinases ; Nerve Growth Factors/pharmacology ; PC12 Cells ; Protein-Serine-Threonine Kinases/*metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-raf ; Rats ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology ; ras Proteins/*pharmacology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 7
    facet.materialart.
    Unbekannt
    Watching the brain remake itself (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-02
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1475-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985011" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/*physiology ; Fear/physiology ; Humans ; Learning/physiology ; Motor Cortex/physiology ; Nerve Growth Factors/physiology ; Nerve Net/*physiology ; Neural Pathways/physiology ; Neuronal Plasticity/*physiology ; Pain/physiopathology ; Rats ; Synapses/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 8
    facet.materialart.
    Unbekannt
    Stimulation and inhibition of angiogenesis by placental proliferin and proliferin-related protein (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-02
    Beschreibung: In many mammalian species, the placenta is the site of synthesis of proteins in the prolactin and growth hormone family. Analysis of two such proteins, proliferin (PLF) and proliferin-related protein (PRP), revealed that they are potent regulators of angiogenesis; PLF stimulated and PRP inhibited endothelial cell migration in cell culture and neovascularization in vivo. The mouse placenta secretes an angiogenic activity during the middle of pregnancy that corresponds primarily to PLF, but later in gestation releases a factor that inhibits angiogenesis, which was identified as PRP. Incubation of placental tissue with PLF led to the specific binding of this hormone to capillary endothelial cells. Thus PLF and PRP may regulate the initiation and then the cessation of placental neovascularization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, D -- Volpert, O V -- Bouck, N -- Linzer, D I -- CA52750/CA/NCI NIH HHS/ -- HD24518/HD/NICHD NIH HHS/ -- HD29962/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527157" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Cattle ; Cell Movement/drug effects ; Cornea/blood supply ; Culture Techniques ; Endothelium, Vascular/*cytology/drug effects/metabolism ; Female ; Fibroblast Growth Factor 2/pharmacology ; Glycoproteins/metabolism/*pharmacology ; Growth Substances/metabolism/*pharmacology ; Intercellular Signaling Peptides and Proteins ; *Neovascularization, Pathologic ; Placenta/*blood supply ; Pregnancy ; Pregnancy Proteins/*pharmacology ; Rats
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 9
    facet.materialart.
    Unbekannt
    Association of insulin receptor substrate-1 with integrins (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-12-02
    Beschreibung: Insulin stimulation was found to promote association of the alpha v beta 3 integrin (a vitronectin receptor) with insulin receptor substrate-1 (IRS-1), an intracellular protein that mediates insulin signaling by binding other signaling molecules, including growth factor receptor-bound protein 2 (Grb2) and phosphatidylinositol-3' kinase. Insulin-treated cells expressing the alpha v beta 3 integrin showed 2.5 times more DNA synthesis when plated on vitronectin than on other substrates, whereas cells expressing another vitronectin receptor, alpha v beta 5, did not show this difference. The association between integrin and IRS-1 may be a mechanism for the synergistic action of growth factor and extracellular matrix receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vuori, K -- Ruoslahti, E -- CA 28896/CA/NCI NIH HHS/ -- CA 30199/CA/NCI NIH HHS/ -- CA 42507/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1576-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research Center, La Jolla Cancer Research Foundation, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527156" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Cell Line ; Collagen ; DNA/biosynthesis ; Glycoproteins ; Humans ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Integrins/*metabolism ; Molecular Sequence Data ; Phosphoproteins/*metabolism ; Phosphorylation ; Rats ; Receptor, Insulin ; Receptors, Cytoadhesin/*metabolism ; Receptors, Vitronectin ; Transfection ; Tumor Cells, Cultured ; Vitronectin
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
  • 10
    facet.materialart.
    Unbekannt
    Long-term behavioral recovery in parkinsonian rats by an HSV vector expressing tyrosine hydroxylase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1994-11-25
    Beschreibung: One therapeutic approach to treating Parkinson's disease is to convert endogenous striatal cells into levo-3,4-dihydroxyphenylalanine (L-dopa)-producing cells. A defective herpes simplex virus type 1 vector expressing human tyrosine hydroxylase was delivered into the partially denervated striatum of 6-hydroxydopamine-lesioned rats, used as a model of Parkinson's disease. Efficient behavioral and biochemical recovery was maintained for 1 year after gene transfer. Biochemical recovery included increases in both striatal tyrosine hydroxylase enzyme activity and in extracellular dopamine concentrations. Persistence of human tyrosine hydroxylase was revealed by expression of RNA and immunoreactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉During, M J -- Naegele, J R -- O'Malley, K L -- Geller, A I -- EY09749/EY/NEI NIH HHS/ -- NS06208/NS/NINDS NIH HHS/ -- NS28227/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1399-403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7669103" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Base Sequence ; Corpus Striatum/*enzymology/metabolism ; Denervation ; Disease Models, Animal ; Dopamine/metabolism ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Humans ; Levodopa/metabolism ; Male ; Molecular Sequence Data ; *Motor Activity ; Neurons/enzymology ; Parkinson Disease/metabolism/*therapy ; Rats ; Rats, Sprague-Dawley ; Simplexvirus/*genetics ; Tyrosine 3-Monooxygenase/*genetics/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    AKTUELLE ARTIKEL
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...