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  • Rats  (19)
  • American Association for the Advancement of Science (AAAS)  (19)
  • Springer Nature
  • 2000-2004
  • 1995-1999  (19)
  • 1940-1944
  • 1995  (19)
Sammlung
Schlagwörter
Verlag/Herausgeber
  • American Association for the Advancement of Science (AAAS)  (19)
  • Springer Nature
Erscheinungszeitraum
  • 2000-2004
  • 1995-1999  (19)
  • 1940-1944
Jahr
  • 1
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    Inhibition of ras-induced proliferation and cellular transformation by p16INK4 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-01-13
    Beschreibung: The cyclin-dependent kinase 4 (CDK4) regulates progression through the G1 phase of the cell cycle. The activity of CDK4 is controlled by the opposing effects of the D-type cyclin, an activating subunit, and p16INK4, an inhibitory subunit. Ectopic expression of p16INK4 blocked entry into S phase of the cell cycle induced by oncogenic Ha-Ras, and this block was relieved by coexpression of a catalytically inactive CDK4 mutant. Expression of p16INK4 suppressed cellular transformation of primary rat embryo fibroblasts by oncogenic Ha-Ras and Myc, but not by Ha-Ras and E1a. Together, these observations provide direct evidence that p16INK4 can inhibit cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serrano, M -- Gomez-Lahoz, E -- DePinho, R A -- Beach, D -- Bar-Sagi, D -- CA55360/CA/NCI NIH HHS/ -- EY09300-01/EY/NEI NIH HHS/ -- HD28317-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1995 Jan 13;267(5195):249-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7809631" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenovirus E1A Proteins/genetics/physiology ; Animals ; Carrier Proteins/genetics/*physiology ; *Cell Division ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinase Inhibitor p16 ; *Cyclin-Dependent Kinases ; Genes, Reporter ; Genes, Retinoblastoma ; Genes, myc ; Genes, ras ; Plasmids ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; *Proto-Oncogene Proteins ; Rats ; Retinoblastoma Protein/physiology ; S Phase ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; ras Proteins/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)
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  • 2
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    Crystal structure of DCoH, a bifunctional, protein-binding transcriptional coactivator (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-04-28
    Beschreibung: DCoH, the dimerization cofactor of hepatocyte nuclear factor-1, stimulates gene expression by associating with specific DNA binding proteins and also catalyzes the dehydration of the biopterin cofactor of phenylalanine hydroxylase. The x-ray crystal structure determined at 3 angstrom resolution reveals that DCoH forms a tetramer containing two saddle-shaped grooves that comprise likely macromolecule binding sites. Two equivalent enzyme active sites flank each saddle, suggesting that there is a spatial connection between the catalytic and binding activities. Structural similarities between the DCoH fold and nucleic acid-binding proteins argue that the saddle motif has evolved to bind diverse ligands or that DCoH unexpectedly may bind nucleic acids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Endrizzi, J A -- Cronk, J D -- Wang, W -- Crabtree, G R -- Alber, T -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):556-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley 94720-3206, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725101" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Sequence ; Animals ; Binding Sites ; Computer Graphics ; Crystallography, X-Ray ; Gene Expression Regulation ; Hydro-Lyases/*chemistry/metabolism ; Models, Molecular ; Molecular Sequence Data ; Protein Conformation ; Protein Folding ; Protein Structure, Secondary ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Transcription Factors/*chemistry/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)
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  • 3
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    Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-10-06
    Beschreibung: Furosemide, a chloride cotransport inhibitor, reversibly blocked synchronized burst discharges in hippocampal slices without reducing the pyramidal cell response to single electrical stimuli. Images of the intrinsic optical signal acquired during these slice experiments indicated that furosemide coincidentally blocked changes in extracellular space. In urethane-anesthetized rats, systemically injected furosemide blocked kainic acid-induced electrical discharges recorded from cortex. These results suggest that (i) neuronal synchronization involved in epileptiform activity can be dissociated from synaptic excitability; (ii) nonsynaptic mechanisms, possibly associated with furosemide-sensitive cell volume regulation, may be critical for synchronization of neuronal activity; and (iii) agents that affect extracellular volume may have clinical utility as antiepileptic drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hochman, D W -- Baraban, S C -- Owens, J W -- Schwartzkroin, P A -- NS07144/NS/NINDS NIH HHS/ -- NS15317/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Oct 6;270(5233):99-102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of Washington, Seattle 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569957" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 4-Aminopyridine/pharmacology ; Animals ; Anticonvulsants/*pharmacology ; Bicuculline/pharmacology ; Electric Stimulation ; Entorhinal Cortex/physiology ; Extracellular Space/drug effects/physiology ; Female ; Furosemide/*pharmacology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Kainic Acid/pharmacology ; Magnesium/pharmacology ; Male ; Membrane Potentials/drug effects ; Potassium/pharmacology ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus/chemically induced/*physiopathology ; Synaptic Transmission/drug effects
    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)
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  • 4
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    A region of adenylyl cyclase 2 critical for regulation by G protein beta gamma subunits (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-05-26
    Beschreibung: Receptor-mediated activation of heterotrimeric guanine nucleotide-binding proteins (G proteins) results in the dissociation of alpha from beta gamma subunits, thereby allowing both to regulate effectors. Little is known about the regions of effectors required for recognition of G beta gamma. A peptide encoding residues 956 to 982 of adenylyl cyclase 2 specifically blocked G beta gamma stimulation of adenylyl cyclase 2, phospholipase C-beta 3, potassium channels, and beta-adrenergic receptor kinase as well as inhibition of calmodulin-stimulated adenylyl cyclases, but had no effect on interactions between G beta gamma and G alpha o. Substitutions in this peptide identified a functionally important motif, Gln-X-X-Glu-Arg, that is also conserved in regions of potassium channels and beta-adrenergic receptor kinases that participate in G beta gamma interactions. Thus, the region defined by residues 956 to 982 of adenylyl cyclase 2 may contain determinants important for receiving signals from G beta gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, J -- DeVivo, M -- Dingus, J -- Harry, A -- Li, J -- Sui, J -- Carty, D J -- Blank, J L -- Exton, J H -- Stoffel, R H -- CA-44998/CA/NCI NIH HHS/ -- DK-37219/DK/NIDDK NIH HHS/ -- DK-38761/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 May 26;268(5214):1166-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Mount Sinai School of Medicine, City University of New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761832" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/*chemistry/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Enzyme Activation/physiology ; GTP-Binding Proteins/chemistry/*physiology ; Guanosine Triphosphate/physiology ; In Vitro Techniques ; Molecular Sequence Data ; Peptide Fragments/chemical synthesis/chemistry/physiology ; Potassium Channels/physiology ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptors, Adrenergic, beta/metabolism ; Signal Transduction/physiology ; Structure-Activity Relationship ; Type C Phospholipases/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)
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  • 5
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    Induction of MHC class I genes in neurons (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-07-28
    Beschreibung: Whether neurons express major histocompatibility complex (MHC) class I genes has not been firmly established. The techniques of confocal laser microscopy, patch clamp electrophysiology, and reverse transcriptase-polymerase chain reaction were combined here to directly examine the inducibility of MHC class I genes in individual cultured rat hippocampal neurons. Transcription of MHC class I genes was very rare in neurons with spontaneous action potentials. In electrically silent neurons, transcription was noted, with expression of beta 2-microglobulin under tighter control than in class I heavy chain molecules. Surface expression of class I molecules occurred only in electrically silent neurons treated with interferon gamma. Immunosurveillance by cytotoxic T cells may be focused on functionally impaired neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neumann, H -- Cavalie, A -- Jenne, D E -- Wekerle, H -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):549-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroimmunology, Max Planck Institute for Psychiatry, Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624779" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials/drug effects ; Animals ; Base Sequence ; Cells, Cultured ; *Gene Expression Regulation ; *Genes, MHC Class I ; Hippocampus/cytology ; Histocompatibility Antigens Class I/biosynthesis/genetics ; Interferon-gamma/pharmacology ; Molecular Sequence Data ; Patch-Clamp Techniques ; Polymerase Chain Reaction ; Pyramidal Cells/cytology/*metabolism/physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Inbred Lew ; Tetrodotoxin/pharmacology ; Transcription, Genetic ; beta 2-Microglobulin/biosynthesis/genetics
    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)
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  • 6
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    Synaptic activation of voltage-gated channels in the dendrites of hippocampal pyramidal neurons (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-04-14
    Beschreibung: Activation of dendritic voltage-gated ion channels by local synaptic input was tested by simultaneous dendrite-attached patch-clamp recordings and whole-cell somatic voltage recordings made from CA1 pyramidal neurons in hippocampal slices. Schaffer collateral stimulation elicited subthreshold excitatory postsynaptic potentials (EPSPs) that opened voltage-gated sodium and calcium channels in the apical dendrites. The EPSP-activated sodium channels opened near the peak of the EPSP, whereas low voltage-activated calcium channels opened near the EPSP peak and during the decay phase. Dendritic high voltage-activated channels required somatic action potential generation or suprathreshold synaptic trains for activation. Dendritic voltage-gated channels are, therefore, likely to participate in dendritic integration of synaptic events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magee, J C -- Johnston, D -- MH44754/MH/NIMH NIH HHS/ -- NS09482/NS/NINDS NIH HHS/ -- NS11535/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Apr 14;268(5208):301-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716525" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Action Potentials ; Animals ; Calcium Channels/metabolism ; Dendrites/*physiology ; *Ion Channel Gating ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Sodium Channels/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Tetrodotoxin/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)
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  • 7
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    Steroid hormone--and neurotransmitter-induced rat sexual behavior: addendum (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-06-30
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mani, S K -- Allen, J M -- Clark, J H -- Blaustein, J D -- O'Malley, B W -- New York, N.Y. -- Science. 1995 Jun 30;268(5219):1833.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7604251" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Estradiol/*pharmacology ; Female ; Male ; Neurotransmitter Agents/*physiology ; Rats ; Sexual Behavior, Animal/drug effects/*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)
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  • 8
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    Superresolution three-dimensional images of fluorescence in cells with minimal light exposure (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-06-09
    Beschreibung: Fluorescent probes offer insight into the highly localized and rapid molecular events that underlie cell function. However, methods are required that can efficiently transform the limited signals from such probes into high-resolution images. An algorithm has now been developed that produces highly accurate images of fluorescent probe distribution inside cells with minimal light exposure and a conventional light microscope. This method provides resolution nearly four times greater than that currently available from any fluorescence microscope and was used to study several biological problems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carrington, W A -- Lynch, R M -- Moore, E D -- Isenberg, G -- Fogarty, K E -- Fay, F S -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1483-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine, University of Massachusetts Medical School, Worcester 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7770772" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Animals ; Calcium Channels/analysis ; Cell Line ; Cell Physiological Phenomena ; Cells/*chemistry/*ultrastructure ; Cells, Cultured ; Fluorescence ; *Fluorescent Dyes ; Guinea Pigs ; Hexokinase/analysis ; *Image Processing, Computer-Assisted ; Light ; Microscopy, Fluorescence ; Microtubules/ultrastructure ; Muscle Proteins/analysis ; Muscle, Smooth/cytology/enzymology ; Rats ; Ryanodine Receptor Calcium Release Channel
    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)
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  • 9
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    Association of protein kinase A and protein phosphatase 2B with a common anchoring protein (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-01-06
    Beschreibung: Specificity of protein kinases and phosphatases may be achieved through compartmentalization with preferred substrates. In neurons, adenosine 3', 5'-monophosphate (cAMP)-dependent protein kinase (PKA) is localized at postsynaptic densities by association of its regulatory subunit with an A kinase anchor protein, AKAP79. Interaction cloning experiments demonstrated that AKAP79 also binds protein phosphatase 2B, or calcineurin (CaN). A ternary complex of PKA, AKAP, and CaN was isolated from bovine brain, and colocalization of the kinase and the phosphatase was established in neurites of cultured hippocampal neurons. The putative CaN-binding domain of AKAP79 is similar to that of the immunophilin FKBP-12, and AKAP79 inhibited CaN phosphatase activity. These results suggest that both PKA and CaN are targeted to subcellular sites by association with a common anchor protein and thereby regulate the phosphorylation state of key neuronal substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coghlan, V M -- Perrino, B A -- Howard, M -- Langeberg, L K -- Hicks, J B -- Gallatin, W M -- Scott, J D -- DK09059/DK/NIDDK NIH HHS/ -- GM48231/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jan 6;267(5194):108-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7528941" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): A Kinase Anchor Proteins ; *Adaptor Proteins, Signal Transducing ; Amino Acid Sequence ; Animals ; Binding Sites ; *Brain Chemistry ; Calcineurin ; Calmodulin-Binding Proteins/analysis/antagonists & inhibitors/*metabolism ; Carrier Proteins/analysis ; Cattle ; Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/analysis/*metabolism ; Hippocampus/chemistry ; Molecular Sequence Data ; Neurites/chemistry ; Phosphoprotein Phosphatases/analysis/antagonists & inhibitors/*metabolism ; Phosphorylation ; Proteins/*metabolism/pharmacology ; Rats ; Recombinant Proteins/pharmacology ; Tacrolimus/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)
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  • 10
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    The ARF1 GTPase-activating protein: zinc finger motif and Golgi complex localization (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 1995-12-22
    Beschreibung: Hydrolysis of guanosine triphosphate (GTP) by the small guanosine triphosphatase (GTPase) adenosine diphosphate ribosylation factor-1 (ARF1) depends on a GTPase-activating protein (GAP). A complementary DNA encoding the ARF1 GAP was cloned from rat liver and predicts a protein with a zinc finger motif near the amino terminus. The GAP function required an intact zinc finger and additional amino-terminal residues. The ARF1 GAP was localized to the Golgi complex and was redistributed into a cytosolic pattern when cells were treated with brefeldin A, a drug that prevents ARF1-dependent association of coat proteins with the Golgi. Thus, the GAP is likely to be recruited to the Golgi by an ARF1-dependent mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cukierman, E -- Huber, I -- Rotman, M -- Cassel, D -- New York, N.Y. -- Science. 1995 Dec 22;270(5244):1999-2002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Technion-Israel Institute of Technology, Haifa, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8533093" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): ADP-Ribosylation Factor 1 ; ADP-Ribosylation Factors ; Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Brefeldin A ; Cloning, Molecular ; Cyclopentanes/pharmacology ; Cytosol/metabolism ; DNA, Complementary ; GTP-Binding Proteins/*metabolism ; GTPase-Activating Proteins ; Golgi Apparatus/*metabolism ; Guanosine Triphosphate/metabolism ; Liver/metabolism ; Molecular Sequence Data ; Proteins/chemistry/genetics/isolation & purification/*metabolism ; Rats ; *Zinc Fingers
    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)
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