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  • Rats  (60)
  • American Association for the Advancement of Science (AAAS)  (60)
  • American Geophysical Union
  • Cambridge University Press
  • 2005-2009
  • 1995-1999  (60)
  • 1990-1994
  • 1970-1974
  • 1995  (60)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (60)
  • American Geophysical Union
  • Cambridge University Press
  • Springer  (2)
  • Wiley-Blackwell  (1)
Years
  • 2005-2009
  • 1995-1999  (60)
  • 1990-1994
  • 1970-1974
Year
  • 1
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    Crystal structure of DCoH, a bifunctional, protein-binding transcriptional coactivator (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-28
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-24
    Description: Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xia, Z -- Dickens, M -- Raingeaud, J -- Davis, R J -- Greenberg, M E -- CA43855/CA/NCI NIH HHS/ -- CA65861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 24;270(5240):1326-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481820" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/pharmacology ; Animals ; *Apoptosis ; Calcium-Calmodulin-Dependent Protein Kinases/*antagonists & ; inhibitors/genetics/*metabolism ; Cell Differentiation ; Enzyme Activation ; Genes, jun ; *JNK Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 3 ; MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinases ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Nerve Growth Factors/pharmacology ; Neurons/*cytology/enzymology ; PC12 Cells ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/genetics/metabolism ; Rats ; *Signal Transduction ; Staurosporine ; Sympathetic Nervous System/cytology ; p38 Mitogen-Activated Protein Kinases
    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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    The control of calcium release in heart muscle (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-19
    Description: The control of calcium release from intracellular stores (the sarcoplasmic reticulum) in cardiac muscle was examined with the use of a confocal microscope and voltage clamp techniques. Depolarization evoked graded calcium release by altering the extent of spatial and temporal summation of elementary calcium release events called "calcium sparks." These evoked sparks were triggered by local L-type calcium channel currents in a stochastic manner, were similar at different potentials, and resembled spontaneous calcium sparks. Once triggered, the calcium release from the sarcoplasmic reticulum during a calcium spark was independent of the duration of the triggering calcium influx. These results were used to develop a unifying model for cardiac excitation-contraction coupling that explains the large (but paradoxically stable) amplification of the trigger calcium influx by a combination of digital and analog behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannell, M B -- Cheng, H -- Lederer, W J -- HL25675/HL/NHLBI NIH HHS/ -- HL36974/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 May 19;268(5213):1045-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754384" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/*physiology ; In Vitro Techniques ; Ion Channel Gating/physiology ; Membrane Potentials/physiology ; Microscopy, Confocal ; Muscle Proteins/physiology ; Myocardium/*metabolism ; Patch-Clamp Techniques ; Probability ; Rats ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/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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  • 4
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    Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-31
    Description: Nerve growth factor (NGF) induces both differentiation and survival of neurons by binding to the Trk receptor protein tyrosine kinase. Although Ras is required for differentiation, it was not required for NGF-mediated survival of rat pheochromocytoma PC-12 cells in serum-free medium. However, the ability of NGF to prevent apoptosis (programmed cell death) was inhibited by wortmannin or LY294002, two specific inhibitors of phosphatidylinositol (Pl)-3 kinase. Moreover, platelet-derived growth factor (PDGF) prevented apoptosis of PC-12 cells expressing the wild-type PDGF receptor, but not of cells expressing a mutant receptor that failed to activate Pl-3 kinase. Cell survival thus appears to be mediated by a Pl-3 kinase signaling pathway distinct from the pathway that mediates differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yao, R -- Cooper, G M -- R01 CA 18689/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 31;267(5206):2003-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Genetics, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7701324" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; Apoptosis/*drug effects ; Cell Differentiation ; Cell Survival/drug effects ; Enzyme Activation ; Nerve Growth Factors/*pharmacology ; PC12 Cells ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/*metabolism ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Receptors, Platelet-Derived Growth Factor/metabolism ; *Signal Transduction ; ras Proteins/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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  • 5
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    Key NASA lab under fire for animal care practices (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, A -- New York, N.Y. -- Science. 1995 Jun 23;268(5218):1692.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7792586" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Welfare/*standards ; Animals ; Rats ; Research/*standards ; United States ; *United States National Aeronautics and Space Administration
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-06
    Description: 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〉
    Keywords: 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
    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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    Calcium sparks in vascular smooth muscle: relaxation regulators (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fay, F S -- HL14523/HL/NHLBI NIH HHS/ -- HL47530/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Oct 27;270(5236):588-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Massachusetts Medical School, Worchester 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7570016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cell Membrane/metabolism ; Cerebral Arteries/physiology ; Membrane Potentials ; Muscle Proteins/metabolism ; *Muscle Relaxation ; Muscle, Smooth, Vascular/metabolism/*physiology ; Potassium Channels/metabolism ; Protein Kinases/metabolism ; Rats ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/metabolism ; Vasoconstriction ; Vasodilation
    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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  • 8
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    Cytostatic gene therapy for vascular proliferative disorders with a constitutively active form of the retinoblastoma gene product (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-27
    Description: Vascular smooth muscle cell (SMC) proliferation in response to injury is an important etiologic factor in vascular proliferative disorders such as atherosclerosis and restenosis after balloon angioplasty. The retinoblastoma gene product (Rb) is present in the unphosphorylated and active form in quiescent primary arterial SMCs, but is rapidly inactivated by phosphorylation in response to growth factor stimulation in vitro. A replication-defective adenovirus encoding a nonphosphorylatable, constitutively active form of Rb was constructed. Infection of cultured primary rat aortic SMCs with this virus inhibited growth factor-stimulated cell proliferation in vitro. Localized arterial infection with the virus at the time of balloon angioplasty significantly reduced SMC proliferation and neointima formation in both the rat carotid and porcine femoral artery models of restenosis. These results demonstrate the role of Rb in regulating vascular SMC proliferation and suggest a gene therapy approach for vascular proliferative disorders associated with arterial injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, M W -- Barr, E -- Seltzer, J -- Jiang, Y Q -- Nabel, G J -- Nabel, E G -- Parmacek, M S -- Leiden, J M -- New York, N.Y. -- Science. 1995 Jan 27;267(5197):518-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, IL 60637.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7824950" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Angioplasty, Balloon ; Animals ; Base Sequence ; Blood ; Carotid Arteries/virology ; Cell Division ; Disease Models, Animal ; Femoral Artery/virology ; *Genes, Retinoblastoma ; *Genetic Therapy ; Genetic Vectors ; Humans ; Molecular Sequence Data ; Muscle, Smooth, Vascular/*cytology/pathology/virology ; Rats ; Rats, Sprague-Dawley ; Retinoblastoma Protein/*physiology ; Swine ; Vascular Diseases/pathology/*therapy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Regeneration and mammalian auditory hair cells (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-02-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chardin, S -- Romand, R -- New York, N.Y. -- Science. 1995 Feb 3;267(5198):707-11.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7839151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival/drug effects ; Cilia/ultrastructure ; Culture Media ; Hair Cells, Auditory, Inner/drug effects/*physiology/ultrastructure ; Hair Cells, Auditory, Outer/drug effects/*physiology/ultrastructure ; Neomycin/pharmacology ; Organ Culture Techniques ; Organ of Corti/drug effects/physiology/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Regeneration/*drug effects ; Tretinoin/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    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
    Publication Date: 1995-05-26
    Description: 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〉
    Keywords: 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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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