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  • Rats
  • Theoretical, Physical and Computational Chemistry
  • American Association for the Advancement of Science (AAAS)  (60)
  • Wiley-Blackwell  (1)
  • 1995-1999  (61)
  • 1980-1984
  • 1945-1949
  • 1995  (61)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (60)
  • Wiley-Blackwell  (1)
  • Springer  (2)
Years
  • 1995-1999  (61)
  • 1980-1984
  • 1945-1949
Year
  • 1
    Electronic Resource
    Electronic Resource
    Targeting of endogenous sulfated glycoprotein-1 and -2 to lysosomes within nonciliated cells of the efferent ducts during postnatal development of the rat (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 41 (1995), S. 287-299 
    Details
    ISSN: 1040-452X
    Keywords: SGP-1 ; SGP-2 ; Postnatal development ; Nonciliated cells ; Efferent ducts ; Rats ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Sulfated glycoprotein (SGP) -1 and -2, secretory products of Sertoli cells, are secreted into the lumen of seminiferous tubules where they bind to late spermatids. Once released, the spermatozoa traverse the efferent ducts where these proteins detach from their surface and are endocytosed by the nonciliated cells. In adult animals, SGP-1 and SGP-2 are also synthesized by nonciliated cells and targeted from the Golgi apparatus to lysosomes. The purpose of the present study was to determine the pattern of expression of SGP-1 and SGP-2 within nonciliated cells during postnatal development. The efferent ducts of animals at different postnatal ages were prepared for an electron microscopic immunocytochemical quantitative analysis as well as for Northern blot analysis. The data expressed as labeling content (no. gold particles/μm2 and taking into account the volume of the endocytic or-ganelles and the cell) revealed that anti-SGP-1 labeling in endosomes of nonciliated cells was minimal at 15, 21, and 29 days of age. On the other hand, the lysosomal labeling content showed a significant increase by day 29 compared to 15 and 21-day-old animals indicating that an endogenous form of SGP-1 was being synthesized by nonciliated cells and targeted to lysosomes. By day 39 a significant increase in endosomal labeling occurred; this was attributed to the endocytosis of Sertoli-derived SGP-1 which coincided with the entry of spermatozoa into the lumen of these ducts at this age. Lysosomal labeling showed further significant increases at days 39, 49, and then again at day 90. Northern blot analysis detected SGP-1 mRNA transcripts at all postnatal ages examined. While decreases or increases in transcripts could not be determined due to the greater amount of tissue present with increasing age, these data taken together support the idea of an endogenous form of SGP-1 being synthesized by nonciliated cells and targeted to lysosomes during postnatal development.In the case of SGP-2, endosomal labeling was minimal at 15, 21, and 29 days of age but was significantly increased by day 39, with similar values at all subsequent ages. The high value at day 39 was attributed to the endocytosis of SGP-2 which coincided with the entry of spermatozoa into the lumen at this age. Lysosomal labeling, on the other hand, was low at days 15 and 21 but peaked at day 29 at a time when endosomal labeling was minimal. These results suggested the synthesis of an endogenous form of SGP-2 which was being targeted to lysosomes. Similar values for SGP-2 lysosomal labeling comparable to that at day 29 were obtained at all other ages. Since SGP-2 endosomal labeling was significantly increased at day 39 and maintained thereafter, it is suggested that labeling in lysosomes at this and subsequent ages could also be due to the endocytosis of Sertoli-derived SGP-2. However, Northern blot analysis confirmed the presence of mRNA transcripts for SGP-2 at all postnatal ages examined, although increases or decreases in their amount were not determined. These results thus consolidate the hypothesis of an endogenous form of SGP-2 being synthesized by nonciliated cells and targeted to lysosomes. Finally, since the amounts of endogenous SGP-1 and SGP-2 peak at different ages, it is suggested that different factors are involved in regulation of these two proteins during postnatal development. © 1995 Wiley-Liss, Inc.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080410303
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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
    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
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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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    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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  • 5
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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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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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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    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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    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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    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
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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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    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
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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
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    Monitoring release of neurotrophic activity in the brains of awake rats (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-07-28
    Description: Intracerebral microdialysis of awake rats was used to monitor the possible release of neurotrophic factors from brain cells in response to injury and excitation. Perfusates were tested with ganglia bioassays and enzyme immunoassay. Trophic activity was released after implantation of the microdialysis probe into the hippocampus but not into the striatum, as assessed by increased nerve fiber outgrowth from Remak's ganglion. Kainic acid treatment significantly increased the release of trophic activity from hippocampal sites. These findings suggest that the brain responds to mechanical injury as well as to certain excitatory stimuli by regional extracellular release of neurotrophic activity that is not identical to the actions of known neurotrophic factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Humpel, C -- Lindqvist, E -- Soderstrom, S -- Kylberg, A -- Ebendal, T -- Olson, L -- New York, N.Y. -- Science. 1995 Jul 28;269(5223):552-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Assay ; Chick Embryo ; Corpus Striatum/drug effects/*metabolism ; Ganglia/drug effects/physiology ; Hippocampus/drug effects/*metabolism ; Immunoenzyme Techniques ; Kainic Acid/pharmacology ; Microdialysis ; Nerve Fibers/drug effects/physiology ; Nerve Growth Factors/*metabolism/pharmacology ; Neurotrophin 3 ; Rats
    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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  • 13
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    CFTR as a cAMP-dependent regulator of sodium channels (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-11
    Description: Cystic fibrosis transmembrane regulator (CFTR), the gene product that is mutated in cystic fibrosis (CF) patients, has a well-recognized function as a cyclic adenosine 3',5'-monophosphate (cAMP)-regulated chloride channel, but this property does not account for the abnormally high basal rate and cAMP sensitivity of sodium ion absorption in CF airway epithelia. Expression of complementary DNAs for rat epithelial Na+ channel (rENaC) alone in Madin Darby canine kidney (MDCK) epithelial cells generated large amiloride-sensitive sodium currents that were stimulated by cAMP, whereas coexpression of human CFTR with rENaC generated smaller basal sodium currents that were inhibited by cAMP. Parallel studies that measured regulation of sodium permeability in fibroblasts showed similar results. In CF airway epithelia, the absence of this second function of CFTR as a cAMP-dependent regulator likely accounts for abnormal sodium transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stutts, M J -- Canessa, C M -- Olsen, J C -- Hamrick, M -- Cohn, J A -- Rossier, B C -- Boucher, R C -- CFF R026/PHS HHS/ -- HL 34322/HL/NHLBI NIH HHS/ -- HL 42384/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 11;269(5225):847-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina at Chapel Hill 27599-7020, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7543698" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Absorption ; Amiloride/pharmacology ; Animals ; Cell Line ; Cell Membrane Permeability ; Chloride Channels/metabolism ; Cyclic AMP/*metabolism ; Cystic Fibrosis/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA, Complementary ; Dogs ; Humans ; Membrane Proteins/*metabolism ; Mice ; Patch-Clamp Techniques ; Rats ; Sodium/metabolism ; Sodium Channels/*metabolism ; Transfection
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  • 14
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    Glutamate receptor RNA editing in vitro by enzymatic conversion of adenosine to inosine (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-10
    Description: RNA encoding the B subunit of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of ionotropic glutamate receptor (GluR-B) undergoes a posttranscriptional modification in which a genomically encoded adenosine is represented as a guanosine in the GluR-B complementary DNA. In vitro editing of GluR-B RNA transcripts with HeLa cell nuclear extracts was found to result from an activity that converts adenosine to inosine in regions of double-stranded RNA by enzymatic base modification. This activity is consistent with that of a double-stranded RNA-specific adenosine deaminase previously described in Xenopus oocytes and widely distributed in mammalian tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rueter, S M -- Burns, C M -- Coode, S A -- Mookherjee, P -- Emeson, R B -- ES00267/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232-6600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7878468" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Animals ; Base Sequence ; Cell Line ; Codon ; Exons ; HeLa Cells ; Humans ; Inosine/*metabolism ; Inosine Monophosphate/metabolism ; Mice ; Molecular Sequence Data ; *RNA Editing ; RNA Precursors/metabolism ; RNA, Double-Stranded/metabolism ; Rats ; Receptors, AMPA/*genetics ; Repetitive Sequences, Nucleic Acid ; Tumor Cells, Cultured
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  • 15
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    Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-17
    Description: A member of the inwardly rectifying potassium channel family was cloned here. The channel, called BIR (Kir6.2), was expressed in large amounts in rat pancreatic islets and glucose-responsive insulin-secreting cell lines. Coexpression with the sulfonylurea receptor SUR reconstituted an inwardly rectifying potassium conductance of 76 picosiemens that was sensitive to adenosine triphosphate (ATP) (IKATP) and was inhibited by sulfonylureas and activated by diazoxide. The data indicate that these pancreatic beta cell potassium channels are a complex composed of at least two subunits--BIR, a member of the inward rectifier potassium channel family, and SUR, a member of the ATP-binding cassette superfamily. Gene mapping data show that these two potassium channel subunit genes are clustered on human chromosome 11 at position 11p15.1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inagaki, N -- Gonoi, T -- Clement, J P 4th -- Namba, N -- Inazawa, J -- Gonzalez, G -- Aguilar-Bryan, L -- Seino, S -- Bryan, J -- DK44311/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 17;270(5239):1166-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Medicine, Chiba University School of Medicine, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502040" target="_blank"〉PubMed〈/a〉
    Keywords: *ATP-Binding Cassette Transporters ; Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; Cloning, Molecular ; Cricetinae ; Diazoxide/pharmacology ; Humans ; Islets of Langerhans/metabolism ; KATP Channels ; Mice ; Molecular Sequence Data ; Potassium/*metabolism ; Potassium Channels/*chemistry/genetics/*metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Drug/*chemistry/metabolism ; Rubidium/metabolism ; Sulfonylurea Compounds/pharmacology ; Sulfonylurea Receptors
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  • 16
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    Induction of MHC class I genes in neurons (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-07-28
    Description: 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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Behavioral effects and gene delivery in a rat model of Parkinson's disease (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isacson, O -- New York, N.Y. -- Science. 1995 Aug 11;269(5225):856-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7638605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Corpus Striatum/cytology ; Gene Expression ; Gene Transfer Techniques ; *Genetic Therapy ; *Genetic Vectors ; *Motor Activity ; Neurons/cytology/enzymology/virology ; Parkinson Disease/*therapy ; Rats ; Simplexvirus/*genetics/physiology ; Tyrosine 3-Monooxygenase/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Selective opioid inhibition of small nociceptive neurons (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-11-24
    Description: Opioid analgesia, the selective suppression of pain without effects on other sensations, also distinguishes between different types of pain: severe, persistent pain is potently inhibited by opioids, but they fail to cohceal the sensation of a pinprick. The cellular basis for this specificity was analyzed by means of patch-clamp experiments performed on fluorescently labeled nociceptive neurons (nociceptors) that innervate rat tooth pulp. Activation of the mu opioid receptor inhibited calcium channels on almost all small nociceptors but had minimal effect on large nociceptors. Somatostatin had the opposite specificity, preferentially inhibiting calcium channels on the large cells. Because persistent pain is mediated by slow-conducting, small nociceptors, opioids are thus likely to inhibit neurotransmitter release only at those primary synapses specialized for persistent pain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taddese, A -- Nah, S Y -- McCleskey, E W -- New York, N.Y. -- Science. 1995 Nov 24;270(5240):1366-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7481826" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/*pharmacology ; Animals ; Calcium Channels/drug effects ; Cells, Cultured ; Dental Pulp/innervation ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)- ; Enkephalins/*pharmacology ; Male ; Neurons, Afferent/*drug effects/physiology ; Neurotransmitter Agents/metabolism ; Nociceptors/*drug effects/physiology ; Patch-Clamp Techniques ; Presynaptic Terminals/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, mu/*physiology ; Receptors, Somatostatin/physiology ; Sodium Channel Blockers ; Somatostatin/pharmacology
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  • 19
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    Zinc and Alzheimer's disease (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maggio, J E -- Esler, W P -- Stimson, E R -- Jennings, J M -- Ghilardi, J R -- Mantyh, P W -- New York, N.Y. -- Science. 1995 Jun 30;268(5219):1920-1; author reply 1921-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7604269" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Humans ; Protein Binding ; Rats ; Solubility ; Zinc/*metabolism/pharmacology
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  • 20
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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
    Publication Date: 1995-04-14
    Description: 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〉
    Keywords: 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
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  • 21
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    Steroid hormone--and neurotransmitter-induced rat sexual behavior: addendum (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-06-30
    Description: 〈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〉
    Keywords: Animals ; Estradiol/*pharmacology ; Female ; Male ; Neurotransmitter Agents/*physiology ; Rats ; Sexual Behavior, Animal/drug effects/*physiology
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  • 22
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    KAI1, a metastasis suppressor gene for prostate cancer on human chromosome 11p11.2 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-12
    Description: A gene from human chromosome 11p11.2 was isolated and was shown to suppress metastasis when introduced into rat AT6.1 prostate cancer cells. Expression of this gene, designated KAI1, was reduced in human cell lines derived from metastatic prostate tumors. KAI1 specifies a protein of 267 amino acids, with four hydrophobic and presumably transmembrane domains and one large extracellular hydrophilic domain with three potential N-glycosylation sites. KAI1 is evolutionarily conserved, is expressed in many human tissues, and encodes a member of a structurally distinct family of leukocyte surface glycoproteins. Decreased expression of this gene may be involved in the malignant progression of prostate and other cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dong, J T -- Lamb, P W -- Rinker-Schaeffer, C W -- Vukanovic, J -- Ichikawa, T -- Isaacs, J T -- Barrett, J C -- CA 58236/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 May 12;268(5212):884-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754374" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD/chemistry/*genetics/physiology ; Antigens, CD82 ; Base Sequence ; Biological Evolution ; *Chromosomes, Human, Pair 11 ; Gene Expression ; *Genes, Tumor Suppressor ; Humans ; Male ; Membrane Glycoproteins/chemistry/*genetics/physiology ; Mice ; Mice, SCID ; Molecular Sequence Data ; Neoplasm Metastasis/*genetics ; Prostatic Neoplasms/*genetics/pathology ; *Proto-Oncogene Proteins ; Rats ; Transfection ; Tumor Cells, Cultured
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  • 23
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    Ionic mechanisms of neuronal excitation by inhibitory GABAA receptors (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-08-18
    Description: Gamma-aminobutyric acid A (GABAA) receptors are the principal mediators of synaptic inhibition, and yet when intensely activated, dendritic GABAA receptors excite rather than inhibit neurons. The membrane depolarization mediated by GABAA receptors is a result of the differential, activity-dependent collapse of the opposing concentration gradients of chloride and bicarbonate, the anions that permeate the GABAA ionophore. Because this depolarization diminishes the voltage-dependent block of the N-methyl-D-aspartate (NMDA) receptor by magnesium, the activity-dependent depolarization mediated by GABA is sufficient to account for frequency modulation of synaptic NMDA receptor activation. Anionic gradient shifts may represent a mechanism whereby the rate and coherence of synaptic activity determine whether dendritic GABAA receptor activation is excitatory or inhibitory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Staley, K J -- Soldo, B L -- Proctor, W R -- AA03527/AA/NIAAA NIH HHS/ -- HD27827/HD/NICHD NIH HHS/ -- NS01573/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 18;269(5226):977-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of Colorado Health Sciences Center, Denver 80262, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7638623" target="_blank"〉PubMed〈/a〉
    Keywords: Acetazolamide/pharmacology ; Amiloride/pharmacology ; Animals ; Bicarbonates/*metabolism ; Chlorides/*metabolism ; Dendrites/metabolism ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Magnesium/pharmacology ; Membrane Potentials ; Muscimol/pharmacology ; Neurons/*metabolism ; Pyramidal Cells/metabolism ; Rats ; Receptors, GABA-A/*metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; gamma-Aminobutyric Acid/*metabolism/pharmacology
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  • 24
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    Regulation of hippocampal transmitter release during development and long-term potentiation (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-09-22
    Description: Developmental changes in rat hippocampal transmitter release and synaptic plasticity were investigated. Recordings from pairs of pyramidal neurons in slices showed that an action potential in a CA3 neuron released only a single quantum of transmitter onto a CA1 neuron. Failures of synaptic transmission reflected probabilistic transmitter release. The probability of release (Pr) was 0.9 in 4- to 8-day-old rats and decreased to less than 0.5 at 2 to 3 weeks. Long-term potentiation (LTP) in 2- to 3-week-old rats was associated with an increase in Pr from a single synaptic site. The high initial Pr in 4- to 8-day-old rats normally occludes the expression of LTP at this stage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bolshakov, V Y -- Siegelbaum, S A -- New York, N.Y. -- Science. 1995 Sep 22;269(5231):1730-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569903" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Aging/physiology ; Animals ; Animals, Newborn ; Calcium/metabolism ; Hippocampus ; In Vitro Techniques ; *Long-Term Potentiation ; Neuronal Plasticity ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Presynaptic Terminals/physiology ; Probability ; Pyramidal Cells/metabolism/*physiology ; Rats ; Rats, Sprague-Dawley ; *Synaptic Transmission ; Synaptic Vesicles/physiology
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  • 25
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    Domain interaction between NMDA receptor subunits and the postsynaptic density protein PSD-95 (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-09-22
    Description: The N-methyl-D-aspartate (NMDA) receptor subserves synaptic glutamate-induced transmission and plasticity in central neurons. The yeast two-hybrid system was used to show that the cytoplasmic tails of NMDA receptor subunits interact with a prominent postsynaptic density protein PSD-95. The second PDZ domain in PSD-95 binds to the seven-amino acid, COOH-terminal domain containing the terminal tSXV motif (where S is serine, X is any amino acid, and V is valine) common to NR2 subunits and certain NR1 splice forms. Transcripts encoding PSD-95 are expressed in a pattern similar to that of NMDA receptors, and the NR2B subunit co-localizes with PSD-95 in cultured rat hippocampal neurons. The interaction of these proteins may affect the plasticity of excitatory synapses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kornau, H C -- Schenker, L T -- Kennedy, M B -- Seeburg, P H -- NS-28710/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 22;269(5231):1737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular Biology (ZMBH), University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569905" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Cytoplasm/chemistry ; Genes, Reporter ; Hippocampus/*metabolism ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Molecular Sequence Data ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neuronal Plasticity ; Neurons/*metabolism ; RNA Splicing ; Rats ; Receptors, N-Methyl-D-Aspartate/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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  • 26
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    Excision of deoxyribose phosphate residues by DNA polymerase beta during DNA repair (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-08-04
    Description: Eukaryotic DNA polymerase beta (pol beta) can catalyze DNA synthesis during base excision DNA repair. It is shown here that pol beta also catalyzes release of 5'-terminal deoxyribose phosphate (dRP) residues from incised apurinic-apyrimidinic sites, which are common intermediate products in base excision repair. The catalytic domain for this activity resides within an amino-terminal 8-kilodalton fragment of pol beta, which comprises a distinct structural domain of the enzyme. Magnesium is required for the release of dRP from double-stranded DNA but not from a single-stranded oligonucleotide. Analysis of the released products indicates that the excision reaction occurs by beta-elimination rather than hydrolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, Y -- Kim, K -- CA06927/CA/NCI NIH HHS/ -- CA63154/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Aug 4;269(5224):699-702.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apurinic Acid ; Base Sequence ; Binding Sites ; DNA/*metabolism ; DNA Ligases/metabolism ; DNA Polymerase I/*metabolism ; *DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase ; Deoxyribonuclease IV (Phage T4-Induced) ; Edetic Acid/pharmacology ; Hydrolysis ; Lyases/metabolism ; Molecular Sequence Data ; Polynucleotides ; Protein Structure, Tertiary ; Rats ; Ribosemonophosphates/*metabolism ; Xenopus laevis
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    Flaws in risk assessments (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abelson, P H -- New York, N.Y. -- Science. 1995 Oct 13;270(5234):215.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569958" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Eating ; Gene Frequency ; Humans ; Longevity ; Mice ; Rats ; Reproducibility of Results ; Risk Assessment ; *Toxicity Tests ; United States ; United States Environmental Protection Agency
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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
    Publication Date: 1995-06-09
    Description: 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〉
    Keywords: 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
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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
    Publication Date: 1995-01-06
    Description: 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〉
    Keywords: 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
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    Stable transfection of malaria parasite blood stages (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Genetic manipulation of malaria parasites would revolutionize the study of this group of pathogens and have implications for vaccine and drug development. This report describes the stable, drug-selectable genetic transformation of the clinically relevant intracellular blood stages of a malaria parasite. A plasmid transfection vector carrying the gene locus that encodes a drug-resistant form of the bifunctional enzyme dihydrofolate reductase-thymidylate synthase from the rodent malaria parasite Plasmodium berghei was constructed. Derivatives of this vector were introduced into merozoites of P. berghei by electroporation, and parasites were selected for successful transformation in the rodent host on the basis of resistance to pyrimethamine. The plasmids were present in a circular, unrearranged form that replicated episomally to an observed maximum of 15 copies per cell in drug-resistant populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Dijk, M R -- Waters, A P -- Janse, C J -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1358-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Parasitology, University of Leiden, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA Replication ; Drug Resistance ; Electroporation ; Erythrocytes/parasitology ; Genes, Protozoan ; Genetic Vectors ; Molecular Sequence Data ; Multienzyme Complexes/*genetics ; Plasmids ; Plasmodium berghei/drug effects/*genetics/growth & development ; Point Mutation ; Pyrimethamine/*pharmacology ; Rats ; Rats, Wistar ; Replication Origin ; Tetrahydrofolate Dehydrogenase/*genetics ; Thymidylate Synthase/*genetics ; *Transfection
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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
    Publication Date: 1995-12-22
    Description: 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〉
    Keywords: 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
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    Pineal serotonin N-acetyltransferase: expression cloning and molecular analysis (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-12-08
    Description: Pineal serotonin N-acetyltransferase (arylalkylamine N-acetyltransferase, or AA-NAT) generates the large circadian rhythm in melatonin, the hormone that coordinates daily and seasonal physiology in some mammals. Complementary DNA encoding ovine AA-NAT was cloned. The abundance of AA-NAT messenger RNA (mRNA) during the day was high in the ovine pineal gland and somewhat lower in retina. AA-NAT mRNA was found unexpectedly in the pituitary gland and in some brain regions. The night-to-day ratio of ovine pineal AA-NAT mRNA is less than 2. In contrast, the ratio exceeds 150 in rats. AA-NAT represents a family within a large superfamily of acetyltransferases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coon, S L -- Roseboom, P H -- Baler, R -- Weller, J L -- Namboodiri, M A -- Koonin, E V -- Klein, D C -- New York, N.Y. -- Science. 1995 Dec 8;270(5242):1681-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7502081" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arylamine N-Acetyltransferase/*genetics/metabolism ; Brain/metabolism ; Cell Line ; Circadian Rhythm ; *Cloning, Molecular ; DNA, Complementary/genetics ; Molecular Sequence Data ; Pineal Gland/*enzymology/metabolism ; Pituitary Gland/metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Retina/metabolism ; Sequence Alignment ; Sheep ; Transfection
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    Presynaptic component of long-term potentiation visualized at individual hippocampal synapses (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-16
    Description: Long-term potentiation has previously been studied with electrophysiological techniques that do not readily separate presynaptic and postsynaptic contributions. Changes in exocytotic-endocytotic cycling have now been monitored at synapses between cultured rat hippocampal neurons by measuring the differential uptake of antibodies that recognize the intraluminal domain of the synaptic vesicle protein synaptotagmin. Vesicular cycling increased markedly during glutamate-induced long-term potentiation. The degree of potentiation was heterogeneous, appearing greater at synapses at which the initial extent of vesicular turnover was low. Thus, changes in presynaptic activity were visualized directly and the spatial distribution of potentiation could be determined at the level of single synaptic boutons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malgaroli, A -- Ting, A E -- Wendland, B -- Bergamaschi, A -- Villa, A -- Tsien, R W -- Scheller, R H -- D.016/Telethon/Italy -- New York, N.Y. -- Science. 1995 Jun 16;268(5217):1624-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scientific Institute San Raffaele, Milan, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7777862" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Calcium-Binding Proteins ; Cells, Cultured ; Glutamic Acid/pharmacology ; Hippocampus/*cytology/physiology ; Long-Term Potentiation/drug effects/*physiology ; Membrane Glycoproteins/analysis/immunology ; Molecular Sequence Data ; Nerve Tissue Proteins/analysis/immunology ; Neurons/*physiology ; Patch-Clamp Techniques ; Potassium/pharmacology ; Presynaptic Terminals/drug effects/*physiology ; Pyrroles/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; *Synaptic Transmission/drug effects ; Synaptic Vesicles/chemistry/metabolism ; Synaptotagmins
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    New clue to prostate cancer spread (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1995 May 12;268(5212):799-800.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754364" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor/analysis ; Cell Adhesion ; Chromosomes, Human, Pair 11 ; Cloning, Molecular ; *Genes, Tumor Suppressor ; Humans ; Male ; Mice ; Neoplasm Metastasis/*genetics ; Prostatic Neoplasms/*genetics/pathology/therapy ; Rats
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    Requirement for generation of H2O2 for platelet-derived growth factor signal transduction (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-13
    Description: Stimulation of rat vascular smooth muscle cells (VSMCs) by platelet-derived growth factor (PDGF) transiently increased the intracellular concentration of hydrogen peroxide (H2O2). This increase could be blunted by increasing the intracellular concentration of the scavenging enzyme catalase or by the chemical antioxidant N-acetylcysteine. The response of VSMCs to PDGF, which includes tyrosine phosphorylation, mitogen-activated protein kinase stimulation, DNA synthesis, and chemotaxis, was inhibited when the growth factor-stimulated rise in H2O2 concentration was blocked. These results suggest that H2O2 may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sundaresan, M -- Yu, Z X -- Ferrans, V J -- Irani, K -- Finkel, T -- New York, N.Y. -- Science. 1995 Oct 13;270(5234):296-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1650, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569979" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcysteine/pharmacology ; Adenoviridae/genetics/physiology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Catalase/metabolism ; Cell Line ; Cells, Cultured ; Chemotaxis/drug effects ; Endopeptidase K ; Free Radical Scavengers/pharmacology ; Humans ; Hydrogen Peroxide/*metabolism ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; *Mitogen-Activated Protein Kinases ; Muscle, Smooth, Vascular/cytology/drug effects/*metabolism/virology ; Phosphorylation ; Phosphotyrosine/metabolism ; Platelet-Derived Growth Factor/*pharmacology ; Protein-Tyrosine Kinases/metabolism ; Rats ; Serine Endopeptidases/metabolism ; *Signal Transduction
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    Central command neurons of the sympathetic nervous system: basis of the fight-or-flight response (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-27
    Description: During stress, the activity of the sympathetic nervous system is changed in a global fashion, leading to an increase in cardiovascular function and a release of adrenal catecholamines. This response is thought to be regulated by a common set of brain neurons that provide a dual input to the sympathetic preganglionic neurons regulating cardiac and adrenal medullary functions. By using a double-virus transneuronal labeling technique, the existence of such a set of central autonomic neurons in the hypothalamus and brainstem was demonstrated. These neurons innervate both of the sympathetic outflow systems and likely function in circumstances where parallel sympathetic processing occurs, such as in the fight-or-flight response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jansen, A S -- Nguyen, X V -- Karpitskiy, V -- Mettenleiter, T C -- Loewy, A D -- HL-25449/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Oct 27;270(5236):644-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7570024" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/innervation ; Animals ; Brain Mapping ; Brain Stem/cytology/*physiology ; Catecholamines/metabolism ; Choline O-Acetyltransferase/metabolism ; *Escape Reaction ; Female ; Heart/innervation ; Herpesvirus 1, Suid/physiology ; Hypothalamus/cytology/*physiology ; Male ; Neural Pathways ; Neurons/metabolism/*physiology/virology ; Rats ; Rats, Sprague-Dawley ; Serotonin/metabolism ; Spinal Cord/cytology ; Stellate Ganglion ; Stress, Physiological/physiopathology ; Sympathetic Nervous System/cytology/*physiology
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    Relaxation of arterial smooth muscle by calcium sparks (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-27
    Description: Local increases in intracellular calcium ion concentration ([Ca2+]i) resulting from activation of the ryanodine-sensitive calcium-release channel in the sarcoplasmic reticulum (SR) of smooth muscle cause arterial dilation. Ryanodine-sensitive, spontaneous local increases in [Ca2+]i (Ca2+ sparks) from the SR were observed just under the surface membrane of single smooth muscle cells from myogenic cerebral arteries. Ryanodine and thapsigargin inhibited Ca2+ sparks and Ca(2+)-dependent potassium (KCa) currents, suggesting that Ca2+ sparks activate KCa channels. Furthermore, KCa channels activated by Ca2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of KCa channels. Ca2+ sparks indirectly cause vasodilation through activation of KCa channels, but have little direct effect on spatially averaged [Ca2+]i, which regulates contraction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, M T -- Cheng, H -- Rubart, M -- Santana, L F -- Bonev, A D -- Knot, H J -- Lederer, W J -- HL25675/HL/NHLBI NIH HHS/ -- HL44455/HL/NHLBI NIH HHS/ -- HL51728/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Oct 27;270(5236):633-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Vermont, Colchester 05446, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7570021" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Pyridinecarboxylic acid, ; 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ; ester/pharmacology ; Animals ; Cadmium/pharmacology ; Calcium/*metabolism ; Calcium Channel Agonists/pharmacology ; Calcium Channels/*metabolism ; Cell Membrane/metabolism ; Cerebral Arteries/physiology ; Membrane Potentials ; Muscle Contraction ; *Muscle Relaxation ; Muscle, Smooth, Vascular/cytology/*physiology ; Peptides/pharmacology ; Potassium Channels/*metabolism ; Rats ; Ryanodine/pharmacology ; Sarcoplasmic Reticulum/metabolism ; Terpenes/pharmacology ; Thapsigargin ; Vasodilation
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    Single cells as biosensors for chemical separations (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-06
    Description: A biosensor system based on the response of living cells was demonstrated that can detect specific components of a complex mixture fractionated by a microcolumn separation technique. This system uses ligand-receptor binding and signal-transduction pathways to biochemically amplify the presence of an analyte after electrophoretic separation. The transduced signal was measured by means of two approaches: (i) fluorescence determination of intracellular calcium concentrations in one or more rat PC-12 cells and (ii) measurement of transmembrane current in a Xenopus laevis oocyte microinjected with messenger RNA that encodes a specific receptor. This analysis system has the potential to identify biologically active ligands present in a complex mixture with exceptional sensitivity and selectivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shear, J B -- Fishman, H A -- Allbritton, N L -- Garigan, D -- Zare, R N -- Scheller, R H -- MH45324-05/MH/NIMH NIH HHS/ -- MH45423-03/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1995 Jan 6;267(5194):74-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7809609" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/analysis/isolation & purification ; Adenosine Triphosphate/analysis/isolation & purification ; Animals ; *Biosensing Techniques ; Bradykinin/analysis/isolation & purification ; Calcium/analysis ; Chemistry Techniques, Analytical/*methods ; Electrophoresis ; Ligands ; Microscopy, Fluorescence ; Oocytes ; PC12 Cells ; Patch-Clamp Techniques ; Rats ; Reproducibility of Results ; Sensitivity and Specificity ; Serotonin/analysis/isolation & purification ; Signal Transduction ; Xenopus laevis
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    Dendrites shed their dull image (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1995 Apr 14;268(5208):200-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7536341" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Dendrites/*physiology ; Ion Channels/physiology ; Neuronal Plasticity ; Patch-Clamp Techniques ; Rats ; *Synaptic Transmission
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    Chemical characterization of a family of brain lipids that induce sleep (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-09
    Description: A molecule isolated from the cerebrospinal fluid of sleep-deprived cats has been chemically characterized and identified as cis-9,10-octadecenoamide. Other fatty acid primary amides in addition to cis-9,10-octadecenoamide were identified as natural constituents of the cerebrospinal fluid of cat, rat, and human, indicating that these compounds compose a distinct family of brain lipids. Synthetic cis-9,10-octadecenoamide induced physiological sleep when injected into rats. Together, these results suggest that fatty acid primary amides may represent a previously unrecognized class of biological signaling molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cravatt, B F -- Prospero-Garcia, O -- Siuzdak, G -- Gilula, N B -- Henriksen, S J -- Boger, D L -- Lerner, R A -- 1 S10 RR07273-01/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1506-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Scripps Research Institute, La Jolla, CA 92307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7770779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cats ; Cerebrosides/*cerebrospinal fluid/chemistry/pharmacology ; Humans ; Lipids/*cerebrospinal fluid/chemistry/pharmacology ; Magnetic Resonance Spectroscopy ; Mass Spectrometry ; Molecular Weight ; Oleic Acids/*cerebrospinal fluid/chemistry/pharmacology ; Rats ; Signal Transduction ; *Sleep/drug effects ; Spectrometry, Mass, Fast Atom Bombardment ; Spectrophotometry, Infrared
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    Modulation of chemotropism in the developing spinal cord by substance P (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-02-10
    Description: Developing axons find their targets through direct contact with cues in the extracellular environment and in response to gradients of diffusible factors. The floor plate, a neuroepithelial structure, guides developing commissural axons in the spinal cord by release of chemoattractants. Floor plate cells express neurokinin-1 receptors, and a transiently appearing subpopulation of commissural axons contains substance P, the neuropeptide ligand for this receptor. Substance P increases the amount of axon outgrowth from dorsal horn explants cocultured with floor plate explants. Results of experiments with embryonic rats suggest that substance P released from pioneering neuronal pathways may regulate the release of chemoattractants from floor plate cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Felipe, C -- Pinnock, R D -- Hunt, S P -- New York, N.Y. -- Science. 1995 Feb 10;267(5199):899-902.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Medical Research Council, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7531367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/physiology/ultrastructure ; Calcium/metabolism ; Central Nervous System/chemistry/cytology/*embryology/metabolism ; Chemotactic Factors/*metabolism ; Culture Techniques ; Neurons/chemistry/*physiology/ultrastructure ; Rats ; Receptors, Neurokinin-1/analysis/metabolism ; Spinal Cord/cytology/*embryology ; Substance P/analysis/*metabolism/pharmacology
    Print ISSN: 0036-8075
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    Identification of a stimulator of steroid hormone synthesis isolated from testis (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-16
    Description: Gonadal steroidogenesis is regulated by pituitary gonadotropins and a locally produced, unidentified factor. A 70-kilodalton (kD) protein complex secreted from rat Sertoli cells was isolated. The complex, composed of 28- and 38-kD proteins, stimulated steroidogenesis by Leydig cells and ovarian granulosa cells in a dose-dependent and adenosine 3',5'-monophosphate-independent manner. The follicle-stimulating hormone-induced 28-kD protein appeared to be responsible for the bioactivity, but the 38-kD protein was indispensable for maximal activity. The 28- and 38-kD proteins were shown to be identical to the tissue inhibitor of metalloproteinase-1 (TIMP-1) and the proenzyme form of cathepsin L, respectively. Thus, a TIMP-1-procathepsin L complex is a potent activator of steroidogenesis and may regulate steroid concentrations and, thus, germ cell development in both males and females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boujrad, N -- Ogwuegbu, S O -- Garnier, M -- Lee, C H -- Martin, B M -- Papadopoulos, V -- HD01031/HD/NICHD NIH HHS/ -- HD24633/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 16;268(5217):1609-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Georgetown University Medical Center, Washington, DC 20007, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7777858" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cathepsin L ; Cathepsins/chemistry/*isolation & purification/pharmacology/physiology ; Cells, Cultured ; Culture Media, Conditioned ; Cyclic AMP/metabolism ; Enzyme Precursors/chemistry/*isolation & purification/pharmacology/physiology ; Female ; Follicle Stimulating Hormone/pharmacology ; Glycoproteins/chemistry/genetics/*isolation & ; purification/pharmacology/physiology ; Granulosa Cells/drug effects/metabolism ; Leydig Cells/drug effects/metabolism ; Male ; Molecular Sequence Data ; Molecular Weight ; Pregnenolone/*biosynthesis ; Progesterone/*biosynthesis ; Rats ; Rats, Sprague-Dawley ; Sertoli Cells/*chemistry ; Tissue Inhibitor of Metalloproteinases ; Transfection
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  • 43
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    Muscle-derived neurotrophin-4 as an activity-dependent trophic signal for adult motor neurons (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-09
    Description: The production of neurotrophin-4 (NT-4) in rat skeletal muscle was found to depend on muscle activity. The amounts of NT-4 messenger RNA present decreased after blockade of neuromuscular transmission with alpha-bungarotoxin and increased during postnatal development and after electrical stimulation in a dose-dependent manner. NT-4 immunoreactivity was detected in slow, type I muscle fibers. Intramuscular administration of NT-4 induced sprouting of intact adult motor nerves. Thus, muscle-derived NT-4 acted as an activity-dependent neurotrophic signal for growth and remodeling of adult motor neuron innervation. NT-4 may thus be partly responsible for the effects of exercise and electrical stimulation on neuromuscular performance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funakoshi, H -- Belluardo, N -- Arenas, E -- Yamamoto, Y -- Casabona, A -- Persson, H -- Ibanez, C F -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1495-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7770776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bungarotoxins/pharmacology ; Cell Line ; Electric Stimulation ; Gene Expression Regulation ; Motor Neurons/*physiology ; Muscle Denervation ; Muscle Development ; Muscle Fibers, Slow-Twitch/chemistry ; Muscle, Skeletal/chemistry/growth & development/innervation/*physiology ; Nerve Growth Factors/biosynthesis/genetics/pharmacology/*physiology ; Neuromuscular Junction/physiology ; RNA, Messenger/analysis/biosynthesis/genetics ; Rats ; Rats, Inbred F344 ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Nerve Growth Factor ; Receptor, trkB ; Receptors, Nerve Growth Factor/metabolism ; Receptors, Neuropeptide/metabolism ; Sciatic Nerve/physiology ; Synaptic Transmission
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    Sensorimotor encoding by synchronous neural ensemble activity at multiple levels of the somatosensory system (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-02
    Description: Neural ensemble processing of sensorimotor information during behavior was investigated by simultaneously recording up to 48 single neurons at multiple relays of the rat trigeminal somatosensory system. Cortical, thalamic, and brainstem neurons exhibited widespread 7- to 12-hertz synchronous oscillations, which began during attentive immobility and reliably predicted the imminent onset of rhythmic whisker twitching. Each oscillatory cycle began as a traveling wave of neural activity in the cortex that then spread to the thalamus. Just before the onset of rhythmic whisker twitching, the oscillations spread to the spinal trigeminal brainstem complex. Thereafter, the oscillations at all levels were synchronous with whisker protraction. Neural structures manifesting these rhythms also exhibited distributed spatiotemporal patterns of neuronal ensemble activity in response to tactile stimulation. Thus, multilevel synchronous activity in this system may encode not only sensory information but also the onset and temporal domain of tactile exploratory movements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicolelis, M A -- Baccala, L A -- Lin, R C -- Chapin, J K -- DE11121-01/DE/NIDCR NIH HHS/ -- NS-26722/NS/NINDS NIH HHS/ -- NS-29161/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 2;268(5215):1353-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Electromyography ; Electrophysiology ; Motor Cortex/physiology ; Nerve Net/*physiology ; Neural Pathways ; Neurons, Afferent/*physiology ; Rats ; Somatosensory Cortex/physiology ; Thalamic Nuclei/physiology ; Touch/*physiology ; Trigeminal Ganglion/physiology ; Trigeminal Nuclei/physiology ; Vibrissae/*innervation/physiology
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  • 45
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    Synaptic desensitization of NMDA receptors by calcineurin (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-10
    Description: Desensitization is a phenomenon that is common to many ligand-gated ion channels but has been demonstrated only rarely with physiological stimulation. Numerous studies describe desensitization of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor by exogenous agonists, but whether synaptic stimulation causes desensitization has been unknown. Synaptic stimulation of NMDA receptors on rat hippocampal neurons resulted in desensitization that was prevented by intracellular 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), adenosine-5'-O-(3-thiotriphosphate) (ATP-gamma-S), or inhibitors of phosphatase 2B (calcineurin), but not by inhibitors of phosphatases 1 and 2A or of tyrosine phosphatases. Synaptic NMDA receptors may fluctuate between phosphorylated and dephosphorylated forms, depending on the rate of synaptic stimulation and the magnitude of the associated influx of calcium through NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tong, G -- Shepherd, D -- Jahr, C E -- NS21419/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 10;267(5203):1510-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland 97201-3098.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7878472" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Adenosine Triphosphate/analogs & derivatives/pharmacology ; Animals ; Calcineurin ; Calcium/metabolism ; Calmodulin-Binding Proteins/*pharmacology ; Cells, Cultured ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Glycine/pharmacology ; Hippocampus ; Membrane Potentials ; Neurons/physiology ; Patch-Clamp Techniques ; Phosphoprotein Phosphatases/*pharmacology ; Phosphorylation ; Rats ; Receptors, N-Methyl-D-Aspartate/*drug effects/physiology ; Synapses/*physiology
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  • 46
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    Identification and characterization of a prostaglandin transporter (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-05-12
    Description: Carrier-mediated prostaglandin transport has been postulated to occur in many tissues. On the basis of sequence homology, the protein of unknown function encoded by the rat matrin F/G complementary DNA was predicted to be an organic anion transporter. Expression of the matrin F/G complementary DNA in HeLa cells or Xenopus oocytes conferred the property of specific transport of prostaglandins. The tissue distribution of matrin F/G messenger RNA and the sensitivity of matrin F/G-induced prostaglandin transport to inhibitors were similar to those of endogenous prostaglandin transport. The protein encoded by the matrin F/G complementary DNA is thus preferably called PGT because it is likely to function as a prostaglandin transporter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanai, N -- Lu, R -- Satriano, J A -- Bao, Y -- Wolkoff, A W -- Schuster, V L -- DK-38095/DK/NIDDK NIH HHS/ -- DK23026/DK/NIDDK NIH HHS/ -- DK41296/DK/NIDDK NIH HHS/ -- R01 DK049688/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1995 May 12;268(5212):866-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754369" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Antiporters ; Base Sequence ; Biological Transport/drug effects ; Carrier Proteins/chemistry/genetics/*metabolism ; Codon ; Colon/metabolism ; DNA, Complementary/genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Epithelium/metabolism ; HeLa Cells ; Humans ; Kidney Medulla/metabolism ; Molecular Sequence Data ; Organic Anion Transporters ; Prostaglandins/*metabolism ; RNA, Messenger/analysis ; Rats ; Xenopus
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  • 47
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    Separation of caveolae from associated microdomains of GPI-anchored proteins (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-08
    Description: In situ coating of the surface of endothelial cells in rat lung with cationic colloidal silica particles was used to separate caveolae from detergent-insoluble membranes rich in glycosyl phosphatidylinositol (GPI)-anchored proteins but devoid of caveolin. Immunogold electron microscopy showed that ganglioside GM1-enriched caveolae associated with an annular plasmalemmal domain enriched in GPI-anchored proteins. The purified caveolae contained molecular components required for regulated transport, including various lipid-anchored signaling molecules. Such specialized distinct microdomains may exist separately or together in the plasma membrane to organize signaling molecules and to process surface-bound ligands differentially.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schnitzer, J E -- McIntosh, D P -- Dvorak, A M -- Liu, J -- Oh, P -- AI33372/AI/NIAID NIH HHS/ -- HL43278/HL/NHLBI NIH HHS/ -- HL52766/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Sep 8;269(5229):1435-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Beth Israel Hospital, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7660128" target="_blank"〉PubMed〈/a〉
    Keywords: 5'-Nucleotidase/analysis ; Animals ; Caveolin 1 ; *Caveolins ; Cell Fractionation ; Cell Membrane/*chemistry/*ultrastructure ; Colloids ; Detergents ; Endothelium, Vascular/ultrastructure ; Glycosylphosphatidylinositols/*analysis ; Membrane Proteins/*analysis ; Microscopy, Immunoelectron ; Rats ; Receptors, Cell Surface/analysis ; Receptors, Urokinase Plasminogen Activator ; Signal Transduction ; Silicon Dioxide ; Solubility
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  • 48
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    Long-lasting neurotrophin-induced enhancement of synaptic transmission in the adult hippocampus (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-17
    Description: The neurotrophins are signaling factors important for the differentiation and survival of distinct neuronal populations during development. To test whether the neurotrophins also function in the mature nervous system, the effects of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophic factor 3 (NT-3) on the strength of synaptic transmission in hippocampal slices were determined. Application of BDNF or NT-3 produced a dramatic and sustained (2 to 3 hours) enhancement of synaptic strength at the Schaffer collateral-CA1 synapses; NGF was without significant effect. The enhancement was blocked by K252a, an inhibitor of receptor tyrosine kinases. BDNF and NT-3 decreased paired-pulse facilitation, which is consistent with a possible presynaptic modification. Long-term potentiation could still be elicited in slices previously potentiated by exposure to the neurotrophic factors, which implies that these two forms of plasticity may use at least partially independent cellular mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, H -- Schuman, E M -- New York, N.Y. -- Science. 1995 Mar 17;267(5204):1658-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology 216-76, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7886457" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Brain-Derived Neurotrophic Factor ; Carbazoles/pharmacology ; Dose-Response Relationship, Drug ; Hippocampus/*drug effects/physiology ; In Vitro Techniques ; Indole Alkaloids ; Long-Term Potentiation/drug effects ; Male ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/*pharmacology ; Neuronal Plasticity/drug effects ; Neurotrophin 3 ; Protein Kinase C/antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Synapses/drug effects/physiology ; Synaptic Transmission/*drug effects
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  • 49
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    Control of proton sensitivity of the NMDA receptor by RNA splicing and polyamines (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-05-12
    Description: The function of the N-methyl-D-aspartate (NMDA)-preferring glutamate receptor can be regulated by extracellular pH, a process that may be important during ischemia in the brain or during seizures. Protons inhibit NMDA receptor function by 50 percent at pH 7.3 through interactions with the NR1 subunit, and both polyamines and NR1 exon 5 potentiate receptor function through relief of the tonic proton inhibition present at physiological pH. A single amino acid (lysine 211) was identified that mediates the effects of exon 5 in the rat brain. Electroneutral substitutions at this position restored pH sensitivity and, consequently, polyamine relief of tonic inhibition. This effect, together with the structural similarities between polyamines and the surface loop encoded by exon 5, suggest that exon 5 may act as a tethered pH-sensitive constitutive modulator of NMDA receptor function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Traynelis, S F -- Hartley, M -- Heinemann, S F -- NS08549/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 May 12;268(5212):873-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Emory University, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7754371" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Amino Acid Sequence ; Animals ; Cell Line ; Exons ; Hydrogen-Ion Concentration ; Lysine/physiology ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Oocytes ; Protein Structure, Secondary ; *Protons ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & ; inhibitors/chemistry/genetics/*physiology ; Spermine/*pharmacology ; Xenopus
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  • 50
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    NASA's space biology program shows signs of life (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-04-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):497-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725092" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallization ; Humans ; Intracranial Pressure ; Postural Balance ; Proteins/chemistry ; Rats ; *Space Flight ; United States ; United States National Aeronautics and Space Administration ; *Weightlessness
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  • 51
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    Tissue plasminogen activator induction in Purkinje neurons after cerebellar motor learning (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-12-22
    Description: The cerebellar cortex is implicated in the learning of complex motor skills. This learning may require synaptic remodeling of Purkinje cell inputs. An extracellular serine protease, tissue plasminogen activator (tPA), is involved in remodeling various nonneural tissues and is associated with developing and regenerating neurons. In situ hybridization showed that expression of tPA messenger RNA was increased in the Purkinje neurons of rats within an hour of their being trained for a complex motor task. Antibody to tPA also showed the induction of tPA protein associated with cerebellar Purkinje cells. Thus, the induction of tPA during motor learning may play a role in activity-dependent synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeds, N W -- Williams, B L -- Bickford, P C -- AG-04418/AG/NIA NIH HHS/ -- NS-09818/NS/NINDS NIH HHS/ -- T32-GM 08497/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1995 Dec 22;270(5244):1992-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Colorado Health Sciences Center, Denver 80262, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8533091" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebellum/enzymology ; Enzyme Induction ; In Situ Hybridization ; Learning/*physiology ; Male ; Motor Skills/*physiology ; Neuronal Plasticity ; Physical Conditioning, Animal ; Psychomotor Performance/*physiology ; Purkinje Cells/*enzymology ; Rats ; Rats, Inbred F344 ; Tissue Plasminogen Activator/*biosynthesis/genetics
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  • 52
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    New clue to brain wiring mystery (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1995 Oct 27;270(5236):581.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7570014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology ; Brain-Derived Neurotrophic Factor ; Cell Communication ; Cell Survival ; Cells, Cultured ; Models, Neurological ; Nerve Growth Factors/pharmacology/*physiology ; Nerve Tissue Proteins/pharmacology/physiology ; Neural Pathways ; Neurons/*cytology/*physiology ; Rats
    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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  • 53
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    Requirement for phosphatidylinositol transfer protein in epidermal growth factor signaling (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-05-26
    Description: Stimulation of phosphatidylinositol-4,5-bisphosphate (PIP2) hydrolysis is a widespread mechanism for receptor-mediated signaling in eukaryotes. Cytosolic phosphatidylinositol transfer protein (PITP) is necessary for guanosine triphosphate (GTP)-dependent hydrolysis of PIP2 by phospholipase C-beta (PLC-beta), but the role of PITP is unclear. Stimulation of phospholipase C-gamma (PLC-gamma) in A431 human epidermoid carcinoma cells treated with epidermal growth factor (EGF) required PITP. Stimulation of PI-4 kinase in cells treated with EGF also required PITP. Coprecipitation studies revealed an EGF-dependent association of PITP with the EGF receptor, with PI-4 kinase, and with PLC-gamma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kauffmann-Zeh, A -- Thomas, G M -- Ball, A -- Prosser, S -- Cunningham, E -- Cockcroft, S -- Hsuan, J J -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1995 May 26;268(5214):1188-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Biochemistry Group, Ludwig Institute for Cancer Research, University College London School of Medicine, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7761838" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Phosphatidylinositol 4-Kinase ; Animals ; Carrier Proteins/metabolism/*physiology ; Cytosol/metabolism ; Epidermal Growth Factor/metabolism/*physiology ; Humans ; Isoenzymes/metabolism/physiology ; *Membrane Proteins ; Phosphatidylinositols/metabolism ; Phospholipase C gamma ; Phospholipid Transfer Proteins ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Protein Binding ; Rats ; Receptor, Epidermal Growth Factor/metabolism ; Signal Transduction/*physiology ; Tumor Cells, Cultured ; Type C Phospholipases/metabolism/physiology
    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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  • 54
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    Receptors find work as guides (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1995 Sep 22;269(5231):1668-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7569889" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes ; Axons/*physiology ; Cell Movement ; Cells, Cultured ; Chickens ; Ephrin-A2 ; Glycosylphosphatidylinositols/physiology ; Ligands ; Nervous System Physiological Phenomena ; Proteins/metabolism/*physiology ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism/*physiology ; Receptor, EphA8 ; Retina/*physiology ; Superior Colliculi/*physiology
    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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  • 55
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    Receptor endocytosis and dendrite reshaping in spinal neurons after somatosensory stimulation (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-16
    Description: In vivo somatosensory stimuli evoked the release of substance P from primary afferent neurons that terminate in the spinal cord and stimulated endocytosis of substance P receptors in rat spinal cord neurons. The distal dendrites that showed substance P receptor internalization underwent morphological reorganization, changing from a tubular structure to one characterized by swollen varicosities connected by thin segments. This internalization and dendritic structural reorganization provided a specific image of neurons activated by substance P. Thus receptor internalization can drive reversible structural changes in central nervous system neurons in vivo. Both of these processes may be involved in neuronal plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- DeMaster, E -- Malhotra, A -- Ghilardi, J R -- Rogers, S D -- Mantyh, C R -- Liu, H -- Basbaum, A I -- Vigna, S R -- Maggio, J E -- NS14627/NS/NINDS NIH HHS/ -- NS21445/NS/NINDS NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Jun 16;268(5217):1629-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, Veterans Administration Medical Center, Minneapolis, MN 55417, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7539937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin/pharmacology ; Dendrites/metabolism/*ultrastructure ; *Endocytosis ; GTP-Binding Proteins/metabolism ; Male ; Neuronal Plasticity ; Neurons/*metabolism/ultrastructure ; Physical Stimulation ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/*metabolism ; Spinal Cord/cytology/*metabolism ; Substance P/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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  • 56
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    Researchers broaden the attack on Parkinson's disease (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinapa, M -- New York, N.Y. -- Science. 1995 Jan 27;267(5197):455-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7824944" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Tissue Transplantation ; Cell Differentiation ; Central Nervous System/cytology/embryology ; Dopamine/*biosynthesis ; Embryonic Induction ; *Fetal Tissue Transplantation ; Fibroblast Growth Factor 2/*biosynthesis ; Genetic Engineering ; Glial Cell Line-Derived Neurotrophic Factor ; Graft Survival ; Humans ; Mesencephalon/cytology/embryology ; Nerve Growth Factors/therapeutic use ; Nerve Tissue Proteins/*therapeutic use ; Neurons/cytology/*metabolism/transplantation ; Parkinson Disease/drug therapy/surgery/*therapy ; Rats
    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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  • 57
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    Role of B61, the ligand for the Eck receptor tyrosine kinase, in TNF-alpha-induced angiogenesis (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-28
    Description: B61, a cytokine-inducible endothelial gene product, is the ligand for the Eck receptor protein tyrosine kinase (RPTK). Expression of a B61-immunoglobulin chimera showed that B61 could act as an angiogenic factor in vivo and a chemoattractant for endothelial cells in vitro. The Eck RPTK was activated by tumor necrosis factor-alpha (TNF-alpha) through induction of B61, and an antibody to B61 attenuated angiogenesis induced by TNF-alpha but not by basic fibroblast growth factor. This finding suggests the existence of an autocrine or paracrine loop involving activation of the Eck RPTK by its inducible ligand B61 after an inflammatory stimulus, the net effect of which would be to promote angiogenesis, a hallmark of chronic inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pandey, A -- Shao, H -- Marks, R M -- Polverini, P J -- Dixit, V M -- DK 39255/DK/NIDDK NIH HHS/ -- HL 39926/HL/NHLBI NIH HHS/ -- P0 1AI331890004/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):567-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7536959" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cells, Cultured ; Chemotaxis ; Endothelium, Vascular/cytology/*physiology ; Enzyme Activation ; Ephrin-A1 ; Female ; Humans ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Neovascularization, Pathologic/*etiology ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proteins/*physiology ; Rats ; Rats, Inbred F344 ; Receptor, EphA2 ; Recombinant Fusion Proteins ; Tumor Necrosis Factor-alpha/*pharmacology
    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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  • 58
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    Reliability of spike timing in neocortical neurons (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-09
    Description: It is not known whether the variability of neural activity in the cerebral cortex carries information or reflects noisy underlying mechanisms. In an examination of the reliability of spike generation using recordings from neurons in rat neocortical slices, the precision of spike timing was found to depend on stimulus transients. Constant stimuli led to imprecise spike trains, whereas stimuli with fluctuations resembling synaptic activity produced spike trains with timing reproducible to less than 1 millisecond. These data suggest a low intrinsic noise level in spike generation, which could allow cortical neurons to accurately transform synaptic input into spike sequences, supporting a possible role for spike timing in the processing of cortical information by the neocortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mainen, Z F -- Sejnowski, T J -- New York, N.Y. -- Science. 1995 Jun 9;268(5216):1503-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7770778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; *Evoked Potentials ; In Vitro Techniques ; Neurons/*physiology ; Occipital Lobe/cytology/*physiology ; Rats ; Rats, Sprague-Dawley ; *Synaptic Transmission
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    Inhibition of ras-induced proliferation and cellular transformation by p16INK4 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-13
    Description: 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〉
    Keywords: 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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 60
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    Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites (1995)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1995-04-14
    Description: The temporal and spatial profile of activity-evoked changes in membrane potential and intracellular calcium concentration in the dendrites of hippocampal CA1 pyramidal neurons was examined with simultaneous somatic and dendritic patch-pipette recording and calcium imaging experiments. Action potentials are initiated close to the soma of these neurons and backpropagate into the dendrites in an activity-dependent manner; those occurring early in a train propagate actively, whereas those occurring later fail to actively invade the distal dendrites. Consistent with this finding, dendritic calcium transients evoked by single action potentials do not significantly attenuate with distance from the soma, whereas those evoked by trains attenuate substantially. Failure of action potential propagation into the distal dendrites often occurs at branch points. Consequently, neighboring regions of the dendritic tree can experience different voltage and calcium signals during repetitive action potential firing. The influence of backpropagating action potentials on synaptic integration and plasticity will therefore depend on both the extent of dendritic branching and the pattern of neuronal activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spruston, N -- Schiller, Y -- Stuart, G -- Sakmann, B -- New York, N.Y. -- Science. 1995 Apr 14;268(5208):297-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur medizinische Forschung, Abteilung Zellphysiologie, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716524" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Dendrites/metabolism/*physiology ; Ion Channel Gating ; Neuronal Plasticity ; Patch-Clamp Techniques ; Pyramidal Cells/metabolism/*physiology ; Rats ; Rats, Wistar ; Sodium Channels/metabolism ; Synapses/physiology ; Tetrodotoxin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Glycobiology: more functions for oligosaccharides (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dwek, R A -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1234-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Glycobiology Institute, University of Oxford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD2/*chemistry ; Glycoproteins/*chemistry ; Glycosylation ; Humans ; Models, Molecular ; Oligosaccharides/*chemistry ; *Protein Conformation ; Rats ; Ribonucleases/chemistry
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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