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  • 1
    Publication Date: 2000-03-10
    Description: The first artery and vein of the vertebrate embryo assemble in the trunk by migration and coalescence of angioblasts to form endothelial tubes. The gridlock (grl) mutation in zebrafish selectively perturbs assembly of the artery (the aorta). Here it is shown that grl encodes a basic helix-loop-helix (bHLH) protein belonging to the Hairy/Enhancer of the split family of bHLH proteins. The grl gene is expressed in lateral plate mesoderm before vessel formation, and thereafter in the aorta and not in the vein. These results suggest that the arterial endothelial identity is established even before the onset of blood flow and implicate the grl gene in assignment of vessel-specific cell fate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhong, T P -- Rosenberg, M -- Mohideen, M A -- Weinstein, B -- Fishman, M C -- R01DK55383/DK/NIDDK NIH HHS/ -- R01RR0888/RR/NCRR NIH HHS/ -- T32HL07208/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1820-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital-Harvard Medical School, 149 13th Street, 4th floor, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710309" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aorta/*embryology/metabolism ; Basic Helix-Loop-Helix Transcription Factors ; Cloning, Molecular ; Embryo, Nonmammalian/metabolism ; Embryonic Development ; Endothelium, Vascular/embryology/metabolism ; Gene Expression ; Genotype ; *Helix-Loop-Helix Motifs ; Humans ; Mesoderm/metabolism ; Molecular Sequence Data ; Morphogenesis/genetics ; Mutation ; Phenotype ; Physical Chromosome Mapping ; Proteins/chemistry/*genetics/*physiology ; Sequence Alignment ; Stem Cells/cytology/metabolism ; Zebrafish/embryology/*genetics ; *Zebrafish Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fishman, M C -- New York, N.Y. -- Science. 2001 Nov 9;294(5545):1290-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital and Harvard Medical School, Cardiovascular Division, Boston, MA 02114, USA. mcfishman@partners.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11701913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Body Patterning ; Central Nervous System/physiology ; Cloning, Molecular ; Embryo, Nonmammalian/physiology ; Evolution, Molecular ; *Genome ; Genomics ; Humans ; Mutation ; Phenotype ; Signal Transduction ; Synteny ; Zebrafish/*embryology/*genetics ; Zebrafish Proteins/genetics/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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  • 3
    Publication Date: 1989-06-09
    Description: The neuron-specific protein GAP-43 is associated with the membrane of the nerve growth cone and thus may be important to the activity of this distinctive neuronal structure. Transient transfection of COS and NIH 3T3 cells with appropriate vectors resulted in expression of GAP-43 in these non-neuronal cells; as in neurons, transfected GAP-43 associated with the membrane. In addition, many long fine filopodial processes extended from the periphery of such transfected cells. Stable CHO cell lines expressing GAP-43 also exhibited processes that were more numerous, far longer, and more complex than those of CHO cell lines not transfected or transfected with control plasmids. Thus GAP-43 may directly contribute to growth cone activity by regulating cell membrane structure and enhancing extension of filopodial processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zuber, M X -- Goodman, D W -- Karns, L R -- Fishman, M C -- New York, N.Y. -- Science. 1989 Jun 9;244(4909):1193-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Laboratory, Massachusetts General Hospital Cancer Center, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2658062" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Membrane/*ultrastructure ; Cells, Cultured ; Fluorescent Antibody Technique ; GAP-43 Protein ; Growth Substances/*physiology ; Membrane Proteins/genetics/*physiology ; Mice ; Nerve Tissue Proteins/genetics/*physiology ; Recombinant Proteins/pharmacology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1993-01-01
    Description: During development, motion of nerve growth cones ceases on contact with particular targets. The signaling mechanism is unknown. In culture, growth cone collapse can be caused by solubilized embryonic brain membranes, central nervous system myelin, a 35-kilodalton protein isolated from myelin, and mastoparan. Collapse induced by each of these is blocked by pertussis toxin. Thus, collapse of growth cones is mediated by G protein-coupled receptors, which may be activated by proteins associated with the cell surface as well as by soluble ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Igarashi, M -- Strittmatter, S M -- Vartanian, T -- Fishman, M C -- New York, N.Y. -- Science. 1993 Jan 1;259(5091):77-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Laboratory, Massachusetts General Hospital-East, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8418498" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Cell Membrane/drug effects/physiology/ultrastructure ; Chick Embryo ; GTP-Binding Proteins/*metabolism ; Ganglia, Spinal/*physiology ; Myelin Proteins/physiology ; Neurons/drug effects/*physiology/ultrastructure ; Organ Culture Techniques ; Peptides ; Pertussis Toxin ; *Signal Transduction ; Virulence Factors, Bordetella/pharmacology ; Wasp Venoms/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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  • 5
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1996-10-11
    Description: The mechanisms that maintain the epithelial integrity of the gastrointestinal tract remain largely undefined. The gene encoding intestinal trefoil factor (ITF), a protein secreted throughout the small intestine and colon, was rendered nonfunctional in mice by targeted disruption. Mice lacking ITF had impaired mucosal healing and died from extensive colitis after oral administration of dextran sulfate sodium, an agent that causes mild epithelial injury in wild-type mice. ITF-deficient mice manifested poor epithelial regeneration after injury. These findings reveal a central role for ITF in the maintenance and repair of the intestinal mucosa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mashimo, H -- Wu, D C -- Podolsky, D K -- Fishman, M C -- P30DK43351/DK/NIDDK NIH HHS/ -- R01DK46906/DK/NIDDK NIH HHS/ -- T32DK07191/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Oct 11;274(5285):262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Jackson 7, Massachusetts General Hospital, Fruit Street, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8824194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Movement ; Colitis/etiology/pathology ; Colon/drug effects/pathology/physiology ; Dextran Sulfate/pharmacology ; Gene Targeting ; Growth Substances/genetics/pharmacology/*physiology ; Intestinal Mucosa/drug effects/pathology/*physiology ; Mice ; Molecular Sequence Data ; *Mucins ; *Muscle Proteins ; *Neuropeptides ; Peptides/genetics/pharmacology/*physiology ; Recombinant Proteins/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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  • 7
    Publication Date: 1996-06-21
    Description: Gamma-aminobutyrate acid, L-glutamate, and N-methyl-D-aspartate were separated by capillary electrophoresis and detected by the use of whole-cell and outside-out patch-clamp techniques on freshly dissociated rat olfactory interneurons. These neuroactive compounds could be identified from their electrophoretic migration times, unitary channel conductances, and power spectra that yielded corner frequencies and mean single-channel conductances characteristic for each of the different agonist-receptor interactions. This technique has the sensitivity to observe the opening of a single ion channel for agonists separated by capillary electrophoresis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orwar, O -- Jardemark, K -- Jacobson, I -- Moscho, A -- Fishman, H A -- Scheller, R H -- Zare, R N -- DA 09873-01/DA/NIDA NIH HHS/ -- MH 45423-06/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Stanford University, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosensing Techniques ; Electrophoresis, Capillary ; Glutamic Acid/*analysis/isolation & purification ; Interneurons/*chemistry ; Ion Channels/physiology ; N-Methylaspartate/*analysis/isolation & purification ; Olfactory Bulb/cytology ; Patch-Clamp Techniques ; Rats ; Receptors, GABA/physiology ; Receptors, Glutamate/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Sensitivity and Specificity ; gamma-Aminobutyric Acid/*analysis/isolation & purification
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 1994-09-23
    Description: The proposal that nitric oxide (NO) or its reactant products mediate toxicity in brain remains controversial in part because of the use of nonselective agents that block NO formation in neuronal, glial, and vascular compartments. In mutant mice deficient in neuronal NO synthase (NOS) activity, infarct volumes decreased significantly 24 and 72 hours after middle cerebral artery occlusion, and the neurological deficits were less than those in normal mice. This result could not be accounted for by differences in blood flow or vascular anatomy. However, infarct size in the mutant became larger after endothelial NOS inhibition by nitro-L-arginine administration. Hence, neuronal NO production appears to exacerbate acute ischemic injury, whereas vascular NO protects after middle cerebral artery occlusion. The data emphasize the importance of developing selective inhibitors of the neuronal isoform.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Z -- Huang, P L -- Panahian, N -- Dalkara, T -- Fishman, M C -- Moskowitz, M A -- NS10828/NS/NINDS NIH HHS/ -- NS2636/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1883-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stroke Research Laboratory, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522345" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/deficiency/*metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Brain/enzymology/*metabolism ; Brain Ischemia/complications/*metabolism ; Cerebral Infarction/*etiology ; Cerebrovascular Circulation ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Neurons/*enzymology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1994-02-11
    Description: Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gagliardini, V -- Fernandez, P A -- Lee, R K -- Drexler, H C -- Rotello, R J -- Fishman, M C -- Yuan, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):826-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303301" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 1 ; Cells, Cultured ; Chickens ; Ganglia, Spinal ; Gene Expression ; Metalloendopeptidases/*genetics/physiology ; Microinjections ; Nerve Growth Factors/pharmacology ; Neurons, Afferent/*cytology/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Serpins/*genetics/physiology ; *Viral Proteins
    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
    Publication Date: 1994-07-22
    Description: Long-term potentiation (LTP) is a persistent increase in synaptic strength implicated in certain forms of learning and memory. In the CA1 region of the hippocampus, LTP is thought to involve the release of one or more retrograde messengers from the postsynaptic cell that act on the presynaptic terminal to enhance transmitter release. One candidate retrograde messenger is the membrane-permeant gas nitric oxide (NO), which in the brain is released after activation of the neuronal-specific NO synthase isoform (nNOS). To assess the importance of NO in hippocampal synaptic plasticity, LTP was examined in mice where the gene encoding nNOS was disrupted by gene targeting. In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal except for a slight reduction in comparison to that in wild-type mice and was blocked by NOS inhibitors, just as it was in wild-type mice. Immunocytochemical studies indicate that in the nNOS- mice as in wild-type mice, the endothelial form of NOS (eNOS) is expressed in CA1 neurons. These findings suggest that eNOS, rather than nNOS, generates NO within the postsynaptic cell during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Dell, T J -- Huang, P L -- Dawson, T M -- Dinerman, J L -- Snyder, S H -- Kandel, E R -- Fishman, M C -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- MH-45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):542-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518615" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/genetics/*metabolism ; Animals ; Arginine/*analogs & derivatives/pharmacology ; Electric Stimulation ; Endothelium/enzymology ; Hippocampus/drug effects/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Mice ; Mutation ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine ; Pyramidal Cells/drug effects/enzymology/*physiology ; 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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