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  • Rats  (355)
  • Mutation  (260)
  • Cells, Cultured  (175)
  • *Biological Evolution
  • *Ecosystem
  • American Association for the Advancement of Science (AAAS)  (820)
  • American Meteorological Society
  • MDPI Publishing
  • 1990-1994  (820)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (820)
  • American Meteorological Society
  • MDPI Publishing
  • Springer  (39)
  • Wiley-Blackwell  (2)
Years
Year
  • 1
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    Microtubule severing by elongation factor 1 alpha (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: An activity that severs stable microtubules is thought to be involved in microtubule reorganization during the cell cycle. Here, a 48-kilodalton microtubule-severing protein was purified from Xenopus eggs and identified as translational elongation factor 1 alpha (EF-1 alpha). Bacterially expressed human EF-1 alpha also displayed microtubule-severing activity in vitro and, when microinjected into fibroblasts, induced rapid and transient fragmentation of cytoplasmic microtubule arrays. Thus, EF-1 alpha, an essential component of the eukaryotic translational apparatus, appears to have a second role as a regulator of cytoskeletal rearrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shiina, N -- Gotoh, Y -- Kubomura, N -- Iwamatsu, A -- Nishida, E -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):282-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Molecular Biology, Kyoto University, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939665" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Guanosine Triphosphate/analogs & derivatives/metabolism ; Humans ; Microtubules/drug effects/*metabolism ; Molecular Sequence Data ; Molecular Weight ; Oocytes ; Peptide Elongation Factor 1 ; Peptide Elongation Factors/chemistry/isolation & purification/*physiology ; Rats ; Recombinant Proteins/pharmacology ; Ribonucleoproteins/chemistry/isolation & purification/*physiology ; Sepharose/analogs & derivatives/metabolism ; 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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  • 2
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    Delocalization of Vg1 mRNA from the vegetal cortex in Xenopus oocytes after destruction of Xlsirt RNA (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: The Xlsirts are a family of transcribed repeat sequence genes that do not code for protein. Xlsirt RNAs become localized to the vegetal cortex of Xenopus oocytes early in oogenesis, before the localization of the messenger RNA Vg1, which encodes a transforming growth factor-beta-like molecule involved in mesoderm formation, and coincident with the localization of Xcat2 transcripts, which encode a nanos-like molecule. Destruction of the localized Xlsirts by injection of antisense oligodeoxynucleotides into stage 4 oocytes resulted in the release of Vg1 transcripts but not Xcat2 transcripts from the vegetal cortex. Xlsirt RNAs, which may be a structural component of the vegetal cortex, are a crucial part of a genetic pathway necessary for the proper localization of Vg1 that leads to subsequent normal pattern formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kloc, M -- Etkin, L D -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1101-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Texas, M.D. Anderson Cancer Center, Houston 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Glycoproteins/*genetics ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; Oogenesis ; RNA/*genetics ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/genetics ; Repetitive Sequences, Nucleic Acid ; Transforming Growth Factor beta/genetics ; Xenopus ; *Xenopus Proteins ; Zinc Fingers
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Structures of ternary complexes of rat DNA polymerase beta, a DNA template-primer, and ddCTP (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: Two ternary complexes of rat DNA polymerase beta (pol beta), a DNA template-primer, and dideoxycytidine triphosphate (ddCTP) have been determined at 2.9 A and 3.6 A resolution, respectively. ddCTP is the triphosphate of dideoxycytidine (ddC), a nucleoside analog that targets the reverse transcriptase of human immunodeficiency virus (HIV) and is at present used to treat AIDS. Although crystals of the two complexes belong to different space groups, the structures are similar, suggesting that the polymerase-DNA-ddCTP interactions are not affected by crystal packing forces. In the pol beta active site, the attacking 3'-OH of the elongating primer, the ddCTP phosphates, and two Mg2+ ions are all clustered around Asp190, Asp192, and Asp256. Two of these residues, Asp190 and Asp256, are present in the amino acid sequences of all polymerases so far studied and are also spatially similar in the four polymerases--the Klenow fragment of Escherichia coli DNA polymerase I, HIV-1 reverse transcriptase, T7 RNA polymerase, and rat DNA pol beta--whose crystal structures are now known. A two-metal ion mechanism is described for the nucleotidyl transfer reaction and may apply to all polymerases. In the ternary complex structures analyzed, pol beta binds to the DNA template-primer in a different manner from that recently proposed for other polymerase-DNA models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pelletier, H -- Sawaya, M R -- Kumar, A -- Wilson, S H -- Kraut, J -- CA17374/CA/NCI NIH HHS/ -- ES06839/ES/NIEHS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1891-903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, San Diego 92093-0317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Binding Sites ; Crystallization ; Crystallography, X-Ray ; DNA/chemistry/metabolism ; DNA Polymerase I/*chemistry/metabolism ; DNA Primers/*chemistry/metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxycytosine Nucleotides/*chemistry/metabolism ; Dideoxynucleotides ; HIV Reverse Transcriptase ; Humans ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Rats ; Recombinant Proteins ; Templates, Genetic ; Thymine Nucleotides/chemistry/metabolism ; Viral Proteins ; Zidovudine/analogs & derivatives/chemistry/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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  • 4
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    Abnormal fear response and aggressive behavior in mutant mice deficient for alpha-calcium-calmodulin kinase II (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Mice deficient for the gene encoding alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII knockout mice) provide a promising tool to link behavioral and cellular abnormalities with a specific molecular lesion. The heterozygous mouse exhibited a well-circumscribed syndrome of behavioral abnormalities, consisting primarily of a decreased fear response and an increase in defensive aggression, in the absence of any measured cognitive deficits. Unlike the heterozygote, the homozygote displayed abnormal behavior in all paradigms tested. At the cellular level, both extracellular and whole-cell patch clamp recordings indicated that serotonin release in putative serotonergic neurons of the dorsal raphe was reduced. Thus, alpha-CaMKII knockout mice, in particular the heterozygote, may provide a model for studying the molecular and cellular basis underlying emotional disorders involving fear and aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C -- Rainnie, D G -- Greene, R W -- Tonegawa, S -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939668" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Animals ; Behavior, Animal ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/deficiency/genetics/*physiology ; *Fear ; Fluoxetine/pharmacology ; Gene Dosage ; Heterozygote ; Homozygote ; In Vitro Techniques ; Membrane Potentials ; Mice ; Mice, Knockout ; Mutation ; Neurons/metabolism ; Patch-Clamp Techniques ; Raphe Nuclei/metabolism ; Serotonin/metabolism/pharmacology ; 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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  • 5
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    Functional consequences of posttranslational isomerization of Ser46 in a calcium channel toxin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The venom of the funnel-web spider Agelenopsis aperta contains several peptides that paralyze prey by blocking voltage-sensitive calcium channels. Two peptides, omega-Aga-IVB (IVB) and omega-Aga-IVC (IVC), have identical amino acid sequences, yet have opposite absolute configurations at serine 46. These toxins had similar selectivities for blocking voltage-sensitive calcium channel subtypes but different potencies for blocking P-type voltage-sensitive calcium channels in rat cerebellar Purkinje cells as well as calcium-45 influx into rat brain synaptosomes. An enzyme purified from venom converts IVC to IVB by isomerizing serine 46, which is present in the carboxyl-terminal tail, from the L to the D configuration. Unlike the carboxyl terminus of IVC, that of IVB was resistant to the major venom protease. These results show enzymatic activities in A. aperta venom being used in an unprecedented strategy for coproduction of necessary neurotoxins that possess enhanced stability and potency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heck, S D -- Siok, C J -- Krapcho, K J -- Kelbaugh, P R -- Thadeio, P F -- Welch, M J -- Williams, R D -- Ganong, A H -- Kelly, M E -- Lanzetti, A J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1065-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉NPS Pharmaceuticals Incorporated, Salt Lake City, Utah 84108.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973665" target="_blank"〉PubMed〈/a〉
    Keywords: Agatoxins ; Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Calcium Channel Blockers/chemistry/*metabolism/toxicity ; Calcium Channels/*metabolism ; Isomerases/metabolism ; Molecular Sequence Data ; *Protein Processing, Post-Translational ; Purkinje Cells/metabolism ; Rats ; Serine/*metabolism ; Spider Venoms/chemistry/enzymology/*metabolism/toxicity ; Stereoisomerism ; Structure-Activity Relationship ; Synaptosomes/metabolism
    Print ISSN: 0036-8075
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  • 6
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    Functional participation of the IL-2 receptor gamma chain in IL-7 receptor complexes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: The gamma chain of the interleukin-2 (IL-2) receptor is shared with the functional IL-4 receptor and is causatively related to X-linked severe combined immunodeficiency (XSCID), which is ascribed to a profound T cell defect. Studies with monoclonal antibodies specific for the IL-2 receptor gamma chain showed that the gamma chain participates in the functional high-affinity receptor complexes for IL-7 that are involved in the differentiation of T and B cells. Participation of the gamma subunit in more than one receptor may enable the elucidation of the mechanisms of XSCID development and lymphocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, M -- Takeshita, T -- Higuchi, M -- Nakamura, M -- Sudo, T -- Nishikawa, S -- Sugamura, K -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1453-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Tohoku University School of Medicine, Sendai, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128231" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; B-Lymphocytes/*immunology ; Cell Line ; Cells, Cultured ; Female ; Genetic Linkage ; Interleukin-7/*metabolism/pharmacology ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin/*metabolism ; Receptors, Interleukin-2/genetics/immunology/*metabolism ; Receptors, Interleukin-7 ; Severe Combined Immunodeficiency/genetics/immunology ; T-Lymphocytes/*immunology ; X Chromosome
    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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  • 7
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    Inhibitory CA1-CA3-hilar region feedback in the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-16
    Description: The organization of the hippocampus is generally thought of as a series of cell groups that form a unidirectionally excited chain, regulated by localized inhibitory circuits. With the use of in vivo intracellular labeling, histochemical, and extracellular tracing methods, a longitudinally widespread, inhibitory feedback in rat brain from the CA1 area to the CA3 and hilar regions was observed. This long-range, cross-regional inhibition may allow precise synchronization of population activity by timing the occurrence of action potentials in the principal cells and may contribute to the coordinated induction of synaptic plasticity in distributed networks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sik, A -- Ylinen, A -- Penttonen, M -- Buzsaki, G -- New York, N.Y. -- Science. 1994 Sep 16;265(5179):1722-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8085161" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Dendrites/ultrastructure ; Feedback ; Hippocampus/cytology/*physiology ; Interneurons/*physiology/ultrastructure ; Membrane Potentials ; *Neural Inhibition ; Neural Pathways ; Pyramidal Cells/*physiology/ultrastructure ; Rats ; Synapses/ultrastructure
    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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  • 8
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    Circadian clock mutants of cyanobacteria (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: A diverse set of circadian clock mutants was isolated in a cyanobacterial strain that carries a bacterial luciferase reporter gene attached to a clock-controlled promoter. Among 150,000 clones of chemically mutagenized bioluminescent cells, 12 mutants were isolated that exhibit a broad spectrum of periods (between 16 and 60 hours), and 5 mutants were found that show a variety of unusual patterns, including arrhythmia. These mutations appear to be clock-specific. Moreover, it was demonstrated that in this cyanobacterium it is possible to clone mutant genes by complementation, which provides a means to genetically dissect the circadian mechanism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, T -- Tsinoremas, N F -- Golden, S S -- Johnson, C H -- Kutsuna, S -- Ishiura, M -- GM37040/GM/NIGMS NIH HHS/ -- MH43836/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1233-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute for Basic Biology, Okazaki, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973706" target="_blank"〉PubMed〈/a〉
    Keywords: Circadian Rhythm/*genetics ; Cloning, Molecular ; Cyanobacteria/*genetics/growth & development/physiology ; Darkness ; *Genes, Bacterial ; Genetic Complementation Test ; Light ; Luminescent Measurements ; Mutagenesis ; Mutation ; Temperature
    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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  • 9
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    Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-16
    Description: Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pettit, D L -- Perlman, S -- Malinow, R -- New York, N.Y. -- Science. 1994 Dec 16;266(5192):1881-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program, University of Iowa, Iowa City 52242.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7997883" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Cell Line ; Genetic Vectors ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Membrane Potentials ; Patch-Clamp Techniques ; Pyramidal Cells/enzymology/*physiology ; Rats ; Recombinant Proteins/metabolism ; Synaptic Transmission/drug effects/*physiology ; Transfection ; Vaccinia virus/genetics/physiology
    Print ISSN: 0036-8075
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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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    GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present in the limb bud. Members of the neurotrophin family are currently the best candidates for such neurotrophic factors, but inactivation of their receptor genes leads to only partial loss of motoneurons, which suggests that other factors are involved. Glial cell line-derived neurotrophic factor (GDNF), originally identified as a trophic factor specific for dopaminergic neurons, was found to be 75-fold more potent than the neurotrophins in supporting the survival of purified embryonic rat motoneurons in culture. GDNF messenger RNA was found in the immediate vicinity of motoneurons during the period of cell death in development. In vivo, GDNF rescues and prevents the atrophy of facial motoneurons that have been deprived of target-derived survival factors by axotomy. GDNF may therefore be a physiological trophic factor for spinal motoneurons. Its potency and specificity in vitro and in vivo also make it a good candidate for treatment of motoneuron disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henderson, C E -- Phillips, H S -- Pollock, R A -- Davies, A M -- Lemeulle, C -- Armanini, M -- Simmons, L -- Moffet, B -- Vandlen, R A -- Simpson LC corrected to Simmons, L -- Koliatsos, V E -- Rosenthal, A -- NS 10580/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1062-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U.382, IBDM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor ; Cell Death ; Cell Survival/drug effects ; Cells, Cultured ; Ciliary Neurotrophic Factor ; Face/innervation ; Glial Cell Line-Derived Neurotrophic Factor ; Growth Inhibitors/pharmacology ; *Interleukin-6 ; Leukemia Inhibitory Factor ; Lymphokines/pharmacology ; Molecular Sequence Data ; Motor Neurons/*cytology/drug effects ; Muscle Fibers, Skeletal/*metabolism ; Nerve Growth Factors/analysis/biosynthesis/genetics/*pharmacology ; Nerve Tissue Proteins/*analysis/biosynthesis/genetics/*pharmacology ; Neurons, Afferent/cytology/drug effects ; Peripheral Nerves/*metabolism ; RNA, Messenger/analysis/genetics ; Rats ; Schwann Cells/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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  • 11
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    Violence study hits a nerve in Germany (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simm, M -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):653.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171314" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes/*organization & administration ; Aggression ; Behavioral Research ; Dissent and Disputes ; *Genetics, Behavioral ; Germany ; Group Processes ; Humans ; *Molecular Biology ; Mutation ; National Socialism ; *Violence
    Print ISSN: 0036-8075
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  • 12
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    Detection of endogenous malondialdehyde-deoxyguanosine adducts in human liver (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: Endogenous DNA adducts may contribute to the etiology of human genetic disease and cancer. One potential source of endogenous DNA adducts is lipid peroxidation, which generates mutagenic carbonyl compounds such as malondialdehyde. A sensitive mass spectrometric method permitted detection and quantitation of the major malondialdehyde-DNA adduct, a pyrimidopurinone derived from deoxyguanosine. DNA from disease-free human liver was found to contain 5400 adducts per cell, a frequency comparable to that of adducts formed by exogenous carcinogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chaudhary, A K -- Nokubo, M -- Reddy, G R -- Yeola, S N -- Morrow, J D -- Blair, I A -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- GM42056/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1580-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A. B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt University School of Medicine, Nashville, TN 37232-0146.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079172" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Carbon Tetrachloride/toxicity ; DNA/*chemistry ; DNA Damage ; Deoxyguanosine/*analogs & derivatives/analysis/*metabolism ; Female ; Gas Chromatography-Mass Spectrometry ; Humans ; Lipid Peroxidation ; Liver/*chemistry ; Male ; Malondialdehyde/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 13
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    Anthropology. Putting a new spin on the birth of human birth (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischman, J -- New York, N.Y. -- Science. 1994 May 20;264(5162):1082-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178166" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Female ; *Fossils ; Hominidae/*anatomy & histology ; Humans ; *Labor, Obstetric ; Pelvic Bones/*anatomy & histology ; Pelvimetry ; Pregnancy
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  • 14
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    Molecule of the year: the DNA repair enzyme (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koshland, D E Jr -- New York, N.Y. -- Science. 1994 Dec 23;266(5193):1925.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7801114" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Damage ; *DNA Ligases ; *DNA Repair ; DNA Replication ; Humans ; Mutation ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    Insights from the study of animals lacking functional estrogen receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Estrogen hormones produce physiological actions within a variety of target sites in the body and during development by activating a specific receptor protein. Hormone responsiveness for the estrogen receptor protein was investigated at different stages of development with the use of gene knockout techniques because no natural genetic mutants have been described. A mutant mouse line without a functional estrogen receptor was created and is being used to assess estrogen responsiveness. Both sexes of these mutant animals are infertile and show a variety of phenotypic changes, some of which are associated with the gonads, mammary glands, reproductive tracts, and skeletal tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korach, K S -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1524-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estrogens/*physiology ; Female ; Heterozygote ; Homozygote ; Humans ; Infertility, Female/etiology ; Infertility, Male/etiology ; Male ; Mice ; Mice, Knockout ; Mutation ; Phenotype ; Receptors, Estrogen/genetics/*physiology ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Determination of intrinsic transcription termination efficiency by RNA polymerase elongation rate (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: Transcription terminators recognized by several RNA polymerases include a DNA segment encoding uridine-rich RNA and, for bacterial RNA polymerase, a hairpin loop located immediately upstream. Here, mutationally altered Escherichia coli RNA polymerase enzymes that have different termination efficiencies were used to show that the extent of transcription through the uridine-rich encoding segment is controlled by the substrate concentration of nucleoside triphosphate. This result implies that the rate of elongation determines the probability of transcript release. Moreover, the position of release sites suggests an important spatial relation between the RNA hairpin and the boundary of the terminator.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDowell, J C -- Roberts, J W -- Jin, D J -- Gross, C -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):822-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7526463" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA-Directed RNA Polymerases/genetics/*metabolism ; Escherichia coli/enzymology/genetics ; Molecular Sequence Data ; Mutation ; Nucleic Acid Conformation ; Nucleotides/metabolism ; RNA, Bacterial/*genetics/metabolism ; *Terminator Regions, Genetic ; *Transcription, Genetic ; Uridine Triphosphate/metabolism
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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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    Rules for alpha-helix termination by glycine (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-20
    Description: A predictive rule for protein folding is presented that involves two recurrent glycine-based motifs that cap the carboxyl termini of alpha helices. In proteins, helices that terminated in glycine residues were found predominantly in one of these two motifs. These glycine structures had a characteristic pattern of polar and apolar residues. Visual inspection of known helical sequences was sufficient to distinguish the two motifs from each other and from internal glycines that fail to terminate helices. These glycine motifs--in which the local sequence selects between available structures--represent an example of a stereochemical rule for protein folding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aurora, R -- Srinivasan, R -- Rose, G D -- GM 29458/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 20;264(5162):1126-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178170" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Glycine/*chemistry ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Oligopeptides/chemistry ; *Protein Folding ; *Protein Structure, Secondary
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  • 18
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    Promoter-selective transcriptional defect in cell cycle mutant ts13 rescued by hTAFII250 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: The TAFII250 subunit of the human transcription factor IID (TFIID) rescues the temperature-sensitive hamster cell line ts13 and overcomes a G1 arrest. Investigation of the transcriptional properties of ts13 nuclear extracts in vitro showed that activation by the site-specific regulators Sp1 and Gal4VP16 is temperature sensitive in ts13 extracts, whereas basal transcription remains unaffected. This transcriptional defect can be rescued by purified human TFIID or by expression of wild-type TAFII250 in ts13 cells. Expression from the cyclin A but not c-fos promoter is temperature sensitive in these mutant cells. Thus, the mutation in TAFII250 appears to have gene-specific effects that may lead to the ts13 cell cycle phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, E H -- Tjian, R -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):811-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cyclins/genetics ; DNA-Binding Proteins/*genetics/physiology ; Fungal Proteins/physiology ; *G1 Phase ; Genes, fos ; Genetic Complementation Test ; Genetic Vectors ; Histone Acetyltransferases ; Humans ; Mutation ; Nuclear Proteins/*genetics/physiology ; *Promoter Regions, Genetic ; Sp1 Transcription Factor/physiology ; *TATA-Binding Protein Associated Factors ; Temperature ; Trans-Activators/physiology ; Transcription Factor TFIID ; Transcription Factors/pharmacology ; *Transcription, Genetic ; Transfection
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  • 19
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    A genetic linkage map for the zebrafish (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: To facilitate molecular genetic analysis of vertebrate development, haploid genetics was used to construct a recombination map for the zebrafish Danio (Brachydanio) rerio. The map consists of 401 random amplified polymorphic DNAs (RAPDs) and 13 simple sequence repeats spaced at an average interval of 5.8 centimorgans. Strategies that exploit the advantages of haploid genetics and RAPD markers were developed that quickly mapped lethal and visible mutations and that placed cloned genes on the map. This map is useful for the position-based cloning of mutant genes, the characterization of chromosome rearrangements, and the investigation of evolution in vertebrate genomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Postlethwait, J H -- Johnson, S L -- Midson, C N -- Talbot, W S -- Gates, M -- Ballinger, E W -- Africa, D -- Andrews, R -- Carl, T -- Eisen, J S -- 1RO1AI26734/AI/NIAID NIH HHS/ -- HD07470/HD/NICHD NIH HHS/ -- NS23915/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):699-703.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurosciences, University of Oregon, Eugene 97403.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Cloning, Molecular ; Female ; Genetic Markers ; Genotype ; Male ; Mutation ; Phenotype ; Polymerase Chain Reaction ; Repetitive Sequences, Nucleic Acid ; Software ; Zebrafish/*genetics
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  • 20
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    Tetrad analysis possible in Arabidopsis with mutation of the QUARTET (QRT) genes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: Two Arabidopsis thaliana genes, QRT1 and QRT2, are required for pollen separation during normal development. In qrt mutants, the outer walls of the four meiotic products of the pollen mother cell are fused, and pollen grains are released in tetrads. Pollen is viable and fertile, and the cytoplasmic pollen contents are discrete. Pollination with a single tetrad usually yields four seeds, and genetic analysis confirmed that marker loci segregate in a 2:2 ratio within these tetrads. These mutations allow tetrad analysis to be performed in Arabidopsis and define steps in pollen cell wall development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Preuss, D -- Rhee, S Y -- Davis, R W -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1458-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University, CA 94305-5307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197459" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/physiology/ultrastructure ; Cell Wall/ultrastructure ; Chromosome Mapping ; *Genes, Plant ; Genetic Markers ; Glucuronidase/genetics ; Heterozygote ; Meiosis ; Microscopy, Electron, Scanning ; Mutation ; Phenotype ; Pollen/*physiology/ultrastructure
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  • 21
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    Structural clues to prion replication (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, F E -- Pan, K M -- Huang, Z -- Baldwin, M -- Fletterick, R J -- Prusiner, S B -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):530-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco 94143-0518.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Mice ; Mice, Transgenic ; Models, Biological ; Mutation ; PrPSc Proteins ; Prion Diseases/*metabolism/transmission ; Prions/*biosynthesis/chemistry/genetics/metabolism ; Protein Conformation ; Protein Structure, Secondary
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  • 22
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    Changes of induction and competence during the evolution of vulva development in nematodes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: In Caenorhabditis, the vulva is formed in the central body region from three of six equivalent cells and is induced by the gonad. In some nematodes, however, the vulva is located in the posterior body region. Vulval development has been analyzed in three such genera. The same precursor cells give rise to the vulva in Caenorhabditis and in the posterior vulva species, but in the latter the cells first migrate posteriorly. In two such species, the vulva is not induced by the gonad, but instead relies on intrinsic properties of precursor cells. Thus, evolution of organ position involves changes in induction and competence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sommer, R J -- Sternberg, P W -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):114-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, California Institute of Technology, Pasadena 91125.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016644" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Caenorhabditis elegans/cytology/*growth & development ; Cell Communication ; Cell Differentiation ; Female ; Gonads/cytology/physiology ; Rhabditoidea/cytology/*growth & development ; Species Specificity ; Vulva/cytology/growth & development
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  • 23
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    Carcinogenicity of chloroform (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messing, R B -- Gust, L D -- Petersen, D W -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1518-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Carcinogenicity Tests ; Chloroform/administration & dosage/*toxicity ; Female ; Humans ; Kidney Neoplasms/*chemically induced ; Rats ; Risk Factors ; *Water Supply
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  • 24
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    Potential role of human cytomegalovirus and p53 interaction in coronary restenosis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: A subset of patients who have undergone coronary angioplasty develop restenosis, a vessel renarrowing characterized by excessive proliferation of smooth muscle cells (SMCs). Of 60 human restenosis lesions examined, 23 (38 percent) were found to have accumulated high amounts of the tumor suppressor protein p53, and this correlated with the presence of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the lesions expressed HCMV protein IE84 and high amounts of p53. HCMV infection of cultured SMCs enhanced p53 accumulation, which correlated temporally with IE84 expression. IE84 also bound to p53 and abolished its ability to transcriptionally activate a reporter gene. Thus, HCMV, and IE84-mediated inhibition of p53 function, may contribute to the development of restenosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speir, E -- Modali, R -- Huang, E S -- Leon, M B -- Shawl, F -- Finkel, T -- Epstein, S E -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cardiology Branch, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023160" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Aged, 80 and over ; *Angioplasty, Balloon ; Antigens, Viral/*metabolism ; Atherectomy, Coronary ; Base Sequence ; Cells, Cultured ; Coronary Disease/*etiology/pathology/therapy ; Coronary Vessels/cytology/metabolism/microbiology ; Cytomegalovirus/*physiology ; Genes, p53 ; Humans ; Immediate-Early Proteins/*metabolism ; Middle Aged ; Molecular Sequence Data ; Muscle, Smooth, Vascular/cytology/metabolism/microbiology ; Recurrence ; Transcriptional Activation ; Transfection ; Tumor Suppressor Protein p53/genetics/*metabolism
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  • 25
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    Alzheimer's disease and possible gene interaction (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St George-Hyslop, P -- McLachlan, D C -- Tsuda, T -- Rogaev, E -- Karlinsky, H -- Lippa, C F -- Pollen, D -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):537.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8290965" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Amyloid beta-Protein Precursor/*genetics ; Apolipoprotein E4 ; Apolipoproteins E/*genetics ; Genotype ; Humans ; Mutation ; Phenotype
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  • 26
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    The prion connection: now in yeast? (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-04-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weissmann, C -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Molecularbiologie I, Universitat Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909168" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid/analogs & derivatives/metabolism ; Fungal Proteins/chemistry/*genetics ; Genes, Fungal ; Glutathione Peroxidase ; Mutation ; PrPSc Proteins ; Prions/chemistry/genetics ; Protein Conformation ; Saccharomyces cerevisiae/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins
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  • 27
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    Innervation of the heart and its central medullary origin defined by viral tracing (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: The vagus nerve exerts a profound influence on the heart, regulating the heart rate and rhythm. An extensive vagal innervation of the cardiac ventricles and the central origin and extent of this innervation was demonstrated by transynaptic transport of pseudorabies virus with a virulent and two attenuated pseudorabies viral strains. The neurons that innervate the ventricles are numerous, and their distribution within the nucleus ambiguus and dorsal motor nucleus of the vagus is similar to that of neurons innervating other cardiac targets, such as the sino-atrial node. These data provide a neuroanatomical correlate to the physiological influence of the vagus nerve on ventricular function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Standish, A -- Enquist, L W -- Schwaber, J S -- MH-43787/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):232-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neural Computation Group, E. I. DuPont de Nemours & Co., Wilmington, DE 19880-0323.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284675" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Heart Ventricles/*innervation/microbiology ; Herpesvirus 1, Suid/pathogenicity/*physiology ; Interneurons/cytology ; Medulla Oblongata/*anatomy & histology/microbiology ; Motor Neurons/cytology ; Neural Pathways ; Rats ; Rats, Wistar ; Vagus Nerve/*anatomy & histology/microbiology ; Virulence
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  • 28
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    Watching the brain remake itself (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1475-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Fear/physiology ; Humans ; Learning/physiology ; Motor Cortex/physiology ; Nerve Growth Factors/physiology ; Nerve Net/*physiology ; Neural Pathways/physiology ; Neuronal Plasticity/*physiology ; Pain/physiopathology ; Rats ; Synapses/physiology
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  • 29
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    Roles of N-type and Q-type Ca2+ channels in supporting hippocampal synaptic transmission (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: Several types of calcium channels found in the central nervous system are possible participants in triggering neurotransmitter release. Synaptic transmission between hippocampal CA3 and CA1 neurons was mediated by N-type calcium channels, together with calcium channels whose pharmacology differs from that of L- and P-type channels but resembles that of the Q-type channel encoded by the alpha 1A subunit gene. Blockade of either population of channels strongly increased enhancement of synaptic transmission with repetitive stimuli. Even after complete blockade of N-type channels, transmission was strongly modulated by stimulation of neurotransmitter receptors or protein kinase C. These findings suggest a role for alpha 1A subunits in synaptic transmission and support the idea that neurotransmitter release may depend on multiple types of calcium channels under physiological conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, D B -- Randall, A -- Tsien, R W -- MH48108-02/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):107-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Beckman Center for Molecular and Genetic Medicine, Stanford University School of Medicine, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7832825" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects/*physiology ; Hippocampus/drug effects/*physiology ; In Vitro Techniques ; Peptides/pharmacology ; Phorbol 12,13-Dibutyrate/pharmacology ; Protein Kinase C/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholinergic/metabolism ; Receptors, GABA-B/metabolism ; Receptors, Glutamate/metabolism ; Receptors, Purinergic P1/metabolism ; Spider Venoms/pharmacology ; *Synaptic Transmission/drug effects ; omega-Agatoxin IVA ; omega-Conotoxin GVIA ; *omega-Conotoxins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Genetic control of programmed cell death in Drosophila (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: A gene, reaper (rpr), that appears to play a central control function for the initiation of programmed cell death (apoptosis) in Drosophila was identified. Virtually all programmed cell death that normally occurs during Drosophila embryogenesis was blocked in embryos homozygous for a small deletion that includes the reaper gene. Mutant embryos contained many extra cells and failed to hatch, but many other aspects of development appeared quite normal. Deletions that include reaper also protected embryos from apoptosis caused by x-irradiation and developmental defects. However, high doses of x-rays induced some apoptosis in mutant embryos, and the resulting corpses were phagocytosed by macrophages. These data suggest that the basic cell death program is intact although it was not activated in mutant embryos. The DNA encompassed by the deletion was cloned and the reaper gene was identified on the basis of the ability of cloned DNA to restore apoptosis to cell death defective embryos in germ line transformation experiments. The reaper gene appears to encode a small peptide that shows no homology to known proteins, and reaper messenger RNA is expressed in cells destined to undergo apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, K -- Grether, M E -- Abrams, J M -- Young, L -- Farrell, K -- Steller, H -- 5 F32 NS08536/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):677-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Brain and Cognitive Sciences, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171319" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/*genetics ; Base Sequence ; Cloning, Molecular ; DNA Primers ; Drosophila/cytology/embryology/*genetics ; *Drosophila Proteins ; Embryo, Nonmammalian/cytology ; *Genes, Insect ; Models, Genetic ; Molecular Sequence Data ; Mutation ; Nervous System/cytology ; Neurons/cytology ; Peptides/chemistry/*genetics/physiology
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    Neuroscience. To sleep, perchance to ... learn? New studies say yes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):603-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036508" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Learning/*physiology ; Memory/physiology ; Rats ; Sleep/*physiology ; Sleep, REM/physiology
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    p53: a glimpse at the puppet behind the shadow play (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friend, S -- New York, N.Y. -- Science. 1994 Jul 15;265(5170):334-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MGH Cancer Center, Massachusetts General Hospital, Charlestown.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8023155" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallization ; Crystallography, X-Ray ; DNA/metabolism ; Genes, p53 ; Hydrogen Bonding ; Mutation ; *Protein Conformation ; Protein Structure, Secondary ; Tumor Suppressor Protein p53/*chemistry/genetics/metabolism
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    Will molecular data set the stage for a synthesis? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, J -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):758.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303291" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Computer Simulation ; DNA, Mitochondrial/genetics ; HLA Antigens/analysis/genetics ; Humans ; *Molecular Biology ; Turtles/genetics
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    [URE3] as an altered URE2 protein: evidence for a prion analog in Saccharomyces cerevisiae (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-22
    Description: A cytoplasmically inherited element, [URE3], allows yeast to use ureidosuccinate in the presence of ammonium ion. Chromosomal mutations in the URE2 gene produce the same phenotype. [URE3] depends for its propagation on the URE2 product (Ure2p), a negative regulator of enzymes of nitrogen metabolism. Saccharomyces cerevisiae strains cured of [URE3] with guanidium chloride were shown to return to the [URE3]-carrying state without its introduction from other cells. Overproduction of Ure2p increased the frequency with which a strain became [URE3] by 100-fold. In analogy to mammalian prions, [URE3] may be an altered form of Ure2p that is inactive for its normal function but can convert normal Ure2p to the altered form. The genetic evidence presented here suggests that protein-based inheritance, involving a protein unrelated to the mammalian prion protein, can occur in a microorganism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickner, R B -- New York, N.Y. -- Science. 1994 Apr 22;264(5158):566-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7909170" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid/analogs & derivatives/metabolism ; Base Sequence ; Crosses, Genetic ; Fungal Proteins/chemistry/*genetics/metabolism ; Genes, Dominant ; Genes, Fungal ; Genes, Recessive ; Glutathione Peroxidase ; Guanidine ; Guanidines/pharmacology ; Molecular Sequence Data ; Mutation ; Phenotype ; Plasmids ; PrPSc Proteins ; Prions/chemistry/genetics/metabolism ; Saccharomyces cerevisiae/*genetics/metabolism ; *Saccharomyces cerevisiae Proteins
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    Neurotrophic factors enter the clinic (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 May 6;264(5160):772-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171331" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy ; Amyotrophic Lateral Sclerosis/drug therapy ; Animals ; Clinical Trials as Topic ; Humans ; Insulin-Like Growth Factor I/therapeutic use ; Nerve Growth Factors/*therapeutic use ; Nerve Tissue Proteins/*therapeutic use ; Nervous System Diseases/*drug therapy ; Neurons/drug effects ; Parkinson Disease/drug therapy ; Peripheral Nervous System Diseases/drug therapy ; Rats
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    Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    Cell suicide: by ICE, not fire (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):754-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303290" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caenorhabditis elegans/genetics ; Caspase 1 ; Cells, Cultured ; Free Radicals/metabolism ; Metalloendopeptidases/*genetics/metabolism ; Mice ; Mice, Knockout ; Neurons/cytology ; Oxygen/metabolism ; Proto-Oncogene Proteins/genetics/physiology ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; bcl-2-Associated X Protein ; bcl-X Protein
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    Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: In this study, a protein that interacts with sequences encoded by the first exon of the protein kinase Bcr was cloned. The Bcr-associated protein 1 (Bap-1) is a member of the 14-3-3 family of proteins. Bap-1 interacts with full-length c-Bcr and with the chimeric Bcr-Abl tyrosine kinase of Philadelphia chromosome (Ph1)-positive human leukemias. Bap-1 is a substrate for the Bcr serine-threonine kinase and is also phosphorylated on tyrosine by Bcr-Abl but not by c-Abl. Bap-1 may function in the regulation of c-Bcr and may contribute to the transforming activity of Bcr-Abl in vivo. 14-3-3 proteins are essential for cell proliferation and have a role in determining the timing of mitosis in yeast. Through direct binding to sequences present in Bcr and in other proteins implicated in signaling, the mammalian 14-3-3 proteins may link specific signaling protein components to mitogenic and cell-cycle control pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reuther, G W -- Fu, H -- Cripe, L D -- Collier, R J -- Pendergast, A M -- CA61033/CA/NCI NIH HHS/ -- DK01965/DK/NIDDK NIH HHS/ -- GM07184/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):129-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939633" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Animals ; Cell Division ; Cell Line ; Cell Transformation, Neoplastic ; Fusion Proteins, bcr-abl/*metabolism ; Humans ; Mice ; Phosphorylation ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Tyrosine Kinases/*metabolism ; Proteins/isolation & purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcr ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; *Tyrosine 3-Monooxygenase
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    Degeneration of a nonrecombining chromosome (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-01-14
    Description: Comparative studies suggest that sex chromosomes begin as ordinary autosomes that happen to carry a major sex determining locus. Over evolutionary time the Y chromosome is selected to stop recombining with the X chromosome, perhaps in response to accumulation of alleles beneficial to the heterogametic but harmful to the homogametic sex. Population genetic theory predicts that a nonrecombining Y chromosome should degenerate. Here this prediction is tested by application of specific selection pressures to Drosophila melanogaster populations. Results demonstrate the decay of a nonrecombining, nascent Y chromosome and the capacity for recombination to ameliorate such decay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rice, W R -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):230-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Santa Cruz 95064.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8284674" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crosses, Genetic ; Drosophila melanogaster/*genetics/physiology ; Female ; Haplotypes ; Male ; Mutation ; *Recombination, Genetic ; *Y Chromosome
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    Risk from low-dose exposures (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monro, A M -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1141.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogenicity Tests/*statistics & numerical data ; Carcinogens/*administration & dosage/toxicity ; Dose-Response Relationship, Drug ; Female ; Humans ; Male ; Mice ; Mutagenicity Tests ; Neoplasms/*chemically induced ; Rats ; Risk Assessment
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    The Drosophila saxophone gene: a serine-threonine kinase receptor of the TGF-beta superfamily (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-25
    Description: The Drosophila decapentaplegic (dpp) gene encodes a transforming growth factor-beta (TGF-beta)-like protein that plays a key role in several aspects of development. Transduction of the DPP signal was investigated by cloning of serine-threonine kinase transmembrane receptors from Drosophila because this type of receptor is specific for the TGF-beta-like ligands. Here evidence is provided demonstrating that the Drosophila saxophone (sax) gene, a previously identified female sterile locus, encodes a TGF-beta-like type I receptor. Embryos from sax mothers and dpp embryos exhibit similar mutant phenotypes during early gastrulation, and these two loci exhibit genetic interactions, which suggest that they are utilized in the same pathway. These data suggest that sax encodes a receptor for dpp.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, T -- Finelli, A L -- Padgett, R W -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1756-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute, Rutgers University, Piscataway, NJ 08855-0759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134837" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; Drosophila/embryology/*genetics/metabolism ; *Drosophila Proteins ; Embryo, Nonmammalian/metabolism ; Female ; *Genes, Insect ; Insect Hormones/genetics/*metabolism ; Male ; Molecular Sequence Data ; Mutation ; Protein-Serine-Threonine Kinases/chemistry/*genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/*genetics/metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics/*metabolism
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    Arabidopsis ABA response gene ABI1: features of a calcium-modulated protein phosphatase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-03
    Description: The Arabidopsis ABI1 locus is essential for a wide spectrum of abscisic acid (ABA) responses throughout plant development. Here, ABI1 was shown to regulate stomatal aperture in leaves and mitotic activity in root meristems. The ABI1 gene was cloned and predicted to encode a signaling protein. Although its carboxyl-terminal domain is related to serine-threonine phosphatase 2C, the ABI1 protein has a unique amino-terminal extension containing an EF hand calcium-binding site. These results suggest that the ABI1 protein is a Ca(2+)-modulated phosphatase and functions to integrate ABA and Ca2+ signals with phosphorylation-dependent response pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, J -- Bouvier-Durand, M -- Morris, P C -- Guerrier, D -- Chefdor, F -- Giraudat, J -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1448-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut des Sciences Vegetales, Centre National de la Recherche Scientifique UPR 40, Gif-sur-Yvette, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7910981" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Arabidopsis/chemistry/cytology/*genetics/physiology ; *Arabidopsis Proteins ; Calcium/*metabolism ; Cloning, Molecular ; *Genes, Plant ; Mitosis ; Molecular Sequence Data ; Mutation ; Phenotype ; Phosphoprotein Phosphatases/chemistry/*genetics/*metabolism ; Phosphorylation ; Plants, Genetically Modified ; Polymorphism, Restriction Fragment Length ; Signal Transduction ; Transformation, Genetic
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    Stimulation and inhibition of angiogenesis by placental proliferin and proliferin-related protein (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: In many mammalian species, the placenta is the site of synthesis of proteins in the prolactin and growth hormone family. Analysis of two such proteins, proliferin (PLF) and proliferin-related protein (PRP), revealed that they are potent regulators of angiogenesis; PLF stimulated and PRP inhibited endothelial cell migration in cell culture and neovascularization in vivo. The mouse placenta secretes an angiogenic activity during the middle of pregnancy that corresponds primarily to PLF, but later in gestation releases a factor that inhibits angiogenesis, which was identified as PRP. Incubation of placental tissue with PLF led to the specific binding of this hormone to capillary endothelial cells. Thus PLF and PRP may regulate the initiation and then the cessation of placental neovascularization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, D -- Volpert, O V -- Bouck, N -- Linzer, D I -- CA52750/CA/NCI NIH HHS/ -- HD24518/HD/NICHD NIH HHS/ -- HD29962/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1581-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cell Movement/drug effects ; Cornea/blood supply ; Culture Techniques ; Endothelium, Vascular/*cytology/drug effects/metabolism ; Female ; Fibroblast Growth Factor 2/pharmacology ; Glycoproteins/metabolism/*pharmacology ; Growth Substances/metabolism/*pharmacology ; Intercellular Signaling Peptides and Proteins ; *Neovascularization, Pathologic ; Placenta/*blood supply ; Pregnancy ; Pregnancy Proteins/*pharmacology ; Rats
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    Sequential interactions of the TCR with two distinct cytoplasmic tyrosine kinases (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: The T cell antigen receptor (TCR) initiates signals by interacting with cytoplasmic protein tyrosine kinases (PTKs) through a 17-residue sequence motif [called the antigen recognition activation motif (ARAM)] that is contained in the TCR zeta and CD3 chains. TCR stimulation induces the tyrosine phosphorylation of several cellular substrates, including the ARAMs. Lck kinase activity is required for phosphorylation of two conserved tyrosine residues in an ARAM. This phosphorylation leads to the recruitment of a second cytoplasmic PTK, ZAP-70, through both of the ZAP-70 Src homology 2 domains and its phosphorylation. Thus, TCR signal transduction is initiated by the sequential interaction of two PTKs with TCR ARAMs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iwashima, M -- Irving, B A -- van Oers, N S -- Chan, A C -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1136-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7509083" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD8/metabolism ; Cell Line ; Cytoplasm/enzymology ; Haplorhini ; Humans ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) ; Membrane Proteins/*metabolism ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Phosphotyrosine ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Signal Transduction ; Tumor Cells, Cultured ; Tyrosine/analogs & derivatives/metabolism ; ZAP-70 Protein-Tyrosine Kinase
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  • 45
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    A designed peptide ligase for total synthesis of ribonuclease A with unnatural catalytic residues (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: An engineered variant of subtilisin BPN', termed subtiligase, which efficiently ligates esterified peptides in aqueous solution, was used for the complete synthesis of ribonuclease (RNase) A that contains unnatural catalytic residues. Fully active RNase A (124 residues long) was produced in milligram quantities by stepwise ligation of six esterified peptide fragments (each 12 to 30 residues long) at yields averaging 70 percent per ligation. Variants of RNase A were produced in which the catalytic histidines at positions 12 and 119 were substituted with the unnatural amino acid 4-fluorohistidine, which has a pKa of 3.5 compared to 6.8 for histidine. Large changes in the profile of the pH as it affects rate occurred for the single and double mutants with surprisingly little change in the kcat for either the RNA cleavage or hydrolysis steps. The data indicate that these imidazoles function as general acids and bases, but that the proton transfer steps are not rate-limiting when the imidazoles are present in their correct protonation states. These studies indicate the potential of subtiligase for the blockwise synthesis of large proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, D Y -- Burnier, J -- Quan, C -- Stanley, M -- Tom, J -- Wells, J A -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):243-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Protein Engineering, Genentech, Inc., South San Francisco, CA 94080.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939659" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Esterification ; Histidine/analogs & derivatives/analysis ; Hydrogen-Ion Concentration ; Molecular Sequence Data ; Mutation ; Nucleotides, Cyclic/metabolism ; Protein Engineering/*methods ; Ribonuclease, Pancreatic/*chemical synthesis/chemistry/isolation & purification ; Subtilisins/chemistry/genetics/*metabolism ; Uridine Monophosphate/metabolism
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  • 46
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    Two identical noninteracting sites in an ion channel revealed by proton transfer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: The functional consequences of single proton transfers occurring in the pore of a cyclic nucleotide-gated channel were observed with patch recording techniques. These results led to three conclusions about the chemical nature of ion binding sites in the conduction pathway: The channel contains two identical titratable sites, even though there are more than two (probably four) identical subunits; the sites are formed by glutamate residues that have a pKa (where K(a) is the acid constant) of 7.6; and protonation of one site does not perturb the pKa of the other. These properties point to an unusual arrangement of carboxyl side-chain residues in the pore of a cation channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Root, M J -- MacKinnon, R -- 5 T32 GM083113/GM/NIGMS NIH HHS/ -- GM47400/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1852-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522344" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Calcium Channels/metabolism ; Catfishes ; Electric Conductivity ; Hydrogen-Ion Concentration ; Ion Channel Gating ; Ion Channels/chemistry/genetics/*metabolism ; Kinetics ; Molecular Sequence Data ; Mutation ; *Protons ; Sodium/metabolism ; Xenopus
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  • 47
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    A molecular determinant for submillisecond desensitization in glutamate receptors (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: The decay of excitatory postsynaptic currents in central neurons mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors is likely to be shaped either by receptor desensitization or by offset after removal of glutamate from the synaptic cleft. Native AMPA receptors show desensitization time constants of 1 to about 10 milliseconds, but the underlying molecular determinants of these large differences are unknown. Cloned AMPA receptors carrying the "flop" splice variants of glutamate receptor subtype C (GluR-C) and GluR-D are shown to have desensitization time constants of around 1 millisecond, whereas those with the "flip" variants are about four times slower. Cerebellar granule cells switch their expression of GluR-D splice variants from mostly flip forms in early stages to predominantly flop forms in the adult rat brain. These findings suggest that rapid desensitization of AMPA receptors can be regulated by the expression and alternative splicing of GluR-D gene transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosbacher, J -- Schoepfer, R -- Monyer, H -- Burnashev, N -- Seeburg, P H -- Ruppersberg, J P -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1059-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur medizinische Forschung, Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973663" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; Cerebellum/cytology/metabolism ; Cloning, Molecular ; Glutamic Acid/*pharmacology ; In Situ Hybridization ; Oocytes ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/drug effects/genetics/*physiology ; Recombinant Proteins ; Synaptic Transmission ; Xenopus laevis
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  • 48
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    Calcineurin inhibition of dynamin I GTPase activity coupled to nerve terminal depolarization (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: Dynamin I is a nerve terminal phosphoprotein with intrinsic guanosine triphosphatase (GTPase) activity that is required for endocytosis. Upon depolarization and synaptic vesicle recycling, dynamin I undergoes a rapid dephosphorylation. Dynamin I was found to be a specific high-affinity substrate for calcineurin in vitro. At low concentrations, calcineurin dephosphorylated dynamin I that had been phosphorylated by protein kinase C. The dephosphorylation inhibited dynamin I GTPase activity in vitro and after depolarization of nerve terminals. The effect in nerve terminals was prevented by the calcineurin inhibitor cyclosporin A. This suggests that in nerve terminals, calcineurin serves as a Ca(2+)-sensitive switch for depolarization-evoked synaptic vesicle recycling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, J P -- Sim, A T -- Robinson, P J -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):970-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Unit, John Hunter Hospital, NSW, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052858" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin ; Calcium/metabolism ; Calmodulin-Binding Proteins/metabolism/*pharmacology ; Cyclosporine/pharmacology ; Dynamin I ; Dynamins ; Endocytosis ; GTP Phosphohydrolases/*antagonists & inhibitors/metabolism ; Nerve Endings/enzymology/*metabolism ; Phosphoprotein Phosphatases/metabolism/*pharmacology ; Phosphorylation ; Rats ; Synaptic Vesicles/*metabolism ; Synaptosomes/enzymology/*metabolism
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  • 49
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    Nitric oxide activation of poly(ADP-ribose) synthetase in neurotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Poly(adenosine 5'-diphosphoribose) synthetase (PARS) is a nuclear enzyme which, when activated by DNA strand breaks, adds up to 100 adenosine 5'-diphosphoribose (ADP-ribose) units to nuclear proteins such as histones and PARS itself. This activation can lead to cell death through depletion of beta-nicotinamide adenine dinucleotide (the source of ADP-ribose) and adenosine triphosphate. Nitric oxide (NO) stimulated ADP-ribosylation of PARS in rat brain. Benzamide and other derivatives, which inhibit PARS, blocked N-methyl-D-aspartate- and NO-mediated neurotoxicity with relative potencies paralleling their ability to inhibit PARS. Thus, NO appeared to elicit neurotoxicity by activating PARS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, J -- Dawson, V L -- Dawson, T M -- Snyder, S H -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- DA-271-90-7408/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8080500" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/pharmacology ; Brain/cytology/drug effects/enzymology ; Cell Death/drug effects ; Cell Line ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/enzymology ; DNA Damage ; Enzyme Activation ; Humans ; N-Methylaspartate/*toxicity ; Neurons/cytology/*drug effects/enzymology ; Nitric Oxide/*toxicity ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly(ADP-ribose) Polymerases/*metabolism ; Rats ; Rats, Sprague-Dawley
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  • 50
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    Functional role of type I and type II interferons in antiviral defense (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: Mice lacking the known subunit of the type I interferon (IFN) receptor were completely unresponsive to type I IFNs, suggesting that this receptor chain is essential for type I IFN-mediated signal transduction. These mice showed no overt anomalies but were unable to cope with viral infections, despite otherwise normal immune responses. Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, U -- Steinhoff, U -- Reis, L F -- Hemmi, S -- Pavlovic, J -- Zinkernagel, R M -- Aguet, M -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1918-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Biology I, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009221" target="_blank"〉PubMed〈/a〉
    Keywords: Alphavirus Infections/immunology ; Animals ; Antibodies, Viral/biosynthesis ; Disease Susceptibility ; Immunity, Innate ; Interferon Type I/*physiology ; Interferon-gamma/*physiology ; Lymphocytic Choriomeningitis/immunology ; Membrane Proteins ; Mice ; Mutation ; Receptor, Interferon alpha-beta ; Receptors, Interferon/genetics/*physiology ; Rhabdoviridae Infections/immunology ; Semliki forest virus ; Signal Transduction ; T-Lymphocytes/immunology ; Vesicular stomatitis Indiana virus ; Virus Diseases/*immunology
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    Visualization of quantal synaptic transmission by dendritic calcium imaging (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: As changes in synaptic strength are thought to be critical for learning and memory, it would be useful to monitor the activity of individual identified synapses on mammalian central neurons. Calcium imaging of cortical neurons grown in primary culture was used to visualize the activation of individual postsynaptic elements by miniature excitatory synaptic currents elicited by spontaneous quantal release. This approach revealed that the probability of spontaneous activity differed among synapses on the same dendrite. Furthermore, synapses that undergo changes in activity induced by glutamate or phorbol ester treatment were identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, T H -- Baraban, J M -- Wier, W G -- Blatter, L A -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):529-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7904774" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Cells, Cultured ; Cerebral Cortex ; Dendrites/*metabolism ; Glutamates/pharmacology ; Glutamic Acid ; Kinetics ; Microelectrodes ; Neuronal Plasticity ; Neurons/*physiology ; Phorbol Esters/pharmacology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/*physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
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  • 52
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    Correction of lethal intestinal defect in a mouse model of cystic fibrosis by human CFTR (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-12-09
    Description: Cystic fibrosis (CF) is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). A potential animal model of CF, the CFTR-/- mouse, has had limited utility because most mice die from intestinal obstruction during the first month of life. Human CFTR (hCFTR) was expressed in CFTR-/- mice under the control of the rat intestinal fatty acid-binding protein gene promoter. The mice survived and showed functional correction of ileal goblet cell and crypt cell hyperplasia and cyclic adenosine monophosphate-stimulated chloride secretion. These results support the concept that transfer of the hCFTR gene may be a useful strategy for correcting physiologic defects in patients with CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, L -- Dey, C R -- Wert, S E -- DuVall, M D -- Frizzell, R A -- Whitsett, J A -- DK38518/DK/NIDDK NIH HHS/ -- HL49004/HL/NHLBI NIH HHS/ -- HL51832/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1705-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, OH 45229-3039.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527588" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Carrier Proteins/genetics ; Chlorides/metabolism ; Colforsin/pharmacology ; Colon/chemistry/pathology ; Cystic Fibrosis/genetics/metabolism/pathology/*therapy ; Cystic Fibrosis Transmembrane Conductance Regulator ; Disease Models, Animal ; Fatty Acid-Binding Proteins ; Gene Expression ; *Genetic Therapy ; Humans ; Intestinal Mucosa/chemistry/*pathology/secretion ; Intestine, Small/chemistry/pathology ; Membrane Proteins/analysis/*genetics/physiology ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neoplasm Proteins ; *Nerve Tissue Proteins ; Promoter Regions, Genetic ; RNA, Messenger/analysis/genetics ; Rats ; Recombinant Proteins/biosynthesis ; *Tumor Suppressor Proteins
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  • 53
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    Interaction of IL-2R beta and gamma c chains with Jak1 and Jak3: implications for XSCID and XCID (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-11
    Description: Interleukin-2 (IL-2) signaling requires the dimerization of the IL-2 receptor beta.(IL-2R beta) and common gamma (gamma c) chains. Mutations of gamma c can result in X-linked severe combined immunodeficiency (XSCID). IL-2, IL-4, IL-7 (whose receptors are known to contain gamma c), and IL-9 (whose receptor is shown here to contain gamma c) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3. Jak1 and Jak3 associated with IL-2R beta and gamma c, respectively; IL-2 induced Jak3-IL-2R beta and increased Jak3-gamma c associations. Truncations of gamma c, and a gamma c, point mutation causing moderate X-linked combined immunodeficiency (XCID), decreased gamma c-Jak3 association. Thus, gamma c mutations in at least some XSCID and XCID patients prevent normal Jak3 activation, suggesting that mutations of Jak3 may result in an XSCID-like phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Johnston, J A -- Noguchi, M -- Kawamura, M -- Bacon, C M -- Friedmann, M -- Berg, M -- McVicar, D W -- Witthuhn, B A -- Silvennoinen, O -- P30 CA21765/CA/NCI NIH HHS/ -- R01 DK42932/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):1042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973658" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Enzyme Activation ; Humans ; Interleukin-2/pharmacology ; Janus Kinase 1 ; Janus Kinase 3 ; Mutation ; Phosphorylation ; Point Mutation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Interleukin-2/genetics/*metabolism ; Severe Combined Immunodeficiency/genetics/*immunology/metabolism ; Transfection ; Tyrosine/metabolism
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    Rewriting--and redating--prehistory (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1087-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108724" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Biological Evolution ; *Fossils ; History, Ancient ; *Hominidae ; Humans ; Indonesia
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  • 55
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    Control of kinetic properties of AMPA receptor channels by nuclear RNA editing (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-12-09
    Description: AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor channels mediate the fast component of excitatory postsynaptic currents in the central nervous system. Site-selective nuclear RNA editing controls the calcium permeability of these channels, and RNA editing at a second site is shown here to affect the kinetic aspects of these channels in rat brain. In three of the four AMPA receptor subunits (GluR-B, -C, and -D), intronic elements determine a codon switch (AGA, arginine, to GGA, glycine) in the primary transcripts in a position termed the R/G site, which immediately precedes the alternatively spliced modules "flip" and "flop." The extent of editing at this site progresses with brain development in a manner specific for subunit and splice form, and edited channels possess faster recovery rates from desensitization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lomeli, H -- Mosbacher, J -- Melcher, T -- Hoger, T -- Geiger, J R -- Kuner, T -- Monyer, H -- Higuchi, M -- Bach, A -- Seeburg, P H -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1709-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7992055" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Animals ; Base Sequence ; Brain/embryology/*metabolism ; Cell Nucleus/metabolism ; Exons ; Glutamic Acid/pharmacology ; Glycine/genetics ; Introns ; Kinetics ; Membrane Potentials ; Molecular Sequence Data ; Oocytes ; PC12 Cells ; Patch-Clamp Techniques ; *RNA Editing ; Rats ; Rats, Wistar ; Receptors, AMPA/*genetics/*metabolism ; Recombinant Proteins/metabolism ; Xenopus
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  • 56
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    Direct signaling from astrocytes to neurons in cultures of mammalian brain cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-25
    Description: Although astrocytes have been considered to be supportive, rather than transmissive, in the adult nervous system, recent studies have challenged this assumption by demonstrating that astrocytes possess functional neurotransmitter receptors. Astrocytes are now shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons. When a focal electric field potential was applied to single astrocytes in mixed cultures of rat forebrain astrocytes and neurons, a prompt elevation of calcium occurred in the target cell. This in turn triggered a wave of calcium increase, which propagated from astrocyte to astrocyte. Neurons resting on these astrocytes responded with large increases in their concentration of cytosolic calcium. The gap junction blocker octanol attenuated the neuronal response, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically. This neuronal response to local astrocytic stimulation may mediate local intercellular communication within the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, M -- New York, N.Y. -- Science. 1994 Mar 25;263(5154):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8134839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/drug effects/*metabolism ; Calcium/*metabolism ; Cell Communication ; Cells, Cultured ; Electric Stimulation ; Excitatory Amino Acid Antagonists ; Gap Junctions/physiology ; Kynurenic Acid/pharmacology ; Neurons/drug effects/*metabolism ; Nifedipine/pharmacology ; Octanols/pharmacology ; Prosencephalon/*cytology/embryology ; Rats ; *Signal Transduction ; Synapses/metabolism ; Tetrodotoxin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Age of the earliest known hominids in Java, Indonesia (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-02-25
    Description: 40Ar/39Ar laser-incremental heating of hornblende separated from pumice recovered at two hominid sites in Java, Indonesia, has yielded well-defined plateaus with weighted mean ages of 1.81 +/- 0.04 and 1.66 +/- 0.04 million years ago (Ma). The hominid fossils, a juvenile calvaria of Pithecanthropus and a partial face and cranial fragments of Meganthropus, commonly considered part of the Asian Homo erectus hypodigm, are at least 0.6 million years older than fossils referred to as Homo erectus (OH-9) from Olduvai Gorge, Tanzania, and comparable in age with the oldest Koobi Fora Homo cf. erectus (Homo ergaster) in Kenya. These ages lend further credence to the view that Homo erectus may have evolved outside of Africa. If the ancestor of Homo erectus ventured out of Africa before 1.8 Ma, the dispersal would have predated the advent of the Acheulean culture at 1.4 Ma, possibly explaining the absence of these characteristic stone cleavers and hand axes in East Asia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swisher, C C 3rd -- Curtis, G H -- Jacob, T -- Getty, A G -- Suprijo, A -- Widiasmoro -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geochronology Center, Institute of Human Origins, Berkeley, CA 94709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108729" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; *Biological Evolution ; *Fossils ; History, Ancient ; *Hominidae ; Humans ; Indonesia
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    Colon cancer screening (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danks, D M -- New York, N.Y. -- Science. 1994 Apr 1;264(5155):13-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8140413" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, Pair 2 ; Colorectal Neoplasms, Hereditary Nonpolyposis/*diagnosis/genetics ; *Genetic Testing ; Humans ; Mutation
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    Requirement of a critical period of transcription for induction of a late phase of LTP (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-08-19
    Description: Repeated high-frequency trains of stimuli induce long-term potentiation (LTP) in the CA1 region that persists for up to 8 hours in hippocampal slices and for days in intact animals. This long time course has made LTP an attractive model for certain forms of long-term memory in the mammalian brain. A hallmark of long-term memory in the intact animal is a requirement for transcription, and thus whether the late phase of LTP (L-LTP) requires transcription was investigated here. With the use of different inhibitors, it was found in rat hippocampal slices that the induction of L-LTP [produced either by tetanic stimulation or by application of the cyclic adenosine monophosphate (cAMP) analog Sp-cAMPS (Sp-cyclic adenosine 3',5'-monophosphorothioate)] was selectively prevented when transcription was blocked immediately after tetanization or during application of cAMP. As with behavioral memory, this requirement for transcription had a critical time window. Thus, the late phase of LTP in the CA1 region requires transcription during a critical period, perhaps because cAMP-inducible genes must be expressed during this period.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nguyen, P V -- Abel, T -- Kandel, E R -- GM32099/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1104-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, New York, NY.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8066450" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/analogs & derivatives/metabolism/pharmacology ; Dactinomycin/pharmacology ; Dichlororibofuranosylbenzimidazole/pharmacology ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Pyramidal Cells/metabolism ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; *Transcription, Genetic/drug effects
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    Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-22
    Description: Two molecular mechanisms of T cell-mediated cytotoxicity, one perforin-based, the other Fas-based, have been demonstrated. To determine the extent of their contribution to T cell-mediated cytotoxicity, a range of effector cells from normal control or perforin-deficient mice were tested against a panel of target cells with various levels of Fas expression. All cytotoxicity observed was due to either of these mechanisms, and no third mechanism was detected. Thus, the perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kagi, D -- Vignaux, F -- Ledermann, B -- Burki, K -- Depraetere, V -- Nagata, S -- Hengartner, H -- Golstein, P -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):528-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518614" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, CD95 ; Antigens, Surface/*immunology ; Cells, Cultured ; Concanavalin A/pharmacology ; *Cytotoxicity, Immunologic ; Ionomycin/pharmacology ; Leukemia L1210 ; Lymphocyte Culture Test, Mixed ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Cells, Cultured
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    Enhanced aggressive behavior in mice lacking 5-HT1B receptor (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-09-23
    Description: The neuromodulator serotonin (5-hydroxytryptamine, 5-HT) has been associated with mood disorders such as depression, anxiety, and impulsive violence. To define the contribution of 5-HT receptor subtypes to behavior, mutant mice lacking the 5-HT1B receptor were generated by homologous recombination. These mice did not exhibit any obvious developmental or behavioral defects. However, the hyperlocomotor effect of the 5-HT1A/1B agonist RU24969 was absent in mutant mice, indicating that this effect is mediated by 5-HT1B receptors. Moreover, when confronted with an intruder, mutant mice attacked the intruder faster and more intensely than did wild-type mice, suggesting the participation of 5-HT1B receptors in aggressive behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saudou, F -- Amara, D A -- Dierich, A -- LeMeur, M -- Ramboz, S -- Segu, L -- Buhot, M C -- Hen, R -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1875-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, U184 de l'INSERM, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091214" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*physiology ; Animals ; Brain Chemistry ; Chimera ; Female ; Indoles/pharmacology ; Male ; Mice ; Motor Activity/drug effects ; Mutation ; Pindolol/analogs & derivatives/metabolism ; Receptor, Serotonin, 5-HT1B ; Receptors, Serotonin/analysis/genetics/*physiology ; Recombination, Genetic ; Serotonin Receptor Agonists/pharmacology
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    p53 status and the efficacy of cancer therapy in vivo (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-04
    Description: The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowe, S W -- Bodis, S -- McClatchey, A -- Remington, L -- Ruley, H E -- Fisher, D E -- Housman, D E -- Jacks, T -- 5R27CA17575/CA/NCI NIH HHS/ -- CA14051/CA/NCI NIH HHS/ -- R01CA40602/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):807-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Doxorubicin/*therapeutic use ; Drug Resistance ; Fibrosarcoma/drug therapy/*genetics/radiotherapy/*therapy ; *Gamma Rays ; *Genes, p53/genetics ; Immunocompromised Host ; Mice ; Mice, Nude ; Mutation ; Neoplasm Recurrence, Local ; Neoplasm Transplantation ; Radiation Tolerance
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    Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-03
    Description: Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darnell, J E Jr -- Kerr, I M -- Stark, G R -- New York, N.Y. -- Science. 1994 Jun 3;264(5164):1415-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8197455" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; DNA-Binding Proteins/*metabolism ; Genes ; Genetic Complementation Test ; Humans ; Interferon-Stimulated Gene Factor 3 ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; Interferon-alpha/*pharmacology ; Interferon-gamma/*pharmacology ; Molecular Sequence Data ; Mutation ; Protein-Tyrosine Kinases/metabolism ; Regulatory Sequences, Nucleic Acid ; *Signal Transduction ; Transcription Factors/*metabolism ; *Transcriptional Activation
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    Crystal structure of rat DNA polymerase beta: evidence for a common polymerase mechanism (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-24
    Description: Structures of the 31-kilodalton catalytic domain of rat DNA polymerase beta (pol beta) and the whole 39-kilodalton enzyme were determined at 2.3 and 3.6 angstrom resolution, respectively. The 31-kilodalton domain is composed of fingers, palm, and thumb subdomains arranged to form a DNA binding channel reminiscent of the polymerase domains of the Klenow fragment of Escherichia coli DNA polymerase I, HIV-1 reverse transcriptase, and bacteriophage T7 RNA polymerase. The amino-terminal 8-kilodalton domain is attached to the fingers subdomain by a flexible hinge. The two invariant aspartates found in all polymerase sequences and implicated in catalytic activity have the same geometric arrangement within structurally similar but topologically distinct palms, indicating that the polymerases have maintained, or possibly re-evolved, a common nucleotidyl transfer mechanism. The location of Mn2+ and deoxyadenosine triphosphate in pol beta confirms the role of the invariant aspartates in metal ion and deoxynucleoside triphosphate binding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawaya, M R -- Pelletier, H -- Kumar, A -- Wilson, S H -- Kraut, J -- CA17374/CA/NCI NIH HHS/ -- ES06839/ES/NIEHS NIH HHS/ -- GM10928/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1930-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, San Diego 92093-0317.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7516581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cloning, Molecular ; Crystallization ; Crystallography, X-Ray ; DNA/metabolism ; DNA Polymerase I/*chemistry/metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxyadenine Nucleotides/chemistry/metabolism ; Deoxycytosine Nucleotides/chemistry/metabolism ; Dideoxynucleotides ; HIV Reverse Transcriptase ; Protein Folding ; Protein Structure, Secondary ; RNA-Directed DNA Polymerase/chemistry/metabolism ; Rats ; Recombinant Proteins/chemistry ; Viral Proteins
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    Modulation of epithelial cell growth by intraepithelial gamma delta T cells (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-11-18
    Description: The role played in immune surveillance by gamma delta T cells residing in various epithelia has not been clear. It is shown here that activated gamma delta T cells obtained from skin and intestine express the epithelial cell mitogen keratinocyte growth factor (KGF). In contrast, intraepithelial alpha beta T cells, as well as all lymphoid alpha beta and gamma delta T cell populations tested, did not produce KGF or promote the growth of cultured epithelial cells. These results suggest that intraepithelial gamma delta T cells function in surveillance and in repair of damaged epithelial tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boismenu, R -- Havran, W L -- AI32751/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1994 Nov 18;266(5188):1253-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Division ; Cell Line ; Cells, Cultured ; Cloning, Molecular ; Dendritic Cells/*physiology ; Epithelial Cells ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; *Fibroblast Growth Factors ; Growth Substances/*biosynthesis/genetics ; Keratinocytes/*cytology ; Lymphocyte Activation ; Mice ; Molecular Sequence Data ; *Receptors, Antigen, T-Cell, gamma-delta ; T-Lymphocyte Subsets/immunology/metabolism/*physiology
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    Regulation of melanin biosynthesis in the human epidermis by tetrahydrobiopterin (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-03-11
    Description: The participation of (6R) 5,6,7,8-tetrahydrobiopterin (6-BH4) in regulating the tyrosine supply for melanin biosynthesis was investigated by the examination of human keratinocytes, melanocytes, and epidermal suction blisters from normal human skin and from patients with the depigmentation disorder vitiligo. Cells, as well as total epidermis, contained high phenylalanine hydroxylase activities and also displayed the capacity to synthesize and recycle 6-BH4, the essential cofactor for this enzyme. In vitiligo, 4a-hydroxy-BH4 dehydratase activity was extremely low or absent, yielding an accumulation of the nonenzymatic by-product 7-tetrahydrobiopterin (7-BH4) at concentrations up to 8 x 10(-6) M in the epidermis. This by-product is a potent competitive inhibitor in the phenylalanine hydroxylase reaction with an inhibition constant of 10(-6) M. Thus, 6-BH4 seems to control melanin biosynthesis in the human epidermis, whereas 7-BH4 may initiate depigmentation in patients with vitiligo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schallreuter, K U -- Wood, J M -- Pittelkow, M R -- Gutlich, M -- Lemke, K R -- Rodl, W -- Swanson, N N -- Hitzemann, K -- Ziegler, I -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1444-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Hamburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128228" target="_blank"〉PubMed〈/a〉
    Keywords: Biopterin/*analogs & derivatives/biosynthesis/metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Epidermis/*metabolism ; GTP Cyclohydrolase/metabolism ; Humans ; Keratinocytes/metabolism ; Melanins/*biosynthesis ; Melanocytes/metabolism ; Phenylalanine Hydroxylase/antagonists & inhibitors/metabolism ; Tyrosine/biosynthesis ; Vitiligo/*metabolism
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    Padlock probes: circularizing oligonucleotides for localized DNA detection (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-09-30
    Description: Nucleotide sequence information derived from DNA segments of the human and other genomes is accumulating rapidly. However, it frequently proves difficult to use such short DNA segments to identify clones in genomic libraries or fragments in blots of the whole genome or for in situ analysis of chromosomes. Oligonucleotide probes, consisting of two target-complementary segments, connected by a linker sequence, were designed. Upon recognition of the specific nucleic acid molecule the ends of the probes were joined through the action of a ligase, creating circular DNA molecules catenated to the target sequence. These probes thus provide highly specific detection with minimal background.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nilsson, M -- Malmgren, H -- Samiotaki, M -- Kwiatkowski, M -- Chowdhary, B P -- Landegren, U -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2085-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beijer Laboratory, Department of Medical Genetics, Biomedical Center, Uppsala, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7522346" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cells, Cultured ; Chromosomes, Human, Pair 12 ; Cystic Fibrosis Transmembrane Conductance Regulator ; DNA/*analysis ; DNA, Circular/*analysis ; Genetic Vectors ; Humans ; In Situ Hybridization ; Lymphocytes ; Membrane Proteins/genetics ; Models, Molecular ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Oligonucleotide Probes/chemistry ; Repetitive Sequences, Nucleic Acid ; Templates, Genetic
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    Digenic retinitis pigmentosa due to mutations at the unlinked peripherin/RDS and ROM1 loci (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-06-10
    Description: In spite of recent advances in identifying genes causing monogenic human disease, very little is known about the genes involved in polygenic disease. Three families were identified with mutations in the unlinked photoreceptor-specific genes ROM1 and peripherin/RDS, in which only double heterozygotes develop retinitis pigmentosa (RP). These findings indicate that the allelic and nonallelic heterogeneity known to be a feature of monogenic RP is complicated further by interactions between unlinked mutations causing digenic RP. Recognition of the inheritance pattern exemplified by these three families might facilitate the identification of other examples of digenic inheritance in human disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kajiwara, K -- Berson, E L -- Dryja, T P -- EY00169/EY/NEI NIH HHS/ -- EY08683/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1604-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman-Gund Laboratory for the Study of Retinal Degenerations, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202715" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Base Sequence ; Electroretinography ; Eye Proteins/chemistry/*genetics ; Female ; Genes, Dominant ; Genes, Recessive ; Genetic Linkage ; Heterozygote ; Humans ; Intermediate Filament Proteins/chemistry/*genetics ; Male ; *Membrane Glycoproteins ; Membrane Proteins/chemistry/*genetics ; Molecular Sequence Data ; Mutation ; *Nerve Tissue Proteins ; Pedigree ; Peripherins ; Retinitis Pigmentosa/*genetics ; Rod Cell Outer Segment/chemistry ; Tetraspanins
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    Gem: an induced, immediate early protein belonging to the Ras family (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-07-08
    Description: A gene encoding a 35-kilodalton guanosine triphosphate (GTP)-binding protein, Gem, was cloned from mitogen-induced human peripheral blood T cells. Gem and Rad, the product of a gene overexpressed in skeletal muscle in individuals with Type II diabetes, constitute a new family of Ras-related GTP-binding proteins. The distinct structural features of this family include the G3 GTP-binding motif, extensive amino- and carboxyl-terminal extensions beyond the Ras-related domain, and a motif that determines membrane association. Gem was transiently expressed in human peripheral blood T cells in response to mitogenic stimulation; the protein was phosphorylated on tyrosine residues and localized to the cytosolic face of the plasma membrane. Deregulated Gem expression prevented proliferation of normal and transformed 3T3 cells. These results suggest that Gem is a regulatory protein, possibly participating in receptor-mediated signal transduction at the plasma membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maguire, J -- Santoro, T -- Jensen, P -- Siebenlist, U -- Yewdell, J -- Kelly, K -- New York, N.Y. -- Science. 1994 Jul 8;265(5169):241-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7912851" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CD4-Positive T-Lymphocytes/metabolism ; Cell Death ; Cell Division ; Cell Line ; Cell Line, Transformed ; Cell Membrane/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Genes, ras ; Guanosine Triphosphate/metabolism ; Humans ; Immediate-Early Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; *Monomeric GTP-Binding Proteins ; Mutation ; RNA, Messenger/genetics/metabolism ; Transfection ; *ras Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The sex determination process in maize (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-02
    Description: Maize partitions the sexes into different flowers on the plant, a condition called monoecy, which facilitates outcrossing. Sex determination in maize is a complex process involving an interplay between genetic determinants, the environment, and hormones. Unisexuality of flowers is achieved by the process of selective arrest and abortion of the inappropriate organ primordia within a bisexual floral meristem. Floral organ abortion is associated with the degeneration of cells within an immature primordia. Masculinizing genes are required for gynoecial abortion, feminizing genes arrest stamen development, and both types also control secondary sexual traits involving morphological characteristics of floral tissues. Gibberellins, steroid-like plant hormones, appear to play a pivotal role in the stamen abortion process and the feminization of floral tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellaporta, S L -- Calderon-Urrea, A -- GM38148/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 2;266(5190):1501-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Yale University, New Haven, CT 06520-8104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7985019" target="_blank"〉PubMed〈/a〉
    Keywords: *Genes, Plant ; Gibberellins/biosynthesis/metabolism ; Models, Biological ; Mutation ; Zea mays/*genetics/*growth & development
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    Cloning of a T cell growth factor that interacts with the beta chain of the interleukin-2 receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: A cytokine was identified that stimulated the proliferation of T lymphocytes, and a complementary DNA clone encoding this new T cell growth factor was isolated. The cytokine, designated interleukin-15 (IL-15), is produced by a wide variety of cells and tissues and shares many biological properties with IL-2. Monoclonal antibodies to the beta chain of the IL-2 receptor inhibited the biological activity of IL-15, and IL-15 competed for binding with IL-2, indicating that IL-15 uses components of the IL-2 receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grabstein, K H -- Eisenman, J -- Shanebeck, K -- Rauch, C -- Srinivasan, S -- Fung, V -- Beers, C -- Richardson, J -- Schoenborn, M A -- Ahdieh, M -- New York, N.Y. -- Science. 1994 May 13;264(5161):965-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunex Research and Development Corporation, Seattle, WA 98101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178155" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; *Cloning, Molecular ; Haplorhini ; Humans ; Interleukin-15 ; Interleukin-2/immunology/metabolism/pharmacology ; Interleukins/chemistry/*genetics/metabolism/pharmacology ; Killer Cells, Lymphokine-Activated/immunology ; Leukocytes, Mononuclear/immunology/metabolism ; Lymphocyte Activation ; Lymphocyte Culture Test, Mixed ; Molecular Sequence Data ; Protein Structure, Secondary ; Receptors, Interleukin-2/immunology/*metabolism ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology
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    Resetting the biological clock: mediation of nocturnal circadian shifts by glutamate and NO (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-12-09
    Description: Circadian rhythms of mammals are timed by an endogenous clock with a period of about 24 hours located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Light synchronizes this clock to the external environment by daily adjustments in the phase of the circadian oscillation. The mechanism has been thought to involve the release of excitatory amino acids from retinal afferents to the SCN. Brief treatment of rat SCN in vitro with glutamate (Glu), N-methyl-D-aspartate (NMDA), or nitric oxide (NO) generators produced lightlike phase shifts of circadian rhythms. The SCN exhibited calcium-dependent nitric oxide synthase (NOS) activity. Antagonists of NMDA or NOS pathways blocked Glu effects in vitro, and intracerebroventricular injection of a NOS inhibitor in vivo blocked the light-induced resetting of behavioral rhythms. Together, these data indicate that Glu release, NMDA receptor activation, NOS stimulation, and NO production link light activation of the retina to cellular changes within the SCN mediating the phase resetting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, J M -- Chen, D -- Weber, E T -- Faiman, L E -- Rea, M A -- Gillette, M U -- NS22155/NS/NINDS NIH HHS/ -- R01 NS022155/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Dec 9;266(5191):1713-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Structural Biology, University of Illinois, Urbana 61801.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7527589" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/metabolism ; Animals ; Arginine/analogs & derivatives/pharmacology ; Biological Clocks/drug effects/*physiology ; Circadian Rhythm/drug effects/*physiology ; Glutamic Acid/*metabolism/pharmacology ; In Vitro Techniques ; Light ; N-Methylaspartate/pharmacology ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent/physiology ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Rats ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Retina/physiology ; Signal Transduction ; Suprachiasmatic Nucleus/drug effects/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Recombination between viral RNA and transgenic plant transcripts (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-11
    Description: Transformed plants expressing the 3' two-thirds of the cowpea chlorotic mottle virus (CCMV) capsid gene were inoculated with a CCMV deletion mutant lacking the 3' one-third of the capsid gene. Although the deletion inoculum replicates in inoculated cells, systemic infections occur only if recombination restores a functional capsid gene. Four of 125 inoculated transgenic plants, representing three different transgenic lines, became systemically infected. Analysis of viral RNA confirmed that RNA recombination had united the transgenic messenger RNA and the challenging virus through aberrant homologous recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, A E -- Allison, R F -- New York, N.Y. -- Science. 1994 Mar 11;263(5152):1423-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Botany and Plant Pathology, Michigan State University, East Lansing 48824-1312.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128222" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Bromovirus/*genetics/physiology ; Capsid/genetics ; Gene Deletion ; Genes, Viral ; Molecular Sequence Data ; Mutation ; Plants, Genetically Modified/genetics/*microbiology ; Plants, Toxic ; RNA, Messenger/*genetics ; RNA, Viral/*genetics ; *Recombination, Genetic ; Tobacco/genetics/microbiology ; Virus Replication
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Breast cancer gene offers surprises (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1796-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091205" target="_blank"〉PubMed〈/a〉
    Keywords: BRCA1 Protein ; Breast Neoplasms/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 17 ; Female ; Genes ; Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; Humans ; Molecular Sequence Data ; Mutation ; Neoplasm Proteins/*genetics ; Transcription Factors/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Activation of the sphingomyelin cycle through the low-affinity neurotrophin receptor (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-09
    Description: The role of the low-affinity neurotrophin receptor (p75NTR) in signal transduction is undefined. Nerve growth factor can activate the sphingomyelin cycle, generating the putative-lipid second messenger ceramide. In T9 glioma cells, addition of a cell-permeable ceramide analog mimicked the effects of nerve growth factor on cell growth inhibition and process formation. This signaling pathway appears to be mediated by p75NTR in T9 cells and NIH 3T3 cells overexpressing p75NTR. Expression of an epidermal growth factor receptor-p75NTR chimera in T9 cells imparted to epidermal growth factor the ability to activate the sphingomyelin cycle. These data demonstrate that p75NTR is capable of signaling independently of the trk neurotrophin receptor (p140trk) and that ceramide may be a mediator in neurotrophin biology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dobrowsky, R T -- Werner, M H -- Castellino, A M -- Chao, M V -- Hannun, Y A -- AG05531/AG/NIA NIH HHS/ -- GM43825/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 9;265(5178):1596-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Cell Biology, Duke University Medical Center, Durham, NC 27710.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8079174" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Astrocytes/cytology/*metabolism ; Ceramides/metabolism/pharmacology ; Epidermal Growth Factor/pharmacology ; Glioblastoma ; Mice ; Nerve Growth Factors/pharmacology ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor/metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/*metabolism ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; Sphingomyelins/*metabolism ; Tumor Cells, Cultured
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    T cells and suppression in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, B -- Kaye, J -- Lo, D -- New York, N.Y. -- Science. 1994 Oct 21;266(5184):464-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; *Clonal Anergy ; *Lymphocyte Activation ; Mice ; Mice, Transgenic ; T-Lymphocytes, Regulatory/*immunology
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    Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-01
    Description: Deletion of the promoter and the first exon of the DNA polymerase beta gene (pol beta) in the mouse germ line results in a lethal phenotype. With the use of the bacteriophage-derived, site-specific recombinase Cre in a transgenic approach, the same mutation can be selectively introduced into a particular cellular compartment-in this case, T cells. The impact of the mutation on those cells can then be analyzed because the mutant animals are viable.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, H -- Marth, J D -- Orban, P C -- Mossmann, H -- Rajewsky, K -- New York, N.Y. -- Science. 1994 Jul 1;265(5168):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8016642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA Nucleotidyltransferases/genetics/metabolism ; DNA Polymerase I/*genetics/metabolism ; Female ; *Gene Deletion ; Genetic Engineering/*methods ; Homozygote ; *Integrases ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Recombination, Genetic ; Stem Cells/enzymology ; T-Lymphocytes/*enzymology ; Transfection ; *Viral Proteins
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    Nicotine scrutinized as FDA seeks to regulate cigarettes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nowak, R -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1555-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dopamine/metabolism ; Drug and Narcotic Control ; Humans ; Limbic System/drug effects/metabolism ; *Nicotine/pharmacology ; Rats ; Receptors, Cholinergic/drug effects/metabolism ; *Smoking ; *Substance-Related Disorders ; United States ; *United States Food and Drug Administration
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    Animal tests take back seat to clinical data (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seachrist, L -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1525.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/chemically induced/prevention & control ; Endometrial Neoplasms/chemically induced ; Female ; Humans ; Liver Neoplasms, Experimental/chemically induced ; Rats ; Tamoxifen/therapeutic use/*toxicity
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    Long-term behavioral recovery in parkinsonian rats by an HSV vector expressing tyrosine hydroxylase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-25
    Description: One therapeutic approach to treating Parkinson's disease is to convert endogenous striatal cells into levo-3,4-dihydroxyphenylalanine (L-dopa)-producing cells. A defective herpes simplex virus type 1 vector expressing human tyrosine hydroxylase was delivered into the partially denervated striatum of 6-hydroxydopamine-lesioned rats, used as a model of Parkinson's disease. Efficient behavioral and biochemical recovery was maintained for 1 year after gene transfer. Biochemical recovery included increases in both striatal tyrosine hydroxylase enzyme activity and in extracellular dopamine concentrations. Persistence of human tyrosine hydroxylase was revealed by expression of RNA and immunoreactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2638002/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉During, M J -- Naegele, J R -- O'Malley, K L -- Geller, A I -- EY09749/EY/NEI NIH HHS/ -- NS06208/NS/NINDS NIH HHS/ -- NS28227/NS/NINDS NIH HHS/ -- R01 NS034025/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 25;266(5189):1399-403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Yale University School of Medicine, New Haven, CT 06510.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7669103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Corpus Striatum/*enzymology/metabolism ; Denervation ; Disease Models, Animal ; Dopamine/metabolism ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; Humans ; Levodopa/metabolism ; Male ; Molecular Sequence Data ; *Motor Activity ; Neurons/enzymology ; Parkinson Disease/metabolism/*therapy ; Rats ; Rats, Sprague-Dawley ; Simplexvirus/*genetics ; Tyrosine 3-Monooxygenase/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Effective tumor vaccine generated by fusion of hepatoma cells with activated B cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-28
    Description: Fusion of BERH-2 rat hepatocellular carcinoma cells with activated B cells produced hybrid cells that lost their tumorigenicity and became immunogenic. Syngeneic rats injected with BERH-2-B hybrid cells became resistant to challenge with parental BERH-2 cells, and rats with established BERH-2 hepatomas were cured by subsequent injection of BERH-2-B cells. Both CD4+ and CD8+ cells were essential for the induction of protective immunity; however, only CD8+ cells were required for the eradication of BERH-2 tumors. The generation of hybrid tumor cells that elicit antitumor immune responses may be a useful strategy for cancer immunotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Y -- Wu, M -- Chen, H -- Wang, X -- Liu, G -- Li, G -- Ma, J -- Sy, M S -- New York, N.Y. -- Science. 1994 Jan 28;263(5146):518-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumor Immunology and Biotherapy Center, Eastern Institute of Hepatobiliary Surgery, Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7507262" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD80/analysis ; B-Lymphocytes/*immunology ; CD4-Positive T-Lymphocytes/immunology ; Cell Fusion ; Female ; Histocompatibility Antigens Class II/analysis ; Hybrid Cells/*immunology ; Immunotherapy, Active ; Liver Neoplasms, Experimental/*immunology/prevention & control/therapy ; Lymphocyte Activation ; Neoplasm Transplantation ; Rats ; Rats, Wistar ; T-Lymphocyte Subsets/immunology ; Tumor Cells, Cultured ; Vaccination ; Vaccines/*immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Rapid induction of Alzheimer A beta amyloid formation by zinc (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-02
    Description: A beta 1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM). Thus, physiological factors which induce A beta amyloid formation could provide clues to the pathogenesis of the disease. It has been shown that human A beta specifically and saturably binds zinc. Here, concentrations of zinc above 300 nM rapidly destabilized human A beta 1-40 solutions, inducing tinctorial amyloid formation. However, rat A beta 1-40 binds zinc less avidly and is immune to these effects, perhaps explaining the scarcity with which these animals form cerebral A beta amyloid. These data suggest a role for cerebral zinc metabolism in the neuropathogenesis of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bush, A I -- Pettingell, W H -- Multhaup, G -- d Paradis, M -- Vonsattel, J P -- Gusella, J F -- Beyreuther, K -- Masters, C L -- Tanzi, R E -- R01 AG11899-01/AG/NIA NIH HHS/ -- R01 NS30428-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1464-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics and Aging, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073293" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/etiology/*metabolism ; Amyloid beta-Peptides/chemistry/*metabolism ; Animals ; Brain/metabolism ; Edetic Acid/pharmacology ; Humans ; Kinetics ; Mice ; Peptide Fragments/chemistry/*metabolism ; Rats ; Solubility ; Zinc/*metabolism/pharmacology
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    Noradrenergic regulation of cholinergic differentiation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: When the sympathetic nerves that innervate rat sweat glands reach their targets, they are induced to switch from using norepinephrine as their neurotransmitter to acetylcholine. Catecholamines (such as norepinephrine) released by nerves growing to the sweat gland induce this phenotypic conversion by stimulating production of a cholinergic differentiation factor [sweat gland factor (SGF)] by gland cells. Here, culture of gland cells with sympathetic, but not sensory, neurons induced SGF production. Blockage of alpha 1- or beta-adrenergic receptors prevented acquisition of the cholinergic phenotype in sympathetic neurons co-cultured with sweat glands, and sweat glands from sympathectomized animals lacked SGF. Thus, reciprocal instructive interactions, mediated in part by small molecule neurotransmitters, direct the development of this synapse.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habecker, B A -- Landis, S C -- NS-023678/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1602-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4975.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202714" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Base Sequence ; Cell Differentiation ; Cells, Cultured ; Culture Media, Conditioned ; Glycoproteins/*biosynthesis ; Molecular Sequence Data ; Neuregulins ; Neurons/cytology/physiology ; Neurons, Afferent/cytology/physiology ; Parasympathetic Nervous System/cytology/*physiology ; Phenotype ; Rats ; Receptors, Adrenergic/*physiology ; Sweat Glands/cytology/*innervation/metabolism ; Sympathectomy ; Sympathetic Nervous System/cytology/*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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  • 84
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    On the trail of a second susceptibility gene (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Brien, C -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1798.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8091206" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 13 ; Female ; Genes, Tumor Suppressor ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Male ; Mutation
    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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  • 85
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    Glia: the brain's other cells (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Travis, J -- New York, N.Y. -- Science. 1994 Nov 11;266(5187):970-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973679" target="_blank"〉PubMed〈/a〉
    Keywords: Astrocytes/physiology ; Brain/*cytology/physiology ; Calcium/metabolism ; Cell Communication ; Cells, Cultured ; Humans ; Nerve Growth Factors/biosynthesis ; Neuroglia/*physiology ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Synapses/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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  • 86
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    Of flies and fishes (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nusslein-Volhard, C -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Entwicklungsbiologie, Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila/embryology/*genetics ; *Embryonic Development ; *Genes ; *Genes, Insect ; Mutation ; Point Mutation ; Zebrafish/embryology/*genetics
    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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  • 87
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    RNA editing: transfer of genetic information from gRNA to precursor mRNA in vitro (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-07
    Description: RNA editing in the mitochondrion of Trypanosoma brucei extensively alters the adenosine triphosphate synthase (ATPase) subunit 6 precursor messenger RNA (pre-mRNA) by addition of 447 uridines and removal of 28 uridines. In vivo, the guide RNA gA6[14] is thought to specify the deletion of two uridines from the editing site closest to the 3' end. In this study, an in vitro system was developed that accurately removed uridines from this editing site in synthetic ATPase 6 pre-mRNA when gA6[14] and ATP were added. Mutations in both the guide RNA and the pre-mRNA editing site suggest that base-pairing interactions control the number of uridines deleted in vitro. Thus, guide RNAs are required for RNA editing and for the transfer of genetic information to pre-mRNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seiwert, S D -- Stuart, K -- GM 42188/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Oct 7;266(5182):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06536-0182.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7524149" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/genetics ; Adenosine Triphosphate/metabolism ; Animals ; Base Composition ; Base Sequence ; Mitochondria/genetics ; Molecular Sequence Data ; Mutation ; RNA/chemistry/*genetics/metabolism ; *RNA Editing ; RNA Precursors/chemistry/*genetics/metabolism ; RNA, Guide/chemistry/*genetics/metabolism ; RNA, Protozoan/chemistry/genetics/metabolism ; Trypanosoma brucei brucei/*genetics/metabolism ; Uridine/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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  • 88
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    The mating of a fly (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: Courtship in Drosophila is influenced by a wide variety of genes, in that many different kinds of pleiotropic mutations lead to defective courtship. This may seem to be a truism, but the broad temporal and spatial expression of most of the fly's "neuro genes" makes it difficult to exclude elements of such genes' actions as materially underlying reproductive behavior. "Courtship genes" that seem to play more particular roles were originally identified as sensory, learning, or rhythm mutations; their reproductive abnormalities have been especially informative for revealing components of male or female actions that might otherwise have gone unnoticed. Further behavioral mutations seemed originally to be courtship-specific, turned out not to have that property, and have led to a broadened perspective on the nature and action of Drosophila's sex-determination genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, J C -- GM-21473/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1702-14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254-9110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drosophila melanogaster/anatomy & histology/*genetics/physiology ; Female ; *Genes, Insect ; Male ; Mutation ; Nervous System Physiological Phenomena ; Phenotype ; Sex Characteristics ; Sex Determination Analysis ; *Sexual Behavior, Animal
    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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  • 89
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    What are we? Where did we come from? Where are we going? (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Neill, L -- Murphy, M -- Gallagher, R B -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):181-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Trinity College, Dublin, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7506843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Humans ; *Mental Processes ; *Origin of Life ; *Rna
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 90
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    Treating brain cancers (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maruyama, Y -- Fontanesi, J -- Porter, A T -- Wierzbicki, J G -- Gaspar, L -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):714-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Boron Neutron Capture Therapy ; Brain Neoplasms/*radiotherapy ; Californium/*therapeutic use ; Humans ; Neutron Capture Therapy/*methods ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 91
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    Stalking the start of colon cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, R F -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1559-60.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128240" target="_blank"〉PubMed〈/a〉
    Keywords: *Adenosine Triphosphatases ; Bacterial Proteins/genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 2 ; *Chromosomes, Human, Pair 3 ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; *DNA Repair ; DNA, Complementary/genetics ; *DNA-Binding Proteins ; Databases, Factual ; *Escherichia coli Proteins ; *Genes ; Humans ; MutS Homolog 2 Protein ; Mutation ; Proto-Oncogene Proteins/genetics
    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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  • 92
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    New tumor suppressor may rival p53 (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):344-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153613" target="_blank"〉PubMed〈/a〉
    Keywords: Carrier Proteins/*genetics ; Chromosomes, Human, Pair 9 ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinase Inhibitor p16 ; *Cyclin-Dependent Kinases ; Gene Deletion ; *Genes, Tumor Suppressor ; Genes, p53 ; Humans ; Melanoma/genetics ; Mutation ; Neoplasms/*genetics ; Protein Kinase Inhibitors ; *Proto-Oncogene Proteins ; Tumor Cells, Cultured
    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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  • 93
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    Mutation of a mutL homolog in hereditary colon cancer (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-03-18
    Description: Some cases of hereditary nonpolyposis colorectal cancer (HNPCC) are due to alterations in a mutS-related mismatch repair gene. A search of a large database of expressed sequence tags derived from random complementary DNA clones revealed three additional human mismatch repair genes, all related to the bacterial mutL gene. One of these genes (hMLH1) resides on chromosome 3p21, within 1 centimorgan of markers previously linked to cancer susceptibility in HNPCC kindreds. Mutations of hMLH1 that would disrupt the gene product were identified in such kindreds, demonstrating that this gene is responsible for the disease. These results suggest that defects in any of several mismatch repair genes can cause HNPCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papadopoulos, N -- Nicolaides, N C -- Wei, Y F -- Ruben, S M -- Carter, K C -- Rosen, C A -- Haseltine, W A -- Fleischmann, R D -- Fraser, C M -- Adams, M D -- CA35494/CA/NCI NIH HHS/ -- CA47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Mar 18;263(5153):1625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johns Hopkins Oncology Center, Baltimore, MD 21231.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8128251" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; *Adenosine Triphosphatases ; Amino Acid Sequence ; Bacterial Proteins/chemistry/*genetics ; Base Sequence ; Carrier Proteins ; Chromosome Mapping ; *Chromosomes, Human, Pair 3 ; Codon ; Colorectal Neoplasms, Hereditary Nonpolyposis/*genetics ; *DNA Repair ; *DNA-Binding Proteins ; *Escherichia coli Proteins ; Female ; Frameshift Mutation ; *Genes ; Genetic Markers ; Humans ; Male ; Molecular Sequence Data ; MutS Homolog 2 Protein ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; Nuclear Proteins ; Open Reading Frames ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/genetics ; Sequence Deletion ; Tumor Cells, Cultured
    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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  • 94
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    Genetic engineering. Safety concerns halt U.K. study (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kingman, S -- New York, N.Y. -- Science. 1994 Feb 11;263(5148):748.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303287" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Advisory Committees ; Cells, Cultured ; *Containment of Biohazards ; *Genetic Engineering ; *Government Regulation ; Great Britain ; Humans ; *Oncogenes ; Simian virus 40/*genetics
    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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  • 95
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    Mouse model found for ALS (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J -- New York, N.Y. -- Science. 1994 Jun 17;264(5166):1663-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8209242" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/enzymology/*genetics ; Animals ; *Disease Models, Animal ; Mice ; *Mice, Transgenic ; Mutation ; Superoxide Dismutase/*genetics/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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  • 96
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    Developmental evolution: insights from studies of insect segmentation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-28
    Description: Rapid advances have been made in the understanding of the genetic basis of development and pattern formation in a variety of model systems. By examining the extent to which these developmental systems are conserved or altered between different organisms, insight can be gained into the evolutionary events that have generated the diversity of organisms around us. The molecular and genetic basis of early pattern formation in Drosophila melanogaster has been particularly well studied, and comparisons to other insects have revealed conservation of some aspects of development, as well as differences that may explain variations in early patterning events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, N H -- New York, N.Y. -- Science. 1994 Oct 28;266(5185):581-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Embryology, Carnegie Institution of Washington, Baltimore, MD 21210-3399.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila melanogaster/*embryology/genetics ; *Embryonic Development ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; *Genes, Insect ; Insects/embryology/genetics ; Morphogenesis ; Phylogeny ; Signal Transduction
    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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  • 97
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    Activity-dependent changes in the intrinsic properties of cultured neurons (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-13
    Description: Learning and memory arise through activity-dependent modifications of neural circuits. Although the activity dependence of synaptic efficacy has been studied extensively, less is known about how activity shapes the intrinsic electrical properties of neurons. Lobster stomatogastric ganglion neurons fire in bursts when receiving synaptic and modulatory input but fire tonically when pharmacologically isolated. Long-term isolation in culture changed their intrinsic activity from tonic firing to burst firing. Rhythmic stimulation reversed this transition through a mechanism that was mediated by a rise in intracellular calcium concentration. These data suggest that neurons regulate their conductances to maintain stable activity patterns and that the intrinsic properties of a neuron depend on its recent history of activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Turrigiano, G -- Abbott, L F -- Marder, E -- MH46742/MH/NIMH NIH HHS/ -- NS17813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1994 May 13;264(5161):974-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Brandeis University, Waltham, MA 02254.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8178157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cells, Cultured ; Egtazic Acid/analogs & derivatives/pharmacology ; Electric Stimulation ; Electrophysiology ; Ganglia, Invertebrate/cytology ; Membrane Potentials ; Nephropidae ; Neurites/physiology ; Neurons/cytology/*physiology ; Synapses/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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  • 98
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    ZAP-70 deficiency in an autosomal recessive form of severe combined immunodeficiency (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-10
    Description: Protein tyrosine kinases (PTKs) play an integral role in T cell activation and differentiation. Defects in the Src-family PTKs in mice and in T cell lines have resulted in variable defects in thymic development and in T cell antigen receptor (TCR) signal transduction. Here, three siblings are described with an autosomal recessive form of severe combined immunodeficiency disease (SCID) in which ZAP-70, a non-Src PTK, is absent as a result of mutations in the ZAP-70 gene. This absence is associated with defects in TCR signal transduction, suggesting an important functional role for ZAP-70.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, A C -- Kadlecek, T A -- Elder, M E -- Filipovich, A H -- Kuo, W L -- Iwashima, M -- Parslow, T G -- Weiss, A -- AR-20684/AR/NIAMS NIH HHS/ -- GM39553/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Jun 10;264(5165):1599-601.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8202713" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Calcium/metabolism ; Cell Line ; Child ; Female ; Gene Deletion ; *Genes, Recessive ; Humans ; Lymphocyte Activation ; Male ; Molecular Sequence Data ; Mutation ; Point Mutation ; Protein-Tyrosine Kinases/deficiency/*genetics/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Severe Combined Immunodeficiency/*genetics/immunology ; *Signal Transduction ; T-Lymphocyte Subsets/immunology ; ZAP-70 Protein-Tyrosine Kinase
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    RNA editing and the evolution of parasites (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-06-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simpson, L -- Maslov, D A -- New York, N.Y. -- Science. 1994 Jun 24;264(5167):1870-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Los Angeles, CA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8009214" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Kinetoplastida/*genetics ; Phylogeny ; *RNA Editing ; RNA, Protozoan/genetics/metabolism ; Trypanosomatina/*genetics
    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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  • 100
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    Co-opting a blind watchmaker (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flam, F -- New York, N.Y. -- Science. 1994 Aug 19;265(5175):1032-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7520602" target="_blank"〉PubMed〈/a〉
    Keywords: Biochemistry/*methods ; *Biological Evolution ; Biotechnology/*methods ; Drug Design ; Enzymes/*metabolism ; Escherichia coli/enzymology/genetics ; Mutation ; RNA/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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