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  • Signal Transduction  (1,508)
  • *Biological Evolution  (1,390)
  • American Association for the Advancement of Science (AAAS)  (2,886)
  • Cell Press
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  • 1
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2016-09-03
    Description: Author: L. Bryan Ray
    Keywords: Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-08-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, Michael -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):945-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA. mlynch@bio.indiana.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12169715" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Caenorhabditis elegans/genetics ; Chromosomes/genetics ; Chromosomes, Human/genetics ; *Gene Duplication ; Gene Rearrangement ; Gene Silencing ; *Genes, Duplicate ; *Genome, Human ; Genomics ; Humans ; Mutation ; Selection, Genetic
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-01-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moffat, Anne Simon -- New York, N.Y. -- Science. 2002 Jan 25;295(5555):613-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11809953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Color Perception ; Feeding Behavior ; Female ; *Fossils ; Haplorhini ; Male ; Plant Leaves ; *Primates/anatomy & histology ; Skeleton
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2002-05-04
    Description: There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillaber, Inge -- Rammes, Gerhard -- Zimmermann, Stephan -- Mahal, Beatrice -- Zieglgansberger, Walter -- Wurst, Wolfgang -- Holsboer, Florian -- Spanagel, Rainer -- New York, N.Y. -- Science. 2002 May 3;296(5569):931-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany. sillaber@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988580" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; *Alcohol Drinking ; Alcoholism/*etiology/genetics ; Animals ; Brain/metabolism ; Corticotropin-Releasing Hormone/physiology ; Ethanol/blood ; Female ; Hippocampus/physiology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Models, Animal ; Mutation ; Receptors, AMPA/metabolism ; Receptors, Corticotropin-Releasing Hormone/*genetics/*physiology ; Receptors, Kainic Acid/metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Signal Transduction ; Stress, Physiological/physiopathology ; Stress, Psychological/*physiopathology ; Up-Regulation
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-06-18
    Description: Hundreds of coral species coexist sympatrically on reefs, reproducing in mass-spawning events where hybridization appears common. In the Caribbean, DNA sequence data from all three sympatric Acropora corals show that mass spawning does not erode species barriers. Species A. cervicornis and A. palmata are distinct at two nuclear loci or share ancestral alleles. Morphotypes historically given the name Acropora prolifera are entirely F(1) hybrids of these two species, showing morphologies that depend on which species provides the egg for hybridization. Although selection limits the evolutionary potential of hybrids, F(1) individuals can reproduce asexually and form long-lived, potentially immortal hybrids with unique morphologies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vollmer, Steven V -- Palumbi, Stephen R -- New York, N.Y. -- Science. 2002 Jun 14;296(5575):2023-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA. svollmer@oeb.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12065836" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bayes Theorem ; *Biological Evolution ; Calmodulin/genetics ; Caribbean Region ; Cnidaria/anatomy & histology/*classification/*genetics/physiology ; Collagen/genetics ; DNA, Mitochondrial/genetics ; *Ecosystem ; Environment ; *Genetic Variation ; Haplotypes ; *Hybridization, Genetic ; Introns ; Likelihood Functions ; Polymorphism, Genetic ; Reproduction ; Reproduction, Asexual ; Sequence Analysis, DNA ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2003-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brivanlou, Ali H -- Gage, Fred H -- Jaenisch, Rudolf -- Jessell, Thomas -- Melton, Douglas -- Rossant, Janet -- New York, N.Y. -- Science. 2003 May 9;300(5621):913-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021, USA. brvnlou@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12738841" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; Cell Culture Techniques/methods ; Cell Differentiation ; Cell Division ; *Cell Line ; Culture Media ; Culture Media, Conditioned ; Databases, Factual ; *Embryo Research ; Embryo, Mammalian/*cytology ; Humans ; Quality Control ; Registries ; Research/standards ; Signal Transduction ; Stem Cell Transplantation ; *Stem Cells/cytology/physiology ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2002-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Funes, Soledad -- Davidson, Edgar -- Reyes-Prieto, Adrian -- Magallon, Susana -- Herion, Pascal -- King, Michael P -- Gonzalez-Halphen, Diego -- HL59646/HL/NHLBI NIH HHS/ -- TW01176/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Dec 13;298(5601):2155.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico (UNAM), 04510 D.F., Mexico.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12481129" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apicomplexa/enzymology/*genetics/ultrastructure ; *Biological Evolution ; Cell Nucleus/genetics ; Chlamydomonas reinhardtii/enzymology/genetics ; Chlorophyta/enzymology/*genetics ; Cloning, Molecular ; DNA, Mitochondrial/genetics ; Electron Transport Complex IV/chemistry/*genetics ; *Gene Transfer, Horizontal ; Genes ; Genes, Protozoan ; Molecular Sequence Data ; Phylogeny ; Plastids/*genetics ; Symbiosis ; Toxoplasma/enzymology/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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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-07-06
    Description: Fishery management plans ignore the potential for evolutionary change in harvestable biomass. We subjected populations of an exploited fish (Menidia menidia) to large, small, or random size-selective harvest of adults over four generations. Harvested biomass evolved rapidly in directions counter to the size-dependent force of fishing mortality. Large-harvested populations initially produced the highest catch but quickly evolved a lower yield than controls. Small-harvested populations did the reverse. These shifts were caused by selection of genotypes with slower or faster rates of growth. Management tools that preserve natural genetic variation are necessary for long-term sustainable yield.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conover, David O -- Munch, Stephan B -- New York, N.Y. -- Science. 2002 Jul 5;297(5578):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marine Sciences Research Center, State University of New York, Stony Brook, NY 11794-5000, USA. dconover@notes.cc.sunysb.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12098697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Biomass ; Body Constitution ; Body Weight ; Conservation of Natural Resources ; *Fisheries ; Fishes/anatomy & histology/*genetics/*growth & development ; Genetic Variation ; Population Dynamics ; Regression Analysis ; *Selection, Genetic ; Time Factors
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-05-11
    Description: Breast cancer manifests itself in the mammary epithelium, yet there is a growing recognition that mammary stromal cells also play an important role in tumorigenesis. During its developmental cycle, the mammary gland displays many of the properties associated with breast cancer, and many of the stromal factors necessary for mammary development also promote or protect against breast cancer. Here we review our present knowledge of the specific factors and cell types that contribute to epithelial-stromal crosstalk during mammary development. To find cures for diseases like breast cancer that rely on epithelial-stromal crosstalk, we must understand how these different cell types communicate with each other.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788989/" 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/PMC2788989/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wiseman, Bryony S -- Werb, Zena -- CA57621/CA/NCI NIH HHS/ -- R01 CA057621/CA/NCI NIH HHS/ -- R01 CA057621-07/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 May 10;296(5570):1046-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12004111" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/physiology ; Animals ; Apoptosis ; Breast/cytology/embryology/*growth & development/physiology ; Breast Neoplasms/pathology/*physiopathology ; Cell Communication ; Epithelial Cells/physiology ; Extracellular Matrix/physiology ; Female ; Humans ; Mammary Glands, Animal/cytology/embryology/*growth & development/physiology ; Mammary Neoplasms, Animal/pathology/*physiopathology ; Morphogenesis ; Neoplasm Metastasis ; Pregnancy ; Signal Transduction ; Stromal Cells/*physiology
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, J K M -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1680-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Disease and Stress Biology, John Innes Centre, Norwich, NR4 7UH, UK. james.brown@bbsrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637729" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Basidiomycota/genetics/*pathogenicity/physiology ; *Biological Evolution ; Flax/genetics/*microbiology/physiology ; Genes, Fungal ; Genes, Plant ; *Genetic Variation ; Models, Genetic ; Plant Diseases/*microbiology ; Reproduction ; Spores, Fungal ; Virulence/*genetics
    Print ISSN: 0036-8075
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Kathryn -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645825" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Biological Evolution ; Desert Climate ; Ecosystem ; Environment ; Genes, Plant ; Helianthus/*genetics/growth & development/physiology ; History, 20th Century ; History, 21st Century ; *Hybridization, Genetic ; Mutation ; Phenotype ; Sodium Chloride/pharmacology ; United States
    Print ISSN: 0036-8075
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1142.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Constitution ; Diet ; *Dogs/anatomy & histology ; Jaw/anatomy & histology ; Paleontology ; *Predatory Behavior ; Time
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dunbar, Robin -- New York, N.Y. -- Science. 2003 Nov 14;302(5648):1160-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Liverpool, Liverpool L69 7ZB, UK. rimd@liv.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14615522" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Wild ; *Biological Evolution ; *Cognition ; Endorphins/physiology ; Female ; Grooming ; Hierarchy, Social ; Language ; Neocortex/anatomy & histology/physiology ; Papio/physiology/*psychology ; *Reproduction ; *Social Behavior ; Social Dominance ; Social Support ; Vocalization, Animal
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  • 14
    Publication Date: 2003-03-15
    Description: Captive breeding and release programs, widely used to supplement populations of declining species, minimize juvenile mortality to achieve rapid population growth. However, raising animals in benign environments may promote traits that are adaptive in captivity but maladaptive in nature. In chinook salmon, hatchery rearing relaxes natural selection favoring large eggs, allowing fecundity selection to drive exceptionally rapid evolution of small eggs. Trends toward small eggs are also evident in natural populations heavily supplemented by hatcheries, but not in minimally supplemented populations. Unintentional selection in captivity can lead to rapid changes in critical life-history traits that may reduce the success of supplementation or reintroduction programs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heath, Daniel D -- Heath, John W -- Bryden, Colleen A -- Johnson, Rachel M -- Fox, Charles W -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1738-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Great Lakes Institute for Environmental Research and Department of Biological Sciences, University of Windsor, 401 Sunset Avenue, Windsor, Ontario N9B 3P4, Canada. dheath@uwindsor.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Constitution ; Body Weight ; *Breeding ; Conservation of Natural Resources ; Environment ; Female ; Fertility ; *Fisheries ; Ovum/*physiology ; Salmon/genetics/*physiology ; Selection, Genetic
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roff, Derek -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):58-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, Riverside, CA 92521, USA. derek.roff@ucr.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843382" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Australia ; *Biological Evolution ; Climate ; Dehydration ; Drosophila/*genetics/*physiology ; Ecosystem ; Environment ; *Genetic Variation ; *Greenhouse Effect ; Selection, Genetic ; Trees
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  • 16
    Publication Date: 2003-02-22
    Description: Placoderms are extinct jawed fishes of the class Placodermi and are basal among jawed vertebrates. It is generally thought that teeth are absent in placoderms and that the phylogenetic origin of teeth occurred after the evolution of jaws. However, we now report the presence of tooth rows in more derived placoderms, the arthrodires. New teeth are composed of gnathostome-type dentine and develop at specific locations. Hence, it appears that these placoderm teeth develop and are regulated as in other jawed vertebrates. Because tooth development occurs only in derived forms of placoderms, we suggest that teeth evolved at least twice, through a mechanism of convergent evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Moya Meredith -- Johanson, Zerina -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1235-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Craniofacial Development, Dental Institute, King's College London, Guy's Campus, London Bridge, London SE1 9RT, UK. moya.smith@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595693" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Dentition ; Fishes/*anatomy & histology ; *Fossils ; *Paleodontology ; Phylogeny ; *Tooth ; Western Australia
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-08-09
    Description: Large-scale genome sequencing is providing a comprehensive view of the complex evolutionary forces that have shaped the structure of eukaryotic chromosomes. Comparative sequence analyses reveal patterns of apparently random rearrangement interspersed with regions of extraordinarily rapid, localized genome evolution. Numerous subtle rearrangements near centromeres, telomeres, duplications, and interspersed repeats suggest hotspots for eukaryotic chromosome evolution. This localized chromosomal instability may play a role in rapidly evolving lineage-specific gene families and in fostering large-scale changes in gene order. Computational algorithms that take into account these dynamic forces along with traditional models of chromosomal rearrangement show promise for reconstructing the natural history of eukaryotic chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eichler, Evan E -- Sankoff, David -- GM58815/GM/NIGMS NIH HHS/ -- HD43569/HD/NICHD NIH HHS/ -- HG02385/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):793-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Center for Human Genetics and Center for Computational Genomics, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, OH 44106, USA. eee@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907789" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Centromere/physiology ; Chromosome Aberrations ; *Chromosomes/genetics/physiology/ultrastructure ; Computational Biology ; DNA Transposable Elements ; Eukaryotic Cells/physiology/*ultrastructure ; Gene Duplication ; Genome ; Humans ; Recombination, Genetic ; Synteny ; Telomere/physiology
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintz, Nathaniel -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):59-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Rockefeller University, New York, NY 10021, USA. heintz@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843383" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Substitution ; Animals ; Ataxin-1 ; Ataxins ; Cell Nucleus/metabolism ; Disease Progression ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Nuclear Proteins/*chemistry/genetics/*metabolism ; Peptides ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Purkinje Cells/metabolism/ultrastructure ; Signal Transduction ; Spinocerebellar Ataxias/etiology/genetics/pathology/*physiopathology ; *Trinucleotide Repeat Expansion ; Tyrosine 3-Monooxygenase/*metabolism
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  • 19
    Publication Date: 2003-06-14
    Description: In eukaryotes, the combinatorial association of sequence-specific DNA binding proteins is essential for transcription. We have used protein arrays to test 492 pairings of a nearly complete set of coiled-coil strands from human basic-region leucine zipper (bZIP) transcription factors. We find considerable partnering selectivity despite the bZIPs' homologous sequences. The interaction data are of high quality, as assessed by their reproducibility, reciprocity, and agreement with previous observations. Biophysical studies in solution support the relative binding strengths observed with the arrays. New associations provide insights into the circadian clock and the unfolded protein response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, John R S -- Keating, Amy E -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2097-101. Epub 2003 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12805554" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Basic-Leucine Zipper Transcription Factors ; Chromatography, High Pressure Liquid ; Circadian Rhythm ; Circular Dichroism ; Cyclic AMP Response Element-Binding Protein/chemistry/metabolism ; DNA-Binding Proteins/chemistry/isolation & purification/*metabolism ; Dimerization ; G-Box Binding Factors ; Humans ; *Leucine Zippers ; Peptides/chemistry/isolation & purification/metabolism ; *Protein Array Analysis ; Protein Binding ; Protein Folding ; Protein Structure, Tertiary ; Signal Transduction ; Temperature ; Thermodynamics ; Transcription Factors/*chemistry/isolation & purification/*metabolism
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elena, Santiago F -- Sanjuan, Rafael -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2074-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Biologia Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cientificas-UPV, 46022 Valencia, Spain. sfelena@ibmcp.upv.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684807" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Biological Evolution ; Chlamydomonas/physiology ; Darkness ; *Ecosystem ; Environment ; *Genetic Variation ; Genotype ; Light ; Mutation ; Phenotype ; Pseudomonas fluorescens/genetics/*physiology ; RNA Viruses/physiology ; Selection, Genetic
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  • 21
    Publication Date: 2003-08-16
    Description: Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, Marc T -- Stein, Monica -- Hou, Bi-Huei -- Vogel, John P -- Edwards, Herb -- Somerville, Shauna C -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):969-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920300" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/cytology/genetics/*metabolism/*microbiology ; Ascomycota/*physiology ; Cell Death ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Genes, Plant ; Glucans/metabolism ; Glucosyltransferases/*genetics/metabolism ; *Membrane Proteins ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; *Plant Diseases ; Plant Leaves/metabolism ; Salicylic Acid/*metabolism ; *Schizosaccharomyces pombe Proteins ; Signal Transduction
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  • 22
    Publication Date: 2003-07-05
    Description: Raf kinases have been linked to endothelial cell survival. Here, we show that basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) differentially activate Raf, resulting in protection from distinct pathways of apoptosis in human endothelial cells and chick embryo vasculature. bFGF activated Raf-1 via p21-activated protein kinase-1 (PAK-1) phosphorylation of serines 338 and 339, resulting in Raf-1 mitochondrial translocation and endothelial cell protection from the intrinsic pathway of apoptosis, independent of the mitogen-activated protein kinase kinase-1 (MEK1). In contrast, VEGF activated Raf-1 via Src kinase, leading to phosphorylation of tyrosines 340 and 341 and MEK1-dependent protection from extrinsic-mediated apoptosis. These findings implicate Raf-1 as a pivotal regulator of endothelial cell survival during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alavi, Alireza -- Hood, John D -- Frausto, Ricardo -- Stupack, Dwayne G -- Cheresh, David A -- CA45726/CA/NCI NIH HHS/ -- CA50286/CA/NCI NIH HHS/ -- CA75924/CA/NCI NIH HHS/ -- P01 CA78045/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):94-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/*cytology/drug effects ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Flavonoids/pharmacology ; Humans ; Intercellular Signaling Peptides and Proteins/pharmacology ; Lymphokines/pharmacology ; MAP Kinase Kinase 1 ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Neovascularization, Pathologic ; *Neovascularization, Physiologic/drug effects ; Phosphorylation ; Point Mutation ; Protein Transport ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins B-raf ; Proto-Oncogene Proteins c-raf/chemistry/genetics/*metabolism ; Signal Transduction ; Umbilical Veins ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; p21-Activated Kinases ; src-Family Kinases/antagonists & inhibitors/metabolism
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  • 23
    Publication Date: 2003-07-05
    Description: The ability of sensitive rainforest species to evolve in response to climate change is largely unknown. We show that the Australian tropical rainforest fly Drosophila birchii exhibits clinal variation in desiccation resistance, but the most resistant population lacks the ability to evolve further resistance even after intense selection for over 30 generations. Parent-offspring comparisons indicate low heritable variation for this trait but high levels of genetic variation for morphology. D. birchii also exhibits abundant genetic variation at microsatellite loci. The low potential for resistance evolution highlights the importance of assessing evolutionary potential in targeted ecological traits and species from threatened habitats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, A A -- Hallas, R J -- Dean, J A -- Schiffer, M -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):100-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Environmental Stress and Adaptation Research, La Trobe University, Bundoora, Victoria 3086, Australia. A.Hoffmann@latrobe.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843394" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Australia ; *Biological Evolution ; *Climate ; Crosses, Genetic ; Dehydration ; Drosophila/*genetics/*physiology ; Ecosystem ; Environment ; Female ; *Genetic Variation ; Geography ; Inbreeding ; Male ; Microsatellite Repeats ; Selection, Genetic ; Trees
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-03-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allen, John F -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1530-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biochemistry, Center for Chemistry and Chemical Engineering, Box 124, Lund University, SE-221 00 Lund, Sweden. john.allen@plantbio.lu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12624254" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/chemistry/genetics/isolation & purification/metabolism ; Animals ; Binding Sites ; Chlamydomonas reinhardtii/*enzymology/genetics/metabolism ; Chlorophyll/metabolism ; Electron Transport ; Fluorescence ; Gene Library ; Light ; Light-Harvesting Protein Complexes ; Models, Biological ; Mutation ; Oxidation-Reduction ; Phosphorylation ; Photosynthesis ; Photosynthetic Reaction Center Complex Proteins/*metabolism ; Plastoquinone/metabolism ; Protein-Serine-Threonine Kinases/chemistry/genetics/*isolation & ; purification/*metabolism ; Signal Transduction ; Thylakoids/*enzymology ; Transcription, Genetic
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-04-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altshuler, Douglas L -- Clark, Christopher James -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):588-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, California Institute of Technology, Pasadena, CA 91104, USA. doug@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beak/*anatomy & histology ; *Biological Evolution ; Birds/*anatomy & histology/physiology ; Body Constitution ; Dominica ; Ecosystem ; Feeding Behavior ; Female ; Flowers/*anatomy & histology ; Heliconiaceae/*anatomy & histology ; Male ; Pigmentation ; Saint Lucia ; *Sex Characteristics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, Carl -- New York, N.Y. -- Science. 2003 May 30;300(5624):1363.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775815" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; *Communicable Disease Control ; Corynebacterium diphtheriae/pathogenicity ; Diphtheria/microbiology/prevention & control ; Diphtheria Toxin/biosynthesis ; Diphtheria Toxoid ; Humans ; Immunization Programs ; *Vaccines ; *Virulence
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  • 27
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-05-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, Carl -- New York, N.Y. -- Science. 2003 May 30;300(5624):1362-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12775814" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Cholera/epidemiology/microbiology/transmission ; Communicable Disease Control ; Communicable Diseases/*microbiology/*parasitology/transmission/virology ; Humans ; Influenza, Human/epidemiology/transmission/virology ; *Models, Biological ; Myxoma virus/pathogenicity ; Sanitation ; Vibrio cholerae/pathogenicity ; *Virulence
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  • 28
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Caroni, P -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1465-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute, Basel, Switzerland. caroni@fmi.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750116" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Animals ; Axons/*physiology ; Brain-Derived Neurotrophic Factor/physiology ; Calcium/metabolism ; Cell Movement ; Cyclic AMP/*physiology ; Cyclic GMP/*physiology ; Glycoproteins/physiology ; Nerve Growth Factors/physiology ; Neurons/*physiology ; Neurotrophin 3 ; Semaphorin-3A ; Signal Transduction ; Tumor Suppressor Proteins
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-02-07
    Description: The Son of Sevenless (Sos) proteins control receptor-mediated activation of Ras by catalyzing the exchange of guanosine diphosphate for guanosine triphosphate on Ras. The NH2-terminal region of Sos contains a Dbl homology (DH) domain in tandem with a pleckstrin homology (PH) domain. In COS-1 cells, the DH domain of Sos stimulated guanine nucleotide exchange on Rac but not Cdc42 in vitro and in vivo. The tandem DH-PH domain of Sos (DH-PH-Sos) was defective in Rac activation but regained Rac stimulating activity when it was coexpressed with activated Ras. Ras-mediated activation of DH-PH-Sos did not require activation of mitogen-activated protein kinase but it was dependent on activation of phosphoinositide 3-kinase. These results reveal a potential mechanism for coupling of Ras and Rac signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimnual, A S -- Yatsula, B A -- Bar-Sagi, D -- CA09176/CA/NCI NIH HHS/ -- CA28146/CA/NCI NIH HHS/ -- CA55360/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):560-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438849" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; COS Cells ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Membrane/ultrastructure ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; Membrane Proteins/chemistry/*metabolism ; *Mitogen-Activated Protein Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins ; Recombinant Fusion Proteins/metabolism ; Retroviridae Proteins, Oncogenic/chemistry ; Signal Transduction ; Son of Sevenless Proteins ; Transfection ; cdc42 GTP-Binding Protein ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors ; ras Proteins/*metabolism
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-18
    Description: During T cell activation, the engagement of costimulatory molecules is often crucial to the development of an effective immune response, but the mechanism by which this is achieved is not known. Here, it is shown that beads attached to the surface of a T cell translocate toward the interface shortly after the start of T cell activation. This movement appears to depend on myosin motor proteins and requires the engagement of the major costimulatory receptor pairs, B7-CD28 and ICAM-1-LFA-1. This suggests that the engagement of costimulatory receptors triggers an active accumulation of molecules at the interface of the T cell and the antigen-presenting cell, which then increases the overall amplitude and duration of T cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wulfing, C -- Davis, M M -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2266-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens, CD/*metabolism ; Antigens, CD28/metabolism ; Antigens, CD86 ; Biotinylation ; CHO Cells ; Calcium/metabolism ; Cricetinae ; Cytoskeleton/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; *Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Microspheres ; Molecular Motor Proteins/physiology ; Myosins/physiology ; Phosphatidylinositol 3-Kinases/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism/ultrastructure ; Tumor Cells, Cultured
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chess, A -- New York, N.Y. -- Science. 1998 Mar 27;279(5359):2067-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. chess@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9537917" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; CD4-Positive T-Lymphocytes/*immunology ; DNA Replication ; *Gene Expression Regulation ; Genes, Immunoglobulin ; Interleukin-2/*genetics ; Lymphocyte Activation ; Mice ; Polymerase Chain Reaction ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; Transcription, Genetic
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, A -- New York, N.Y. -- Science. 1998 May 1;280(5364):675-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Evolution, Molecular ; Fossils ; History, Ancient ; Mammals/*genetics ; *Paleontology
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  • 33
    Publication Date: 1998-04-16
    Description: FADD (also known as Mort-1) is a signal transducer downstream of cell death receptor CD95 (also called Fas). CD95, tumor necrosis factor receptor type 1 (TNFR-1), and death receptor 3 (DR3) did not induce apoptosis in FADD-deficient embryonic fibroblasts, whereas DR4, oncogenes E1A and c-myc, and chemotherapeutic agent adriamycin did. Mice with a deletion in the FADD gene did not survive beyond day 11.5 of embryogenesis; these mice showed signs of cardiac failure and abdominal hemorrhage. Chimeric embryos showing a high contribution of FADD null mutant cells to the heart reproduce the phenotype of FADD-deficient mutants. Thus, not only death receptors, but also receptors that couple to developmental programs, may use FADD for signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeh, W C -- de la Pompa, J L -- McCurrach, M E -- Shu, H B -- Elia, A J -- Shahinian, A -- Ng, M -- Wakeham, A -- Khoo, W -- Mitchell, K -- El-Deiry, W S -- Lowe, S W -- Goeddel, D V -- Mak, T W -- CA13106/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1954-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Amgen Institute, University of Toronto, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506948" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/physiology ; *Apoptosis ; Carrier Proteins/genetics/*physiology ; Cell Transformation, Neoplastic ; Cells, Cultured ; Doxorubicin/pharmacology ; *Embryonic and Fetal Development ; Endothelium, Vascular/embryology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression ; Gene Targeting ; Heart/*embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncogenes ; Receptors, Tumor Necrosis Factor/genetics/physiology ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, G A -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1047-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841447" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Culture ; Female ; Hominidae/psychology ; Humans ; Male ; *Sexual Behavior ; Sexual Behavior, Animal ; *Sexual Partners
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  • 35
    Publication Date: 1998-06-25
    Description: Signaling pathways that stabilize interleukin-2 (IL-2) messenger RNA (mRNA) in activated T cells were examined. IL-2 mRNA contains at least two cis elements that mediated its stabilization in response to different signals, including activation of c-Jun amino-terminal kinase (JNK). This response was mediated through a cis element encompassing the 5' untranslated region (UTR) and the beginning of the coding region. IL-2 transcripts lacking this 5' element no longer responded to JNK activation but were still responsive to other signals generated during T cell activation, which were probably sensed through the 3' UTR. Thus, multiple elements within IL-2 mRNA modulate its stability in a combinatorial manner, and the JNK pathway controls turnover as well as synthesis of IL-2 mRNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C Y -- Del Gatto-Konczak, F -- Wu, Z -- Karin, M -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1945-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9632395" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, CD28/immunology ; Antigens, CD3/immunology ; Calcimycin/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cyclosporine/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; *Gene Expression Regulation ; Humans ; Imidazoles/pharmacology ; Interleukin-2/*genetics ; JNK Mitogen-Activated Protein Kinases ; Jurkat Cells ; Lymphocyte Activation ; MAP Kinase Kinase 1 ; MAP Kinase Kinase 7 ; *Mitogen-Activated Protein Kinase Kinases ; *Mitogen-Activated Protein Kinases ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Pyridines/pharmacology ; RNA, Messenger/chemistry/genetics/*metabolism ; Signal Transduction ; T-Lymphocytes/immunology/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transgenes ; p38 Mitogen-Activated Protein Kinases
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  • 36
    Publication Date: 1998-09-25
    Description: The development of the Drosophila eye has served as a model system for investigations of tissue patterning and cell-cell communication; however, early eye development has not been well understood. The results presented here indicate that specialized cells are established along the dorsal-ventral midline of the developing eye by Notch-mediated signaling between dorsal and ventral cells, and that Notch activation at the midline plays an essential role both in promoting the growth of the eye primordia and in regulating eye patterning. These observations imply that the developmental homology between Drosophila wings and vertebrate limbs extends to Drosophila eyes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulos, V -- Tomlinson, A -- Panin, V M -- Rauskolb, C -- Irvine, K D -- GM-R01-54594/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2031-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers, The State University, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748163" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning ; Calcium-Binding Proteins ; Drosophila/genetics/*growth & development/metabolism ; *Drosophila Proteins ; Eye Proteins/genetics ; Gene Expression Regulation, Developmental ; Genes, Insect ; Homeodomain Proteins ; Insect Proteins/genetics/physiology ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Larva/growth & development ; Ligands ; Membrane Proteins/genetics/*physiology ; Morphogenesis ; Mutation ; *N-Acetylglucosaminyltransferases ; Photoreceptor Cells, Invertebrate/cytology/*growth & development ; Receptors, Notch ; Signal Transduction ; *Transcription Factors
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-25
    Description: Evolutionary conflict occurs when the deterministic spread of an allele lowers the fitness either of its bearer or of other individuals in the population, leading to selection for suppressors. Sex promotes conflict because associations between alleles are temporary. Differing selection on males and females, sexual selection, and differences in transmission patterns between classes of nuclear and cytoplasmic genes can all give rise to conflict. Inert Y chromosomes, uniparental inheritance of cytoplasmic genes, mating strains and sexes, and many features of sexual behavior may have evolved in part as a result of evolutionary conflict. Estimates of its quantitative importance, however, are still needed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Partridge, L -- Hurst, L D -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2003-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Galton Laboratory, Department of Biology, University College London, London NW1 2HE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748155" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; *Biological Evolution ; Female ; Male ; Meiosis ; Organelles/genetics ; *Selection, Genetic ; *Sex ; Sex Characteristics ; Sexual Behavior, Animal ; Y Chromosome/genetics
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abramson, P R -- Pinkerton, S D -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):1993-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9874650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura/*genetics/physiology ; *Biological Evolution ; Male ; Selection, Genetic ; *Sexual Behavior, Animal ; *Vocalization, Animal
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-28
    Description: The OxyR transcription factor is sensitive to oxidation and activates the expression of antioxidant genes in response to hydrogen peroxide in Escherichia coli. Genetic and biochemical studies revealed that OxyR is activated through the formation of a disulfide bond and is deactivated by enzymatic reduction with glutaredoxin 1 (Grx1). The gene encoding Grx1 is regulated by OxyR, thus providing a mechanism for autoregulation. The redox potential of OxyR was determined to be -185 millivolts, ensuring that OxyR is reduced in the absence of stress. These results represent an example of redox signaling through disulfide bond formation and reduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, M -- Aslund, F -- Storz, G -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1718-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497290" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Bacterial Proteins/genetics/metabolism ; Base Sequence ; Cysteine/metabolism ; *DNA-Binding Proteins ; Disulfides/*metabolism ; Escherichia coli/genetics/*metabolism ; Escherichia coli Proteins ; Gene Expression Regulation, Bacterial ; Glutaredoxins ; Glutathione/metabolism ; Glutathione Disulfide/metabolism ; Glutathione Reductase/metabolism ; Hydrogen Peroxide/*metabolism/pharmacology ; Molecular Sequence Data ; Oxidation-Reduction ; Oxidative Stress ; *Oxidoreductases ; Proteins/genetics/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Thioredoxins/metabolism ; Transcription Factors/genetics/*metabolism
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  • 40
    Publication Date: 1998-05-09
    Description: Hormones and neurotransmitters may mediate common responses through receptors that couple to the same class of heterotrimeric guanine nucleotide-binding (G) protein. For example, several receptors that couple to Gq class proteins can induce cardiomyocyte hypertrophy. Class-specific inhibition of Gq-mediated signaling was produced in the hearts of transgenic mice by targeted expression of a carboxyl-terminal peptide of the alpha subunit Galphaq. When pressure overload was surgically induced, the transgenic mice developed significantly less ventricular hypertrophy than control animals. The data demonstrate the role of myocardial Gq in the initiation of myocardial hypertrophy and indicate a possible strategy for preventing pathophysiological signaling by simultaneously blocking multiple receptors coupled to Gq.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akhter, S A -- Luttrell, L M -- Rockman, H A -- Iaccarino, G -- Lefkowitz, R J -- Koch, W J -- HL-03041/HL/NHLBI NIH HHS/ -- HL-09436/HL/NHLBI NIH HHS/ -- HL-16037/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554846" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/pharmacology ; Animals ; Atrial Natriuretic Factor/genetics ; COS Cells ; Diglycerides/metabolism ; Enzyme Activation ; GTP-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Gene Expression Regulation ; Gene Targeting ; Hypertrophy, Left Ventricular/*metabolism/prevention & control ; Inositol Phosphates/metabolism ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 1/metabolism ; Myocardium/*metabolism ; Peptide Fragments/genetics/metabolism ; Phenylephrine/pharmacology ; Receptors, Adrenergic, alpha/*metabolism ; Signal Transduction ; Transfection ; Transgenes ; Ventricular Pressure
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1438-9, 1441.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750112" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Cadherins/metabolism ; Cell Nucleus/metabolism ; Colorectal Neoplasms/etiology/genetics ; Cytoskeletal Proteins/metabolism ; *Gene Expression Regulation, Neoplastic ; *Genes, APC ; *Genes, myc ; Humans ; Neoplasms/*etiology/genetics ; Proto-Oncogene Proteins/*genetics/physiology ; Proto-Oncogene Proteins c-myc/metabolism ; Signal Transduction ; *Trans-Activators ; Transcription Factors/metabolism ; Wnt Proteins ; *Zebrafish Proteins ; beta Catenin
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-11-13
    Description: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells. To investigate whether this property can be exploited for cancer therapy, severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells were treated with the virus. A single intratumoral injection of virus resulted in regression of tumors in 65 to 80 percent of the mice. Treatment of immune-competent C3H mice bearing tumors established from ras-transformed C3H-10T1/2 cells also resulted in tumor regression, although a series of injections were required. These results suggest that, with further work, reovirus may have applicability in the treatment of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coffey, M C -- Strong, J E -- Forsyth, P A -- Lee, P W -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1332-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Research Group and Department of Microbiology and Infectious Diseases, University of Calgary Health Science Centre, Calgary, Alberta, T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812900" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Viral/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Genes, erbB ; *Genes, ras ; Humans ; Male ; Mammalian orthoreovirus 3/immunology/*physiology ; Mice ; Mice, Inbred C3H ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism/pathology/*therapy/virology ; Signal Transduction ; Tumor Cells, Cultured ; Virus Replication ; ras Proteins/*metabolism
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):477-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9454345" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase/physiology ; Animals ; Calcium-Binding Proteins/metabolism ; *Carrier Proteins ; Cdc20 Proteins ; *Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosomes/*physiology ; Fungal Proteins/metabolism ; Humans ; Kinetochores/*physiology ; Microtubules/metabolism ; *Mitosis ; Nuclear Proteins ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Signal Transduction ; Spindle Apparatus/metabolism
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  • 44
    Publication Date: 1998-04-16
    Description: Photoactive yellow protein (PYP) is a member of the xanthopsin family of eubacterial blue-light photoreceptors. On absorption of light, PYP enters a photocycle that ultimately transduces the energy contained in a light signal into an altered biological response. Nanosecond time-resolved x-ray crystallography was used to determine the structure of the short-lived, red-shifted, intermediate state denoted [pR], which develops within 1 nanosecond after photoelectronic excitation of the chromophore of PYP by absorption of light. The resulting structural model demonstrates that the [pR] state possesses the cis conformation of the 4-hydroxyl cinnamic thioester chromophore, and that the process of trans to cis isomerization is accompanied by the specific formation of new hydrogen bonds that replace those broken upon excitation of the chromophore. Regions of flexibility that compose the chromophore-binding pocket serve to lower the activation energy barrier between the dark state, denoted pG, and [pR], and help initiate entrance into the photocycle. Direct structural evidence is provided for the initial processes of transduction of light energy, which ultimately translate into a physiological signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perman, B -- Srajer, V -- Ren, Z -- Teng, T -- Pradervand, C -- Ursby, T -- Bourgeois, D -- Schotte, F -- Wulff, M -- Kort, R -- Hellingwerf, K -- Moffat, K -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1946-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506946" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Proteins/*chemistry/metabolism ; Chromatiaceae/chemistry ; Crystallography, X-Ray ; Energy Metabolism ; Fourier Analysis ; Hydrogen Bonding ; Isomerism ; Kinetics ; *Light ; Models, Molecular ; *Photoreceptors, Microbial ; *Protein Conformation ; Signal Transduction
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-02-07
    Description: The actin cytoskeleton mediates a variety of essential biological functions in all eukaryotic cells. In addition to providing a structural framework around which cell shape and polarity are defined, its dynamic properties provide the driving force for cells to move and to divide. Understanding the biochemical mechanisms that control the organization of actin is thus a major goal of contemporary cell biology, with implications for health and disease. Members of the Rho family of small guanosine triphosphatases have emerged as key regulators of the actin cytoskeleton, and furthermore, through their interaction with multiple target proteins, they ensure coordinated control of other cellular activities such as gene transcription and adhesion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):509-14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology, Cancer Research Campaign Oncogene and Signal Transduction Group, University College London, Gower Street, London WC1E 6BT, UK. alan.hall@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438836" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Animals ; Cell Adhesion ; Cell Cycle ; Cell Movement ; Cytoskeleton/*metabolism/physiology/*ultrastructure ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Gene Expression Regulation ; Humans ; Membrane Proteins/*metabolism ; Signal Transduction ; rhoB GTP-Binding Protein
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  • 46
    Publication Date: 1998-06-20
    Description: Two- and three-dimensional computer imaging shows that endocranial capacity in an approximately 2.8- to 2.6-million-year-old early hominid cranium (Stw 505) from Sterkfontein, South Africa, tentatively assigned to Australopithecus africanus, is approximately 515 cubic centimeters. Although this is the largest endocranial capacity recorded for this species, it is still markedly less than anecdotal reports of endocranial capacity exceeding 600 cubic centimeters. No australopithecine has an endocranial capacity approaching, let alone exceeding, 600 cubic centimeters. Some currently accepted estimates of early hominid endocranial capacity may be inflated, suggesting that the tempo and mode of early hominid brain evolution may need reevaluation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conroy, G C -- Weber, G W -- Seidler, H -- Tobias, P V -- Kane, A -- Brunsden, B -- New York, N.Y. -- Science. 1998 Jun 12;280(5370):1730-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology and Department of Anthropology, Washington University School of Medicine, St. Louis, MO 63110, USA. conroyg@thalamus.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9624045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Brain/*anatomy & histology ; Computer Simulation ; *Fossils ; History, Ancient ; Hominidae/*anatomy & histology ; Humans ; Image Processing, Computer-Assisted ; *Models, Anatomic ; Skull/*anatomy & histology ; South Africa ; Tomography, X-Ray Computed
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hall, A -- New York, N.Y. -- Science. 1998 Jun 26;280(5372):2074-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK. Alan.Hall@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9669963" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Cytoskeleton/metabolism ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Protein alpha Subunits, G12-G13 ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Morphogenesis ; Myosins/metabolism ; Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/metabolism ; Rho Guanine Nucleotide Exchange Factors ; Signal Transduction
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  • 48
    Publication Date: 1999-01-15
    Description: Mutator genotypes with increased mutation rates may be especially important in microbial evolution if genetic adaptation is generally limited by the supply of mutations. In experimental populations of the bacterium Escherichia coli, the rate of evolutionary adaptation was proportional to the mutation supply rate only in particular circumstances of small or initially well-adapted populations. These experiments also demonstrate a "speed limit" on adaptive evolution in asexual populations, one that is independent of the mutation supply rate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arjan, J A -- Visser, M -- Zeyl, C W -- Gerrish, P J -- Blanchard, J L -- Lenski, R E -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):404-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Microbial Ecology, Michigan State University, East Lansing, MI 48824, USA. arjan.devisser@algemeen.micr.wau.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888858" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Biological Evolution ; Escherichia coli/*genetics/physiology ; Genetics, Population ; Genotype ; Linear Models ; *Models, Biological ; *Mutation
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Appenzeller, T -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2108-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409068" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; *Biological Evolution ; Culture Media ; *Ecosystem ; Escherichia coli/*genetics/physiology ; Glucose/metabolism ; Maltose/metabolism ; *Mutation ; Pseudomonas fluorescens/*genetics/physiology ; Selection, Genetic
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitehead, F -- New York, N.Y. -- Science. 1999 Oct 22;286(5440):681.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577223" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Education/legislation & jurisprudence/standards ; Kansas ; *Politics ; Religion and Science ; Science/*education
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):14-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism ; Cells, Cultured ; Dimerization ; Drug Design ; Humans ; Neurons/*metabolism ; Potassium Channels/metabolism ; Rats ; Receptors, GABA-B/*chemistry/*metabolism ; Signal Transduction ; gamma-Aminobutyric Acid/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culotta, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):572-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328732" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Ethiopia ; Facial Bones/anatomy & histology ; *Fossils ; History, Ancient ; *Hominidae/anatomy & histology/classification ; Humans ; Paleodontology ; Skull/anatomy & histology ; Tooth/anatomy & histology
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  • 53
    Publication Date: 1999-09-18
    Description: The antifungal defense of Drosophila is controlled by the spaetzle/Toll/cactus gene cassette. Here, a loss-of-function mutation in the gene encoding a blood serine protease inhibitor, Spn43Ac, was shown to lead to constitutive expression of the antifungal peptide drosomycin, and this effect was mediated by the spaetzle and Toll gene products. Spaetzle was cleaved by proteolytic enzymes to its active ligand form shortly after immune challenge, and cleaved Spaetzle was constitutively present in Spn43Ac-deficient flies. Hence, Spn43Ac negatively regulates the Toll signaling pathway, and Toll does not function as a pattern recognition receptor in the Drosophila host defense.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levashina, E A -- Langley, E -- Green, C -- Gubb, D -- Ashburner, M -- Hoffmann, J A -- Reichhart, J M -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1917-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UPR 9022 CNRS, Institut de Biologie Moleculaire et Cellulaire, 15 Rue Rene Descartes, Strasbourg 67084, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10489372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antifungal Agents/*metabolism ; *Antimicrobial Cationic Peptides ; Body Patterning ; Drosophila/embryology/genetics/*immunology ; *Drosophila Proteins ; Escherichia coli/genetics/immunology ; Genes, Insect ; Hemolymph/metabolism ; Insect Proteins/*biosynthesis/genetics/metabolism/*physiology ; Membrane Glycoproteins/genetics/*physiology ; Micrococcus luteus/immunology ; Molecular Sequence Data ; Mutagenesis ; Peptides/genetics/metabolism ; *Receptors, Cell Surface ; Recombinant Fusion Proteins/genetics/metabolism ; Serine Proteinase Inhibitors/genetics/*metabolism ; Serpins/genetics/*metabolism ; Signal Transduction ; Toll-Like Receptors ; Up-Regulation
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-02-05
    Description: Traditionally, the interest of population and evolutionary biologists in infectious diseases has been almost exclusively in their role as agents of natural selection in higher organisms. Recently, this interest has expanded to include the genetic structure and evolution of microparasite populations, the mechanisms of pathogenesis and the immune response, and the population biology, ecology, and evolutionary consequences of medical and public health interventions. This article describes recent work in these areas, emphasizing the ways in which quantitative, population-biological approaches have been contributing to the understanding of infectious disease and the design and evaluation of interventions for their treatment and prevention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levin, B R -- Lipsitch, M -- Bonhoeffer, S -- New York, N.Y. -- Science. 1999 Feb 5;283(5403):806-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Emory University, 1510 Clifton Road, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9933155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Physiological Phenomena ; *Biological Evolution ; Drug Resistance, Microbial ; Humans ; Infection/immunology/*microbiology ; Molecular Epidemiology ; Parasites/genetics/physiology ; Parasitic Diseases/immunology/*parasitology ; Population Dynamics ; Vaccination ; Virus Physiological Phenomena
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  • 55
    Publication Date: 1999-01-23
    Description: The plant hormone abscisic acid (ABA) regulates potassium and chloride ion channels at the plasma membrane of guard cells, leading to stomatal closure that reduces transpirational water loss from the leaf. The tobacco Nt-SYR1 gene encodes a syntaxin that is associated with the plasma membrane. Syntaxins and related SNARE proteins aid intracellular vesicle trafficking, fusion, and secretion. Disrupting Nt-Syr1 function by cleavage with Clostridium botulinum type C toxin or competition with a soluble fragment of Nt-Syr1 prevents potassium and chloride ion channel response to ABA in guard cells and implicates Nt-Syr1 in an ABA-signaling cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leyman, B -- Geelen, D -- Quintero, F J -- Blatt, M R -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):537-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Plant Physiology and Biophysics, University of London, Wye College, Wye, Kent TN25 5AH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915701" target="_blank"〉PubMed〈/a〉
    Keywords: Abscisic Acid/*pharmacology ; Amino Acid Sequence ; Animals ; Botulinum Toxins/metabolism ; Cell Membrane/physiology ; Chloride Channels/*physiology ; Genes, Plant ; Genetic Complementation Test ; Ion Channel Gating/drug effects ; Membrane Proteins/chemistry/genetics/*physiology ; Molecular Sequence Data ; Oocytes ; Patch-Clamp Techniques ; Plant Growth Regulators/*pharmacology ; Plant Leaves/*physiology ; *Plants, Toxic ; Potassium Channels/*physiology ; Qa-SNARE Proteins ; Saccharomyces cerevisiae/genetics/growth & development ; Signal Transduction ; Tobacco/genetics/*physiology ; Xenopus
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  • 56
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wojcik, J F -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):663.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10454918" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Humans ; *Religion and Science
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  • 57
    Publication Date: 1999-11-05
    Description: Glutamatergic neurotransmission is controlled by presynaptic metabotropic glutamate receptors (mGluRs). A subdomain in the intracellular carboxyl-terminal tail of group III mGluRs binds calmodulin and heterotrimeric guanosine triphosphate-binding protein (G protein) betagamma subunits in a mutually exclusive manner. Mutations interfering with calmodulin binding and calmodulin antagonists inhibit G protein-mediated modulation of ionic currents by mGluR 7. Calmodulin antagonists also prevent inhibition of excitatory neurotransmission via presynaptic mGluRs. These results reveal a novel mechanism of presynaptic modulation in which Ca(2+)-calmodulin is required to release G protein betagamma subunits from the C-tail of group III mGluRs in order to mediate glutamatergic autoinhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Connor, V -- El Far, O -- Bofill-Cardona, E -- Nanoff, C -- Freissmuth, M -- Karschin, A -- Airas, J M -- Betz, H -- Boehm, S -- New York, N.Y. -- Science. 1999 Nov 5;286(5442):1180-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurochemistry, Max Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10550060" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Calmodulin/antagonists & inhibitors/*metabolism ; Cells, Cultured ; Dimerization ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; GTP-Binding Proteins/*metabolism ; Glutamic Acid/*metabolism ; Hippocampus/cytology/metabolism ; Humans ; Mice ; Molecular Sequence Data ; Neurons/metabolism ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Presynaptic Terminals/metabolism ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/antagonists & inhibitors/*metabolism ; Recombinant Fusion Proteins/metabolism ; Sesterterpenes ; Signal Transduction ; Swine ; *Synaptic Transmission ; Terpenes/pharmacology
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  • 58
    Publication Date: 1999-05-29
    Description: Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, D Y -- Sorensen, L K -- Brooke, B S -- Urness, L D -- Davis, E C -- Taylor, D G -- Boak, B B -- Wendel, D P -- K08 HL03490-03/HL/NHLBI NIH HHS/ -- T35 HL07744-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 28;284(5419):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD31/analysis ; Blood Vessels/cytology/*embryology/metabolism ; Cell Differentiation ; Crosses, Genetic ; Endothelium, Vascular/cytology/*embryology/metabolism ; Female ; Gene Targeting ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Muscle, Smooth, Vascular/cytology/*embryology ; *Neovascularization, Physiologic ; Receptors, Cell Surface ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Vascular Cell Adhesion Molecule-1/genetics/*physiology ; Yolk Sac/ultrastructure
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  • 59
    Publication Date: 1999-07-31
    Description: Many immune receptors are composed of separate ligand-binding and signal-transducing subunits. In natural killer (NK) and T cells, DAP10 was identified as a cell surface adaptor protein in an activating receptor complex with NKG2D, a receptor for the stress-inducible and tumor-associated major histocompatibility complex molecule MICA. Within the DAP10 cytoplasmic domain, an Src homology 2 (SH2) domain-binding site was capable of recruiting the p85 subunit of the phosphatidylinositol 3-kinase (PI 3-kinase), providing for NKG2D-dependent signal transduction. Thus, NKG2D-DAP10 receptor complexes may activate NK and T cell responses against MICA-bearing tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, J -- Song, Y -- Bakker, A B -- Bauer, S -- Spies, T -- Lanier, L L -- Phillips, J H -- AI30581/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):730-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Binding Sites ; Cell Line ; Cytotoxicity, Immunologic ; Humans ; Killer Cells, Natural/*immunology/metabolism ; Ligands ; *Lymphocyte Activation ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Molecular Sequence Data ; NK Cell Lectin-Like Receptor Subfamily K ; Neoplasms/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Receptors, Immunologic/chemistry/genetics/*metabolism ; Receptors, Natural Killer Cell ; Signal Transduction ; T-Lymphocytes/*immunology/metabolism ; Tumor Cells, Cultured ; src Homology Domains
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  • 60
    Publication Date: 1999-07-03
    Description: Lymphocyte development is critically influenced by self-antigens. T cells are subject to both positive and negative selection, depending on their degree of self-reactivity. Although B cells are subject to negative selection, it has been difficult to test whether self-antigen plays any positive role in B cell development. A murine model system of naturally generated autoreactive B cells with a germ line gene-encoded specificity for the Thy-1 (CD90) glycoprotein was developed, in which the presence of self-antigen promotes B cell accumulation and serum autoantibody secretion. Thus, B cells can be subject to positive selection, generated, and maintained on the basis of their autoreactivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayakawa, K -- Asano, M -- Shinton, S A -- Gui, M -- Allman, D -- Stewart, C L -- Silver, J -- Hardy, R R -- New York, N.Y. -- Science. 1999 Jul 2;285(5424):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Research, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111, USA. K_Hayakawa@fccc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10390361" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Animals ; Antigens, CD5/analysis ; Antigens, Thy-1/*immunology ; Autoantibodies/*biosynthesis/blood/immunology ; Autoantigens/*immunology ; B-Lymphocyte Subsets/*immunology ; Genes, Immunoglobulin ; Hybridomas ; Immunity, Innate ; Immunologic Surveillance ; Mice ; Mice, SCID ; Mice, Transgenic ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction ; T-Lymphocytes/immunology
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  • 61
    Publication Date: 1999-04-09
    Description: Phosphorylation of inhibitor of kappa B (IkappaB) proteins is an important step in the activation of the transcription nuclear factor kappa B (NF-kappaB) and requires two IkappaB kinases, IKK1 (IKKalpha) and IKK2 (IKKbeta). Mice that are devoid of the IKK2 gene had extensive liver damage from apoptosis and died as embryos, but these mice could be rescued by the inactivation of the gene encoding tumor necrosis factor receptor 1. Mouse embryonic fibroblast cells that were isolated from IKK2-/- embryos showed a marked reduction in tumor necrosis factor-alpha (TNF-alpha)- and interleukin-1alpha-induced NF-kappaB activity and an enhanced apoptosis in response to TNF-alpha. IKK1 associated with NF-kappaB essential modulator (IKKgamma/IKKAP1), another component of the IKK complex. These results show that IKK2 is essential for mouse development and cannot be substituted with IKK1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Q -- Van Antwerp, D -- Mercurio, F -- Lee, K F -- Verma, I M -- New York, N.Y. -- Science. 1999 Apr 9;284(5412):321-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute, La Jolla, CA 92037, USA. Signal Pharmaceuticals, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10195897" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Line ; DNA-Binding Proteins/metabolism ; Embryonic and Fetal Development ; Gene Targeting ; I-kappa B Kinase ; I-kappa B Proteins ; Interleukin-1/pharmacology ; Liver/cytology/*embryology ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Receptors, Tumor Necrosis Factor/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Signal Transduction ; Transcription Factor RelA ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
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  • 62
    Publication Date: 2000-01-05
    Description: Phytochromes are a family of photoreceptors used by green plants to entrain their development to the light environment. The distribution of these chromoproteins has been expanded beyond photoautotrophs with the discovery of phytochrome-like proteins in the nonphotosynthetic eubacteria Deinococcus radiodurans and Pseudomonas aeruginosa. Like plant phytochromes, the D. radiodurans receptor covalently binds linear tetrapyrroles autocatalytically to generate a photochromic holoprotein. However, the attachment site is distinct, using a histidine to potentially form a Schiff base linkage. Sequence homology and mutational analysis suggest that D. radiodurans bacteriophytochrome functions as a light-regulated histidine kinase, which helps protect the bacterium from visible light.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S J -- Vener, A V -- Vierstra, R D -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2517-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, Cellular and Molecular Biology Program and Department of Horticulture, University of Wisconsin-Madison, 1575 Linden Drive, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617469" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Bacterial Proteins/chemistry/genetics/*metabolism ; Biliverdine/analogs & derivatives/metabolism ; Binding Sites ; Gram-Positive Cocci/genetics/*metabolism ; Histidine/metabolism ; Light ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Photoreceptors, Microbial/chemistry/genetics/*metabolism ; Phytochrome/metabolism ; Protein Kinases/chemistry/genetics/*metabolism ; Pseudomonas aeruginosa/*metabolism ; Signal Transduction
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, H -- New York, N.Y. -- Science. 1999 Sep 17;285(5435):1849.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10515786" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Biology/education ; Kansas ; Science/*education ; Universities/standards
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  • 64
    Publication Date: 1999-01-05
    Description: CmPP16 from Cucurbita maxima was cloned and the protein was shown to possess properties similar to those of viral movement proteins. CmPP16 messenger RNA (mRNA) is present in phloem tissue, whereas protein appears confined to sieve elements (SE). Microinjection and grafting studies revealed that CmPP16 moves from cell to cell, mediates the transport of sense and antisense RNA, and moves together with its mRNA into the SE of scion tissue. CmPP16 possesses the characteristics that are likely required to mediate RNA delivery into the long-distance translocation stream. Thus, RNA may move within the phloem as a component of a plant information superhighway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xoconostle-Cazares, B -- Xiang, Y -- Ruiz-Medrano, R -- Wang, H L -- Monzer, J -- Yoo, B C -- McFarland, K C -- Franceschi, V R -- Lucas, W J -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):94-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Plant Biology, Division of Biological Sciences, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872750" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Biological Transport ; Cloning, Molecular ; Cucumis sativus ; Cucurbitaceae/genetics/*metabolism ; Microinjections ; Molecular Sequence Data ; Plant Leaves/metabolism ; Plant Proteins/chemistry/genetics/*metabolism ; Plant Roots/metabolism ; Plant Stems/metabolism ; Plant Viral Movement Proteins ; RNA, Antisense/metabolism ; RNA, Messenger/*metabolism ; RNA, Plant/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Viral Proteins/chemistry/metabolism
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, T -- DePinho, R A -- CA76027/CA/NCI NIH HHS/ -- HD 348880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1999 Feb 12;283(5404):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10075559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Aging ; *Cell Division ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Neoplasms/enzymology/metabolism/pathology ; Proto-Oncogene Proteins c-myc/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; Telomerase/genetics/*metabolism ; Telomere/*metabolism ; ras Proteins/metabolism
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  • 66
    Publication Date: 1999-02-26
    Description: Cell proliferation and differentiation are regulated by growth regulatory factors such as transforming growth factor-beta (TGF-beta) and the liphophilic hormone vitamin D. TGF-beta causes activation of SMAD proteins acting as coactivators or transcription factors in the nucleus. Vitamin D controls transcription of target genes through the vitamin D receptor (VDR). Smad3, one of the SMAD proteins downstream in the TGF-beta signaling pathway, was found in mammalian cells to act as a coactivator specific for ligand-induced transactivation of VDR by forming a complex with a member of the steroid receptor coactivator-1 protein family in the nucleus. Thus, Smad3 may mediate cross-talk between vitamin D and TGF-beta signaling pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yanagisawa, J -- Yanagi, Y -- Masuhiro, Y -- Suzawa, M -- Watanabe, M -- Kashiwagi, K -- Toriyabe, T -- Kawabata, M -- Miyazono, K -- Kato, S -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1317-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037600" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Protein Receptors ; Bone Morphogenetic Proteins/pharmacology ; COS Cells ; Calcitriol/*metabolism/pharmacology ; Cell Nucleus/metabolism ; DNA-Binding Proteins/*metabolism ; Histone Acetyltransferases ; Ligands ; Nuclear Receptor Coactivator 1 ; Phosphorylation ; Receptor Cross-Talk ; Receptors, Calcitriol/*metabolism ; Receptors, Cell Surface/metabolism ; *Receptors, Growth Factor ; Receptors, Retinoic Acid/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Retinoid X Receptors ; Signal Transduction ; Smad3 Protein ; Trans-Activators/*metabolism ; Transcription Factors/metabolism ; *Transcriptional Activation ; Transfection ; Transforming Growth Factor beta/*metabolism
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  • 67
    Publication Date: 1999-12-03
    Description: Linker proteins function as molecular scaffolds to localize enzymes with substrates. In B cells, B cell linker protein (BLNK) links the B cell receptor (BCR)-activated Syk kinase to the phosphoinositide and mitogen-activated kinase pathways. To examine the in vivo role of BLNK, mice deficient in BLNK were generated. B cell development in BLNK-/- mice was blocked at the transition from B220+CD43+ progenitor B to B220+CD43- precursor B cells. Only a small percentage of immunoglobulin M++ (IgM++), but not mature IgMloIgDhi, B cells were detected in the periphery. Hence, BLNK is an essential component of BCR signaling pathways and is required to promote B cell development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pappu, R -- Cheng, A M -- Li, B -- Gong, Q -- Chiu, C -- Griffin, N -- White, M -- Sleckman, B P -- Chan, A C -- AI42787/AI/NIAID NIH HHS/ -- CA71516/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 3;286(5446):1949-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Division of Rheumatology, Department of Medicine, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10583957" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Aging ; Animals ; B-Lymphocyte Subsets/cytology/immunology ; B-Lymphocytes/*cytology/immunology/*metabolism ; Bone Marrow Cells/cytology/immunology ; Carrier Proteins/genetics/*physiology ; Cell Count ; Cell Differentiation ; Cell Separation ; Cell Size ; Flow Cytometry ; Gene Targeting ; Hematopoietic Stem Cells/*cytology/metabolism ; Immunoglobulin M/analysis ; Leukopoiesis ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; *Phosphoproteins ; Receptors, Antigen, B-Cell/*metabolism ; Second Messenger Systems ; Signal Transduction
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  • 68
    Publication Date: 1999-03-05
    Description: Protein tyrosine phosphatase-1B (PTP-1B) has been implicated in the negative regulation of insulin signaling. Disruption of the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP-1B+/+ littermates. The enhanced insulin sensitivity of the PTP-1B-/- mice was also evident in glucose and insulin tolerance tests. The PTP-1B-/- mice showed increased phosphorylation of the insulin receptor in liver and muscle tissue after insulin injection in comparison to PTP-1B+/+ mice. On a high-fat diet, the PTP-1B-/- and PTP-1B+/- mice were resistant to weight gain and remained insulin sensitive, whereas the PTP-1B+/+ mice rapidly gained weight and became insulin resistant. These results demonstrate that PTP-1B has a major role in modulating both insulin sensitivity and fuel metabolism, thereby establishing it as a potential therapeutic target in the treatment of type 2 diabetes and obesity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elchebly, M -- Payette, P -- Michaliszyn, E -- Cromlish, W -- Collins, S -- Loy, A L -- Normandin, D -- Cheng, A -- Himms-Hagen, J -- Chan, C C -- Ramachandran, C -- Gresser, M J -- Tremblay, M L -- Kennedy, B P -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1544-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, McGill University, 3655 Drummond Street, Montreal, Quebec, Canada, H3G 1Y6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066179" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dietary Fats/administration & dosage ; Gene Targeting ; Glucose Tolerance Test ; Insulin/blood/*metabolism/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Muscle, Skeletal/metabolism ; Obesity/*metabolism/therapy ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Tyrosine Phosphatases/*genetics/*metabolism ; Receptor, Insulin/metabolism ; Signal Transduction
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  • 69
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-04-02
    Description: One of the most striking patterns in biology is the formation of animal aggregations. Classically, aggregation has been viewed as an evolutionarily advantageous state, in which members derive the benefits of protection, mate choice, and centralized information, balanced by the costs of limiting resources. Consisting of individual members, aggregations nevertheless function as an integrated whole, displaying a complex set of behaviors not possible at the level of the individual organism. Complexity theory indicates that large populations of units can self-organize into aggregations that generate pattern, store information, and engage in collective decision-making. This begs the question, are all emergent properties of animal aggregations functional or are some simply pattern? Solutions to this dilemma will necessitate a closer marriage of theoretical and modeling studies linked to empirical work addressing the choices, and trajectories, of individuals constrained by membership in the group.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parrish, J K -- Edelstein-Keshet, L -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoology Department, University of Washington, Seattle, WA 98195, USA. jparrish@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; *Biological Evolution ; *Cooperative Behavior ; Mathematics ; Models, Biological
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  • 71
    Publication Date: 1999-10-09
    Description: Ubiquitination of receptor protein-tyrosine kinases (RPTKs) terminates signaling by marking active receptors for degradation. c-Cbl, an adapter protein for RPTKs, positively regulates RPTK ubiquitination in a manner dependent on its variant SRC homology 2 (SH2) and RING finger domains. Ubiquitin-protein ligases (or E3s) are the components of ubiquitination pathways that recognize target substrates and promote their ligation to ubiquitin. The c-Cbl protein acted as an E3 that can recognize tyrosine-phosphorylated substrates, such as the activated platelet-derived growth factor receptor, through its SH2 domain and that recruits and allosterically activates an E2 ubiquitin-conjugating enzyme through its RING domain. These results reveal an SH2-containing protein that functions as a ubiquitin-protein ligase and thus provide a distinct mechanism for substrate targeting in the ubiquitin system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Joazeiro, C A -- Wing, S S -- Huang, H -- Leverson, J D -- Hunter, T -- Liu, Y C -- CA39780/CA/NCI NIH HHS/ -- R01 DK56558/DK/NIDDK NIH HHS/ -- T32CA09523/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Oct 8;286(5438):309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Salk Institute, Molecular Biology and Virology Laboratory, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10514377" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Cell Line ; Humans ; Ligases/chemistry/*metabolism ; Molecular Sequence Data ; Phosphotyrosine/metabolism ; Point Mutation ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Receptor Protein-Tyrosine Kinases/*metabolism ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Recombinant Fusion Proteins/metabolism ; Sequence Alignment ; Signal Transduction ; *Ubiquitin-Conjugating Enzymes ; Ubiquitin-Protein Ligases ; Ubiquitins/*metabolism ; src Homology Domains
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-18
    Description: Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boulanger, L -- Poo, M M -- NS 37831/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 18;284(5422):1982-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10373115" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain-Derived Neurotrophic Factor/*pharmacology ; *Carbazoles ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cycloleucine/analogs & derivatives/pharmacology ; *Excitatory Postsynaptic Potentials/drug effects ; Indoles/pharmacology ; Nerve Growth Factors/pharmacology ; Neuronal Plasticity ; Neurons/cytology/physiology ; Neurotrophin 3 ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Pyrroles/pharmacology ; Signal Transduction ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Thionucleotides/pharmacology ; Xenopus
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  • 73
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: Interactions between species are as evolutionarily malleable as the species themselves and have played a central role in the diversification and organization of life. This malleability creates complex geographic mosaics in interspecific interactions that can evolve rapidly over decades, blurring the distinction between evolutionary time and ecological time and making the study of coevolution crucial for human health and welfare.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, J N -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2116-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Botany and Zoology, Washington State University, Pullman, WA 99164, USA. jnt@wsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drug Resistance, Microbial ; *Ecosystem ; Humans ; Models, Biological ; Parasites/pathogenicity ; *Selection, Genetic ; Virulence/genetics
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-03-19
    Description: The role of localized instability of the actin network in specifying axonal fate was examined with the use of rat hippocampal neurons in culture. During normal neuronal development, actin dynamics and instability polarized to a single growth cone before axon formation. Consistently, global application of actin-depolymerizing drugs and of the Rho-signaling inactivator toxin B to nonpolarized cells produced neurons with multiple axons. Moreover, disruption of the actin network in one individual growth cone induced its neurite to become the axon. Thus, local instability of the actin network restricted to a single growth cone is a physiological signal specifying neuronal polarization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bradke, F -- Dotti, C G -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1931-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉European Molecular Biology Laboratory, Cell Biology Programme, Meyerhofstrasse 1, 69012 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10082468" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism/*physiology ; Animals ; Axons/*physiology/ultrastructure ; *Bacterial Proteins ; Bacterial Toxins/pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Cell Polarity ; Cells, Cultured ; Cytochalasin D/pharmacology ; GTP Phosphohydrolases/antagonists & inhibitors/metabolism ; Growth Cones/drug effects/*physiology/ultrastructure ; Hippocampus ; Microtubules/physiology/ultrastructure ; Neurites/*physiology/ultrastructure ; Phenotype ; Pseudopodia/drug effects/ultrastructure ; Rats ; Signal Transduction ; Thiazoles/pharmacology ; Thiazolidines
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tiedge, H -- Bloom, F E -- Richter, D -- New York, N.Y. -- Science. 1999 Jan 8;283(5399):186-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, State Univeristy of New York Health Science Center at Brooklyn, Brooklyn, NY 11203, USA. tiedge@hscbklyn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9925478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Biological Transport ; Cyclic AMP Response Element-Binding Protein/metabolism ; Dendrites/*metabolism ; Gene Expression Regulation ; *Neuronal Plasticity ; Protein Biosynthesis ; RNA, Messenger/chemistry/genetics/*metabolism ; Ribonucleoproteins/metabolism ; Signal Transduction ; Synapses/metabolism/*physiology
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-04-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1999 Mar 19;283(5409):1825-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10206881" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/*genetics/growth & development/metabolism ; *Arabidopsis Proteins ; *Genes, Plant ; Ligands ; Meristem/growth & development ; Phosphotransferases/genetics/metabolism ; Plant Proteins/chemistry/*genetics/metabolism/physiology ; Signal Transduction
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2081.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10409061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Artiodactyla/*genetics ; *Biological Evolution ; Carnivora/classification/*genetics ; Short Interspersed Nucleotide Elements ; Whales/*genetics
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  • 78
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-11-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dusenbery, D B -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):413-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10577200" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Genetic Variation
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-09-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmer, C -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1335, 1337.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10490402" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones/anatomy & histology ; *Fossils ; History, Ancient ; Hominidae/anatomy & histology/*classification ; Humans ; Kenya ; Paleodontology ; Skeleton ; Terminology as Topic
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 May 21;284(5418):1305-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383313" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/classification/*genetics ; Bacteria/classification/*genetics ; *Biological Evolution ; *Eukaryotic Cells ; Evolution, Molecular ; Genes, rRNA ; *Genome ; *Phylogeny ; Recombination, Genetic
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  • 81
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-05-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):575, 577.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10328733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Fishes/anatomy & histology ; *Fossils ; Jaw/*anatomy & histology ; Neural Crest/cytology/physiology ; *Vertebrates/anatomy & histology
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  • 82
    Publication Date: 1999-03-26
    Description: Transforming growth factor-beta (TGF-beta) signaling is mediated by a complex of type I (TBRI) and type II (TBRII) receptors. The type III receptor (TBRIII) lacks a recognizable signaling domain and has no clearly defined role in TGF-beta signaling. Cardiac endothelial cells that undergo epithelial-mesenchymal transformation express TBRIII, and here TBRIII-specific antisera were found to inhibit mesenchyme formation and migration in atrioventricular cushion explants. Misexpression of TBRIII in nontransforming ventricular endothelial cells conferred transformation in response to TGF-beta2. These results support a model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, C B -- Boyer, A S -- Runyan, R B -- Barnett, J V -- 38649/PHS HHS/ -- 42266/PHS HHS/ -- HL52922/HL/NHLBI NIH HHS/ -- R01 HL052922/HL/NHLBI NIH HHS/ -- R01 HL052922-05/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2080-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN 37232-6600, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092230" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement ; Chick Embryo ; Culture Techniques ; Endocardium/cytology/*embryology/metabolism ; Endothelium/*cytology/embryology/metabolism ; Genetic Vectors ; Heart/*embryology ; Heart Atria/cytology/embryology ; Heart Ventricles/cytology/embryology/virology ; Immune Sera ; Ligands ; Mesoderm/*cytology/metabolism ; Myocardium/cytology/metabolism ; Protein-Serine-Threonine Kinases ; Proteoglycans/immunology/*physiology ; Receptors, Transforming Growth Factor beta/immunology/*physiology ; Retroviridae/genetics/physiology ; Signal Transduction ; Transforming Growth Factor beta/*metabolism/pharmacology
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: Organisms allocate resources to male and female offspring in a process called sex allocation. In a Perspective, Stuart West and colleagues discuss what sex allocation tells us about evolution by natural selection and how sex allocation can be applied to understanding the mating structure of parasitic protozoans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, S A -- Herre, E A -- Sheldon, B C -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):288-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 3JT, UK. stu.west@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11183376" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; *Biological Evolution ; Female ; Inbreeding ; Insects/physiology ; Male ; Plasmodium/physiology ; Selection, Genetic ; *Sex Characteristics ; *Sex Ratio ; Sexual Behavior, Animal
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  • 84
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-08-05
    Description: Reproductive cells that are destined to become sperm or egg undergo meiotic division during which the chromosome number is halved. As Sluder and McCollum explain in their Perspective, new findings (Shonn et al.) in yeast show that there is a spindle checkpoint that operates during meiosis to ensure that an equal number of replicated chromosomes arrives at each pole of the cell. One of the components of this meiotic spindle checkpoint turns out to be Mad2, which gives the signal to halt meiosis if it looks like unequal chromosome segregation is taking place.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sluder, G -- McCollum, D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):254-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA. greenfield.sluder@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917849" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium-Binding Proteins/physiology ; *Carrier Proteins ; Cell Cycle Proteins ; Chromosome Aberrations ; Chromosome Disorders ; Chromosome Segregation ; Fungal Proteins/physiology ; Humans ; Meiosis/*physiology ; Nuclear Proteins ; Saccharomycetales/genetics/physiology ; Signal Transduction
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  • 85
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: Microbiologists often focus on one organism and its relationship to its host at one point in time. But viewed in light of evolution, host-parasite relationships range from deadly to helpful, depending on the communication between them. At a meeting here last month of virologists, bacteriologists, parasitologists, and molecular biologists--each dealing with different microorganisms in distinct ways--researchers lamented that evolution is often considered outside the bailiwick of microbiologists, particularly those studying infectious diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, E -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1491-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/genetics/*pathogenicity ; Bacterial Infections/microbiology ; *Bacterial Physiological Phenomena ; *Biological Evolution ; Escherichia coli/genetics/pathogenicity/physiology ; *Host-Parasite Interactions ; Humans ; Leishmania/pathogenicity/*physiology ; Leishmaniasis/parasitology ; Mutation ; Rhizobium/physiology ; *Symbiosis ; Virulence
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 86
    Publication Date: 2000-08-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, S -- Meier, W -- Lovell, F -- McCoy, A -- Robinove, C J -- Creelan, T F -- Brun, R -- Gordon, I -- MacWest, R -- Collier, I E -- Gish, D T -- Hartmann, W K -- Behe, M J -- New York, N.Y. -- Science. 2000 Aug 11;289(5481):869-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10960317" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; Biology/education ; Religion and Science ; Science/*education
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-08-12
    Description: On page 441 of this issue, evolutionary biologists showcase the purple-throated carib hummingbird as a rare example of food supply--in this case, flower shape--spurring the evolution of a sexual dimorphism, or a feature that differs between males and females. On St. Lucia, an island in the West Indies, female caribs sport bills a third longer and twice as curved as those of their male counterparts--one of the most extreme bill differences between the sexes in any hummingbird species. In the paper, the researchers link these "whoppingly dimorphic bills" to the specific flowers the male and female caribs frequent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, K -- New York, N.Y. -- Science. 2000 Jul 21;289(5478):369-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10939937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beak/*anatomy & histology ; *Biological Evolution ; Birds/*anatomy & histology/physiology ; Ecosystem ; Feeding Behavior ; Female ; Male ; Plant Structures/anatomy & histology ; Saint Lucia ; *Sex Characteristics ; Zingiberales/*anatomy & histology
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  • 88
    Publication Date: 2000-12-16
    Description: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" 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/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD3/genetics/*physiology ; Brain/growth & development/*physiology ; Excitatory Postsynaptic Potentials ; Gene Expression Profiling ; Genes, MHC Class I ; Geniculate Bodies/physiology ; Hippocampus/growth & development/physiology ; Histocompatibility Antigens Class I/genetics/*physiology ; In Situ Hybridization ; Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neural Pathways ; *Neuronal Plasticity ; Neurons/*physiology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Retina/growth & development/physiology ; Retinal Ganglion Cells/physiology ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission ; Visual Pathways
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  • 89
    Publication Date: 1999-12-30
    Description: The Smad proteins mediate transforming growth factor-beta (TGFbeta) signaling from the transmembrane serine-threonine receptor kinases to the nucleus. The Smad anchor for receptor activation (SARA) recruits Smad2 to the TGFbeta receptors for phosphorylation. The crystal structure of a Smad2 MH2 domain in complex with the Smad-binding domain (SBD) of SARA has been determined at 2.2 angstrom resolution. SARA SBD, in an extended conformation comprising a rigid coil, an alpha helix, and a beta strand, interacts with the beta sheet and the three-helix bundle of Smad2. Recognition between the SARA rigid coil and the Smad2 beta sheet is essential for specificity, whereas interactions between the SARA beta strand and the Smad2 three-helix bundle contribute significantly to binding affinity. Comparison of the structures between Smad2 and a comediator Smad suggests a model for how receptor-regulated Smads are recognized by the type I receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, G -- Chen, Y G -- Ozdamar, B -- Gyuricza, C A -- Chong, P A -- Wrana, J L -- Massague, J -- Shi, Y -- CA85171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):92-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10615055" target="_blank"〉PubMed〈/a〉
    Keywords: *Activin Receptors, Type I ; Amino Acid Sequence ; Binding Sites ; Carrier Proteins/*chemistry/*metabolism ; Crystallography, X-Ray ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Hydrogen Bonding ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Phosphorylation ; Point Mutation ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/chemistry/genetics/metabolism ; Receptors, Transforming Growth Factor beta/chemistry/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Signal Transduction ; Smad2 Protein ; Trans-Activators/*chemistry/genetics/*metabolism ; Zinc Fingers
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, E -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2131-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744527" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones/anatomy & histology ; Forearm/anatomy & histology ; Gorilla gorilla/anatomy & histology/physiology ; Hominidae/*anatomy & histology/physiology ; Humans ; Pan troglodytes/anatomy & histology/physiology ; *Walking ; Wrist Joint/*anatomy & histology
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  • 91
    Publication Date: 2000-03-17
    Description: Chronic blockade of dopamine D2 receptors, a common mechanism of action for antipsychotic drugs, down-regulates D1 receptors in the prefrontal cortex and, as shown here, produces severe impairments in working memory. These deficits were reversed in monkeys by short-term coadministration of a D1 agonist, ABT 431, and this improvement was sustained for more than a year after cessation of D1 treatment. These findings indicate that pharmacological modulation of the D1 signaling pathway can produce long-lasting changes in functional circuits underlying working memory. Resetting this pathway by brief exposure to the agonist may provide a valuable strategy for therapeutic intervention in schizophrenia and other dopamine dysfunctional states.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Castner, S A -- Williams, G V -- Goldman-Rakic, P S -- P01DA10160/DA/NIDA NIH HHS/ -- P50MH44866/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2020-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720329" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antipsychotic Agents/*pharmacology ; Cyclic AMP/metabolism ; Dopamine/metabolism ; Dopamine Agonists/*pharmacology ; Dopamine Antagonists/pharmacology ; Down-Regulation ; Female ; Haloperidol/*pharmacology ; Haplorhini ; Memory/*drug effects ; Prefrontal Cortex/drug effects/metabolism ; Psychomotor Performance/drug effects ; Pyridines/*pharmacology ; Receptors, Dopamine D1/agonists/*metabolism ; Signal Transduction ; Tetrahydronaphthalenes/*pharmacology ; Time Factors
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  • 92
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-07-06
    Description: Many evolutionary studies use comparisons across species to detect evidence of natural selection and to examine the rate of character evolution. Statistical analyses in these studies are usually performed by means of a species phylogeny to accommodate the effects of shared evolutionary history. The phylogeny is usually treated as known without error; this assumption is problematic because inferred phylogenies are subject to both stochastic and systematic errors. We describe methods for accommodating phylogenetic uncertainty in evolutionary studies by means of Bayesian inference. The methods are computationally intensive but general enough to be applied in most comparative evolutionary studies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huelsenbeck, J P -- Rannala, B -- Masly, J P -- R01-HG01988/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2349-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Rochester, Rochester, NY 14627, USA. johnh@brahms.biology.rochester.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10875916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Aphids/genetics ; Base Sequence ; Bayes Theorem ; *Biological Evolution ; DNA, Mitochondrial/genetics ; *Evolution, Molecular ; Markov Chains ; Monte Carlo Method ; *Phylogeny ; Probability ; Stochastic Processes
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  • 93
    Publication Date: 2000-09-23
    Description: When DNA replication is inhibited during the synthesis (S) phase of the cell cycle, a signaling pathway (checkpoint) is activated that serves to prevent mitosis from initiating before completion of replication. This replication checkpoint acts by down-regulating the activity of the mitotic inducer cdc2-cyclin B. Here, we report the relation between chromatin structure and induction of the replication checkpoint. Chromatin was competent to initiate a checkpoint response only after the DNA was unwound and DNA polymerase alpha had been loaded. Checkpoint induction did not require new DNA synthesis on the unwound template strand but did require RNA primer synthesis by primase. These findings identify the RNA portion of the primer as an important component of the signal that activates the replication checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michael, W M -- Ott, R -- Fanning, E -- Newport, J -- 52948/PHS HHS/ -- R01GM33523-16/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2133-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California, San Diego, La Jolla, CA 92093-0349, USA. matt@mcb.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphidicolin/pharmacology ; *CDC2-CDC28 Kinases ; Carrier Proteins/metabolism ; Chromatin/*metabolism ; Cyclin E/metabolism ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/metabolism ; DNA Helicases/metabolism ; DNA Polymerase I/antagonists & inhibitors/metabolism ; DNA Primase/*metabolism ; *DNA Replication/drug effects ; DNA, Single-Stranded/metabolism ; DNA-Binding Proteins/metabolism ; Mitosis ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Kinases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA/*biosynthesis ; Recombinant Proteins/metabolism ; S Phase ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Xenopus ; Xenopus Proteins
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  • 94
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milligan, G -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):65-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Scotland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766637" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Cell Line ; Cerebral Cortex/metabolism ; Corpus Striatum/metabolism ; Dimerization ; Energy Transfer ; Fluorescence ; GTP-Binding Proteins/*metabolism ; Ligands ; Rats ; Receptor Cross-Talk ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/agonists/*metabolism ; Receptors, Dopamine D5 ; Receptors, GABA-A/metabolism ; Receptors, Somatostatin/agonists/*metabolism ; Signal Transduction ; Somatostatin/metabolism
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  • 95
    Publication Date: 2000-10-20
    Description: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Binding Sites ; Cell Line ; DNA-Binding Proteins/metabolism ; Ectodermal Dysplasia/genetics ; Ectodysplasins ; Epidermis/embryology/*metabolism ; Humans ; *I-kappa B Proteins ; In Situ Hybridization ; Ligands ; Membrane Proteins/*chemistry/*metabolism ; Mice ; Models, Molecular ; Molecular Sequence Data ; Morphogenesis ; NF-kappa B/metabolism ; Phosphorylation ; Point Mutation ; Protein Conformation ; Proteins/metabolism ; Receptors, Cell Surface/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6 ; Transfection
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  • 96
    Publication Date: 2000-02-11
    Description: Gradients of chemoattractants elicit signaling events at the leading edge of a cell even though chemoattractant receptors are uniformly distributed on the cell surface. In highly polarized Dictyostelium discoideum amoebas, membrane-associated betagamma subunits of heterotrimeric guanine nucleotide-binding proteins (G proteins) were localized in a shallow anterior-posterior gradient. A uniformly applied chemoattractant generated binding sites for pleckstrin homology (PH) domains on the inner surface of the membrane in a pattern similar to that of the Gbetagamma subunits. Loss of cell polarity resulted in uniform distribution of both the Gbetagamma subunits and the sensitivity of PH domain recruitment. These observations indicate that Gbetagamma subunits are not sufficiently localized to restrict signaling events to the leading edge but that their distribution may determine the relative chemotactic sensitivity of polarized cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jin, T -- Zhang, N -- Long, Y -- Parent, C A -- Devreotes, P N -- GM-28007/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1034-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669414" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Membrane/metabolism ; Cell Polarity ; Chemotactic Factors/pharmacology ; Chemotaxis/*physiology ; Cyclic AMP/pharmacology ; Dictyostelium/metabolism/*physiology ; *GTP-Binding Protein beta Subunits ; *GTP-Binding Protein gamma Subunits ; GTP-Binding Proteins/*metabolism ; *Heterotrimeric GTP-Binding Proteins ; Recombinant Fusion Proteins/metabolism ; Signal Transduction
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  • 97
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: Although the development of the inner ear has been a favorite subject for biologists to study, it is not yet clear exactly which molecules are involved in the induction of the otic placode, the plug of embryonic ectoderm that will become the inner ear. In his Perspective, Graham takes us on an inner ear odyssey, explaining how the signaling molecules FGF-19 and Wnt-8c cooperate to induce formation of the otic placode (Ladher et al.).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, A -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1904-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Centre for Developmental Neurobiology, Kings College London, London SE1 1UL, UK. anthony.graham@kcl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11187047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/embryology/metabolism ; Chick Embryo ; Coculture Techniques ; Culture Techniques ; Ear, Inner/*embryology/metabolism ; Ectoderm/metabolism ; *Embryonic Induction ; Fibroblast Growth Factors/genetics/*metabolism ; Gene Expression ; Mesoderm/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Signal Transduction ; Wnt Proteins ; *Zebrafish Proteins
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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, H W -- Cundall, D -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):1939-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, Cornell University, Ithaca, NY 14850-2701, USA. hwg5@cornell.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10755945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Fossils ; Hindlimb/anatomy & histology ; Lizards/anatomy & histology/classification ; Phylogeny ; Skull/anatomy & histology ; *Snakes/anatomy & histology/classification ; Terminology as Topic
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  • 99
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-24
    Description: The elegant architecture of photoreceptor cells in the retina is dependent on organization of the actin cytoskeleton during eye development. But what drives this organization? In an equally elegant Perspective, Colley explains new findings in fruit flies (Chang and Ready) that point to the photopigment rhodopsin and its signaling molecule the Rho GTPase Drac1 as the orchestrators of actin organization and the consequent assembly of the sensory membrane in the photoreceptor cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colley, N J -- R01 EY008768/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 8;290(5498):1902-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, WI 53706, USA. njcolley@facstaff.wisc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11187046" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism/*ultrastructure ; Amino Acid Motifs ; Animals ; Drosophila ; *Drosophila Proteins ; Enzyme Activation ; Humans ; Models, Biological ; Morphogenesis ; Photoreceptor Cells, Invertebrate/cytology/*growth & ; development/metabolism/*ultrastructure ; Retina/growth & development/ultrastructure ; Retinitis Pigmentosa/genetics/metabolism/pathology ; Rhodopsin/chemistry/*metabolism ; Signal Transduction ; rac GTP-Binding Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Apr 7;288(5463):38.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10766632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *DNA Methylation ; France ; *Gene Expression Regulation ; Gene Silencing ; Hair Color/genetics ; History, 18th Century ; History, 19th Century ; Mice ; *Mutation ; Plants/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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