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  • 1
    Publication Date: 2002-09-28
    Description: Molecular genetic studies of Drosophila melanogaster have led to profound advances in understanding the regulation of development. Here we report gene expression patterns for nearly one-third of all Drosophila genes during a complete time course of development. Mutations that eliminate eye or germline tissue were used to further analyze tissue-specific gene expression programs. These studies define major characteristics of the transcriptional programs that underlie the life cycle, compare development in males and females, and show that large-scale gene expression data collected from whole animals can be used to identify genes expressed in particular tissues and organs or genes involved in specific biological and biochemical processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arbeitman, Michelle N -- Furlong, Eileen E M -- Imam, Farhad -- Johnson, Eric -- Null, Brian H -- Baker, Bruce S -- Krasnow, Mark A -- Scott, Matthew P -- Davis, Ronald W -- White, Kevin P -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2002 Sep 27;297(5590):2270-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12351791" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cluster Analysis ; Drosophila Proteins/genetics/physiology ; Drosophila melanogaster/embryology/*genetics/*growth & development ; Embryo, Nonmammalian/physiology ; Female ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; *Genes, Insect ; Germ Cells/physiology ; Larva/genetics ; Life Cycle Stages/*genetics ; Male ; Oligonucleotide Array Sequence Analysis ; Organ Specificity ; Pupa/genetics ; RNA, Messenger/genetics/metabolism ; Sex Characteristics ; Transcription, 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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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-04-25
    Description: This study shows that a corpus of proto-word forms shares four sequential sound patterns with words of modern languages and the first words of infants. Three of the patterns involve intrasyllabic consonant-vowel (CV) co-occurrence: labial (lip) consonants with central vowels, coronal (tongue front) consonants with front vowels, and dorsal (tongue back) consonants with back vowels. The fourth pattern is an intersyllabic preference for initiating words with a labial consonant-vowel-coronal consonant sequence (LC). The CV effects may be primarily biomechanically motivated. The LC effect may be self-organizational, with multivariate causality. The findings support the hypothesis that these four patterns were basic to the origin of words.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacNeilage, P F -- Davis, B L -- R01 HD 27733-07/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 21;288(5465):527-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Department of Communication Sciences and Disorders, University of Texas, Austin, TX 78712, USA. macneilage@psy.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10775113" target="_blank"〉PubMed〈/a〉
    Keywords: Biomechanical Phenomena ; Humans ; Infant ; *Language Development ; Lip/physiology ; Mandible/physiology ; Movement ; *Phonetics ; *Speech ; Tongue/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2001-01-06
    Description: Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S T -- Benson, B G -- Bramson, H N -- Chapman, D E -- Dickerson, S H -- Dold, K M -- Eberwein, D J -- Edelstein, M -- Frye, S V -- Gampe Jr, R T -- Griffin, R J -- Harris, P A -- Hassell, A M -- Holmes, W D -- Hunter, R N -- Knick, V B -- Lackey, K -- Lovejoy, B -- Luzzio, M J -- Murray, D -- Parker, P -- Rocque, W J -- Shewchuk, L -- Veal, J M -- Walker, D H -- Kuyper, L F -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Glaxo Wellcome Research and Development, Research Triangle Park, NC 27709, USA. std41085@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141566" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*chemically induced/*prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents/*toxicity ; Antineoplastic Combined Chemotherapy Protocols/toxicity ; Apoptosis/drug effects ; *CDC2-CDC28 Kinases ; Cell Cycle/drug effects ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclophosphamide/toxicity ; Cytoprotection/drug effects ; DNA/biosynthesis ; Doxorubicin/toxicity ; Drug Design ; Enzyme Inhibitors/chemical synthesis/chemistry/*pharmacology ; Epithelium/drug effects ; Etoposide/toxicity ; Hair Follicle/cytology/*drug effects ; Humans ; Indoles/chemical synthesis/chemistry/*pharmacology ; Mice ; Mice, SCID ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Rats ; Retinoblastoma Protein/metabolism ; Scalp/transplantation ; Sulfonamides/chemical synthesis/chemistry/*pharmacology ; Transplantation, Heterologous
    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: 2000-06-24
    Description: T helper 1 (TH1) cells mediate cellular immunity, whereas TH2 cells potentiate antiparasite and humoral immunity. We used a complementary DNA subtraction method, representational display analysis, to show that the small guanosine triphosphatase Rac2 is expressed selectively in murine TH1 cells. Rac induces the interferon-gamma (IFN-gamma) promoter through cooperative activation of the nuclear factor kappa B and p38 mitogen-activated protein kinase pathways. Tetracycline-regulated transgenic mice expressing constitutively active Rac2 in T cells exhibited enhanced IFN-gamma production. Dominant-negative Rac inhibited IFN-gamma production in murine T cells. Moreover, T cells from Rac2-/- mice showed decreased IFN-gamma production under TH1 conditions in vitro. Thus, Rac2 activates TH1-specific signaling and IFN-gamma gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, B -- Yu, H -- Zheng, W -- Voll, R -- Na, S -- Roberts, A W -- Williams, D A -- Davis, R J -- Ghosh, S -- Flavell, R A -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2219-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, 310 Cedar Street, New Haven, CT 06520-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864872" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cells, Cultured ; Cytokines/biosynthesis/genetics ; Gene Expression Regulation ; Humans ; Interferon-gamma/biosynthesis/*genetics ; JNK Mitogen-Activated Protein Kinases ; Jurkat Cells ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Promoter Regions, Genetic ; Signal Transduction ; Th1 Cells/cytology/*immunology/*metabolism ; Transfection ; p38 Mitogen-Activated Protein Kinases ; rac GTP-Binding Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2000-04-28
    Description: A backbone model of a 10-subunit yeast RNA polymerase II has been derived from x-ray diffraction data extending to 3 angstroms resolution. All 10 subunits exhibit a high degree of identity with the corresponding human proteins, and 9 of the 10 subunits are conserved among the three eukaryotic RNA polymerases I, II, and III. Notable features of the model include a pair of jaws, formed by subunits Rpb1, Rpb5, and Rpb9, that appear to grip DNA downstream of the active center. A clamp on the DNA nearer the active center, formed by Rpb1, Rpb2, and Rpb6, may be locked in the closed position by RNA, accounting for the great stability of transcribing complexes. A pore in the protein complex beneath the active center may allow entry of substrates for polymerization and exit of the transcript during proofreading and passage through pause sites in the DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cramer, P -- Bushnell, D A -- Fu, J -- Gnatt, A L -- Maier-Davis, B -- Thompson, N E -- Burgess, R R -- Edwards, A M -- David, P R -- Kornberg, R D -- GM49985/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 28;288(5466):640-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305-5126, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10784442" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Binding Sites ; Catalytic Domain ; Crystallization ; Crystallography, X-Ray ; DNA, Fungal/chemistry/metabolism ; Enzyme Stability ; Escherichia coli/enzymology ; Humans ; *Models, Molecular ; Protein Binding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; RNA Polymerase II/*chemistry/genetics/metabolism ; RNA, Fungal/chemistry/metabolism ; RNA, Messenger/chemistry/metabolism ; Thermus/enzymology ; Transcription Factors/chemistry/metabolism ; *Transcription Factors, General ; *Transcription, Genetic ; *Transcriptional Elongation Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2000-11-25
    Description: An enduring controversy in neuroscience concerns how the brain "binds" together separately coded stimulus features to form unitary representations of objects. Recent evidence has indicated a close link between this binding process and 40-hertz (gamma-band) oscillations generated by localized neural circuits. In a separate line of research, the ability of young infants to perceive objects as unitary and bounded has become a central focus for debates about the mechanisms of perceptual development. Here we demonstrate that binding-related 40-hertz oscillations are evident in the infant brain around 8 months of age, which is the same age at which behavioral and event-related potential evidence indicates the onset of perceptual binding of spatially separated static visual features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Csibra, G -- Davis, G -- Spratling, M W -- Johnson, M H -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Brain and Cognitive Development, School of Psychology, Birkbeck College, University of London, Malet Street, London WC1E 7HX, UK. g.csibra@bbk.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090357" target="_blank"〉PubMed〈/a〉
    Keywords: *Electroencephalography ; Evoked Potentials, Visual ; Female ; *Form Perception ; Frontal Lobe/*physiology ; Humans ; Infant ; Male ; Occipital Lobe/physiology ; Parietal Lobe/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2001-12-26
    Description: The circadian clock in the suprachiasmatic nucleus (SCN) is thought to drive daily rhythms of behavior by secreting factors that act locally within the hypothalamus. In a systematic screen, we identified transforming growth factor-alpha (TGF-alpha) as a likely SCN inhibitor of locomotion. TGF-alpha is expressed rhythmically in the SCN, and when infused into the third ventricle it reversibly inhibited locomotor activity and disrupted circadian sleep-wake cycles. These actions are mediated by epidermal growth factor (EGF) receptors on neurons in the hypothalamic subparaventricular zone. Mice with a hypomorphic EGF receptor mutation exhibited excessive daytime locomotor activity and failed to suppress activity when exposed to light. These results implicate EGF receptor signaling in the daily control of locomotor activity, and identify a neural circuit in the hypothalamus that likely mediates the regulation of behavior both by the SCN and the retina.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, A -- Yang, F C -- Snodgrass, P -- Li, X -- Scammell, T E -- Davis, F C -- Weitz, C J -- HD-18686/HD/NICHD NIH HHS/ -- MH62589/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2511-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11752569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/drug effects/physiology ; Body Temperature/drug effects ; Cerebral Ventricles/metabolism ; Circadian Rhythm/drug effects/*physiology ; Cricetinae ; Darkness ; Epidermal Growth Factor/pharmacology ; Female ; Hypothalamus/*metabolism ; Ligands ; Light ; Male ; Mesocricetus ; Mice ; *Motor Activity/drug effects ; Neural Pathways/physiology ; Neurons/metabolism ; Point Mutation ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Retina/metabolism ; Retinal Ganglion Cells/metabolism ; Signal Transduction ; Sleep/drug effects/*physiology ; Suprachiasmatic Nucleus/*metabolism ; Transforming Growth Factor alpha/administration & ; dosage/genetics/metabolism/pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2000-11-25
    Description: beta-Arrestins, originally discovered in the context of heterotrimeric guanine nucleotide binding protein-coupled receptor (GPCR) desensitization, also function in internalization and signaling of these receptors. We identified c-Jun amino-terminal kinase 3 (JNK3) as a binding partner of beta-arrestin 2 using a yeast two-hybrid screen and by coimmunoprecipitation from mouse brain extracts or cotransfected COS-7 cells. The upstream JNK activators apoptosis signal-regulating kinase 1 (ASK1) and mitogen-activated protein kinase (MAPK) kinase 4 were also found in complex with beta-arrestin 2. Cellular transfection of beta-arrestin 2 caused cytosolic retention of JNK3 and enhanced JNK3 phosphorylation stimulated by ASK1. Moreover, stimulation of the angiotensin II type 1A receptor activated JNK3 and triggered the colocalization of beta-arrestin 2 and active JNK3 to intracellular vesicles. Thus, beta-arrestin 2 acts as a scaffold protein, which brings the spatial distribution and activity of this MAPK module under the control of a GPCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, P H -- Chow, C W -- Miller, W E -- Laporte, S A -- Field, M E -- Lin, F T -- Davis, R J -- Lefkowitz, R J -- CA65861/CA/NCI NIH HHS/ -- CA85422/CA/NCI NIH HHS/ -- HL16037/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Medicine, Duke University Medical Center, Box 3821, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090355" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/metabolism/pharmacology ; Animals ; Arrestins/genetics/*metabolism ; COS Cells ; Cell Line ; Cell Nucleus/metabolism ; Cytosol/enzymology/metabolism ; Endosomes/enzymology/metabolism ; Enzyme Activation ; Humans ; *MAP Kinase Kinase 4 ; MAP Kinase Kinase Kinase 5 ; MAP Kinase Kinase Kinases/*metabolism ; *MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 10 ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Mutation ; Phosphorylation ; Protein-Tyrosine Kinases/*metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Rats ; Receptor, Angiotensin, Type 1 ; Receptors, Angiotensin/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Two-Hybrid System Techniques
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2001-08-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cifuentes, L -- Borja-Aburto, V H -- Gouveia, N -- Thurston, G -- Davis, D L -- ES00260/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 17;293(5533):1257-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pontificia Universidad Catolica de Chile, Santiago, Chile.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11509711" target="_blank"〉PubMed〈/a〉
    Keywords: *Air Pollution/adverse effects/prevention & control ; Brazil ; Chile ; Developed Countries ; Developing Countries ; Forecasting ; Fossil Fuels ; *Greenhouse Effect ; Health Status ; Humans ; Mexico ; Mortality ; New York City ; Ozone/adverse effects ; *Public Health
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weston, C R -- Davis, R J -- New York, N.Y. -- Science. 2001 Jun 29;292(5526):2439-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Molecular Medicine and Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11431552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axin Protein ; Binding Sites ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & ; inhibitors/chemistry/genetics/*metabolism ; Cell Membrane/metabolism ; Cytoplasm/enzymology ; Cytoskeletal Proteins/metabolism ; Drug Design ; Glycogen Synthase/metabolism ; Glycogen Synthase Kinase 3 ; Humans ; Insulin/*metabolism ; Models, Biological ; Mutation ; Phosphorylation ; Phosphoserine/metabolism ; Protein Conformation ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; *Repressor Proteins ; *Signal Transduction ; Substrate Specificity ; *Trans-Activators ; Wnt Proteins ; *Zebrafish Proteins ; beta Catenin
    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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