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  • 2000-2004  (521)
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  • 1
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    Reversing the inactivation of peroxiredoxins caused by cysteine sulfinic acid formation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-26
    Description: The active-site cysteine of peroxiredoxins is selectively oxidized to cysteine sulfinic acid during catalysis, which leads to inactivation of peroxidase activity. This oxidation was thought to be irreversible. However, by metabolic labeling of mammalian cells with 35S, we show that the sulfinic form of peroxiredoxin I, produced during the exposure of cells to H2O2, is rapidly reduced to the catalytically active thiol form. The mammalian cells' ability to reduce protein sulfinic acid might serve as a mechanism to repair oxidatively damaged proteins or represent a new type of cyclic modification by which the function of various proteins is regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woo, Hyun Ae -- Chae, Ho Zoon -- Hwang, Sung Chul -- Yang, Kap-Seok -- Kang, Sang Won -- Kim, Kanghwa -- Rhee, Sue Goo -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell Signaling Research and Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalysis ; Cell Line ; Cycloheximide/pharmacology ; Cysteine/*analogs & derivatives/*metabolism ; Dimerization ; HeLa Cells ; Humans ; Hydrogen Peroxide/*metabolism ; Methionine/metabolism ; Mice ; Neurotransmitter Agents ; Oxidation-Reduction ; Peroxidases/chemistry/*metabolism ; Peroxiredoxins ; Protein Synthesis Inhibitors/pharmacology ; Spectrometry, Mass, Electrospray Ionization ; Sulfhydryl Compounds/metabolism ; Sulfinic Acids/metabolism ; Tumor Cells, Cultured
    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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    A gene-coexpression network for global discovery of conserved genetic modules (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-23
    Description: To elucidate gene function on a global scale, we identified pairs of genes that are coexpressed over 3182 DNA microarrays from humans, flies, worms, and yeast. We found 22,163 such coexpression relationships, each of which has been conserved across evolution. This conservation implies that the coexpression of these gene pairs confers a selective advantage and therefore that these genes are functionally related. Many of these relationships provide strong evidence for the involvement of new genes in core biological functions such as the cell cycle, secretion, and protein expression. We experimentally confirmed the predictions implied by some of these links and identified cell proliferation functions for several genes. By assembling these links into a gene-coexpression network, we found several components that were animal-specific as well as interrelationships between newly evolved and ancient modules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuart, Joshua M -- Segal, Eran -- Koller, Daphne -- Kim, Stuart K -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):249-55. Epub 2003 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stanford Medical Informatics, 251 Campus Drive, Medical School Office Building X-215, Stanford, CA 94305-5329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12934013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Caenorhabditis elegans/genetics ; Cell Cycle/genetics ; Cell Division/genetics ; Computational Biology ; Conserved Sequence ; Databases, Genetic ; Drosophila melanogaster/genetics ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Fungal ; Genes, Helminth ; Genes, Insect ; Humans ; Models, Statistical ; Mutation ; *Oligonucleotide Array Sequence Analysis ; Proteins/metabolism ; Saccharomyces cerevisiae/genetics ; Signal Transduction/genetics ; Species Specificity ; Tumor Cells, Cultured
    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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    Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta) (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-06-02
    Description: Glucose homeostasis depends on insulin responsiveness in target tissues, most importantly, muscle and liver. The critical initial steps in insulin action include phosphorylation of scaffolding proteins and activation of phosphatidylinositol 3-kinase. These early events lead to activation of the serine-threonine protein kinase Akt, also known as protein kinase B. We show that mice deficient in Akt2 are impaired in the ability of insulin to lower blood glucose because of defects in the action of the hormone on liver and skeletal muscle. These data establish Akt2 as an essential gene in the maintenance of normal glucose homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, H -- Mu, J -- Kim, J K -- Thorvaldsen, J L -- Chu, Q -- Crenshaw, E B 3rd -- Kaestner, K H -- Bartolomei, M S -- Shulman, G I -- Birnbaum, M J -- GM07229/GM/NIGMS NIH HHS/ -- P30 19525/PHS HHS/ -- P30 DK50306/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R01 DK56886/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2001 Jun 1;292(5522):1728-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11387480" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Deoxyglucose/metabolism ; Diabetes Mellitus, Type 2/*metabolism ; Female ; Gene Targeting ; Glucose/*metabolism ; Glucose Clamp Technique ; Glucose Tolerance Test ; Homeostasis ; Insulin/administration & dosage/blood/*metabolism ; *Insulin Resistance/genetics/physiology ; Islets of Langerhans/cytology/physiology ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle, Skeletal/enzymology/metabolism ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Signal Transduction
    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
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    Mechanism of ATP-dependent promoter melting by transcription factor IIH (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-29
    Description: We show that transcription factor IIH ERCC3 subunit, the DNA helicase responsible for adenosine triphosphate (ATP)-dependent promoter melting during transcription initiation, does not interact with the promoter region that undergoes melting but instead interacts with DNA downstream of this region. We show further that promoter melting does not change protein-DNA interactions upstream of the region that undergoes melting but does change interactions within and downstream of this region. Our results rule out the proposal that IIH functions in promoter melting through a conventional DNA-helicase mechanism. We propose that IIH functions as a molecular wrench: rotating downstream DNA relative to fixed upstream protein-DNA interactions, thereby generating torque on, and melting, the intervening DNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, T K -- Ebright, R H -- Reinberg, D -- GM37120/GM/NIGMS NIH HHS/ -- GM53665/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 May 26;288(5470):1418-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Division of Nucleic Acids Enzymology, Department of Biochemistry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10827951" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Base Sequence ; DNA/*chemistry/*metabolism ; DNA Helicases/metabolism ; DNA, Single-Stranded/metabolism ; DNA-Binding Proteins/*metabolism ; Humans ; Models, Genetic ; Molecular Sequence Data ; Nucleic Acid Conformation ; *Promoter Regions, Genetic ; Protein Binding ; RNA Polymerase II/metabolism ; Transcription Factor TFIIH ; Transcription Factors/*metabolism ; *Transcription Factors, TFII ; 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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  • 5
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    Carbon nanotube-based nonvolatile random access memory for molecular computing (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-07
    Description: A concept for molecular electronics exploiting carbon nanotubes as both molecular device elements and molecular wires for reading and writing information was developed. Each device element is based on a suspended, crossed nanotube geometry that leads to bistable, electrostatically switchable ON/OFF states. The device elements are naturally addressable in large arrays by the carbon nanotube molecular wires making up the devices. These reversible, bistable device elements could be used to construct nonvolatile random access memory and logic function tables at an integration level approaching 10(12) elements per square centimeter and an element operation frequency in excess of 100 gigahertz. The viability of this concept is demonstrated by detailed calculations and by the experimental realization of a reversible, bistable nanotube-based bit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rueckes -- Kim -- Joselevich -- Tseng -- Cheung -- Lieber -- New York, N.Y. -- Science. 2000 Jul 7;289(5476):94-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Chemical Biology, Division of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10884232" target="_blank"〉PubMed〈/a〉
    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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    Reading the worm genome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, S K -- New York, N.Y. -- Science. 2000 Jan 7;287(5450):52-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Genetics, Stanford University Medical Center, Stanford, CA 94305-5329, USA. kim@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10644223" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/growth & development/*metabolism ; *Caenorhabditis elegans Proteins ; Female ; Genes, Helminth ; *Genome ; Helminth Proteins/genetics/*metabolism ; Protein Binding ; Repressor Proteins/genetics/metabolism ; Retinoblastoma Protein/metabolism ; Signal Transduction ; *Two-Hybrid System Techniques ; Vulva/growth & development ; Yeasts/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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  • 7
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    A gene expression map for Caenorhabditis elegans (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-09-15
    Description: We have assembled data from Caenorhabditis elegans DNA microarray experiments involving many growth conditions, developmental stages, and varieties of mutants. Co-regulated genes were grouped together and visualized in a three-dimensional expression map that displays correlations of gene expression profiles as distances in two dimensions and gene density in the third dimension. The gene expression map can be used as a gene discovery tool to identify genes that are co-regulated with known sets of genes (such as heat shock, growth control genes, germ line genes, and so forth) or to uncover previously unknown genetic functions (such as genomic instability in males and sperm caused by specific transposons).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, S K -- Lund, J -- Kiraly, M -- Duke, K -- Jiang, M -- Stuart, J M -- Eizinger, A -- Wylie, B N -- Davidson, G S -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2087-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Genetics, Stanford University Medical School, Stanford, CA 94305, USA. kim@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11557892" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Caenorhabditis elegans/*genetics/physiology ; *Computational Biology ; DNA Transposable Elements ; DNA, Complementary ; Databases, Factual ; Female ; *Gene Expression ; *Gene Expression Profiling ; Gene Expression Regulation ; *Genes, Helminth ; Genome ; *Genomics ; Helminth Proteins/biosynthesis/genetics ; Intestines/physiology ; Male ; Muscles/physiology ; Neurons/physiology ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis ; Oocytes/physiology ; RNA, Helminth/genetics ; Software ; Spermatozoa/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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  • 8
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    Positional cloning of the human quantitative trait locus underlying taste sensitivity to phenylthiocarbamide (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: The ability to taste the substance phenylthiocarbamide (PTC) has been widely used for genetic and anthropological studies, but genetic studies have produced conflicting results and demonstrated complex inheritance for this trait. We have identified a small region on chromosome 7q that shows strong linkage disequilibrium between single-nucleotide polymorphism (SNP) markers and PTC taste sensitivity in unrelated subjects. This region contains a single gene that encodes a member of the TAS2R bitter taste receptor family. We identified three coding SNPs giving rise to five haplotypes in this gene worldwide. These haplotypes completely explain the bimodal distribution of PTC taste sensitivity, thus accounting for the inheritance of the classically defined taste insensitivity and for 55 to 85% of the variance in PTC sensitivity. Distinct phenotypes were associated with specific haplotypes, which demonstrates that this gene has a direct influence on PTC taste sensitivity and that sequence variants at different sites interact with each other within the encoded gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Un-kyung -- Jorgenson, Eric -- Coon, Hilary -- Leppert, Mark -- Risch, Neil -- Drayna, Dennis -- M01-RR00064/RR/NCRR NIH HHS/ -- T32 HG00044/HG/NHGRI NIH HHS/ -- Z01-000046-04/PHS HHS/ -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute on Deafness and Other Communication Disorders, National Institutes of Health, 5 Research Court, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595690" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Cebidae/genetics ; Chromosomes, Human, Pair 7/genetics ; Cloning, Molecular ; Computational Biology ; Continental Population Groups/genetics ; Evolution, Molecular ; Female ; Genetic Linkage ; Haplotypes ; Heterozygote ; Hominidae/genetics ; Homozygote ; Humans ; Linkage Disequilibrium ; Macaca fascicularis/genetics ; Male ; *Phenylthiourea ; *Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; Receptors, Cell Surface/chemistry/*genetics/physiology ; Receptors, G-Protein-Coupled ; Sequence Analysis, DNA ; Taste/*genetics ; Taste Threshold
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Acidic mammalian chitinase in asthmatic Th2 inflammation and IL-13 pathway activation (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-12
    Description: Chitin is a surface component of parasites and insects, and chitinases are induced in lower life forms during infections with these agents. Although chitin itself does not exist in humans, chitinases are present in the human genome. We show here that acidic mammalian chitinase (AMCase) is induced via a T helper-2 (Th2)-specific, interleukin-13 (IL-13)-mediated pathway in epithelial cells and macrophages in an aeroallergen asthma model and expressed in exaggerated quantities in human asthma. AMCase neutralization ameliorated Th2 inflammation and airway hyperresponsiveness, in part by inhibiting IL-13 pathway activation and chemokine induction. AMCase may thus be an important mediator of IL-13-induced responses in Th2-dominated disorders such as asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Zhou -- Zheng, Tao -- Homer, Robert J -- Kim, Yoon-Keun -- Chen, Ning Yuan -- Cohn, Lauren -- Hamid, Qutayba -- Elias, Jack A -- P50-HL-56/HL/NHLBI NIH HHS/ -- R01-HL-074095/HL/NHLBI NIH HHS/ -- R01-HL-61904/HL/NHLBI NIH HHS/ -- R01-HL-64242/HL/NHLBI NIH HHS/ -- R01-HL-66571/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jun 11;304(5677):1678-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, Department of Internal Medicine, 300 Cedar Street, TAC S-441, New Haven, CT 06520-8057, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15192232" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Allergens ; Animals ; Asthma/*enzymology/immunology ; Bronchoalveolar Lavage Fluid/chemistry ; Chemokines/metabolism ; Chitin/metabolism ; Chitinase/antagonists & inhibitors/genetics/immunology/*metabolism ; Epithelial Cells/enzymology ; Female ; Humans ; Hydrogen-Ion Concentration ; Immune Sera ; Interleukin-13/*metabolism ; Interleukins/genetics/metabolism ; Lung/*enzymology/immunology ; Macrophages, Alveolar/enzymology ; Mice ; Mice, Inbred Strains ; Mice, Transgenic ; Ovalbumin/immunology ; Respiratory Mucosa/enzymology ; Th2 Cells/*immunology ; 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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  • 10
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    Ablation of insulin-producing neurons in flies: growth and diabetic phenotypes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-11
    Description: In the fruit fly Drosophila, four insulin genes are coexpressed in small clusters of cells [insulin-producing cells (IPCs)] in the brain. Here, we show that ablation of these IPCs causes developmental delay, growth retardation, and elevated carbohydrate levels in larval hemolymph. All of the defects were reversed by ectopic expression of a Drosophila insulin transgene. On the basis of these functional data and the observation that IPCs release insulin into the circulatory system, we conclude that brain IPCs are the main systemic supply of insulin during larval growth. We propose that IPCs and pancreatic islet beta cells are functionally analogous and may have evolved from a common ancestral insulin-producing neuron. Interestingly, the phenotype of flies lacking IPCs includes certain features of diabetes mellitus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rulifson, Eric J -- Kim, Seung K -- Nusse, Roel -- New York, N.Y. -- Science. 2002 May 10;296(5570):1118-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Beckman Center B300, Stanford University, Stanford, CA 94305-5329, USA. rulifson@cmgm.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12004130" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Blood Glucose/*metabolism ; Brain/cytology ; Cell Count ; Cell Size ; Diabetes Mellitus ; Drosophila/anatomy & histology/genetics/growth & development/*physiology ; Drosophila Proteins/genetics/*metabolism ; Gene Expression ; Heart/innervation ; Hemolymph ; Insect Hormones/genetics/metabolism ; Insulin/genetics/*metabolism ; Larva/growth & development ; Myocardium/metabolism ; Neurons/*metabolism ; Neurosecretory Systems/cytology/metabolism ; Oligopeptides/genetics/metabolism ; Phenotype ; Pyrrolidonecarboxylic Acid/analogs & derivatives ; RNA, Messenger/genetics/metabolism ; Transgenes ; Trehalose/*blood ; Wings, Animal/anatomy & histology/cytology/growth & development
    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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