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  • Signal Transduction  (767)
  • Cell Line  (686)
  • Astronomy
  • American Association for the Advancement of Science (AAAS)  (1,379)
  • 2005-2009  (652)
  • 2000-2004  (727)
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  • 1
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    Global analysis of short RNAs reveals widespread promoter-proximal stalling and arrest of Pol II in Drosophila (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Emerging evidence indicates that gene expression in higher organisms is regulated by RNA polymerase II stalling during early transcription elongation. To probe the mechanisms responsible for this regulation, we developed methods to isolate and characterize short RNAs derived from stalled RNA polymerase II in Drosophila cells. Significant levels of these short RNAs were generated from more than one-third of all genes, indicating that promoter-proximal stalling is a general feature of early polymerase elongation. Nucleotide composition of the initially transcribed sequence played an important role in promoting transcriptional stalling by rendering polymerase elongation complexes highly susceptible to backtracking and arrest. These results indicate that the intrinsic efficiency of early elongation can greatly affect gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435875/" 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/PMC3435875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nechaev, Sergei -- Fargo, David C -- dos Santos, Gilberto -- Liu, Liwen -- Gao, Yuan -- Adelman, Karen -- ZIA ES101987-05/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):335-8. doi: 10.1126/science.1181421. Epub 2009 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Composition ; Cell Line ; Drosophila melanogaster ; *Gene Expression Regulation ; *Genes, Insect ; Genome, Insect ; Oligonucleotide Array Sequence Analysis ; *Promoter Regions, Genetic ; RNA/genetics/*metabolism ; RNA Caps/genetics/metabolism ; RNA Polymerase II/*metabolism ; RNA, Messenger/genetics/metabolism ; Transcription Initiation Site ; *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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    Medicine. A reinnervating microRNA (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Robert H -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1494-5. doi: 10.1126/science.1183842.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology, Biochemistry and Molecular Pharmacology and Program in Neuroscience, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. robert.brown@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007892" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Binding Sites ; Carrier Proteins/metabolism ; Disease Models, Animal ; Histone Deacetylases/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Muscle Cells/enzymology ; Muscle Denervation ; Muscle, Skeletal/innervation/metabolism ; Myostatin/genetics ; Neuromuscular Junction/*pathology/*physiology ; RNA Interference ; Sequence Analysis, RNA ; 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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  • 3
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    Norbin is an endogenous regulator of metabotropic glutamate receptor 5 signaling (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" 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/PMC2796550/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong -- Westin, Linda -- Nong, Yi -- Birnbaum, Shari -- Bendor, Jacob -- Brismar, Hjalmar -- Nestler, Eric -- Aperia, Anita -- Flajolet, Marc -- Greengard, Paul -- DA 10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- MH66172/MH/NIMH NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-020002/DA/NIDA NIH HHS/ -- P01 DA010044-030002/DA/NIDA NIH HHS/ -- P01 DA010044-04/DA/NIDA NIH HHS/ -- P01 DA010044-040002/DA/NIDA NIH HHS/ -- P01 DA010044-05/DA/NIDA NIH HHS/ -- P01 DA010044-050002/DA/NIDA NIH HHS/ -- P01 DA010044-06/DA/NIDA NIH HHS/ -- P01 DA010044-060002/DA/NIDA NIH HHS/ -- P01 DA010044-07/DA/NIDA NIH HHS/ -- P01 DA010044-070002/DA/NIDA NIH HHS/ -- P01 DA010044-08/DA/NIDA NIH HHS/ -- P01 DA010044-080002/DA/NIDA NIH HHS/ -- P01 DA010044-09/DA/NIDA NIH HHS/ -- P01 DA010044-090002/DA/NIDA NIH HHS/ -- P01 DA010044-10/DA/NIDA NIH HHS/ -- P01 DA010044-100002/DA/NIDA NIH HHS/ -- P01 DA010044-11/DA/NIDA NIH HHS/ -- P01 DA010044-110005/DA/NIDA NIH HHS/ -- P01 DA010044-12/DA/NIDA NIH HHS/ -- P01 DA010044-120005/DA/NIDA NIH HHS/ -- P01 DA010044-129002/DA/NIDA NIH HHS/ -- P01 DA010044-13/DA/NIDA NIH HHS/ -- P01 DA010044-130005/DA/NIDA NIH HHS/ -- P01 DA010044-139002/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-010001/MH/NIMH NIH HHS/ -- P50 MH074866-020001/MH/NIMH NIH HHS/ -- P50 MH074866-030001/MH/NIMH NIH HHS/ -- P50 MH074866-039001/MH/NIMH NIH HHS/ -- P50 MH074866-040001/MH/NIMH NIH HHS/ -- P50 MH074866-050001/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1554-7. doi: 10.1126/science.1178496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Humans ; Mice ; Mice, Knockout ; Motor Activity ; Nerve Tissue Proteins/genetics/*metabolism ; Neuronal Plasticity ; Protein Binding ; Rats ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/genetics/*metabolism ; Reflex, Startle ; Schizophrenia/physiopathology ; *Signal Transduction ; Synaptic Transmission ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by loss of motor neurons, denervation of target muscles, muscle atrophy, and paralysis. Understanding ALS pathogenesis may require a fuller understanding of the bidirectional signaling between motor neurons and skeletal muscle fibers at neuromuscular synapses. Here, we show that a key regulator of this signaling is miR-206, a skeletal muscle-specific microRNA that is dramatically induced in a mouse model of ALS. Mice that are genetically deficient in miR-206 form normal neuromuscular synapses during development, but deficiency of miR-206 in the ALS mouse model accelerates disease progression. miR-206 is required for efficient regeneration of neuromuscular synapses after acute nerve injury, which probably accounts for its salutary effects in ALS. miR-206 mediates these effects at least in part through histone deacetylase 4 and fibroblast growth factor signaling pathways. Thus, miR-206 slows ALS progression by sensing motor neuron injury and promoting the compensatory regeneration of neuromuscular synapses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796560/" 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/PMC2796560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Andrew H -- Valdez, Gregorio -- Moresi, Viviana -- Qi, Xiaoxia -- McAnally, John -- Elliott, Jeffrey L -- Bassel-Duby, Rhonda -- Sanes, Joshua R -- Olson, Eric N -- 1F32NS061464-01A1/NS/NINDS NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL093039-01A1/HL/NHLBI NIH HHS/ -- T32HL007360/HL/NHLBI NIH HHS/ -- U24 CA126608/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1549-54. doi: 10.1126/science.1181046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007902" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/pathology/*physiopathology ; Animals ; Axons/physiology ; Carrier Proteins/genetics/metabolism ; Disease Models, Animal ; Disease Progression ; Fibroblast Growth Factors/metabolism ; Histone Deacetylases/genetics/metabolism ; Mice ; Mice, Transgenic ; MicroRNAs/genetics/*metabolism ; Motor Neurons/pathology/*physiology ; Muscle Denervation ; Muscle, Skeletal/innervation/*metabolism/pathology ; MyoD Protein/genetics/metabolism ; Myogenin/genetics/metabolism ; Nerve Regeneration ; Neuromuscular Junction/growth & development/*pathology/*physiology ; RNA Interference ; Signal Transduction ; Transcriptional Activation ; 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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    Cell-specific information processing in segregating populations of Eph receptor ephrin-expressing cells (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Cells have self-organizing properties that control their behavior in complex tissues. Contact between cells expressing either B-type Eph receptors or their transmembrane ephrin ligands initiates bidirectional signals that regulate cell positioning. However, simultaneously investigating how information is processed in two interacting cell types remains a challenge. We implemented a proteomic strategy to systematically determine cell-specific signaling networks underlying EphB2- and ephrin-B1-controlled cell sorting. Quantitative mass spectrometric analysis of mixed populations of EphB2- and ephrin-B1-expressing cells that were labeled with different isotopes revealed cell-specific tyrosine phosphorylation events. Functional associations between these phosphotyrosine signaling networks and cell sorting were established with small interfering RNA screening. Data-driven network modeling revealed that signaling between mixed EphB2- and ephrin-B1-expressing cells is asymmetric and that the distinct cell types use different tyrosine kinases and targets to process signals induced by cell-cell contact. We provide systems- and cell-specific network models of contact-initiated signaling between two distinct cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jorgensen, Claus -- Sherman, Andrew -- Chen, Ginny I -- Pasculescu, Adrian -- Poliakov, Alexei -- Hsiung, Marilyn -- Larsen, Brett -- Wilkinson, David G -- Linding, Rune -- Pawson, Tony -- MC_U117532048/Medical Research Council/United Kingdom -- MOP-6849/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1502-9. doi: 10.1126/science.1176615.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute (SLRI), Mount Sinai Hospital, Toronto M5G 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007894" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Algorithms ; Cell Line ; Ephrin-B1/genetics/*metabolism ; Humans ; Ligands ; Mass Spectrometry ; Models, Biological ; PDZ Domains ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Tyrosine Kinases/metabolism ; Proteomics ; RNA, Small Interfering ; Receptor, EphB2/genetics/*metabolism ; *Signal Transduction ; Tyrosine/metabolism ; src Homology Domains
    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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    The Fanconi anemia pathway promotes replication-dependent DNA interstrand cross-link repair (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Fanconi anemia is a human cancer predisposition syndrome caused by mutations in 13 Fanc genes. The disorder is characterized by genomic instability and cellular hypersensitivity to chemicals that generate DNA interstrand cross-links (ICLs). A central event in the activation of the Fanconi anemia pathway is the mono-ubiquitylation of the FANCI-FANCD2 complex, but how this complex confers ICL resistance remains enigmatic. Using a cell-free system, we showed that FANCI-FANCD2 is required for replication-coupled ICL repair in S phase. Removal of FANCD2 from extracts inhibits both nucleolytic incisions near the ICL and translesion DNA synthesis past the lesion. Reversal of these defects requires ubiquitylated FANCI-FANCD2. Our results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia pathway is compromised.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909596/" 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/PMC2909596/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knipscheer, Puck -- Raschle, Markus -- Smogorzewska, Agata -- Enoiu, Milica -- Ho, The Vinh -- Scharer, Orlando D -- Elledge, Stephen J -- Walter, Johannes C -- GM62267/GM/NIGMS NIH HHS/ -- R01 GM062267/GM/NIGMS NIH HHS/ -- R01 GM062267-09/GM/NIGMS NIH HHS/ -- R37 GM044664/GM/NIGMS NIH HHS/ -- R37 GM044664-23/GM/NIGMS NIH HHS/ -- T32CA09216/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 18;326(5960):1698-701. doi: 10.1126/science.1182372. Epub 2009 Nov 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965384" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell-Free System ; Chromatin/metabolism ; DNA/biosynthesis ; DNA Damage ; *DNA Repair ; *DNA Replication ; Fanconi Anemia/genetics/metabolism ; Fanconi Anemia Complementation Group D2 Protein/*metabolism ; Fanconi Anemia Complementation Group Proteins/*metabolism ; Molecular Sequence Data ; Recombinant Proteins/metabolism ; S Phase ; Signal Transduction ; Ubiquitinated Proteins/metabolism ; Ubiquitination ; Xenopus Proteins/*metabolism ; Xenopus laevis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Impact of genome reduction on bacterial metabolism and its regulation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: To understand basic principles of bacterial metabolism organization and regulation, but also the impact of genome size, we systematically studied one of the smallest bacteria, Mycoplasma pneumoniae. A manually curated metabolic network of 189 reactions catalyzed by 129 enzymes allowed the design of a defined, minimal medium with 19 essential nutrients. More than 1300 growth curves were recorded in the presence of various nutrient concentrations. Measurements of biomass indicators, metabolites, and 13C-glucose experiments provided information on directionality, fluxes, and energetics; integration with transcription profiling enabled the global analysis of metabolic regulation. Compared with more complex bacteria, the M. pneumoniae metabolic network has a more linear topology and contains a higher fraction of multifunctional enzymes; general features such as metabolite concentrations, cellular energetics, adaptability, and global gene expression responses are similar, however.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yus, Eva -- Maier, Tobias -- Michalodimitrakis, Konstantinos -- van Noort, Vera -- Yamada, Takuji -- Chen, Wei-Hua -- Wodke, Judith A H -- Guell, Marc -- Martinez, Sira -- Bourgeois, Ronan -- Kuhner, Sebastian -- Raineri, Emanuele -- Letunic, Ivica -- Kalinina, Olga V -- Rode, Michaela -- Herrmann, Richard -- Gutierrez-Gallego, Ricardo -- Russell, Robert B -- Gavin, Anne-Claude -- Bork, Peer -- Serrano, Luis -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1263-8. doi: 10.1126/science.1177263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Genomic Regulation (CRG) and Universitat Pompeu Fabra, Avenida Dr. Aiguader 88, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965476" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Bacterial Proteins/*metabolism ; Culture Media ; Energy Metabolism ; Enzymes/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Bacterial ; *Genome, Bacterial ; Glycolysis ; *Metabolic Networks and Pathways ; Mycoplasma pneumoniae/*genetics/growth & development/*metabolism ; RNA, Bacterial/genetics/metabolism ; Signal Transduction ; Systems Biology ; Transcription, Genetic ; rRNA Operon
    Print ISSN: 0036-8075
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  • 8
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    The extracellular matrix: not just pretty fibrils (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The extracellular matrix (ECM) and ECM proteins are important in phenomena as diverse as developmental patterning, stem cell niches, cancer, and genetic diseases. The ECM has many effects beyond providing structural support. ECM proteins typically include multiple, independently folded domains whose sequences and arrangement are highly conserved. Some of these domains bind adhesion receptors such as integrins that mediate cell-matrix adhesion and also transduce signals into cells. However, ECM proteins also bind soluble growth factors and regulate their distribution, activation, and presentation to cells. As organized, solid-phase ligands, ECM proteins can integrate complex, multivalent signals to cells in a spatially patterned and regulated fashion. These properties need to be incorporated into considerations of the functions of the ECM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536535/" 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/PMC3536535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hynes, Richard O -- P01 HL066105/HL/NHLBI NIH HHS/ -- R01 CA017007/CA/NCI NIH HHS/ -- U54 CA126515/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Nov 27;326(5957):1216-9. doi: 10.1126/science.1176009.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. rohynes@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; *Cell Physiological Processes ; Extracellular Matrix/*physiology ; Extracellular Matrix Proteins/chemistry/*metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Models, Biological ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Structure, Tertiary ; Signal Transduction ; Transforming Growth Factor beta/metabolism
    Print ISSN: 0036-8075
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  • 9
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    The insect neuropeptide PTTH activates receptor tyrosine kinase torso to initiate metamorphosis (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived prothoracicotropic hormone (PTTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rewitz, Kim F -- Yamanaka, Naoki -- Gilbert, Lawrence I -- O'Connor, Michael B -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1403-5. doi: 10.1126/science.1176450.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965758" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bombyx/*genetics/metabolism ; Cell Line ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/embryology/genetics/*growth & development/metabolism ; Embryo, Nonmammalian/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Insect Hormones/chemistry/*metabolism ; Larva/growth & development ; Ligands ; *Metamorphosis, Biological ; Molecular Sequence Data ; Neurons/metabolism ; Phosphorylation ; Pupa/growth & development ; RNA Interference ; Receptor Protein-Tyrosine Kinases/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    How telomeres solve the end-protection problem (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: The ends of eukaryotic chromosomes have the potential to be mistaken for damaged or broken DNA and must therefore be protected from cellular DNA damage response pathways. Otherwise, cells might permanently arrest in the cell cycle, and attempts to "repair" the chromosome ends would have devastating consequences for genome integrity. This end-protection problem is solved by protein-DNA complexes called telomeres. Studies of mammalian cells have recently uncovered the mechanism by which telomeres disguise the chromosome ends. Comparison to unicellular eukaryotes reveals key differences in the DNA damage response systems that inadvertently threaten chromosome ends. Telomeres appear to be tailored to these variations, explaining their variable structure and composition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2819049/" 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/PMC2819049/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- CA076027/CA/NCI NIH HHS/ -- DP1 OD000379/OD/NIH HHS/ -- DP1 OD000379-01/OD/NIH HHS/ -- DP1 OD000379-02/OD/NIH HHS/ -- DP1 OD000379-03/OD/NIH HHS/ -- DP1 OD000379-04/OD/NIH HHS/ -- DP1 OD000379-05/OD/NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R01 CA076027-02/CA/NCI NIH HHS/ -- R01 CA076027-03/CA/NCI NIH HHS/ -- R01 CA076027-04/CA/NCI NIH HHS/ -- R01 CA076027-05A1/CA/NCI NIH HHS/ -- R01 CA076027-06/CA/NCI NIH HHS/ -- R01 CA076027-07/CA/NCI NIH HHS/ -- R01 CA076027-08/CA/NCI NIH HHS/ -- R01 CA076027-09/CA/NCI NIH HHS/ -- R01 CA076027-10/CA/NCI NIH HHS/ -- R01 CA076027-11/CA/NCI NIH HHS/ -- R01 CA076027-11S1/CA/NCI NIH HHS/ -- R01 CA076027-12/CA/NCI NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):948-52. doi: 10.1126/science.1170633.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA. delange@mail.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965504" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes/physiology ; Chromosomes, Mammalian/*physiology/ultrastructure ; Ciliophora/genetics/metabolism ; DNA/biosynthesis/*metabolism ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/metabolism ; Humans ; Repetitive Sequences, Nucleic Acid ; Signal Transduction ; Telomerase/metabolism ; Telomere/*physiology/ultrastructure ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/metabolism ; Yeasts/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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