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  • 1
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    "Fluorescent timer": protein that changes color with time (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2000-11-25
    Beschreibung: We generated a mutant of the red fluorescent protein drFP583. The mutant (E5) changes its fluorescence from green to red over time. The rate of color conversion is independent of protein concentration and therefore can be used to trace time-dependent expression. We used in vivo labeling with E5 to measure expression from the heat shock-dependent promoter in Caenorhabditis elegans and from the Otx-2 promoter in developing Xenopus embryos. Thus, E5 is a "fluorescent timer" that can be used to monitor both activation and down-regulation of target promoters on the whole-organism scale.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Terskikh, A -- Fradkov, A -- Ermakova, G -- Zaraisky, A -- Tan, P -- Kajava, A V -- Zhao, X -- Lukyanov, S -- Matz, M -- Kim, S -- Weissman, I -- Siebert, P -- 1 RO3 TW01362-01/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1585-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Medicine, Stanford University, Stanford, CA 94305, USA. Alexey.Terskikh@Stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090358" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain/embryology/metabolism ; Caenorhabditis elegans/embryology/genetics ; Cell Line ; Color ; Fluorescence ; Gene Expression Profiling/*methods ; *Gene Expression Regulation ; Gene Expression Regulation, Developmental ; Heat-Shock Proteins/genetics ; *Homeodomain Proteins ; Humans ; Luminescent Proteins/*chemistry/*genetics/metabolism ; Mutation ; Nerve Tissue Proteins/genetics ; Otx Transcription Factors ; *Promoter Regions, Genetic ; Temperature ; Time Factors ; Trans-Activators/genetics ; Xenopus laevis/embryology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Somatic mutations affect key pathways in lung adenocarcinoma (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-10-25
    Beschreibung: Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" 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/PMC2694412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Getz, Gad -- Wheeler, David A -- Mardis, Elaine R -- McLellan, Michael D -- Cibulskis, Kristian -- Sougnez, Carrie -- Greulich, Heidi -- Muzny, Donna M -- Morgan, Margaret B -- Fulton, Lucinda -- Fulton, Robert S -- Zhang, Qunyuan -- Wendl, Michael C -- Lawrence, Michael S -- Larson, David E -- Chen, Ken -- Dooling, David J -- Sabo, Aniko -- Hawes, Alicia C -- Shen, Hua -- Jhangiani, Shalini N -- Lewis, Lora R -- Hall, Otis -- Zhu, Yiming -- Mathew, Tittu -- Ren, Yanru -- Yao, Jiqiang -- Scherer, Steven E -- Clerc, Kerstin -- Metcalf, Ginger A -- Ng, Brian -- Milosavljevic, Aleksandar -- Gonzalez-Garay, Manuel L -- Osborne, John R -- Meyer, Rick -- Shi, Xiaoqi -- Tang, Yuzhu -- Koboldt, Daniel C -- Lin, Ling -- Abbott, Rachel -- Miner, Tracie L -- Pohl, Craig -- Fewell, Ginger -- Haipek, Carrie -- Schmidt, Heather -- Dunford-Shore, Brian H -- Kraja, Aldi -- Crosby, Seth D -- Sawyer, Christopher S -- Vickery, Tammi -- Sander, Sacha -- Robinson, Jody -- Winckler, Wendy -- Baldwin, Jennifer -- Chirieac, Lucian R -- Dutt, Amit -- Fennell, Tim -- Hanna, Megan -- Johnson, Bruce E -- Onofrio, Robert C -- Thomas, Roman K -- Tonon, Giovanni -- Weir, Barbara A -- Zhao, Xiaojun -- Ziaugra, Liuda -- Zody, Michael C -- Giordano, Thomas -- Orringer, Mark B -- Roth, Jack A -- Spitz, Margaret R -- Wistuba, Ignacio I -- Ozenberger, Bradley -- Good, Peter J -- Chang, Andrew C -- Beer, David G -- Watson, Mark A -- Ladanyi, Marc -- Broderick, Stephen -- Yoshizawa, Akihiko -- Travis, William D -- Pao, William -- Province, Michael A -- Weinstock, George M -- Varmus, Harold E -- Gabriel, Stacey B -- Lander, Eric S -- Gibbs, Richard A -- Meyerson, Matthew -- Wilson, Richard K -- P50 CA070907/CA/NCI NIH HHS/ -- R01 CA154365/CA/NCI NIH HHS/ -- U19 CA084953/CA/NCI NIH HHS/ -- U19 CA084953-050003/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1069-75. doi: 10.1038/nature07423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948947" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenocarcinoma, Bronchiolo-Alveolar/*genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung Neoplasms/*genetics ; Male ; Mutation/*genetics ; Proto-Oncogenes/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Rational design of a structural and functional nitric oxide reductase (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-11-27
    Beschreibung: Protein design provides a rigorous test of our knowledge about proteins and allows the creation of novel enzymes for biotechnological applications. Whereas progress has been made in designing proteins that mimic native proteins structurally, it is more difficult to design functional proteins. In comparison to recent successes in designing non-metalloproteins, it is even more challenging to rationally design metalloproteins that reproduce both the structure and function of native metalloenzymes. This is because protein metal-binding sites are much more varied than non-metal-containing sites, in terms of different metal ion oxidation states, preferred geometry and metal ion ligand donor sets. Because of their variability, it has been difficult to predict metal-binding site properties in silico, as many of the parameters, such as force fields, are ill-defined. Therefore, the successful design of a structural and functional metalloprotein would greatly advance the field of protein design and our understanding of enzymes. Here we report a successful, rational design of a structural and functional model of a metalloprotein, nitric oxide reductase (NOR), by introducing three histidines and one glutamate, predicted as ligands in the active site of NOR, into the distal pocket of myoglobin. A crystal structure of the designed protein confirms that the minimized computer model contains a haem/non-haem Fe(B) centre that is remarkably similar to that in the crystal structure. This designed protein also exhibits NO reduction activity, and so models both the structure and function of NOR, offering insight that the active site glutamate is required for both iron binding and activity. These results show that structural and functional metalloproteins can be rationally designed in silico.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297211/" 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/PMC4297211/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yeung, Natasha -- Lin, Ying-Wu -- Gao, Yi-Gui -- Zhao, Xuan -- Russell, Brandy S -- Lei, Lanyu -- Miner, Kyle D -- Robinson, Howard -- Lu, Yi -- GM062211/GM/NIGMS NIH HHS/ -- R01 GM062211/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1079-82. doi: 10.1038/nature08620. Epub 2009 Nov 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19940850" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Crystallization ; Iron/metabolism ; Models, Molecular ; Myoglobin/chemistry ; Nitric Oxide/metabolism ; Oxidoreductases/*chemical synthesis/*chemistry/metabolism ; Protein Binding ; Protein Structure, Tertiary
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Live-animal tracking of individual haematopoietic stem/progenitor cells in their niche (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-12-05
    Beschreibung: Stem cells reside in a specialized, regulatory environment termed the niche that dictates how they generate, maintain and repair tissues. We have previously documented that transplanted haematopoietic stem and progenitor cell populations localize to subdomains of bone-marrow microvessels where the chemokine CXCL12 is particularly abundant. Using a combination of high-resolution confocal microscopy and two-photon video imaging of individual haematopoietic cells in the calvarium bone marrow of living mice over time, we examine the relationship of haematopoietic stem and progenitor cells to blood vessels, osteoblasts and endosteal surface as they home and engraft in irradiated and c-Kit-receptor-deficient recipient mice. Osteoblasts were enmeshed in microvessels and relative positioning of stem/progenitor cells within this complex tissue was nonrandom and dynamic. Both cell autonomous and non-autonomous factors influenced primitive cell localization. Different haematopoietic cell subsets localized to distinct locations according to the stage of differentiation. When physiological challenges drove either engraftment or expansion, bone-marrow stem/progenitor cells assumed positions in close proximity to bone and osteoblasts. Our analysis permits observing in real time, at a single cell level, processes that previously have been studied only by their long-term outcome at the organismal level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820276/" 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/PMC2820276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo Celso, Cristina -- Fleming, Heather E -- Wu, Juwell W -- Zhao, Cher X -- Miake-Lye, Sam -- Fujisaki, Joji -- Cote, Daniel -- Rowe, David W -- Lin, Charles P -- Scadden, David T -- R01 EY014106/EY/NEI NIH HHS/ -- R01 EY014106-05/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jan 1;457(7225):92-6. doi: 10.1038/nature07434. Epub 2008 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19052546" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blood Vessels/cytology ; Bone Marrow ; Cell Division ; Cell Separation ; Hematopoietic Stem Cells/*cytology ; Mice ; Mice, Inbred C57BL ; Osteoblasts/cytology ; Proto-Oncogene Proteins c-kit/genetics/metabolism ; Skull/cytology ; Stem Cell Niche/*cytology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    The transcriptional network for mesenchymal transformation of brain tumours (2009)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2009-12-25
    Beschreibung: The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPbeta and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPbeta and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage, whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma, expression of C/EBPbeta and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4011561/" 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/PMC4011561/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carro, Maria Stella -- Lim, Wei Keat -- Alvarez, Mariano Javier -- Bollo, Robert J -- Zhao, Xudong -- Snyder, Evan Y -- Sulman, Erik P -- Anne, Sandrine L -- Doetsch, Fiona -- Colman, Howard -- Lasorella, Anna -- Aldape, Ken -- Califano, Andrea -- Iavarone, Antonio -- 1RC2CA148308-01/CA/NCI NIH HHS/ -- P20 GM075059/GM/NIGMS NIH HHS/ -- P20GM075059/GM/NIGMS NIH HHS/ -- R01 CA085628/CA/NCI NIH HHS/ -- R01 CA101644/CA/NCI NIH HHS/ -- R01 CA109755/CA/NCI NIH HHS/ -- R01 CA127643/CA/NCI NIH HHS/ -- R01 NS061776/NS/NINDS NIH HHS/ -- R01 NS061776-01A2/NS/NINDS NIH HHS/ -- R01 NS061776-02/NS/NINDS NIH HHS/ -- R01CA085628/CA/NCI NIH HHS/ -- R01CA101644/CA/NCI NIH HHS/ -- R01CA109755/CA/NCI NIH HHS/ -- R01NS061776/NS/NINDS NIH HHS/ -- RC2 CA148308/CA/NCI NIH HHS/ -- U01 CA168426/CA/NCI NIH HHS/ -- U54 CA121852/CA/NCI NIH HHS/ -- U54CA121852/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jan 21;463(7279):318-25. doi: 10.1038/nature08712. Epub 2009 Dec 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University Medical Center, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20032975" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Brain Neoplasms/diagnosis/*genetics/*pathology ; CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism ; Cell Differentiation/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/metabolism/pathology ; Cellular Reprogramming/genetics ; Computational Biology ; *Gene Expression Regulation, Neoplastic ; *Gene Regulatory Networks ; Glioma/diagnosis/genetics/pathology ; Humans ; Mesenchymal Stromal Cells/metabolism/pathology ; Mesoderm/*metabolism/*pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Invasiveness/genetics/pathology ; Neurons/metabolism/pathology ; Prognosis ; Reproducibility of Results ; STAT3 Transcription Factor/genetics/metabolism ; *Transcription, Genetic
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2011-07-19
    Beschreibung: The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" 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/PMC3251012/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lan -- Gural, Alexander -- Sun, Xiao-Jian -- Zhao, Xinyang -- Perna, Fabiana -- Huang, Gang -- Hatlen, Megan A -- Vu, Ly -- Liu, Fan -- Xu, Haiming -- Asai, Takashi -- Xu, Hao -- Deblasio, Tony -- Menendez, Silvia -- Voza, Francesca -- Jiang, Yanwen -- Cole, Philip A -- Zhang, Jinsong -- Melnick, Ari -- Roeder, Robert G -- Nimer, Stephen D -- GM62437/GM/NIGMS NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):765-9. doi: 10.1126/science.1201662. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764752" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylation ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; E1A-Associated p300 Protein/antagonists & inhibitors/*metabolism ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoietic Stem Cells/*cytology/physiology ; Humans ; Leukemia, Myeloid, Acute/*metabolism/pathology ; Lysine/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Preleukemia/metabolism/pathology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Transcriptional Activation ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    China's little emperors show signs of success (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2013-02-23
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Xudong -- Ma, Xiquan -- Yao, Yuhong -- Wan, Chonghua -- Ng, Emily -- New York, N.Y. -- Science. 2013 Feb 22;339(6122):905-6. doi: 10.1126/science.339.6122.905-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23430636" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Attitude ; *Behavior ; *Family Planning Policy ; Female ; Humans ; Male ; Only Child/*psychology ; *Personality
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    A draft sequence for the genome of the domesticated silkworm (Bombyx mori) (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2004-12-14
    Beschreibung: We report a draft sequence for the genome of the domesticated silkworm (Bombyx mori), covering 90.9% of all known silkworm genes. Our estimated gene count is 18,510, which exceeds the 13,379 genes reported for Drosophila melanogaster. Comparative analyses to fruitfly, mosquito, spider, and butterfly reveal both similarities and differences in gene content.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xia, Qingyou -- Zhou, Zeyang -- Lu, Cheng -- Cheng, Daojun -- Dai, Fangyin -- Li, Bin -- Zhao, Ping -- Zha, Xingfu -- Cheng, Tingcai -- Chai, Chunli -- Pan, Guoqing -- Xu, Jinshan -- Liu, Chun -- Lin, Ying -- Qian, Jifeng -- Hou, Yong -- Wu, Zhengli -- Li, Guanrong -- Pan, Minhui -- Li, Chunfeng -- Shen, Yihong -- Lan, Xiqian -- Yuan, Lianwei -- Li, Tian -- Xu, Hanfu -- Yang, Guangwei -- Wan, Yongji -- Zhu, Yong -- Yu, Maode -- Shen, Weide -- Wu, Dayang -- Xiang, Zhonghuai -- Yu, Jun -- Wang, Jun -- Li, Ruiqiang -- Shi, Jianping -- Li, Heng -- Li, Guangyuan -- Su, Jianning -- Wang, Xiaoling -- Li, Guoqing -- Zhang, Zengjin -- Wu, Qingfa -- Li, Jun -- Zhang, Qingpeng -- Wei, Ning -- Xu, Jianzhe -- Sun, Haibo -- Dong, Le -- Liu, Dongyuan -- Zhao, Shengli -- Zhao, Xiaolan -- Meng, Qingshun -- Lan, Fengdi -- Huang, Xiangang -- Li, Yuanzhe -- Fang, Lin -- Li, Changfeng -- Li, Dawei -- Sun, Yongqiao -- Zhang, Zhenpeng -- Yang, Zheng -- Huang, Yanqing -- Xi, Yan -- Qi, Qiuhui -- He, Dandan -- Huang, Haiyan -- Zhang, Xiaowei -- Wang, Zhiqiang -- Li, Wenjie -- Cao, Yuzhu -- Yu, Yingpu -- Yu, Hong -- Li, Jinhong -- Ye, Jiehua -- Chen, Huan -- Zhou, Yan -- Liu, Bin -- Wang, Jing -- Ye, Jia -- Ji, Hai -- Li, Shengting -- Ni, Peixiang -- Zhang, Jianguo -- Zhang, Yong -- Zheng, Hongkun -- Mao, Bingyu -- Wang, Wen -- Ye, Chen -- Li, Songgang -- Wang, Jian -- Wong, Gane Ka-Shu -- Yang, Huanming -- Biology Analysis Group -- 1 P50 HG02351/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2004 Dec 10;306(5703):1937-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Southwest Agricultural University, Chongqing Beibei, 400716, China. xiaqy@swau.cq.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15591204" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Algorithms ; Animals ; Anopheles/genetics ; Body Patterning/genetics ; Bombyx/*genetics/growth & development/metabolism ; Butterflies/genetics ; Computational Biology ; DNA Transposable Elements ; Drosophila melanogaster/genetics ; Exocrine Glands/metabolism ; Expressed Sequence Tags ; Female ; Genes, Homeobox ; *Genes, Insect ; *Genome ; Immunity, Innate/genetics ; Insect Hormones/genetics ; Insect Proteins/genetics ; Male ; Molecular Sequence Data ; *Sequence Analysis, DNA ; Sequence Homology, Nucleic Acid ; Sex Determination Processes ; Spiders/genetics ; Wings, Animal/growth & development
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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    A directional switch of integrin signalling and a new anti-thrombotic strategy (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-10-29
    Beschreibung: Integrins have a critical role in thrombosis and haemostasis. Antagonists of the platelet integrin alphaIIbbeta3 are potent anti-thrombotic drugs, but also have the life-threatening adverse effect of causing bleeding. It is therefore desirable to develop new antagonists that do not cause bleeding. Integrins transmit signals bidirectionally. Inside-out signalling activates integrins through a talin-dependent mechanism. Integrin ligation mediates thrombus formation and outside-in signalling, which requires Galpha13 and greatly expands thrombi. Here we show that Galpha13 and talin bind to mutually exclusive but distinct sites within the integrin beta3 cytoplasmic domain in opposing waves. The first talin-binding wave mediates inside-out signalling and also ligand-induced integrin activation, but is not required for outside-in signalling. Integrin ligation induces transient talin dissociation and Galpha13 binding to an EXE motif (in which X denotes any residue), which selectively mediates outside-in signalling and platelet spreading. The second talin-binding wave is associated with clot retraction. An EXE-motif-based inhibitor of Galpha13-integrin interaction selectively abolishes outside-in signalling without affecting integrin ligation, and suppresses occlusive arterial thrombosis without affecting bleeding time. Thus, we have discovered a new mechanism for the directional switch of integrin signalling and, on the basis of this mechanism, designed a potent new anti-thrombotic drug that does not cause bleeding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823815/" 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/PMC3823815/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Bo -- Zhao, Xiaojuan -- O'Brien, Kelly A -- Stojanovic-Terpo, Aleksandra -- Delaney, M Keegan -- Kim, Kyungho -- Cho, Jaehyung -- Lam, Stephen C-T -- Du, Xiaoping -- HL062350/HL/NHLBI NIH HHS/ -- HL080264/HL/NHLBI NIH HHS/ -- HL109439/HL/NHLBI NIH HHS/ -- R01 HL080264/HL/NHLBI NIH HHS/ -- R01 HL109439/HL/NHLBI NIH HHS/ -- T32 HL007829/HL/NHLBI NIH HHS/ -- England -- Nature. 2013 Nov 7;503(7474):131-5. doi: 10.1038/nature12613. Epub 2013 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, Illinois 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24162846" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Antithrombins/adverse effects/*pharmacology/therapeutic use ; Binding Sites ; Bleeding Time ; *Cell Polarity ; Cytoplasm/metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/metabolism ; Hemorrhage/chemically induced ; Humans ; Integrin beta3/chemistry/genetics/metabolism ; Integrins/chemistry/deficiency/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Platelet Glycoprotein GPIIb-IIIa Complex/metabolism ; Protein Binding ; Protein Structure, Tertiary ; Signal Transduction/*drug effects ; Talin/metabolism ; Thrombosis/*drug therapy/metabolism/pathology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Unusual architecture of the p7 channel from hepatitis C virus (2013)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2013-06-07
    Beschreibung: The hepatitis C virus (HCV) has developed a small membrane protein, p7, which remarkably can self-assemble into a large channel complex that selectively conducts cations. We wanted to examine the structural solution that the viroporin adopts in order to achieve selective cation conduction, because p7 has no homology with any of the known prokaryotic or eukaryotic channel proteins. The activity of p7 can be inhibited by amantadine and rimantadine, which are potent blockers of the influenza M2 channel and licensed drugs against influenza infections. The adamantane derivatives have been used in HCV clinical trials, but large variation in drug efficacy among the various HCV genotypes has been difficult to explain without detailed molecular structures. Here we determine the structures of this HCV viroporin as well as its drug-binding site using the latest nuclear magnetic resonance (NMR) technologies. The structure exhibits an unusual mode of hexameric assembly, where the individual p7 monomers, i, not only interact with their immediate neighbours, but also reach farther to associate with the i+2 and i+3 monomers, forming a sophisticated, funnel-like architecture. The structure also points to a mechanism of cation selection: an asparagine/histidine ring that constricts the narrow end of the funnel serves as a broad cation selectivity filter, whereas an arginine/lysine ring that defines the wide end of the funnel may selectively allow cation diffusion into the channel. Our functional investigation using whole-cell channel recording shows that these residues are critical for channel activity. NMR measurements of the channel-drug complex revealed six equivalent hydrophobic pockets between the peripheral and pore-forming helices to which amantadine or rimantadine binds, and compound binding specifically to this position may allosterically inhibit cation conduction by preventing the channel from opening. Our data provide a molecular explanation for p7-mediated cation conductance and its inhibition by adamantane derivatives.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725310/" 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/PMC3725310/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉OuYang, Bo -- Xie, Shiqi -- Berardi, Marcelo J -- Zhao, Xinhao -- Dev, Jyoti -- Yu, Wenjing -- Sun, Bing -- Chou, James J -- GM094608/GM/NIGMS NIH HHS/ -- U54 GM094608/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Jun 27;498(7455):521-5. doi: 10.1038/nature12283. Epub 2013 Jun 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23739335" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adamantane/analogs & derivatives/chemistry/metabolism/pharmacology ; Binding Sites ; Diffusion ; Hepacivirus/*chemistry ; Microscopy, Electron ; Models, Biological ; Models, Molecular ; Nuclear Magnetic Resonance, Biomolecular ; Porosity ; Rimantadine/chemistry/metabolism/pharmacology ; Structure-Activity Relationship ; Viral Proteins/antagonists & inhibitors/*chemistry/metabolism/ultrastructure
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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