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  • Institute of Physics  (182)
  • Oxford University Press  (46)
  • American Association for the Advancement of Science (AAAS)  (19)
  • Taylor & Francis  (12)
  • 2005-2009  (259)
  • 11
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    Small-molecule inhibition of TNF-alpha (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-15
    Description: We have identified a small-molecule inhibitor of tumor necrosis factor alpha (TNF-alpha) that promotes subunit disassembly of this trimeric cytokine family member. The compound inhibits TNF-alpha activity in biochemical and cell-based assays with median inhibitory concentrations of 22 and 4.6 micromolar, respectively. Formation of an intermediate complex between the compound and the intact trimer results in a 600-fold accelerated subunit dissociation rate that leads to trimer dissociation. A structure solved by x-ray crystallography reveals that a single compound molecule displaces a subunit of the trimer to form a complex with a dimer of TNF-alpha subunits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Molly M -- Smith, Annemarie Stroustrup -- Oslob, Johan D -- Flanagan, William M -- Braisted, Andrew C -- Whitty, Adrian -- Cancilla, Mark T -- Wang, Jun -- Lugovskoy, Alexey A -- Yoburn, Josh C -- Fung, Amy D -- Farrington, Graham -- Eldredge, John K -- Day, Eric S -- Cruz, Leslie A -- Cachero, Teresa G -- Miller, Stephan K -- Friedman, Jessica E -- Choong, Ingrid C -- Cunningham, Brian C -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):1022-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sunesis Pharmaceuticals, Incorporated, 341 Oyster Point Boulevard, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284179" target="_blank"〉PubMed〈/a〉
    Keywords: Biotinylation ; Chemistry, Physical ; Crystallography, X-Ray ; Dimerization ; Fluorescence ; Hydrogen/chemistry ; Hydrophobic and Hydrophilic Interactions ; Indoles/chemical synthesis/*chemistry/*pharmacology ; Kinetics ; Mass Spectrometry ; Models, Chemical ; Models, Molecular ; Molecular Conformation ; Molecular Structure ; Physicochemical Phenomena ; Protein Conformation ; Protein Subunits/chemistry ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Tumor Necrosis Factor-alpha/*antagonists & inhibitors/*chemistry/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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  • 12
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    Highly pathogenic H5N1 influenza virus infection in migratory birds (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-08
    Description: H5N1 avian influenza virus (AIV) has emerged as a pathogenic entity for a variety of species, including humans, in recent years. Here we report an outbreak among migratory birds on Lake Qinghaihu, China, in May and June 2005, in which more than a thousand birds were affected. Pancreatic necrosis and abnormal neurological symptoms were the major clinical features. Sequencing of the complete genomes of four H5N1 AIV strains revealed them to be reassortants related to a peregrine falcon isolate from Hong Kong and to have known highly pathogenic characteristics. Experimental animal infections reproduced typical highly pathogenic AIV infection symptoms and pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, J -- Xiao, H -- Lei, F -- Zhu, Q -- Qin, K -- Zhang, X-W -- Zhang, X-L -- Zhao, D -- Wang, G -- Feng, Y -- Ma, J -- Liu, W -- Wang, J -- Gao, G F -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1206. Epub 2005 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Veterinary Medicine, China Agricultural University, Beijing 100094, China. jhl@cau.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16000410" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animal Migration ; Animals ; Birds/virology ; Charadriiformes/*virology ; Chickens ; China/epidemiology ; Disease Outbreaks/*veterinary ; Geese/*virology ; Genome, Viral ; *Influenza A Virus, H5N1 Subtype ; Influenza A virus/classification/genetics/isolation & purification/*pathogenicity ; Influenza in Birds/*epidemiology/pathology/*virology ; Mice ; Molecular Sequence Data ; Phylogeny ; Reassortant Viruses/genetics/pathogenicity ; Virulence
    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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  • 13
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    Comment on "Oscillations in NF-kappaB signaling control the dynamics of gene expression" (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821939/" 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/PMC2821939/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barken, Derren -- Wang, Chiaochun Joanne -- Kearns, Jeff -- Cheong, Raymond -- Hoffmann, Alexander -- Levchenko, Andre -- GM072024-01/GM/NIGMS NIH HHS/ -- P01 GM071862/GM/NIGMS NIH HHS/ -- P01 GM071862-01A20005/GM/NIGMS NIH HHS/ -- R01 GM071573/GM/NIGMS NIH HHS/ -- R01 GM071573-01A1/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):52; author reply 52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry and Bioinformatics Graduate Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802586" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Nucleus/metabolism ; Computer Simulation ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Proteins/metabolism ; Immunohistochemistry ; Models, Biological ; NF-kappa B/*metabolism ; Recombinant Fusion Proteins ; *Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
    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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  • 14
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    Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Lithium is commonly used to treat bipolar disorder, which is associated with altered circadian rhythm. Lithium is a potent inhibitor of glycogen synthase kinase 3 (GSK3), which regulates circadian rhythm in several organisms. In experiments with cultured cells, we show here that GSK3beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erbalpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erbalpha and activation of clock gene Bmal1. A form of Rev-erbalpha that is insensitive to lithium interferes with the expression of circadian genes. Control of Rev-erbalpha protein stability is thus a critical component of the peripheral clock and a biological target of lithium therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yin, Lei -- Wang, Jing -- Klein, Peter S -- Lazar, Mitchell A -- DK 19525/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- MH058324/MH/NIMH NIH HHS/ -- R01 MH058324/MH/NIMH NIH HHS/ -- R01 MH058324-07/MH/NIMH NIH HHS/ -- R01 MH058324-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1002-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, and University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484495" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Amino Acid Sequence ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biological Clocks/*physiology ; Cell Line ; Cell Line, Tumor ; Circadian Rhythm/*physiology ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Down-Regulation ; Gene Expression Regulation ; Glycogen Synthase Kinase 3/antagonists & inhibitors/metabolism ; Humans ; Lithium Chloride/*pharmacology ; Mice ; Molecular Sequence Data ; NIH 3T3 Cells ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Phosphorylation ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Proteasome Inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry/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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  • 15
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    Rheb activates mTOR by antagonizing its endogenous inhibitor, FKBP38 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: The mammalian target of rapamycin, mTOR, is a central regulator of cell growth. Its activity is regulated by Rheb, a Ras-like small guanosine triphosphatase (GTPase), in response to growth factor stimulation and nutrient availability. We show that Rheb regulates mTOR through FKBP38, a member of the FK506-binding protein (FKBP) family that is structurally related to FKBP12. FKBP38 binds to mTOR and inhibits its activity in a manner similar to that of the FKBP12-rapamycin complex. Rheb interacts directly with FKBP38 and prevents its association with mTOR in a guanosine 5'-triphosphate (GTP)-dependent manner. Our findings suggest that FKBP38 is an endogenous inhibitor of mTOR, whose inhibitory activity is antagonized by Rheb in response to growth factor stimulation and nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bai, Xiaochun -- Ma, Dongzhu -- Liu, Anling -- Shen, Xiaoyun -- Wang, Qiming J -- Liu, Yongjian -- Jiang, Yu -- GM068832/GM/NIGMS NIH HHS/ -- R01 CA129821/CA/NCI NIH HHS/ -- R01 GM068832/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):977-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Pittsburgh School of Medicine, E1357 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991864" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Cell Line ; Culture Media ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Mutant Proteins/metabolism ; Neuropeptides/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinases/chemistry/*metabolism ; Protein Structure, Tertiary ; Proteins ; Recombinant Proteins/metabolism ; Serum ; Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/metabolism
    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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  • 16
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    A neoplastic gene fusion mimics trans-splicing of RNAs in normal human cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: Chromosomal rearrangements that create gene fusions are common features of human tumors. The prevailing view is that the resultant chimeric transcripts and proteins are abnormal, tumor-specific products that provide tumor cells with a growth and/or survival advantage. We show that normal endometrial stromal cells contain a specific chimeric RNA joining 5' exons of the JAZF1 gene on chromosome 7p15 to 3' exons of the Polycomb group gene JJAZ1/SUZ12 on chromosome 17q11 and that this RNA is translated into JAZF1-JJAZ1, a protein with anti-apoptotic activity. The JAZF1-JJAZ1 RNA appears to arise from physiologically regulated trans-splicing between precursor messenger RNAs for JAZF1 and JJAZ1. The chimeric RNA and protein are identical to those produced from a gene fusion found in human endometrial stromal tumors. These observations suggest that certain gene fusions may be pro-neoplastic owing to constitutive expression of chimeric gene products normally generated by trans-splicing of RNAs in developing tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Hui -- Wang, Jinglan -- Mor, Gil -- Sklar, Jeffrey -- R01 CA85995/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1357-61. doi: 10.1126/science.1156725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772439" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Hypoxia ; Cell Line ; Cell Line, Tumor ; Chromosome Aberrations ; Chromosomes, Human, Pair 17/genetics ; Chromosomes, Human, Pair 7/genetics ; Deferoxamine/pharmacology ; Endometrial Neoplasms/genetics ; Endometrium/cytology/*metabolism ; Exons ; Female ; *Gene Fusion ; Humans ; Menstrual Cycle ; Mutant Chimeric Proteins/genetics ; Neoplasm Proteins/biosynthesis/*genetics ; Progesterone/pharmacology ; Protein Biosynthesis ; RNA Precursors/*genetics ; RNA, Messenger/genetics ; Stromal Cells/*metabolism ; *Trans-Splicing ; Transcription Factors/biosynthesis/*genetics ; Translocation, Genetic
    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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  • 17
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    Dependence of mouse embryonic stem cells on threonine catabolism (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: Measurements of the abundance of common metabolites in cultured embryonic stem (ES) cells revealed an unusual state with respect to one-carbon metabolism. These findings led to the discovery of copious expression of the gene encoding threonine dehydrogenase (TDH) in ES cells. TDH-mediated catabolism of threonine takes place in mitochondria to generate glycine and acetyl-coenzyme A (CoA), with glycine facilitating one-carbon metabolism via the glycine cleavage system and acetyl-CoA feeding the tricarboxylic acid cycle. Culture media individually deprived of each of the 20 amino acids were applied to ES cells, leading to the discovery that ES cells are critically dependent on one amino acid--threonine. These observations show that ES cells exist in a high-flux backbone metabolic state comparable to that of rapidly growing bacterial cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373593/" 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/PMC4373593/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Jian -- Alexander, Peter -- Wu, Leeju -- Hammer, Robert -- Cleaver, Ondine -- McKnight, Steven L -- R01 DK079862/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):435-9. doi: 10.1126/science.1173288. Epub 2009 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19589965" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Oxidoreductases/genetics/metabolism ; Animals ; Cells, Cultured ; Culture Media ; Embryo, Mammalian/metabolism ; Embryonic Development ; Embryonic Stem Cells/*metabolism ; HeLa Cells ; Humans ; Mice ; NIH 3T3 Cells ; Threonine/*metabolism ; Tissue Culture Techniques
    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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  • 18
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    The E3 ligase TRAF6 regulates Akt ubiquitination and activation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-29
    Description: Akt signaling plays a central role in many biological functions, such as cell proliferation and apoptosis. Because Akt (also known as protein kinase B) resides primarily in the cytosol, it is not known how these signaling molecules are recruited to the plasma membrane and subsequently activated by growth factor stimuli. We found that the protein kinase Akt undergoes lysine-63 chain ubiquitination, which is important for Akt membrane localization and phosphorylation. TRAF6 was found to be a direct E3 ligase for Akt and was essential for Akt ubiquitination, membrane recruitment, and phosphorylation upon growth-factor stimulation. The human cancer-associated Akt mutant displayed an increase in Akt ubiquitination, in turn contributing to the enhancement of Akt membrane localization and phosphorylation. Thus, Akt ubiquitination is an important step for oncogenic Akt activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3008763/" 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/PMC3008763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Wei-Lei -- Wang, Jing -- Chan, Chia-Hsin -- Lee, Szu-Wei -- Campos, Alejandro D -- Lamothe, Betty -- Hur, Lana -- Grabiner, Brian C -- Lin, Xin -- Darnay, Bryant G -- Lin, Hui-Kuan -- R01 CA149321/CA/NCI NIH HHS/ -- R01 CA149321-02/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1134-8. doi: 10.1126/science.1175065.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713527" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Apoptosis ; Cell Line ; Cell Line, Tumor ; Cell Membrane/*metabolism ; Humans ; Insulin-Like Growth Factor I/pharmacology ; Interleukin-1beta/pharmacology ; Lipopolysaccharides/pharmacology ; Mice ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/chemistry/*metabolism ; *Signal Transduction ; TNF Receptor-Associated Factor 6/genetics/*metabolism ; Transplantation, Heterologous ; Ubiquitin-Protein Ligases/*metabolism ; Ubiquitination
    Print ISSN: 0036-8075
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  • 19
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    Physics. Learning and scientific reasoning (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bao, Lei -- Cai, Tianfan -- Koenig, Kathy -- Fang, Kai -- Han, Jing -- Wang, Jing -- Liu, Qing -- Ding, Lin -- Cui, Lili -- Luo, Ying -- Wang, Yufeng -- Li, Lieming -- Wu, Nianle -- New York, N.Y. -- Science. 2009 Jan 30;323(5914):586-7. doi: 10.1126/science.1167740.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Ohio State University, Columbus, OH 43210, USA. bao.15@osu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19179514" target="_blank"〉PubMed〈/a〉
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  • 20
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    FGF: A web tool for Fishing Gene Family in a whole genome database (2007)
    Oxford University Press
    Details
    Publication Date: 2007-05-08
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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