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  • 1
    Publication Date: 2002-04-06
    Description: We have produced a draft sequence of the rice genome for the most widely cultivated subspecies in China, Oryza sativa L. ssp. indica, by whole-genome shotgun sequencing. The genome was 466 megabases in size, with an estimated 46,022 to 55,615 genes. Functional coverage in the assembled sequences was 92.0%. About 42.2% of the genome was in exact 20-nucleotide oligomer repeats, and most of the transposons were in the intergenic regions between genes. Although 80.6% of predicted Arabidopsis thaliana genes had a homolog in rice, only 49.4% of predicted rice genes had a homolog in A. thaliana. The large proportion of rice genes with no recognizable homologs is due to a gradient in the GC content of rice coding sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Jun -- Hu, Songnian -- Wang, Jun -- Wong, Gane Ka-Shu -- Li, Songgang -- Liu, Bin -- Deng, Yajun -- Dai, Li -- Zhou, Yan -- Zhang, Xiuqing -- Cao, Mengliang -- Liu, Jing -- Sun, Jiandong -- Tang, Jiabin -- Chen, Yanjiong -- Huang, Xiaobing -- Lin, Wei -- Ye, Chen -- Tong, Wei -- Cong, Lijuan -- Geng, Jianing -- Han, Yujun -- Li, Lin -- Li, Wei -- Hu, Guangqiang -- Huang, Xiangang -- Li, Wenjie -- Li, Jian -- Liu, Zhanwei -- Li, Long -- Liu, Jianping -- Qi, Qiuhui -- Liu, Jinsong -- Li, Li -- Li, Tao -- Wang, Xuegang -- Lu, Hong -- Wu, Tingting -- Zhu, Miao -- Ni, Peixiang -- Han, Hua -- Dong, Wei -- Ren, Xiaoyu -- Feng, Xiaoli -- Cui, Peng -- Li, Xianran -- Wang, Hao -- Xu, Xin -- Zhai, Wenxue -- Xu, Zhao -- Zhang, Jinsong -- He, Sijie -- Zhang, Jianguo -- Xu, Jichen -- Zhang, Kunlin -- Zheng, Xianwu -- Dong, Jianhai -- Zeng, Wanyong -- Tao, Lin -- Ye, Jia -- Tan, Jun -- Ren, Xide -- Chen, Xuewei -- He, Jun -- Liu, Daofeng -- Tian, Wei -- Tian, Chaoguang -- Xia, Hongai -- Bao, Qiyu -- Li, Gang -- Gao, Hui -- Cao, Ting -- Wang, Juan -- Zhao, Wenming -- Li, Ping -- Chen, Wei -- Wang, Xudong -- Zhang, Yong -- Hu, Jianfei -- Wang, Jing -- Liu, Song -- Yang, Jian -- Zhang, Guangyu -- Xiong, Yuqing -- Li, Zhijie -- Mao, Long -- Zhou, Chengshu -- Zhu, Zhen -- Chen, Runsheng -- Hao, Bailin -- Zheng, Weimou -- Chen, Shouyi -- Guo, Wei -- Li, Guojie -- Liu, Siqi -- Tao, Ming -- Wang, Jian -- Zhu, Lihuang -- Yuan, Longping -- Yang, Huanming -- 1 RO1 ES09909/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 5;296(5565):79-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Beijing Genomics Institute/Center of Genomics and Bioinformatics, Chinese Academy of Sciences, Beijing 101300, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11935017" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics ; Base Composition ; Computational Biology ; Contig Mapping ; DNA Transposable Elements ; DNA, Intergenic ; DNA, Plant/chemistry/genetics ; Databases, Nucleic Acid ; Exons ; Gene Duplication ; Genes, Plant ; *Genome, Plant ; Genomics ; Introns ; Molecular Sequence Data ; Oryza/*genetics ; Plant Proteins/chemistry/genetics ; Polymorphism, Genetic ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Sequence Homology, Nucleic Acid ; Software ; Species Specificity ; Synteny
    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
    Publication Date: 2009-12-25
    Description: The clinical efficacy of epidermal growth factor receptor (EGFR) kinase inhibitors in EGFR-mutant non-small-cell lung cancer (NSCLC) is limited by the development of drug-resistance mutations, including the gatekeeper T790M mutation. Strategies targeting EGFR T790M with irreversible inhibitors have had limited success and are associated with toxicity due to concurrent inhibition of wild-type EGFR. All current EGFR inhibitors possess a structurally related quinazoline-based core scaffold and were identified as ATP-competitive inhibitors of wild-type EGFR. Here we identify a covalent pyrimidine EGFR inhibitor by screening an irreversible kinase inhibitor library specifically against EGFR T790M. These agents are 30- to 100-fold more potent against EGFR T790M, and up to 100-fold less potent against wild-type EGFR, than quinazoline-based EGFR inhibitors in vitro. They are also effective in murine models of lung cancer driven by EGFR T790M. Co-crystallization studies reveal a structural basis for the increased potency and mutant selectivity of these agents. These mutant-selective irreversible EGFR kinase inhibitors may be clinically more effective and better tolerated than quinazoline-based inhibitors. Our findings demonstrate that functional pharmacological screens against clinically important mutant kinases represent a powerful strategy to identify new classes of mutant-selective kinase inhibitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879581/" 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/PMC2879581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Wenjun -- Ercan, Dalia -- Chen, Liang -- Yun, Cai-Hong -- Li, Danan -- Capelletti, Marzia -- Cortot, Alexis B -- Chirieac, Lucian -- Iacob, Roxana E -- Padera, Robert -- Engen, John R -- Wong, Kwok-Kin -- Eck, Michael J -- Gray, Nathanael S -- Janne, Pasi A -- P50CA090578/CA/NCI NIH HHS/ -- R01 CA122794/CA/NCI NIH HHS/ -- R01 CA130876/CA/NCI NIH HHS/ -- R01 CA130876-02/CA/NCI NIH HHS/ -- R01 CA135257/CA/NCI NIH HHS/ -- R01AG2400401/AG/NIA NIH HHS/ -- R01CA080942/CA/NCI NIH HHS/ -- R01CA11446/CA/NCI NIH HHS/ -- R01CA116020/CA/NCI NIH HHS/ -- R01CA130876-02/CA/NCI NIH HHS/ -- R01CA135257/CA/NCI NIH HHS/ -- R01GM070590/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Dec 24;462(7276):1070-4. doi: 10.1038/nature08622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20033049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/chemistry/*pharmacology/toxicity ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Drug Evaluation, Preclinical ; Drug Resistance, Neoplasm/genetics ; Lung/drug effects ; Mice ; Models, Chemical ; Models, Molecular ; Mutation/*genetics ; NIH 3T3 Cells ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/chemistry/*pharmacology/toxicity ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-09-17
    Description: We report genome sequences of 17 inbred strains of laboratory mice and identify almost ten times more variants than previously known. We use these genomes to explore the phylogenetic history of the laboratory mouse and to examine the functional consequences of allele-specific variation on transcript abundance, revealing that at least 12% of transcripts show a significant tissue-specific expression bias. By identifying candidate functional variants at 718 quantitative trait loci we show that the molecular nature of functional variants and their position relative to genes vary according to the effect size of the locus. These sequences provide a starting point for a new era in the functional analysis of a key model organism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276836/" 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/PMC3276836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keane, Thomas M -- Goodstadt, Leo -- Danecek, Petr -- White, Michael A -- Wong, Kim -- Yalcin, Binnaz -- Heger, Andreas -- Agam, Avigail -- Slater, Guy -- Goodson, Martin -- Furlotte, Nicholas A -- Eskin, Eleazar -- Nellaker, Christoffer -- Whitley, Helen -- Cleak, James -- Janowitz, Deborah -- Hernandez-Pliego, Polinka -- Edwards, Andrew -- Belgard, T Grant -- Oliver, Peter L -- McIntyre, Rebecca E -- Bhomra, Amarjit -- Nicod, Jerome -- Gan, Xiangchao -- Yuan, Wei -- van der Weyden, Louise -- Steward, Charles A -- Bala, Sendu -- Stalker, Jim -- Mott, Richard -- Durbin, Richard -- Jackson, Ian J -- Czechanski, Anne -- Guerra-Assuncao, Jose Afonso -- Donahue, Leah Rae -- Reinholdt, Laura G -- Payseur, Bret A -- Ponting, Chris P -- Birney, Ewan -- Flint, Jonathan -- Adams, David J -- 077192/Wellcome Trust/United Kingdom -- 079912/Wellcome Trust/United Kingdom -- 082356/Wellcome Trust/United Kingdom -- 083573/Wellcome Trust/United Kingdom -- 083573/Z/07/Z/Wellcome Trust/United Kingdom -- 085906/Wellcome Trust/United Kingdom -- 085906/Z/08/Z/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 2T15LM007359/LM/NLM NIH HHS/ -- A6997/Cancer Research UK/United Kingdom -- BB/F022697/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0800024/Medical Research Council/United Kingdom -- K25 HL080079/HL/NHLBI NIH HHS/ -- MC_U127561112/Medical Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Sep 14;477(7364):289-94. doi: 10.1038/nature10413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921910" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Laboratory/genetics ; Gene Expression Regulation/*genetics ; Genetic Variation/*genetics ; Genome/*genetics ; Genomics ; Mice/classification/*genetics ; Mice, Inbred C57BL/genetics ; Mice, Inbred Strains/*genetics ; *Phenotype ; Phylogeny ; Quantitative Trait Loci/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-01-30
    Description: Non-small-cell lung cancer is the leading cause of cancer-related death worldwide. Chemotherapies such as the topoisomerase II (TopoII) inhibitor etoposide effectively reduce disease in a minority of patients with this cancer; therefore, alternative drug targets, including epigenetic enzymes, are under consideration for therapeutic intervention. A promising potential epigenetic target is the methyltransferase EZH2, which in the context of the polycomb repressive complex 2 (PRC2) is well known to tri-methylate histone H3 at lysine 27 (H3K27me3) and elicit gene silencing. Here we demonstrate that EZH2 inhibition has differential effects on the TopoII inhibitor response of non-small-cell lung cancers in vitro and in vivo. EGFR and BRG1 mutations are genetic biomarkers that predict enhanced sensitivity to TopoII inhibitor in response to EZH2 inhibition. BRG1 loss-of-function mutant tumours respond to EZH2 inhibition with increased S phase, anaphase bridging, apoptosis and TopoII inhibitor sensitivity. Conversely, EGFR and BRG1 wild-type tumours upregulate BRG1 in response to EZH2 inhibition and ultimately become more resistant to TopoII inhibitor. EGFR gain-of-function mutant tumours are also sensitive to dual EZH2 inhibition and TopoII inhibitor, because of genetic antagonism between EGFR and BRG1. These findings suggest an opportunity for precision medicine in the genetically complex disease of non-small-cell lung cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393352/" 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/PMC4393352/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fillmore, Christine M -- Xu, Chunxiao -- Desai, Pooja T -- Berry, Joanne M -- Rowbotham, Samuel P -- Lin, Yi-Jang -- Zhang, Haikuo -- Marquez, Victor E -- Hammerman, Peter S -- Wong, Kwok-Kin -- Kim, Carla F -- CA120964/CA/NCI NIH HHS/ -- CA122794/CA/NCI NIH HHS/ -- CA140594/CA/NCI NIH HHS/ -- CA154303/CA/NCI NIH HHS/ -- CA163896/CA/NCI NIH HHS/ -- CA166480/CA/NCI NIH HHS/ -- K08 CA163677/CA/NCI NIH HHS/ -- R01 CA140594/CA/NCI NIH HHS/ -- R01 CA163896/CA/NCI NIH HHS/ -- R01 CA166480/CA/NCI NIH HHS/ -- R01 HL090136/HL/NHLBI NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2015 Apr 9;520(7546):239-42. doi: 10.1038/nature14122. Epub 2015 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Stem Cell Program, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2] Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA [3] Harvard Stem Cell Institute, Cambridge, Massachusetts 02138, USA. ; 1] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA. ; Stem Cell Program, Boston Children's Hospital, Boston, Massachusetts 02115, USA. ; Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Chemical Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25629630" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase/drug effects ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology/therapeutic use ; Apoptosis/drug effects ; Carcinoma, Non-Small-Cell Lung/drug therapy/enzymology/genetics/pathology ; Cell Cycle/drug effects ; Cell Line, Tumor ; DNA Helicases/*genetics ; Etoposide/pharmacology/therapeutic use ; Genes, erbB-1/*genetics ; Humans ; Lung Neoplasms/*drug therapy/enzymology/*genetics/pathology ; Mice ; Molecular Targeted Therapy ; Nuclear Proteins/*genetics ; Polycomb Repressive Complex 2/*antagonists & inhibitors ; Topoisomerase II Inhibitors/*pharmacology/*therapeutic use ; Transcription Factors/*genetics ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2011-09-17
    Description: Structural variation is widespread in mammalian genomes and is an important cause of disease, but just how abundant and important structural variants (SVs) are in shaping phenotypic variation remains unclear. Without knowing how many SVs there are, and how they arise, it is difficult to discover what they do. Combining experimental with automated analyses, we identified 711,920 SVs at 281,243 sites in the genomes of thirteen classical and four wild-derived inbred mouse strains. The majority of SVs are less than 1 kilobase in size and 98% are deletions or insertions. The breakpoints of 160,000 SVs were mapped to base pair resolution, allowing us to infer that insertion of retrotransposons causes more than half of SVs. Yet, despite their prevalence, SVs are less likely than other sequence variants to cause gene expression or quantitative phenotypic variation. We identified 24 SVs that disrupt coding exons, acting as rare variants of large effect on gene function. One-third of the genes so affected have immunological functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428933/" 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/PMC3428933/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcin, Binnaz -- Wong, Kim -- Agam, Avigail -- Goodson, Martin -- Keane, Thomas M -- Gan, Xiangchao -- Nellaker, Christoffer -- Goodstadt, Leo -- Nicod, Jerome -- Bhomra, Amarjit -- Hernandez-Pliego, Polinka -- Whitley, Helen -- Cleak, James -- Dutton, Rebekah -- Janowitz, Deborah -- Mott, Richard -- Adams, David J -- Flint, Jonathan -- 079912/Wellcome Trust/United Kingdom -- 082356/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- G0800024/Medical Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Sep 14;477(7364):326-9. doi: 10.1038/nature10432.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Breakpoints ; Exons/genetics ; Female ; Gene Expression ; Genetic Variation/*genetics ; Genome/*genetics ; Genomics ; Genotype ; Male ; Mice ; Mice, Inbred Strains/*genetics/immunology ; Mutagenesis, Insertional/genetics ; *Phenotype ; Quantitative Trait Loci/genetics ; Rats ; Retroelements/genetics ; Sequence Deletion/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2014-11-08
    Description: Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relations hips. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misof, Bernhard -- Liu, Shanlin -- Meusemann, Karen -- Peters, Ralph S -- Donath, Alexander -- Mayer, Christoph -- Frandsen, Paul B -- Ware, Jessica -- Flouri, Tomas -- Beutel, Rolf G -- Niehuis, Oliver -- Petersen, Malte -- Izquierdo-Carrasco, Fernando -- Wappler, Torsten -- Rust, Jes -- Aberer, Andre J -- Aspock, Ulrike -- Aspock, Horst -- Bartel, Daniela -- Blanke, Alexander -- Berger, Simon -- Bohm, Alexander -- Buckley, Thomas R -- Calcott, Brett -- Chen, Junqing -- Friedrich, Frank -- Fukui, Makiko -- Fujita, Mari -- Greve, Carola -- Grobe, Peter -- Gu, Shengchang -- Huang, Ying -- Jermiin, Lars S -- Kawahara, Akito Y -- Krogmann, Lars -- Kubiak, Martin -- Lanfear, Robert -- Letsch, Harald -- Li, Yiyuan -- Li, Zhenyu -- Li, Jiguang -- Lu, Haorong -- Machida, Ryuichiro -- Mashimo, Yuta -- Kapli, Pashalia -- McKenna, Duane D -- Meng, Guanliang -- Nakagaki, Yasutaka -- Navarrete-Heredia, Jose Luis -- Ott, Michael -- Ou, Yanxiang -- Pass, Gunther -- Podsiadlowski, Lars -- Pohl, Hans -- von Reumont, Bjorn M -- Schutte, Kai -- Sekiya, Kaoru -- Shimizu, Shota -- Slipinski, Adam -- Stamatakis, Alexandros -- Song, Wenhui -- Su, Xu -- Szucsich, Nikolaus U -- Tan, Meihua -- Tan, Xuemei -- Tang, Min -- Tang, Jingbo -- Timelthaler, Gerald -- Tomizuka, Shigekazu -- Trautwein, Michelle -- Tong, Xiaoli -- Uchifune, Toshiki -- Walzl, Manfred G -- Wiegmann, Brian M -- Wilbrandt, Jeanne -- Wipfler, Benjamin -- Wong, Thomas K F -- Wu, Qiong -- Wu, Gengxiong -- Xie, Yinlong -- Yang, Shenzhou -- Yang, Qing -- Yeates, David K -- Yoshizawa, Kazunori -- Zhang, Qing -- Zhang, Rui -- Zhang, Wenwei -- Zhang, Yunhui -- Zhao, Jing -- Zhou, Chengran -- Zhou, Lili -- Ziesmann, Tanja -- Zou, Shijie -- Li, Yingrui -- Xu, Xun -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Wang, Jun -- Kjer, Karl M -- Zhou, Xin -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):763-7. doi: 10.1126/science.1257570. Epub 2014 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Abteilung Arthropoda, Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. ; Department of Entomology, Rutgers University, New Brunswick, NJ 08854, USA. ; Department of Biological Sciences, Rutgers University, Newark, NJ 08854, USA. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. ; Institut fur Spezielle Zoologie und Evolutionsbiologie mit Phyletischem Museum Jena, FSU Jena, Germany. ; Steinmann-Institut, Bereich Palaontologie, Universitat Bonn, Germany. ; 2. Zoologische Abteilung (Insekten), Naturhistorisches Museum Wien, Vienna, Austria. Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Institut fur Spezifische Prophylaxe und Tropenmedizin, Medizinische Parasitologie, Medizinische Universitat Wien (MUW), Vienna, Austria. ; Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Manaaki Whenua Landcare Research, Auckland, New Zealand. ; Center for Advanced Modeling, Emergency Medicine Department, Johns Hopkins University, Baltimore, MD 21209, USA. ; BGI-Shenzhen, China. ; Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Evolutionary Morphology Laboratory, Graduate School of Science and Engineering, Ehime University, Japan. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Land and Water Flagship, CSIRO, Canberra, ACT, Australia. ; Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA. ; Entomology, Staatliches Museum fur Naturkunde Stuttgart (SMNS), Germany. ; Ecology Evolution and Genetics, Research School of Biology, Australian National University, Canberra, ACT, Australia. National Evolutionary Synthesis Center, Durham, NC 27705, USA. Department of Biological Sciences, Macquarie University, Sydney, Australia. ; Department fur Botanik und Biodiversitatsforschung, Universitat Wien, Vienna, Austria. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Natural History Museum of Crete, University of Crete, Post Office Box 2208, Gr-71409, Iraklio, and Biology Department, University of Crete, Iraklio, Crete, Greece. ; Department of Biological Sciences and Feinstone Center for Genomic Research, University of Memphis, Memphis, TN 38152, USA. ; Centro Universitario de Ciencias Biologicas y Agropecuarias, Centro de Estudios en Zoologia, Universidad de Guadalajara, Zapopan, Jalisco, Mexico. ; Leibniz Supercomputing Centre of the Bavarian Academy of Sciences and Humanities, Garching, Germany. ; Institute of Evolutionary Biology and Ecology, Zoology and Evolutionary Biology, University of Bonn, Bonn, Germany. ; Department of Life Sciences, The Natural History Museum London, London, UK. ; Abteilung Entomologie, Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Fakultat fur Informatik, Karlsruher Institut fur Technologie, Karlsruhe, Germany. ; California Academy of Sciences, San Francisco, CA 94118, USA. ; Department of Entomology, College of Natural Resources and Environment, South China Agricultural University, China. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. Yokosuka City Museum, Yokosuka, Kanagawa, Japan. ; Department of Entomology, North Carolina State University, Raleigh, NC 27695, USA. ; Systematic Entomology, Hokkaido University, Sapporo, Japan. ; BGI-Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; Department of Ecology, Evolution, and Natural Resources, Rutgers University, New Brunswick, NJ 08854, USA. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25378627" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genetic Code ; Genome, Insect ; Genomics ; Insect Proteins/*classification/genetics ; Insects/*classification/genetics ; *Phylogeny ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2013-12-03
    Description: Thalidomide-like drugs such as lenalidomide are clinically important treatments for multiple myeloma and show promise for other B cell malignancies. The biochemical mechanisms underlying their antitumor activity are unknown. Thalidomide was recently shown to bind to, and inhibit, the cereblon ubiquitin ligase. Cereblon loss in zebrafish causes fin defects reminiscent of the limb defects seen in children exposed to thalidomide in utero. Here we show that lenalidomide-bound cereblon acquires the ability to target for proteasomal degradation two specific B cell transcription factors, Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3). Analysis of myeloma cell lines revealed that loss of IKZF1 and IKZF3 is both necessary and sufficient for lenalidomide's therapeutic effect, suggesting that the antitumor and teratogenic activities of thalidomide-like drugs are dissociable.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070318/" 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/PMC4070318/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Gang -- Middleton, Richard E -- Sun, Huahang -- Naniong, MarkVic -- Ott, Christopher J -- Mitsiades, Constantine S -- Wong, Kwok-Kin -- Bradner, James E -- Kaelin, William G Jr -- R01 CA068490/CA/NCI NIH HHS/ -- R01 CA076120/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 17;343(6168):305-9. doi: 10.1126/science.1244917. Epub 2013 Nov 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24292623" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Cell Line, Tumor ; HEK293 Cells ; Humans ; Ikaros Transcription Factor/genetics/*metabolism ; Multiple Myeloma/*metabolism ; Peptide Hydrolases/genetics/*metabolism ; Proteolysis ; Teratogens/*pharmacology ; Thalidomide/*analogs & derivatives/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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