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  • 1
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    The structural basis for autonomous dimerization of the pre-T-cell antigen receptor (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-15
    Description: The pre-T-cell antigen receptor (pre-TCR), expressed by immature thymocytes, has a pivotal role in early T-cell development, including TCR beta-selection, survival and proliferation of CD4(-)CD8(-) double-negative thymocytes, and subsequent alphabeta T-cell lineage differentiation. Whereas alphabetaTCR ligation by the peptide-loaded major histocompatibility complex initiates T-cell signalling, pre-TCR-induced signalling occurs by means of a ligand-independent dimerization event. The pre-TCR comprises an invariant alpha-chain (pre-Talpha) that pairs with any TCR beta-chain (TCRbeta) following successful TCR beta-gene rearrangement. Here we provide the basis of pre-Talpha-TCRbeta assembly and pre-TCR dimerization. The pre-Talpha chain comprised a single immunoglobulin-like domain that is structurally distinct from the constant (C) domain of the TCR alpha-chain; nevertheless, the mode of association between pre-Talpha and TCRbeta mirrored that mediated by the Calpha-Cbeta domains of the alphabetaTCR. The pre-TCR had a propensity to dimerize in solution, and the molecular envelope of the pre-TCR dimer correlated well with the observed head-to-tail pre-TCR dimer. This mode of pre-TCR dimerization enabled the pre-Talpha domain to interact with the variable (V) beta domain through residues that are highly conserved across the Vbeta and joining (J) beta gene families, thus mimicking the interactions at the core of the alphabetaTCR's Valpha-Vbeta interface. Disruption of this pre-Talpha-Vbeta dimer interface abrogated pre-TCR dimerization in solution and impaired pre-TCR expression on the cell surface. Accordingly, we provide a mechanism of pre-TCR self-association that allows the pre-Talpha chain to simultaneously 'sample' the correct folding of both the V and C domains of any TCR beta-chain, regardless of its ultimate specificity, which represents a critical checkpoint in T-cell development. This unusual dual-chaperone-like sensing function of pre-Talpha represents a unique mechanism in nature whereby developmental quality control regulates the expression and signalling of an integral membrane receptor complex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pang, Siew Siew -- Berry, Richard -- Chen, Zhenjun -- Kjer-Nielsen, Lars -- Perugini, Matthew A -- King, Glenn F -- Wang, Christina -- Chew, Sock Hui -- La Gruta, Nicole L -- Williams, Neal K -- Beddoe, Travis -- Tiganis, Tony -- Cowieson, Nathan P -- Godfrey, Dale I -- Purcell, Anthony W -- Wilce, Matthew C J -- McCluskey, James -- Rossjohn, Jamie -- England -- Nature. 2010 Oct 14;467(7317):844-8. doi: 10.1038/nature09448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Protein Crystallography Unit, Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Clayton, Victoria 3800, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20944746" target="_blank"〉PubMed〈/a〉
    Keywords: Crystallography, X-Ray ; Gene Rearrangement, T-Lymphocyte/genetics ; Humans ; Models, Molecular ; Mutation ; Protein Folding ; *Protein Multimerization ; Protein Structure, Tertiary ; Receptors, Antigen, T-Cell/*chemistry/genetics/*metabolism ; Receptors, Antigen, T-Cell, alpha-beta/chemistry/metabolism ; Signal Transduction ; Solutions ; T-Lymphocytes/cytology/immunology/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Regulation of heterochromatic DNA replication by histone H3 lysine 27 methyltransferases (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: Multiple pathways prevent DNA replication from occurring more than once per cell cycle. These pathways block re-replication by strictly controlling the activity of pre-replication complexes, which assemble at specific sites in the genome called origins. Here we show that mutations in the homologous histone 3 lysine 27 (H3K27) monomethyltransferases, ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6, lead to re-replication of specific genomic locations. Most of these locations correspond to transposons and other repetitive and silent elements of the Arabidopsis genome. These sites also correspond to high levels of H3K27 monomethylation, and mutation of the catalytic SET domain is sufficient to cause the re-replication defect. Mutation of ATXR5 and ATXR6 also causes upregulation of transposon expression and has pleiotropic effects on plant development. These results uncover a novel pathway that prevents over-replication of heterochromatin in Arabidopsis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964344/" 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/PMC2964344/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacob, Yannick -- Stroud, Hume -- Leblanc, Chantal -- Feng, Suhua -- Zhuo, Luting -- Caro, Elena -- Hassel, Christiane -- Gutierrez, Crisanto -- Michaels, Scott D -- Jacobsen, Steven E -- GM075060/GM/NIGMS NIH HHS/ -- R01 GM075060/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Aug 19;466(7309):987-91. doi: 10.1038/nature09290. Epub 2010 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, 915 East Third Street, Bloomington, Indiana 47405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631708" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; *Arabidopsis/cytology/enzymology/genetics ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Catalytic Domain/genetics ; DNA Methylation ; DNA Replication/genetics/*physiology ; DNA Transposable Elements/genetics ; DNA, Plant/analysis/biosynthesis ; Gene Expression Regulation, Plant ; Gene Silencing ; Genome, Plant/genetics ; Heterochromatin/*genetics/metabolism ; Histone-Lysine N-Methyltransferase/*metabolism ; Histones/chemistry/*metabolism ; Lysine/metabolism ; Methylation ; Methyltransferases/chemistry/genetics/*metabolism ; Mutant Proteins/genetics/metabolism ; Mutation ; Replication Origin
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Neurotransmitter/sodium symporter orthologue LeuT has a single high-affinity substrate site (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Neurotransmitter/sodium symporters (NSSs) couple the uptake of neurotransmitter with one or more sodium ions, removing neurotransmitter from the synaptic cleft. NSSs are essential to the function of chemical synapses, are associated with multiple neurological diseases and disorders, and are the targets of therapeutic and illicit drugs. LeuT, a prokaryotic orthologue of the NSS family, is a model transporter for understanding the relationships between molecular mechanism and atomic structure in a broad range of sodium-dependent and sodium-independent secondary transporters. At present there is a controversy over whether there are one or two high-affinity substrate binding sites in LeuT. The first-reported crystal structure of LeuT, together with subsequent functional and structural studies, provided direct evidence for a single, high-affinity, centrally located substrate-binding site, defined as the S1 site. Recent binding, flux and molecular simulation studies, however, have been interpreted in terms of a model where there are two high-affinity binding sites: the central, S1, site and a second, the S2 site, located within the extracellular vestibule. Furthermore, it was proposed that the S1 and S2 sites are allosterically coupled such that occupancy of the S2 site is required for the cytoplasmic release of substrate from the S1 site. Here we address this controversy by performing direct measurement of substrate binding to wild-type LeuT and to S2 site mutants using isothermal titration calorimetry, equilibrium dialysis and scintillation proximity assays. In addition, we perform uptake experiments to determine whether the proposed allosteric coupling between the putative S2 site and the S1 site manifests itself in the kinetics of substrate flux. We conclude that LeuT harbours a single, centrally located, high-affinity substrate-binding site and that transport is well described by a simple, single-substrate kinetic mechanism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079577/" 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/PMC3079577/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Piscitelli, Chayne L -- Krishnamurthy, Harini -- Gouaux, Eric -- R37 MH070039/MH/NIMH NIH HHS/ -- R37 MH070039-07/MH/NIMH NIH HHS/ -- R37 MH070039-08/MH/NIMH NIH HHS/ -- T32 DK007680/DK/NIDDK NIH HHS/ -- T32 DK007680-17/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 23;468(7327):1129-32. doi: 10.1038/nature09581.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179170" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Humans ; Ionophores/pharmacology ; Kinetics ; Leucine/genetics ; Models, Molecular ; Mutation ; Plasma Membrane Neurotransmitter Transport ; Proteins/*chemistry/genetics/*metabolism ; Protein Transport/drug effects ; Valinomycin/pharmacology
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  • 4
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    ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-12
    Description: Gastrointestinal stromal tumour (GIST) is the most common human sarcoma and is primarily defined by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. KIT is highly expressed in interstitial cells of Cajal (ICCs)-the presumed cell of origin for GIST-as well as in haematopoietic stem cells, melanocytes, mast cells and germ cells. Yet, families harbouring germline activating KIT mutations and mice with knock-in Kit mutations almost exclusively develop ICC hyperplasia and GIST, suggesting that the cellular context is important for KIT to mediate oncogenesis. Here we show that the ETS family member ETV1 is highly expressed in the subtypes of ICCs sensitive to oncogenic KIT mediated transformation, and is required for their development. In addition, ETV1 is universally highly expressed in GISTs and is required for growth of imatinib-sensitive and resistant GIST cell lines. Transcriptome profiling and global analyses of ETV1-binding sites suggest that ETV1 is a master regulator of an ICC-GIST-specific transcription network mainly through enhancer binding. The ETV1 transcriptional program is further regulated by activated KIT, which prolongs ETV1 protein stability and cooperates with ETV1 to promote tumorigenesis. We propose that GIST arises from ICCs with high levels of endogenous ETV1 expression that, when coupled with an activating KIT mutation, drives an oncogenic ETS transcriptional program. This differs from other ETS-dependent tumours such as prostate cancer, melanoma and Ewing sarcoma where genomic translocation or amplification drives aberrant ETS expression. It also represents a novel mechanism of oncogenic transcription factor activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955195/" 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/PMC2955195/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Ping -- Chen, Yu -- Zhang, Lei -- Guo, Xingyi -- Wongvipat, John -- Shamu, Tambudzai -- Fletcher, Jonathan A -- Dewell, Scott -- Maki, Robert G -- Zheng, Deyou -- Antonescu, Cristina R -- Allis, C David -- Sawyers, Charles L -- 5F32CA130372/CA/NCI NIH HHS/ -- CA148260/CA/NCI NIH HHS/ -- CA47179/CA/NCI NIH HHS/ -- F32 CA130372/CA/NCI NIH HHS/ -- F32 CA130372-02/CA/NCI NIH HHS/ -- GM40922/GM/NIGMS NIH HHS/ -- K08 CA140946/CA/NCI NIH HHS/ -- K08 CA140946-02/CA/NCI NIH HHS/ -- K08CA140946/CA/NCI NIH HHS/ -- P01 CA047179/CA/NCI NIH HHS/ -- P01 CA047179-169002/CA/NCI NIH HHS/ -- P01CA47179/CA/NCI NIH HHS/ -- R21 MH087840/MH/NIMH NIH HHS/ -- R21 MH087840-01/MH/NIMH NIH HHS/ -- R21MH087840/MH/NIMH NIH HHS/ -- RC2 CA148260-02/CA/NCI NIH HHS/ -- England -- Nature. 2010 Oct 14;467(7317):849-53. doi: 10.1038/nature09409. Epub 2010 Oct 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20927104" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides ; Binding Sites ; Biomarkers, Tumor/genetics/metabolism ; Cell Line, Tumor ; *Cell Lineage ; Cell Survival/drug effects ; *Cell Transformation, Neoplastic ; DNA-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Disease Progression ; Enhancer Elements, Genetic/genetics ; Gastrointestinal Stromal Tumors/*metabolism/*pathology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Imatinib Mesylate ; Interstitial Cells of Cajal/metabolism/pathology ; Mice ; Mutant Proteins/genetics/metabolism ; Mutation ; NIH 3T3 Cells ; Oncogenes/genetics/*physiology ; Piperazines/pharmacology ; Protein Stability ; Proto-Oncogene Proteins c-kit/genetics/*metabolism ; Pyrimidines/pharmacology ; Signal Transduction ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism
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  • 5
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    Sequence space and the ongoing expansion of the protein universe (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-21
    Description: The need to maintain the structural and functional integrity of an evolving protein severely restricts the repertoire of acceptable amino-acid substitutions. However, it is not known whether these restrictions impose a global limit on how far homologous protein sequences can diverge from each other. Here we explore the limits of protein evolution using sequence divergence data. We formulate a computational approach to study the rate of divergence of distant protein sequences and measure this rate for ancient proteins, those that were present in the last universal common ancestor. We show that ancient proteins are still diverging from each other, indicating an ongoing expansion of the protein sequence universe. The slow rate of this divergence is imposed by the sparseness of functional protein sequences in sequence space and the ruggedness of the protein fitness landscape: approximately 98 per cent of sites cannot accept an amino-acid substitution at any given moment but a vast majority of all sites may eventually be permitted to evolve when other, compensatory, changes occur. Thus, approximately 3.5 x 10(9) yr has not been enough to reach the limit of divergent evolution of proteins, and for most proteins the limit of sequence similarity imposed by common function may not exceed that of random sequences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Povolotskaya, Inna S -- Kondrashov, Fyodor A -- England -- Nature. 2010 Jun 17;465(7300):922-6. doi: 10.1038/nature09105. Epub 2010 May 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioinformatics and Genomics Programme, Centre for Genomic Regulation, Calle Dr Aiguader 88, Barcelona Biomedical Research Park Building, 08003 Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485343" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Amino Acids/chemistry ; *Evolution, Molecular ; *Genetic Variation ; Molecular Sequence Data ; Mutation ; Prokaryotic Cells ; Protein Structure, Secondary ; Proteins/*chemistry ; Selection, Genetic/genetics ; Sequence Analysis, Protein ; Sequence Homology, Amino Acid
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  • 6
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    The CRISPR/Cas bacterial immune system cleaves bacteriophage and plasmid DNA (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-05
    Description: Bacteria and Archaea have developed several defence strategies against foreign nucleic acids such as viral genomes and plasmids. Among them, clustered regularly interspaced short palindromic repeats (CRISPR) loci together with cas (CRISPR-associated) genes form the CRISPR/Cas immune system, which involves partially palindromic repeats separated by short stretches of DNA called spacers, acquired from extrachromosomal elements. It was recently demonstrated that these variable loci can incorporate spacers from infecting bacteriophages and then provide immunity against subsequent bacteriophage infections in a sequence-specific manner. Here we show that the Streptococcus thermophilus CRISPR1/Cas system can also naturally acquire spacers from a self-replicating plasmid containing an antibiotic-resistance gene, leading to plasmid loss. Acquired spacers that match antibiotic-resistance genes provide a novel means to naturally select bacteria that cannot uptake and disseminate such genes. We also provide in vivo evidence that the CRISPR1/Cas system specifically cleaves plasmid and bacteriophage double-stranded DNA within the proto-spacer, at specific sites. Our data show that the CRISPR/Cas immune system is remarkably adapted to cleave invading DNA rapidly and has the potential for exploitation to generate safer microbial strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garneau, Josiane E -- Dupuis, Marie-Eve -- Villion, Manuela -- Romero, Dennis A -- Barrangou, Rodolphe -- Boyaval, Patrick -- Fremaux, Christophe -- Horvath, Philippe -- Magadan, Alfonso H -- Moineau, Sylvain -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Nov 4;468(7320):67-71. doi: 10.1038/nature09523.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de biochimie, de microbiologie et de bio-informatique, Faculte des sciences et de genie, Groupe de recherche en ecologie buccale, Faculte de medecine dentaire, Felix d'Herelle Reference Center for Bacterial Viruses, Universite Laval, Quebec City, Quebec G1V 0A6, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21048762" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophages/*genetics/metabolism ; Base Sequence ; DNA, Intergenic/genetics/metabolism ; DNA, Viral/genetics/*metabolism ; Drug Resistance, Bacterial/genetics ; Genetic Loci/*genetics/*immunology ; Interspersed Repetitive Sequences/genetics ; Molecular Sequence Data ; Mutation ; Plasmids/genetics/*metabolism ; RNA, Bacterial/genetics/immunology ; Streptococcus thermophilus/genetics/*immunology/*virology
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  • 7
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    An RNA polymerase II- and AGO4-associated protein acts in RNA-directed DNA methylation (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-23
    Description: DNA methylation is an important epigenetic mark in many eukaryotes. In plants, 24-nucleotide small interfering RNAs (siRNAs) bound to the effector protein, Argonaute 4 (AGO4), can direct de novo DNA methylation by the methyltransferase DRM2 (refs 2, 4-6). Here we report a new regulator of RNA-directed DNA methylation (RdDM) in Arabidopsis: RDM1. Loss-of-function mutations in the RDM1 gene impair the accumulation of 24-nucleotide siRNAs, reduce DNA methylation, and release transcriptional gene silencing at RdDM target loci. RDM1 encodes a small protein that seems to bind single-stranded methyl DNA, and associates and co-localizes with RNA polymerase II (Pol II, also known as NRPB), AGO4 and DRM2 in the nucleus. Our results indicate that RDM1 is a component of the RdDM effector complex and may have a role in linking siRNA production with pre-existing or de novo cytosine methylation. Our results also indicate that, although RDM1 and Pol V (also known as NRPE) may function together at some RdDM target sites in the peri-nucleolar siRNA processing centre, Pol II rather than Pol V is associated with the RdDM effector complex at target sites in the nucleoplasm.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865564/" 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/PMC2865564/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Zhihuan -- Liu, Hai-Liang -- Daxinger, Lucia -- Pontes, Olga -- He, Xinjian -- Qian, Weiqiang -- Lin, Huixin -- Xie, Mingtang -- Lorkovic, Zdravko J -- Zhang, Shoudong -- Miki, Daisuke -- Zhan, Xiangqiang -- Pontier, Dominique -- Lagrange, Thierry -- Jin, Hailing -- Matzke, Antonius J M -- Matzke, Marjori -- Pikaard, Craig S -- Zhu, Jian-Kang -- R01 GM059138/GM/NIGMS NIH HHS/ -- R01 GM059138-12/GM/NIGMS NIH HHS/ -- R01 GM070795/GM/NIGMS NIH HHS/ -- R01 GM070795-06/GM/NIGMS NIH HHS/ -- R01 GM070795-06S1/GM/NIGMS NIH HHS/ -- R01 GM077590/GM/NIGMS NIH HHS/ -- R01 GM093008/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 May 6;465(7294):106-9. doi: 10.1038/nature09025. Epub 2010 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Integrative Genome Biology and Department of Botany and Plant Sciences, University of California, Riverside, California 92521, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20410883" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Argonaute Proteins ; Cell Nucleus/metabolism ; *DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Gene Expression Regulation, Plant ; Gene Silencing/physiology ; Methyltransferases/metabolism ; Mutation ; RNA Polymerase II/*metabolism ; RNA, Plant/*metabolism
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    Inhibition of follicular T-helper cells by CD8(+) regulatory T cells is essential for self tolerance (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-17
    Description: The ability to produce vigorous immune responses that spare self tissues and organs depends on the elimination of autoreactive T and B cells. However, purging of immature and mature self-reactive T and B cells is incomplete and may also require the involvement of cells programmed to suppress immune responses. Regulatory T cells (T(reg)) belonging to the CD4(+) T-cell subset may have a role in preventing untoward inflammatory responses, but T-cell subsets programmed to inhibit the development of autoantibody formation and systemic-lupus-erythematosus-like disease have not yet been defined. Here we delineate a CD8(+) regulatory T-cell lineage that is essential for the maintenance of self tolerance and prevention of murine autoimmune disease. Genetic disruption of the inhibitory interaction between these CD8(+) T cells and their target Qa-1(+) follicular T-helper cells results in the development of a lethal systemic-lupus-erythematosus-like autoimmune disease. These findings define a sublineage of CD8 T cells programmed to suppress rather than activate immunity that represents an essential regulatory element of the immune response and a guarantor of self tolerance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395240/" 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/PMC3395240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Hye-Jung -- Verbinnen, Bert -- Tang, Xiaolei -- Lu, Linrong -- Cantor, Harvey -- AI 037562/AI/NIAID NIH HHS/ -- R01 AI037562/AI/NIAID NIH HHS/ -- T32 CA009382/CA/NCI NIH HHS/ -- T32 CA070083/CA/NCI NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):328-32. doi: 10.1038/nature09370.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Immunology & AIDS, 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/20844537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Antibody Affinity/immunology ; Antigens/immunology ; Antigens, CD44/immunology/metabolism ; Autoantibodies/biosynthesis/immunology ; CD8-Positive T-Lymphocytes/*cytology/*immunology ; Cell Lineage ; Germinal Center/cytology/immunology ; Histocompatibility Antigens Class I/genetics/immunology/metabolism ; Immunoglobulin G/blood ; Lupus Erythematosus, Systemic/immunology ; Mice ; Models, Immunological ; Mutation ; Self Tolerance/*immunology ; T-Lymphocytes, Helper-Inducer/*cytology/*immunology/metabolism ; T-Lymphocytes, Regulatory/cytology/immunology
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    Cancer: Oncogenes in context (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinrich, Michael C -- Corless, Christopher L -- England -- Nature. 2010 Oct 14;467(7317):796-7. doi: 10.1038/467796a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20944735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides ; Cell Survival/drug effects ; Cell Transformation, Neoplastic ; DNA-Binding Proteins/genetics/*metabolism ; Gastrointestinal Stromal Tumors/drug therapy/genetics/*metabolism/*pathology ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Imatinib Mesylate ; Mutation ; Oncogenes/genetics/*physiology ; Piperazines/pharmacology/therapeutic use ; Proto-Oncogene Proteins c-kit/genetics/*metabolism ; Pyrimidines/pharmacology/therapeutic use ; Transcription Factors/genetics/*metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Rare victory in fight against melanoma (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledford, Heidi -- England -- Nature. 2010 Sep 9;467(7312):140-1. doi: 10.1038/467140b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829766" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Humans ; Melanoma/*drug therapy/*genetics ; Mutation ; Proto-Oncogene Proteins B-raf/genetics/metabolism
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    Diversity: Of beans and genes (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisenstein, Michael -- England -- Nature. 2010 Dec 23;468(7327):S13-5. doi: 10.1038/468S13a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179077" target="_blank"〉PubMed〈/a〉
    Keywords: *Culture ; *Diet ; Evolution, Molecular ; *Genetic Variation ; Humans ; Mutation ; Selection, Genetic/*genetics
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  • 12
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    A methyl transferase links the circadian clock to the regulation of alternative splicing (2010)
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    Publication Date: 2010-10-22
    Description: Circadian rhythms allow organisms to time biological processes to the most appropriate phases of the day-night cycle. Post-transcriptional regulation is emerging as an important component of circadian networks, but the molecular mechanisms linking the circadian clock to the control of RNA processing are largely unknown. Here we show that PROTEIN ARGININE METHYL TRANSFERASE 5 (PRMT5), which transfers methyl groups to arginine residues present in histones and Sm spliceosomal proteins, links the circadian clock to the control of alternative splicing in plants. Mutations in PRMT5 impair several circadian rhythms in Arabidopsis thaliana and this phenotype is caused, at least in part, by a strong alteration in alternative splicing of the core-clock gene PSEUDO RESPONSE REGULATOR 9 (PRR9). Furthermore, genome-wide studies show that PRMT5 contributes to the regulation of many pre-messenger-RNA splicing events, probably by modulating 5'-splice-site recognition. PRMT5 expression shows daily and circadian oscillations, and this contributes to the mediation of the circadian regulation of expression and alternative splicing of a subset of genes. Circadian rhythms in locomotor activity are also disrupted in dart5-1, a mutant affected in the Drosophila melanogaster PRMT5 homologue, and this is associated with alterations in splicing of the core-clock gene period and several clock-associated genes. Our results demonstrate a key role for PRMT5 in the regulation of alternative splicing and indicate that the interplay between the circadian clock and the regulation of alternative splicing by PRMT5 constitutes a common mechanism that helps organisms to synchronize physiological processes with daily changes in environmental conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Sabrina E -- Petrillo, Ezequiel -- Beckwith, Esteban J -- Zhang, Xu -- Rugnone, Matias L -- Hernando, C Esteban -- Cuevas, Juan C -- Godoy Herz, Micaela A -- Depetris-Chauvin, Ana -- Simpson, Craig G -- Brown, John W S -- Cerdan, Pablo D -- Borevitz, Justin O -- Mas, Paloma -- Ceriani, M Fernanda -- Kornblihtt, Alberto R -- Yanovsky, Marcelo J -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 4;468(7320):112-6. doi: 10.1038/nature09470. Epub 2010 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IFEVA, Facultad de Agronomia, UBA-CONICET, C1417DSE Buenos Aires, Argentina.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962777" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Arabidopsis/enzymology/genetics/*physiology/radiation effects ; Arabidopsis Proteins/genetics/*metabolism ; Base Sequence ; Circadian Clocks/genetics/*physiology ; Circadian Rhythm/genetics/*physiology ; Darkness ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/enzymology/genetics/*physiology/radiation effects ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Light ; Methylation ; Mutation ; Period Circadian Proteins/genetics ; Phenotype ; Protein Methyltransferases/genetics/*metabolism ; Protein-Arginine N-Methyltransferases/genetics/*metabolism ; RNA Precursors/genetics/metabolism ; RNA Splice Sites/genetics ; RNA, Messenger/genetics/metabolism ; Spliceosomes/metabolism ; Transcription Factors/genetics
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  • 13
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    Bacterial charity work leads to population-wide resistance (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-03
    Description: Bacteria show remarkable adaptability in the face of antibiotic therapeutics. Resistance alleles in drug target-specific sites and general stress responses have been identified in individual end-point isolates. Less is known, however, about the population dynamics during the development of antibiotic-resistant strains. Here we follow a continuous culture of Escherichia coli facing increasing levels of antibiotic and show that the vast majority of isolates are less resistant than the population as a whole. We find that the few highly resistant mutants improve the survival of the population's less resistant constituents, in part by producing indole, a signalling molecule generated by actively growing, unstressed cells. We show, through transcriptional profiling, that indole serves to turn on drug efflux pumps and oxidative-stress protective mechanisms. The indole production comes at a fitness cost to the highly resistant isolates, and whole-genome sequencing reveals that this bacterial altruism is made possible by drug-resistance mutations unrelated to indole production. This work establishes a population-based resistance mechanism constituting a form of kin selection whereby a small number of resistant mutants can, at some cost to themselves, provide protection to other, more vulnerable, cells, enhancing the survival capacity of the overall population in stressful environments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936489/" 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/PMC2936489/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Henry H -- Molla, Michael N -- Cantor, Charles R -- Collins, James J -- DP1 OD003644/OD/NIH HHS/ -- DP1 OD003644-04/OD/NIH HHS/ -- DP1 OD003644-05/OD/NIH HHS/ -- DP1OD003644/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 2;467(7311):82-5. doi: 10.1038/nature09354.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for BioDynamics, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20811456" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-Bacterial Agents/metabolism/pharmacology ; *Drug Resistance, Bacterial ; Escherichia coli/*drug effects/genetics/*growth & development/metabolism ; Gene Expression Profiling ; Genome, Bacterial ; Indoles/metabolism ; Microbial Sensitivity Tests ; Microbial Viability ; Mutation ; Norfloxacin/metabolism/pharmacology
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  • 14
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    Structure of the torque ring of the flagellar motor and the molecular basis for rotational switching (2010)
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    Publication Date: 2010-08-03
    Description: The flagellar motor drives the rotation of flagellar filaments at hundreds of revolutions per second, efficiently propelling bacteria through viscous media. The motor uses the potential energy from an electrochemical gradient of cations across the cytoplasmic membrane to generate torque. A rapid switch from anticlockwise to clockwise rotation determines whether a bacterium runs smoothly forward or tumbles to change its trajectory. A protein called FliG forms a ring in the rotor of the flagellar motor that is involved in the generation of torque through an interaction with the cation-channel-forming stator subunit MotA. FliG has been suggested to adopt distinct conformations that induce switching but these structural changes and the molecular mechanism of switching are unknown. Here we report the molecular structure of the full-length FliG protein, identify conformational changes that are involved in rotational switching and uncover the structural basis for the formation of the FliG torque ring. This allows us to propose a model of the complete ring and switching mechanism in which conformational changes in FliG reverse the electrostatic charges involved in torque generation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159035/" 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/PMC3159035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Lawrence K -- Ginsburg, Michael A -- Crovace, Claudia -- Donohoe, Mhairi -- Stock, Daniela -- MC_U105170645/Medical Research Council/United Kingdom -- P41 RR007707/RR/NCRR NIH HHS/ -- P41 RR007707-17/RR/NCRR NIH HHS/ -- RR007707/RR/NCRR NIH HHS/ -- Y1-CO-1020/CO/NCI NIH HHS/ -- Y1-GM-1104/GM/NIGMS NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Aug 19;466(7309):996-1000. doi: 10.1038/nature09300. Epub 2010 Aug 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Structural and Computational Biology Division, The Victor Chang Cardiac Research Institute, Lowy Packer Building, 405 Liverpool Street, Darlinghurst, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20676082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Bacterial Proteins/*chemistry/genetics/*metabolism ; Flagella/*chemistry/genetics/*physiology ; Models, Molecular ; Molecular Motor Proteins/*chemistry/genetics/metabolism ; Molecular Sequence Data ; Mutation ; Protein Conformation ; Protein Multimerization ; Protein Structure, Tertiary ; *Rotation ; Static Electricity ; Structure-Activity Relationship ; Thermotoga maritima/chemistry ; *Torque
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    Oxidation of methane by a biological dicopper centre (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-23
    Description: Vast world reserves of methane gas are underutilized as a feedstock for the production of liquid fuels and chemicals owing to the lack of economical and sustainable strategies for the selective oxidation of methane to methanol. Current processes to activate the strong C-H bond (104 kcal mol(-1)) in methane require high temperatures, are costly and inefficient, and produce waste. In nature, methanotrophic bacteria perform this reaction under ambient conditions using metalloenzymes called methane monooxygenases (MMOs). MMOs thus provide the optimal model for an efficient, environmentally sound catalyst. There are two types of MMO. Soluble MMO (sMMO) is expressed by several strains of methanotroph under copper-limited conditions and oxidizes methane with a well-characterized catalytic di-iron centre. Particulate MMO (pMMO) is an integral membrane metalloenzyme produced by all methanotrophs and is composed of three subunits, pmoA, pmoB and pmoC, arranged in a trimeric alpha(3)beta(3)gamma(3) complex. Despite 20 years of research and the availability of two crystal structures, the metal composition and location of the pMMO metal active site are not known. Here we show that pMMO activity is dependent on copper, not iron, and that the copper active site is located in the soluble domains of the pmoB subunit rather than within the membrane. Recombinant soluble fragments of pmoB (spmoB) bind copper and have propylene and methane oxidation activities. Disruption of each copper centre in spmoB by mutagenesis indicates that the active site is a dicopper centre. These findings help resolve the pMMO controversy and provide a promising new approach to developing environmentally friendly C-H oxidation catalysts.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999467/" 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/PMC2999467/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balasubramanian, Ramakrishnan -- Smith, Stephen M -- Rawat, Swati -- Yatsunyk, Liliya A -- Stemmler, Timothy L -- Rosenzweig, Amy C -- DK068139/DK/NIDDK NIH HHS/ -- GM070473/GM/NIGMS NIH HHS/ -- R01 DK068139/DK/NIDDK NIH HHS/ -- R01 DK068139-05/DK/NIDDK NIH HHS/ -- R01 GM070473/GM/NIGMS NIH HHS/ -- R01 GM070473-07/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 May 6;465(7294):115-9. doi: 10.1038/nature08992. Epub 2010 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, Illinois 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20410881" target="_blank"〉PubMed〈/a〉
    Keywords: Catalytic Domain ; Copper/*chemistry ; Methane/*metabolism ; Methanol/chemistry ; Methylococcus capsulatus/*enzymology ; Methylosinus trichosporium/enzymology ; *Models, Molecular ; Mutation ; Oxidation-Reduction ; Oxygenases/*chemistry/genetics/metabolism ; Protein Structure, Tertiary
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    International network of cancer genome projects (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-16
    Description: The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902243/" 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/PMC2902243/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉International Cancer Genome Consortium -- Hudson, Thomas J -- Anderson, Warwick -- Artez, Axel -- Barker, Anna D -- Bell, Cindy -- Bernabe, Rosa R -- Bhan, M K -- Calvo, Fabien -- Eerola, Iiro -- Gerhard, Daniela S -- Guttmacher, Alan -- Guyer, Mark -- Hemsley, Fiona M -- Jennings, Jennifer L -- Kerr, David -- Klatt, Peter -- Kolar, Patrik -- Kusada, Jun -- Lane, David P -- Laplace, Frank -- Youyong, Lu -- Nettekoven, Gerd -- Ozenberger, Brad -- Peterson, Jane -- Rao, T S -- Remacle, Jacques -- Schafer, Alan J -- Shibata, Tatsuhiro -- Stratton, Michael R -- Vockley, Joseph G -- Watanabe, Koichi -- Yang, Huanming -- Yuen, Matthew M F -- Knoppers, Bartha M -- Bobrow, Martin -- Cambon-Thomsen, Anne -- Dressler, Lynn G -- Dyke, Stephanie O M -- Joly, Yann -- Kato, Kazuto -- Kennedy, Karen L -- Nicolas, Pilar -- Parker, Michael J -- Rial-Sebbag, Emmanuelle -- Romeo-Casabona, Carlos M -- Shaw, Kenna M -- Wallace, Susan -- Wiesner, Georgia L -- Zeps, Nikolajs -- Lichter, Peter -- Biankin, Andrew V -- Chabannon, Christian -- Chin, Lynda -- Clement, Bruno -- de Alava, Enrique -- Degos, Francoise -- Ferguson, Martin L -- Geary, Peter -- Hayes, D Neil -- Johns, Amber L -- Kasprzyk, Arek -- Nakagawa, Hidewaki -- Penny, Robert -- Piris, Miguel A -- Sarin, Rajiv -- Scarpa, Aldo -- van de Vijver, Marc -- Futreal, P Andrew -- Aburatani, Hiroyuki -- Bayes, Monica -- Botwell, David D L -- Campbell, Peter J -- Estivill, Xavier -- Grimmond, Sean M -- Gut, Ivo -- Hirst, Martin -- Lopez-Otin, Carlos -- Majumder, Partha -- Marra, Marco -- McPherson, John D -- Ning, Zemin -- Puente, Xose S -- Ruan, Yijun -- Stunnenberg, Hendrik G -- Swerdlow, Harold -- Velculescu, Victor E -- Wilson, Richard K -- Xue, Hong H -- Yang, Liu -- Spellman, Paul T -- Bader, Gary D -- Boutros, Paul C -- Flicek, Paul -- Getz, Gad -- Guigo, Roderic -- Guo, Guangwu -- Haussler, David -- Heath, Simon -- Hubbard, Tim J -- Jiang, Tao -- Jones, Steven M -- Li, Qibin -- Lopez-Bigas, Nuria -- Luo, Ruibang -- Muthuswamy, Lakshmi -- Ouellette, B F Francis -- Pearson, John V -- Quesada, Victor -- Raphael, Benjamin J -- Sander, Chris -- Speed, Terence P -- Stein, Lincoln D -- Stuart, Joshua M -- Teague, Jon W -- Totoki, Yasushi -- Tsunoda, Tatsuhiko -- Valencia, Alfonso -- Wheeler, David A -- Wu, Honglong -- Zhao, Shancen -- Zhou, Guangyu -- Lathrop, Mark -- Thomas, Gilles -- Yoshida, Teruhiko -- Axton, Myles -- Gunter, Chris -- Miller, Linda J -- Zhang, Junjun -- Haider, Syed A -- Wang, Jianxin -- Yung, Christina K -- Cros, Anthony -- Liang, Yong -- Gnaneshan, Saravanamuttu -- Guberman, Jonathan -- Hsu, Jack -- Chalmers, Don R C -- Hasel, Karl W -- Kaan, Terry S H -- Lowrance, William W -- Masui, Tohru -- Rodriguez, Laura Lyman -- Vergely, Catherine -- Bowtell, David D L -- Cloonan, Nicole -- deFazio, Anna -- Eshleman, James R -- Etemadmoghadam, Dariush -- Gardiner, Brooke B -- Kench, James G -- Sutherland, Robert L -- Tempero, Margaret A -- Waddell, Nicola J -- Wilson, Peter J -- Gallinger, Steve -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Mukhopadhyay, Debabrata -- DePinho, Ronald A -- Thayer, Sarah -- Shazand, Kamran -- Beck, Timothy -- Sam, Michelle -- Timms, Lee -- Ballin, Vanessa -- Lu, Youyong -- Ji, Jiafu -- Zhang, Xiuqing -- Chen, Feng -- Hu, Xueda -- Yang, Qi -- Tian, Geng -- Zhang, Lianhai -- Xing, Xiaofang -- Li, Xianghong -- Zhu, Zhenggang -- Yu, Yingyan -- Yu, Jun -- Tost, Jorg -- Brennan, Paul -- Holcatova, Ivana -- Zaridze, David -- Brazma, Alvis -- Egevard, Lars -- Prokhortchouk, Egor -- Banks, Rosamonde Elizabeth -- Uhlen, Mathias -- Viksna, Juris -- Ponten, Fredrik -- Skryabin, Konstantin -- Birney, Ewan -- Borg, Ake -- Borresen-Dale, Anne-Lise -- Caldas, Carlos -- Foekens, John A -- Martin, Sancha -- Reis-Filho, Jorge S -- Richardson, Andrea L -- Sotiriou, Christos -- Thoms, Giles -- van't Veer, Laura -- Birnbaum, Daniel -- Blanche, Helene -- Boucher, Pascal -- Boyault, Sandrine -- Masson-Jacquemier, Jocelyne D -- Pauporte, Iris -- Pivot, Xavier -- Vincent-Salomon, Anne -- Tabone, Eric -- Theillet, Charles -- Treilleux, Isabelle -- Bioulac-Sage, Paulette -- Decaens, Thomas -- Franco, Dominique -- Gut, Marta -- Samuel, Didier -- Zucman-Rossi, Jessica -- Eils, Roland -- Brors, Benedikt -- Korbel, Jan O -- Korshunov, Andrey -- Landgraf, Pablo -- Lehrach, Hans -- Pfister, Stefan -- Radlwimmer, Bernhard -- Reifenberger, Guido -- Taylor, Michael D -- von Kalle, Christof -- Majumder, Partha P -- Pederzoli, Paolo -- Lawlor, Rita A -- Delledonne, Massimo -- Bardelli, Alberto -- Gress, Thomas -- Klimstra, David -- Zamboni, Giuseppe -- Nakamura, Yusuke -- Miyano, Satoru -- Fujimoto, Akihiro -- Campo, Elias -- de Sanjose, Silvia -- Montserrat, Emili -- Gonzalez-Diaz, Marcos -- Jares, Pedro -- Himmelbauer, Heinz -- Bea, Silvia -- Aparicio, Samuel -- Easton, Douglas F -- Collins, Francis S -- Compton, Carolyn C -- Lander, Eric S -- Burke, Wylie -- Green, Anthony R -- Hamilton, Stanley R -- Kallioniemi, Olli P -- Ley, Timothy J -- Liu, Edison T -- Wainwright, Brandon J -- 077198/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- 6613/Cancer Research UK/United Kingdom -- K08 DK071329/DK/NIDDK NIH HHS/ -- K08 DK071329-04/DK/NIDDK NIH HHS/ -- K08 DK071329-05/DK/NIDDK NIH HHS/ -- P01 CA117969/CA/NCI NIH HHS/ -- P01 CA117969-04S1/CA/NCI NIH HHS/ -- P01 CA117969-05/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50 CA102701-08/CA/NCI NIH HHS/ -- P50 CA127003/CA/NCI NIH HHS/ -- P50 CA127003-04/CA/NCI NIH HHS/ -- P50 CA127003-05/CA/NCI NIH HHS/ -- R01 HG001806-02/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Apr 15;464(7291):993-8. doi: 10.1038/nature08987.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393554" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Methylation ; DNA Mutational Analysis/trends ; Databases, Genetic ; Genes, Neoplasm/genetics ; Genetics, Medical/*organization & administration/trends ; Genome, Human/*genetics ; Genomics/*organization & administration/trends ; Humans ; Intellectual Property ; *International Cooperation ; Mutation ; Neoplasms/classification/*genetics/pathology/therapy
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    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
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    Details
    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" 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/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Purified human BRCA2 stimulates RAD51-mediated recombination (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-24
    Description: Mutation of the breast cancer susceptibility gene, BRCA2, leads to breast and ovarian cancers. Mechanistic insight into the functions of human BRCA2 has been limited by the difficulty of isolating this large protein (3,418 amino acids). Here we report the purification of full-length BRCA2 and show that it both binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). BRCA2 acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. BRCA2 does not anneal ssDNA complexed with RPA, implying it does not directly function in repair processes that involve ssDNA annealing. Our findings show that BRCA2 is a key mediator of homologous recombination, and they provide a molecular basis for understanding how this DNA repair process is disrupted by BRCA2 mutations, which lead to chromosomal instability and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952063/" 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/PMC2952063/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jensen, Ryan B -- Carreira, Aura -- Kowalczykowski, Stephen C -- GM 62653/GM/NIGMS NIH HHS/ -- R01 GM062653/GM/NIGMS NIH HHS/ -- R01 GM062653-30/GM/NIGMS NIH HHS/ -- R01 GM062653-31/GM/NIGMS NIH HHS/ -- R37 GM062653/GM/NIGMS NIH HHS/ -- R37 GM062653-29/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Oct 7;467(7316):678-83. doi: 10.1038/nature09399.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of California, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20729832" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Apoptosis Regulatory Proteins ; BRCA2 Protein/chemistry/*isolation & purification/*metabolism ; Cell Cycle Proteins/metabolism ; Cell Line ; Chromosomal Instability ; DNA/chemistry/metabolism ; DNA Repair ; DNA, Single-Stranded/chemistry/metabolism ; DNA-Binding Proteins/metabolism ; Humans ; Mutation ; Protein Binding ; Rad51 Recombinase/*metabolism ; *Recombination, Genetic ; Replication Protein A/metabolism ; Sequence Homology, Nucleic Acid ; Substrate Specificity
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 19
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    Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-08
    Description: A role for B-cell-receptor (BCR) signalling in lymphomagenesis has been inferred by studying immunoglobulin genes in human lymphomas and by engineering mouse models, but genetic and functional evidence for its oncogenic role in human lymphomas is needed. Here we describe a form of 'chronic active' BCR signalling that is required for cell survival in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). The signalling adaptor CARD11 is required for constitutive NF-kappaB pathway activity and survival in ABC DLBCL. Roughly 10% of ABC DLBCLs have mutant CARD11 isoforms that activate NF-kappaB, but the mechanism that engages wild-type CARD11 in other ABC DLBCLs was unknown. An RNA interference genetic screen revealed that a BCR signalling component, Bruton's tyrosine kinase, is essential for the survival of ABC DLBCLs with wild-type CARD11. In addition, knockdown of proximal BCR subunits (IgM, Ig-kappa, CD79A and CD79B) killed ABC DLBCLs with wild-type CARD11 but not other lymphomas. The BCRs in these ABC DLBCLs formed prominent clusters in the plasma membrane with low diffusion, similarly to BCRs in antigen-stimulated normal B cells. Somatic mutations affecting the immunoreceptor tyrosine-based activation motif (ITAM) signalling modules of CD79B and CD79A were detected frequently in ABC DLBCL biopsy samples but rarely in other DLBCLs and never in Burkitt's lymphoma or mucosa-associated lymphoid tissue lymphoma. In 18% of ABC DLBCLs, one functionally critical residue of CD79B, the first ITAM tyrosine, was mutated. These mutations increased surface BCR expression and attenuated Lyn kinase, a feedback inhibitor of BCR signalling. These findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845535/" 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/PMC2845535/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, R Eric -- Ngo, Vu N -- Lenz, Georg -- Tolar, Pavel -- Young, Ryan M -- Romesser, Paul B -- Kohlhammer, Holger -- Lamy, Laurence -- Zhao, Hong -- Yang, Yandan -- Xu, Weihong -- Shaffer, Arthur L -- Wright, George -- Xiao, Wenming -- Powell, John -- Jiang, Jian-Kang -- Thomas, Craig J -- Rosenwald, Andreas -- Ott, German -- Muller-Hermelink, Hans Konrad -- Gascoyne, Randy D -- Connors, Joseph M -- Johnson, Nathalie A -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Wilson, Wyndham H -- Delabie, Jan -- Smeland, Erlend B -- Fisher, Richard I -- Braziel, Rita M -- Tubbs, Raymond R -- Cook, J R -- Weisenburger, Dennis D -- Chan, Wing C -- Pierce, Susan K -- Staudt, Louis M -- NIH0011349228/PHS HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2010 Jan 7;463(7277):88-92. doi: 10.1038/nature08638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054396" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Antigens, CD79/chemistry/genetics/metabolism ; B-Lymphocytes/*metabolism/pathology ; CARD Signaling Adaptor Proteins/genetics/metabolism ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Survival ; Guanylate Cyclase/genetics/metabolism ; Humans ; Lymphoma, Large B-Cell, Diffuse/genetics/*metabolism/*pathology ; Mutation ; Protein-Tyrosine Kinases/genetics/metabolism ; RNA Interference ; Receptors, Antigen, B-Cell/deficiency/genetics/*metabolism ; *Signal Transduction ; src-Family Kinases/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 20
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    Molecular biology. Hiding in plain sight (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-22
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033778/" 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/PMC3033778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenberg, Miriam I -- Desplan, Claude -- R01 GM064864/GM/NIGMS NIH HHS/ -- R01 GM064864-07/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):284-5. doi: 10.1126/science.1192769.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Developmental Genetics, Department of Biology, New York University, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647453" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Conserved Sequence ; DNA-Binding Proteins/genetics/*metabolism ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/embryology/*genetics ; Embryo, Nonmammalian/*metabolism ; Epidermis/cytology ; Evolution, Molecular ; *Gene Expression Regulation, Developmental ; Genes, Insect ; Mutation ; Peptides/*genetics/metabolism ; Protein Processing, Post-Translational ; RNA, Untranslated/*genetics ; Transcription Factors/genetics/*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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  • 21
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    Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-04-10
    Description: Arsenic, an ancient drug used in traditional Chinese medicine, has attracted worldwide interest because it shows substantial anticancer activity in patients with acute promyelocytic leukemia (APL). Arsenic trioxide (As2O3) exerts its therapeutic effect by promoting degradation of an oncogenic protein that drives the growth of APL cells, PML-RARalpha (a fusion protein containing sequences from the PML zinc finger protein and retinoic acid receptor alpha). PML and PML-RARalpha degradation is triggered by their SUMOylation, but the mechanism by which As2O3 induces this posttranslational modification is unclear. Here we show that arsenic binds directly to cysteine residues in zinc fingers located within the RBCC domain of PML-RARalpha and PML. Arsenic binding induces PML oligomerization, which increases its interaction with the small ubiquitin-like protein modifier (SUMO)-conjugating enzyme UBC9, resulting in enhanced SUMOylation and degradation. The identification of PML as a direct target of As2O3 provides new insights into the drug's mechanism of action and its specificity for APL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Xiao-Wei -- Yan, Xiao-Jing -- Zhou, Zi-Ren -- Yang, Fei-Fei -- Wu, Zi-Yu -- Sun, Hong-Bin -- Liang, Wen-Xue -- Song, Ai-Xin -- Lallemand-Breitenbach, Valerie -- Jeanne, Marion -- Zhang, Qun-Ye -- Yang, Huai-Yu -- Huang, Qiu-Hua -- Zhou, Guang-Biao -- Tong, Jian-Hua -- Zhang, Yan -- Wu, Ji-Hui -- Hu, Hong-Yu -- de The, Hugues -- Chen, Sai-Juan -- Chen, Zhu -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):240-3. doi: 10.1126/science.1183424.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, 197 Rui Jin Road II, Shanghai 200025, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378816" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenic/*metabolism ; Arsenicals/*metabolism/*pharmacology ; Cell Line ; Humans ; Leukemia, Promyelocytic, Acute/drug therapy/genetics ; Mutant Proteins/chemistry/metabolism ; Mutation ; Nuclear Proteins/chemistry/genetics/*metabolism ; Oncogene Proteins, Fusion/chemistry/genetics/*metabolism ; Oxazines/metabolism ; Oxides/*metabolism/*pharmacology ; Protein Conformation ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Receptors, Retinoic Acid/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Transcription Factors/chemistry/genetics/*metabolism ; Tumor Suppressor Proteins/chemistry/genetics/*metabolism ; Ubiquitination ; Zinc Fingers
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  • 22
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    Cytoplasmic partitioning of P granule components is not required to specify the germline in C. elegans (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: Asymmetric segregation of P granules during the first four divisions of the Caenorhabditis elegans embryo is a classic example of cytoplasmic partitioning of germline determinants. It is thought that asymmetric partitioning of P granule components during mitosis is essential to distinguish germline from soma. We have identified a mutant (pptr-1) in which P granules become unstable during mitosis and P granule proteins and RNAs are distributed equally to somatic and germline blastomeres. Despite symmetric partitioning of P granule components, pptr-1 mutants segregate a germline that uniquely expresses P granules during postembryonic development. pptr-1 mutants are fertile, except at high temperatures. Hence, asymmetric partitioning of maternal P granules is not essential to specify germ cell fate. Instead, it may serve to protect the nascent germline from stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072820/" 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/PMC3072820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallo, Christopher M -- Wang, Jennifer T -- Motegi, Fumio -- Seydoux, Geraldine -- GM080042/GM/NIGMS NIH HHS/ -- HD007276/HD/NICHD NIH HHS/ -- HD037047/HD/NICHD NIH HHS/ -- R01 HD037047/HD/NICHD NIH HHS/ -- R01 HD037047-12/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1685-9. doi: 10.1126/science.1193697. Epub 2010 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Center for Cell Dynamics, Johns Hopkins School of Medicine, 725 North Wolfe Street, PCTB 706, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127218" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastomeres/*physiology ; Caenorhabditis elegans/*embryology/genetics/metabolism ; Caenorhabditis elegans Proteins/genetics/*metabolism/physiology ; Cytoplasm/*metabolism ; Cytoplasmic Granules/*physiology/ultrastructure ; Embryo, Nonmammalian/physiology ; Embryonic Development ; Germ Cells/*physiology ; Interphase ; Microscopy, Confocal ; Mitosis ; Mutation ; Nuclear Proteins/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Helminth/*metabolism ; RNA-Binding Proteins/metabolism ; Recombinant Fusion Proteins/metabolism ; Zygote/physiology
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    Rewiring of genetic networks in response to DNA damage (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: Although cellular behaviors are dynamic, the networks that govern these behaviors have been mapped primarily as static snapshots. Using an approach called differential epistasis mapping, we have discovered widespread changes in genetic interaction among yeast kinases, phosphatases, and transcription factors as the cell responds to DNA damage. Differential interactions uncover many gene functions that go undetected in static conditions. They are very effective at identifying DNA repair pathways, highlighting new damage-dependent roles for the Slt2 kinase, Pph3 phosphatase, and histone variant Htz1. The data also reveal that protein complexes are generally stable in response to perturbation, but the functional relations between these complexes are substantially reorganized. Differential networks chart a new type of genetic landscape that is invaluable for mapping cellular responses to stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006187/" 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/PMC3006187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bandyopadhyay, Sourav -- Mehta, Monika -- Kuo, Dwight -- Sung, Min-Kyung -- Chuang, Ryan -- Jaehnig, Eric J -- Bodenmiller, Bernd -- Licon, Katherine -- Copeland, Wilbert -- Shales, Michael -- Fiedler, Dorothea -- Dutkowski, Janusz -- Guenole, Aude -- van Attikum, Haico -- Shokat, Kevan M -- Kolodner, Richard D -- Huh, Won-Ki -- Aebersold, Ruedi -- Keogh, Michael-Christopher -- Krogan, Nevan J -- Ideker, Trey -- P30CA013330/CA/NCI NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- R01 ES014811/ES/NIEHS NIH HHS/ -- R01 ES014811-01A1/ES/NIEHS NIH HHS/ -- R01 ES014811-02/ES/NIEHS NIH HHS/ -- R01 ES014811-02S1/ES/NIEHS NIH HHS/ -- R01 ES014811-03/ES/NIEHS NIH HHS/ -- R01 ES014811-04/ES/NIEHS NIH HHS/ -- R01 ES014811-05/ES/NIEHS NIH HHS/ -- R01 ES014811-05S1/ES/NIEHS NIH HHS/ -- R01 ES014811-06/ES/NIEHS NIH HHS/ -- R01 GM026017/GM/NIGMS NIH HHS/ -- R01 GM084279/GM/NIGMS NIH HHS/ -- R01 GM084279-01A1/GM/NIGMS NIH HHS/ -- R01 GM084279-02/GM/NIGMS NIH HHS/ -- R01 GM084279-02S1/GM/NIGMS NIH HHS/ -- R01 GM084279-03/GM/NIGMS NIH HHS/ -- R01 GM084279-04/GM/NIGMS NIH HHS/ -- R01 GM084448/GM/NIGMS NIH HHS/ -- R01-ES14811/ES/NIEHS NIH HHS/ -- R01-GM084279/GM/NIGMS NIH HHS/ -- R37 GM026017/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1385-9. doi: 10.1126/science.1195618.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127252" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/metabolism ; *DNA Damage ; DNA Repair/*genetics ; DNA, Fungal/genetics ; *Epistasis, Genetic ; *Gene Regulatory Networks ; Genes, Fungal ; Histones/genetics/metabolism ; Methyl Methanesulfonate/pharmacology ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Mutagens/pharmacology ; Mutation ; Phosphoprotein Phosphatases/genetics/metabolism ; Protein Interaction Mapping ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Saccharomyces cerevisiae/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Signal Transduction ; Transcription Factors/genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Selection at linked sites shapes heritable phenotypic variation in C. elegans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, whereas mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTLs) influencing transcript abundance traits in a cross of two Caenorhabditis elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138179/" 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/PMC3138179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rockman, Matthew V -- Skrovanek, Sonja S -- Kruglyak, Leonid -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-01/GM/NIGMS NIH HHS/ -- R01 GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):372-6. doi: 10.1126/science.1194208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Genomics and Systems Biology, New York University, 100 Washington Square East, New York, NY 10003, USA. mrockman@nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947766" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Caenorhabditis elegans/*genetics/physiology ; Chromosome Mapping ; Chromosomes/*genetics ; Crosses, Genetic ; Evolution, Molecular ; Gene Expression ; Genes, Helminth ; *Genetic Variation ; Logistic Models ; Models, Genetic ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Single Nucleotide ; Population Density ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Recombination, Genetic ; *Selection, Genetic
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    Cell biology. Septins at the nexus (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barral, Yves -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1289-90. doi: 10.1126/science.1195445.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biochemistry, ETH Zurich, 8093 Zurich, Switzerland. yves.barral@bc.biol.ethz.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829470" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/metabolism/ultrastructure ; *Cell Polarity ; Centrioles/metabolism ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/chemistry/*metabolism ; Diffusion ; GTP-Binding Proteins/chemistry/*metabolism ; Glycoproteins/genetics/metabolism ; Hedgehog Proteins/metabolism ; Humans ; Mutant Proteins/metabolism ; Mutation ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Xenopus Proteins/metabolism
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" 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/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
    Print ISSN: 0036-8075
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    The genetic landscape of a cell (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: A genome-scale genetic interaction map was constructed by examining 5.4 million gene-gene pairs for synthetic genetic interactions, generating quantitative genetic interaction profiles for approximately 75% of all genes in the budding yeast, Saccharomyces cerevisiae. A network based on genetic interaction profiles reveals a functional map of the cell in which genes of similar biological processes cluster together in coherent subsets, and highly correlated profiles delineate specific pathways to define gene function. The global network identifies functional cross-connections between all bioprocesses, mapping a cellular wiring diagram of pleiotropy. Genetic interaction degree correlated with a number of different gene attributes, which may be informative about genetic network hubs in other organisms. We also demonstrate that extensive and unbiased mapping of the genetic landscape provides a key for interpretation of chemical-genetic interactions and drug target identification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Costanzo, Michael -- Baryshnikova, Anastasia -- Bellay, Jeremy -- Kim, Yungil -- Spear, Eric D -- Sevier, Carolyn S -- Ding, Huiming -- Koh, Judice L Y -- Toufighi, Kiana -- Mostafavi, Sara -- Prinz, Jeany -- St Onge, Robert P -- VanderSluis, Benjamin -- Makhnevych, Taras -- Vizeacoumar, Franco J -- Alizadeh, Solmaz -- Bahr, Sondra -- Brost, Renee L -- Chen, Yiqun -- Cokol, Murat -- Deshpande, Raamesh -- Li, Zhijian -- Lin, Zhen-Yuan -- Liang, Wendy -- Marback, Michaela -- Paw, Jadine -- San Luis, Bryan-Joseph -- Shuteriqi, Ermira -- Tong, Amy Hin Yan -- van Dyk, Nydia -- Wallace, Iain M -- Whitney, Joseph A -- Weirauch, Matthew T -- Zhong, Guoqing -- Zhu, Hongwei -- Houry, Walid A -- Brudno, Michael -- Ragibizadeh, Sasan -- Papp, Balazs -- Pal, Csaba -- Roth, Frederick P -- Giaever, Guri -- Nislow, Corey -- Troyanskaya, Olga G -- Bussey, Howard -- Bader, Gary D -- Gingras, Anne-Claude -- Morris, Quaid D -- Kim, Philip M -- Kaiser, Chris A -- Myers, Chad L -- Andrews, Brenda J -- Boone, Charles -- 084314/Wellcome Trust/United Kingdom -- GSP-41567/Canadian Institutes of Health Research/Canada -- R01 HG003224/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):425-31. doi: 10.1126/science.1180823.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Banting and Best Department of Medical Research, Terrence Donnelly Centre for Cellular and Biomolecular Research, University of Toronto, Toronto, Ontario M5S 3E1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093466" target="_blank"〉PubMed〈/a〉
    Keywords: Computational Biology ; Gene Duplication ; Gene Expression Regulation, Fungal ; *Gene Regulatory Networks ; Genes, Fungal ; Genetic Fitness ; *Genome, Fungal ; Metabolic Networks and Pathways ; Mutation ; Protein Interaction Mapping ; Saccharomyces cerevisiae/*genetics/*metabolism/physiology ; Saccharomyces cerevisiae Proteins/genetics/*metabolism
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    Changing face of microglia (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-06
    Description: Microglia are resident brain cells that sense pathological tissue alterations. They can develop into brain macrophages and perform immunological functions. However, expression of immune proteins by microglia is not synonymous with inflammation, because these molecules can have central nervous system (CNS)-specific roles. Through their involvement in pain mechanisms, microglia also respond to external threats. Experimental studies support the idea that microglia have a role in the maintenance of synaptic integrity. Analogous to electricians, they are capable of removing defunct axon terminals, thereby helping neuronal connections to stay intact. Microglia in healthy CNS tissue do not qualify as macrophages, and their specific functions are beginning to be explored.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graeber, Manuel B -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):783-8. doi: 10.1126/science.1190929.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia. manuel@graeber.net〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051630" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior ; Behavior, Animal ; Bone Marrow Transplantation ; Brain/*cytology/pathology/physiology ; Brain Diseases/pathology/physiopathology/therapy ; Humans ; Macrophages/cytology/physiology ; Mental Disorders/physiopathology ; Microglia/immunology/*physiology ; Mutation ; Neuralgia/physiopathology ; Neurodegenerative Diseases/pathology/physiopathology/therapy ; Signal Transduction ; Spinal Cord/*cytology/pathology/physiology ; Synapses/physiology
    Print ISSN: 0036-8075
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    The genetic map of Artemisia annua L. identifies loci affecting yield of the antimalarial drug artemisinin (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: Artemisinin is a plant natural product produced by Artemisia annua and the active ingredient in the most effective treatment for malaria. Efforts to eradicate malaria are increasing demand for an affordable, high-quality, robust supply of artemisinin. We performed deep sequencing on the transcriptome of A. annua to identify genes and markers for fast-track breeding. Extensive genetic variation enabled us to build a detailed genetic map with nine linkage groups. Replicated field trials resulted in a quantitative trait loci (QTL) map that accounts for a significant amount of the variation in key traits controlling artemisinin yield. Enrichment for positive QTLs in parents of new high-yielding hybrids confirms that the knowledge and tools to convert A. annua into a robust crop are now available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graham, Ian A -- Besser, Katrin -- Blumer, Susan -- Branigan, Caroline A -- Czechowski, Tomasz -- Elias, Luisa -- Guterman, Inna -- Harvey, David -- Isaac, Peter G -- Khan, Awais M -- Larson, Tony R -- Li, Yi -- Pawson, Tanya -- Penfield, Teresa -- Rae, Anne M -- Rathbone, Deborah A -- Reid, Sonja -- Ross, Joe -- Smallwood, Margaret F -- Segura, Vincent -- Townsend, Theresa -- Vyas, Darshna -- Winzer, Thilo -- Bowles, Dianna -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):328-31. doi: 10.1126/science.1182612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Novel Agricultural Products, Department of Biology, University of York, York YO10 5YW, UK. iag1@york.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075252" target="_blank"〉PubMed〈/a〉
    Keywords: Antimalarials/*metabolism ; Artemisia/*genetics/*metabolism ; Artemisinins/*metabolism ; *Chromosome Mapping ; Crosses, Genetic ; DNA, Complementary ; Gene Expression Profiling ; *Genes, Plant ; Genetic Association Studies ; Humans ; Malaria/drug therapy ; Mutation ; Phenotype ; Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; Sequence Analysis, DNA
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    Permissive secondary mutations enable the evolution of influenza oseltamivir resistance (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: The His274--〉Tyr274 (H274Y) mutation confers oseltamivir resistance on N1 influenza neuraminidase but had long been thought to compromise viral fitness. However, beginning in 2007-2008, viruses containing H274Y rapidly became predominant among human seasonal H1N1 isolates. We show that H274Y decreases the amount of neuraminidase that reaches the cell surface and that this defect can be counteracted by secondary mutations that also restore viral fitness. Two such mutations occurred in seasonal H1N1 shortly before the widespread appearance of H274Y. The evolution of oseltamivir resistance was therefore enabled by "permissive" mutations that allowed the virus to tolerate subsequent occurrences of H274Y. An understanding of this process may provide a basis for predicting the evolution of oseltamivir resistance in other influenza strains.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913718/" 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/PMC2913718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloom, Jesse D -- Gong, Lizhi Ian -- Baltimore, David -- P01 CA132681/CA/NCI NIH HHS/ -- P01 CA132681-01A27259/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1272-5. doi: 10.1126/science.1187816.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522774" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antiviral Agents/*pharmacology ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Drug Resistance, Viral/*genetics ; *Evolution, Molecular ; Genes, Viral ; Genetic Fitness ; Humans ; Influenza A Virus, H1N1 Subtype/*drug effects/*genetics/growth & development ; Influenza, Human/drug therapy/*virology ; Mutation ; Neuraminidase/antagonists & inhibitors/chemistry/genetics/metabolism ; Oseltamivir/*pharmacology ; Phylogeny ; Selection, Genetic
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    Medicine. Poisonous contacts (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-04-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kogan, Scott C -- New York, N.Y. -- Science. 2010 Apr 9;328(5975):184-5. doi: 10.1126/science.1189198.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory Medicine, University of California San Francisco Cancer Center, CA 94143-0100, USA. scott.kogan@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20378808" target="_blank"〉PubMed〈/a〉
    Keywords: Arsenic/*metabolism/*therapeutic use ; Arsenicals/metabolism/*therapeutic use ; Humans ; Leukemia, Promyelocytic, Acute/*drug therapy/genetics ; Mutant Proteins/chemistry/metabolism ; Mutation ; Nuclear Proteins/chemistry/*metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Oxides/metabolism/*therapeutic use ; Protein Multimerization ; Transcription Factors/chemistry/*metabolism ; Tumor Suppressor Proteins/chemistry/*metabolism ; Zinc Fingers
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    D-amino acids trigger biofilm disassembly (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-01
    Description: Bacteria form communities known as biofilms, which disassemble over time. In our studies outlined here, we found that, before biofilm disassembly, Bacillus subtilis produced a factor that prevented biofilm formation and could break down existing biofilms. The factor was shown to be a mixture of D-leucine, D-methionine, D-tyrosine, and D-tryptophan that could act at nanomolar concentrations. D-amino acid treatment caused the release of amyloid fibers that linked cells in the biofilm together. Mutants able to form biofilms in the presence of D-amino acids contained alterations in a protein (YqxM) required for the formation and anchoring of the fibers to the cell. D-amino acids also prevented biofilm formation by Staphylococcus aureus and Pseudomonas aeruginosa. D-amino acids are produced by many bacteria and, thus, may be a widespread signal for biofilm disassembly.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921573/" 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/PMC2921573/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolodkin-Gal, Ilana -- Romero, Diego -- Cao, Shugeng -- Clardy, Jon -- Kolter, Roberto -- Losick, Richard -- CA24487/CA/NCI NIH HHS/ -- GM086258/GM/NIGMS NIH HHS/ -- GM18546/GM/NIGMS NIH HHS/ -- GM58213/GM/NIGMS NIH HHS/ -- R01 GM018568/GM/NIGMS NIH HHS/ -- R01 GM018568-39/GM/NIGMS NIH HHS/ -- R01 GM058213/GM/NIGMS NIH HHS/ -- R01 GM086258/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 30;328(5978):627-9. doi: 10.1126/science.1188628.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20431016" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acids/*metabolism/pharmacology ; Bacillus subtilis/*physiology ; Bacterial Proteins/chemistry/metabolism ; *Biofilms/growth & development ; Cell Wall ; Culture Media, Conditioned ; Genes, Bacterial ; Leucine/metabolism/pharmacology ; Methionine/metabolism/pharmacology ; Molecular Sequence Data ; Mutation ; Pseudomonas aeruginosa/physiology ; Staphylococcus aureus/physiology ; Stereoisomerism ; Tryptophan/metabolism/pharmacology ; Tyrosine/metabolism/pharmacology
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    ATM activation by oxidative stress (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-23
    Description: The ataxia-telangiectasia mutated (ATM) protein kinase is activated by DNA double-strand breaks (DSBs) through the Mre11-Rad50-Nbs1 (MRN) DNA repair complex and orchestrates signaling cascades that initiate the DNA damage response. Cells lacking ATM are also hypersensitive to insults other than DSBs, particularly oxidative stress. We show that oxidation of ATM directly induces ATM activation in the absence of DNA DSBs and the MRN complex. The oxidized form of ATM is a disulfide-cross-linked dimer, and mutation of a critical cysteine residue involved in disulfide bond formation specifically blocked activation through the oxidation pathway. Identification of this pathway explains observations of ATM activation under conditions of oxidative stress and shows that ATM is an important sensor of reactive oxygen species in human cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guo, Zhi -- Kozlov, Sergei -- Lavin, Martin F -- Person, Maria D -- Paull, Tanya T -- 007784/PHS HHS/ -- CA132813/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):517-21. doi: 10.1126/science.1192912.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Genetics and Microbiology, and Institute for Cellular and Molecular Biology (ICMB), University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia/enzymology/genetics ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cysteine/metabolism ; DNA Breaks, Double-Stranded ; DNA Repair ; DNA Repair Enzymes/genetics ; DNA-Binding Proteins/genetics/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide ; Mutation ; Nuclear Proteins/genetics ; *Oxidative Stress ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Tumor Suppressor Proteins/genetics/*metabolism
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    Small peptides switch the transcriptional activity of Shavenbaby during Drosophila embryogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: A substantial proportion of eukaryotic transcripts are considered to be noncoding RNAs because they contain only short open reading frames (sORFs). Recent findings suggest, however, that some sORFs encode small bioactive peptides. Here, we show that peptides of 11 to 32 amino acids encoded by the polished rice (pri) sORF gene control epidermal differentiation in Drosophila by modifying the transcription factor Shavenbaby (Svb). Pri peptides trigger the amino-terminal truncation of the Svb protein, which converts Svb from a repressor to an activator. Our results demonstrate that during Drosophila embryogenesis, Pri sORF peptides provide a strict temporal control to the transcriptional program of epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, T -- Plaza, S -- Zanet, J -- Benrabah, E -- Valenti, P -- Hashimoto, Y -- Kobayashi, S -- Payre, F -- Kageyama, Y -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):336-9. doi: 10.1126/science.1188158.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Okazaki Institute for Integrative Bioscience, National Institute for Basic Biology (NIBB), National Institutes of Natural Sciences, 5-1 Myodaiji-Higashiyama, Okazaki 444-8787, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Nucleus/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/embryology/*genetics/metabolism ; Embryo, Nonmammalian/cytology/*metabolism ; Embryonic Development ; Epidermis/cytology/metabolism ; *Gene Expression Regulation, Developmental ; Genes, Insect ; Mutation ; Open Reading Frames ; Peptides/genetics/*metabolism ; Protein Isoforms/chemistry/genetics/metabolism ; Protein Processing, Post-Translational ; Protein Structure, Tertiary ; RNA, Untranslated/genetics ; Recombinant Fusion Proteins/metabolism ; Transcription Factors/chemistry/genetics/*metabolism ; *Transcription, Genetic
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    Genotype to phenotype: a complex problem (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-04-24
    Description: We generated a high-resolution whole-genome sequence and individually deleted 5100 genes in Sigma1278b, a Saccharomyces cerevisiae strain closely related to reference strain S288c. Similar to the variation between human individuals, Sigma1278b and S288c average 3.2 single-nucleotide polymorphisms per kilobase. A genome-wide comparison of deletion mutant phenotypes identified a subset of genes that were conditionally essential by strain, including 44 essential genes unique to Sigma1278b and 13 unique to S288c. Genetic analysis indicates the conditional phenotype was most often governed by complex genetic interactions, depending on multiple background-specific modifiers. Our comprehensive analysis suggests that the presence of a complex set of modifiers will often underlie the phenotypic differences between individuals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412269/" 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/PMC4412269/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dowell, Robin D -- Ryan, Owen -- Jansen, An -- Cheung, Doris -- Agarwala, Sudeep -- Danford, Timothy -- Bernstein, Douglas A -- Rolfe, P Alexander -- Heisler, Lawrence E -- Chin, Brian -- Nislow, Corey -- Giaever, Guri -- Phillips, Patrick C -- Fink, Gerald R -- Gifford, David K -- Boone, Charles -- DK076284/DK/NIDDK NIH HHS/ -- GM035010/GM/NIGMS NIH HHS/ -- GM069676/GM/NIGMS NIH HHS/ -- P01 NS055923/NS/NINDS NIH HHS/ -- R01 GM035010/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):469. doi: 10.1126/science.1189015.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Computer Science and Artificial Intelligence Laboratory, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413493" target="_blank"〉PubMed〈/a〉
    Keywords: Crosses, Genetic ; Gene Deletion ; *Gene Expression Regulation, Fungal ; Gene Regulatory Networks ; *Genes, Essential ; *Genes, Fungal ; Genetic Variation ; Genome, Fungal ; Genotype ; Mutation ; Phenotype ; Saccharomyces cerevisiae/*genetics ; Sequence Analysis, DNA
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    Poly(A) tail recognition by a viral RNA element through assembly of a triple helix (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: Kaposi's sarcoma-associated herpesvirus produces a highly abundant, nuclear noncoding RNA, polyadenylated nuclear (PAN) RNA, which contains an element that prevents its decay. The 79-nucleotide expression and nuclear retention element (ENE) was proposed to adopt a secondary structure like that of a box H/ACA small nucleolar RNA (snoRNA), with a U-rich internal loop that hybridizes to and protects the PAN RNA poly(A) tail. The crystal structure of a complex between the 40-nucleotide ENE core and oligo(A)(9) RNA at 2.5 angstrom resolution reveals that unlike snoRNAs, the U-rich loop of the ENE engages its target through formation of a major-groove triple helix. A-minor interactions extend the binding interface. Deadenylation assays confirm the functional importance of the triple helix. Thus, the ENE acts as an intramolecular RNA clamp, sequestering the PAN poly(A) tail and preventing the initiation of RNA decay.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074936/" 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/PMC3074936/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitton-Fry, Rachel M -- DeGregorio, Suzanne J -- Wang, Jimin -- Steitz, Thomas A -- Steitz, Joan A -- CA16038/CA/NCI NIH HHS/ -- GM022778/GM/NIGMS NIH HHS/ -- P01 CA016038/CA/NCI NIH HHS/ -- P01 CA016038-38/CA/NCI NIH HHS/ -- P30 EB009998/EB/NIBIB NIH HHS/ -- R01 GM026154/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1244-7. doi: 10.1126/science.1195858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biophysics and Biochemistry (MB&B), Howard Hughes Medical Institute (HHMI), Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536-9812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109672" target="_blank"〉PubMed〈/a〉
    Keywords: Base Pairing ; Cell Nucleus/genetics/metabolism ; Crystallography, X-Ray ; Herpesvirus 8, Human/*genetics ; Mutation ; *Nucleic Acid Conformation ; Poly A/chemistry/*metabolism ; *RNA Stability ; RNA, Messenger/chemistry/genetics/metabolism ; RNA, Nuclear/*chemistry/metabolism ; RNA, Untranslated/*chemistry/genetics/metabolism ; RNA, Viral/*chemistry/genetics/metabolism ; *Regulatory Sequences, Ribonucleic Acid ; Riboswitch
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    Prion strain mutation determined by prion protein conformational compatibility and primary structure (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-15
    Description: Prions are infectious proteins composed of the abnormal disease-causing isoform PrPSc, which induces conformational conversion of the host-encoded normal cellular prion protein PrPC to additional PrPSc. The mechanism underlying prion strain mutation in the absence of nucleic acids remains unresolved. Additionally, the frequency of strains causing chronic wasting disease (CWD), a burgeoning prion epidemic of cervids, is unknown. Using susceptible transgenic mice, we identified two prevalent CWD strains with divergent biological properties but composed of PrPSc with indistinguishable biochemical characteristics. Although CWD transmissions indicated stable, independent strain propagation by elk PrPC, strain coexistence in the brains of deer and transgenic mice demonstrated unstable strain propagation by deer PrPC. The primary structures of deer and elk prion proteins differ at residue 226, which, in concert with PrPSc conformational compatibility, determines prion strain mutation in these cervids.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097672/" 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/PMC4097672/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angers, Rachel C -- Kang, Hae-Eun -- Napier, Dana -- Browning, Shawn -- Seward, Tanya -- Mathiason, Candace -- Balachandran, Aru -- McKenzie, Debbie -- Castilla, Joaquin -- Soto, Claudio -- Jewell, Jean -- Graham, Catherine -- Hoover, Edward A -- Telling, Glenn C -- 1P01AI077774-01/AI/NIAID NIH HHS/ -- 2R01 NS040334-04/NS/NINDS NIH HHS/ -- N01-AI-25491/AI/NIAID NIH HHS/ -- P01 AI077774/AI/NIAID NIH HHS/ -- R01 NS049173/NS/NINDS NIH HHS/ -- T32 AI49795/AI/NIAID NIH HHS/ -- T32 DA022738/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 May 28;328(5982):1154-8. doi: 10.1126/science.1187107. Epub 2010 May 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky Medical Center, Lexington, KY 40536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466881" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/pathology ; Brain Chemistry ; *Deer ; Disease Susceptibility ; Mice ; Mice, Transgenic ; Mutation ; PrPC Proteins/*chemistry/genetics ; PrPSc Proteins/analysis/*chemistry/genetics/pathogenicity ; Protein Conformation ; Protein Folding ; Selection, Genetic ; Serial Passage ; Species Specificity ; *Wasting Disease, Chronic/pathology/transmission
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    Fast vesicle fusion in living cells requires at least three SNARE complexes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-18
    Description: Exocytosis requires formation of SNARE [soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor] complexes between vesicle and target membranes. Recent assessments in reduced model systems have produced divergent estimates of the number of SNARE complexes needed for fusion. Here, we used a titration approach to answer this question in intact, cultured chromaffin cells. Simultaneous expression of wild-type SNAP-25 and a mutant unable to support exocytosis progressively altered fusion kinetics and fusion-pore opening, indicating that both proteins assemble into heteromeric fusion complexes. Expressing different wild-type:mutant ratios revealed a third-power relation for fast (synchronous) fusion and a near-linear relation for overall release. Thus, fast fusion typically observed in synapses and neurosecretory cells requires at least three functional SNARE complexes, whereas slower release might occur with fewer complexes. Heterogeneity in SNARE-complex number may explain heterogeneity in vesicular release probability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mohrmann, Ralf -- de Wit, Heidi -- Verhage, Matthijs -- Neher, Erwin -- Sorensen, Jakob B -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):502-5. doi: 10.1126/science.1193134. Epub 2010 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane Biophysics, Max-Planck Institute for Biophysical Chemistry, Gottingen, Germany. Ralf.Mohrmann@uks.eu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20847232" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Membrane/physiology ; Chromaffin Cells/physiology ; Cytoplasmic Vesicles/physiology ; Exocytosis/*physiology ; Green Fluorescent Proteins/genetics ; Membrane Fusion/*physiology ; Mice ; Mutation ; SNARE Proteins/physiology ; Synaptosomal-Associated Protein 25/genetics/*physiology
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    Virology. Helping the resistance (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, Edward C -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1243-4. doi: 10.1126/science.1190994.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Infectious Disease Dynamics, Department of Biology, The Pennsylvania State University, University Park, PA 16802, USA. ech15@psu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522766" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Antiviral Agents/metabolism/*pharmacology ; Drug Resistance, Viral/*genetics ; *Evolution, Molecular ; Genetic Fitness ; Humans ; Influenza A Virus, H1N1 Subtype/*drug effects/*genetics ; Influenza, Human/drug therapy/*virology ; Mutation ; Neuraminidase/antagonists & inhibitors/chemistry/genetics/metabolism ; Oseltamivir/metabolism/*pharmacology ; Phylogeny ; Selection, Genetic
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    CRISPR/Cas, the immune system of bacteria and archaea (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-09
    Description: Microbes rely on diverse defense mechanisms that allow them to withstand viral predation and exposure to invading nucleic acid. In many Bacteria and most Archaea, clustered regularly interspaced short palindromic repeats (CRISPR) form peculiar genetic loci, which provide acquired immunity against viruses and plasmids by targeting nucleic acid in a sequence-specific manner. These hypervariable loci take up genetic material from invasive elements and build up inheritable DNA-encoded immunity over time. Conversely, viruses have devised mutational escape strategies that allow them to circumvent the CRISPR/Cas system, albeit at a cost. CRISPR features may be exploited for typing purposes, epidemiological studies, host-virus ecological surveys, building specific immunity against undesirable genetic elements, and enhancing viral resistance in domesticated microbes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horvath, Philippe -- Barrangou, Rodolphe -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):167-70. doi: 10.1126/science.1179555.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Danisco France SAS, BP10, F-86220 Dange-Saint-Romain, France. philippe.horvath@danisco.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056882" target="_blank"〉PubMed〈/a〉
    Keywords: Archaea/*genetics/immunology/virology ; Archaeal Proteins/metabolism ; Bacteria/*genetics/immunology/virology ; Bacterial Proteins/metabolism ; Bacteriophages/genetics/physiology ; Base Sequence ; Conserved Sequence ; Gene Transfer, Horizontal ; Genes, Archaeal ; Genes, Bacterial ; *Genetic Loci ; *Genome, Archaeal ; *Genome, Bacterial ; Genome, Viral ; Mutation ; Plasmids ; RNA Interference ; RNA, Archaeal/genetics/metabolism ; RNA, Bacterial/genetics/metabolism ; *Repetitive Sequences, Nucleic Acid
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    Lateral transfer of genes from fungi underlies carotenoid production in aphids (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-01
    Description: Carotenoids are colored compounds produced by plants, fungi, and microorganisms and are required in the diet of most animals for oxidation control or light detection. Pea aphids display a red-green color polymorphism, which influences their susceptibility to natural enemies, and the carotenoid torulene occurs only in red individuals. Unexpectedly, we found that the aphid genome itself encodes multiple enzymes for carotenoid biosynthesis. Phylogenetic analyses show that these aphid genes are derived from fungal genes, which have been integrated into the genome and duplicated. Red individuals have a 30-kilobase region, encoding a single carotenoid desaturase that is absent from green individuals. A mutation causing an amino acid replacement in this desaturase results in loss of torulene and of red body color. Thus, aphids are animals that make their own carotenoids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moran, Nancy A -- Jarvik, Tyler -- New York, N.Y. -- Science. 2010 Apr 30;328(5978):624-7. doi: 10.1126/science.1187113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, 1041 East Lowell Street, University of Arizona, Tucson, AZ 85721, USA. nancy.moran@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20431015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aphids/*genetics/*metabolism/microbiology ; Carotenoids/analysis/*biosynthesis/genetics ; Crosses, Genetic ; Fungi/genetics ; Gene Duplication ; *Gene Transfer, Horizontal ; *Genes, Fungal ; *Genes, Insect ; Genome, Insect ; Heterozygote ; Molecular Sequence Data ; Mutation ; Oxidoreductases/genetics ; Phylogeny ; Pigmentation/genetics ; Pigments, Biological/chemistry ; Polymorphism, Genetic ; Sequence Analysis, DNA
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    RTEL-1 enforces meiotic crossover interference and homeostasis (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-06
    Description: Meiotic crossovers (COs) are tightly regulated to ensure that COs on the same chromosome are distributed far apart (crossover interference, COI) and that at least one CO is formed per homolog pair (CO homeostasis). CO formation is controlled in part during meiotic double-strand break (DSB) creation in Caenorhabditis elegans, but a second level of control must also exist because meiotic DSBs outnumber COs. We show that the antirecombinase RTEL-1 is required to prevent excess meiotic COs, probably by promoting meiotic synthesis-dependent strand annealing. Two distinct classes of meiotic COs are increased in rtel-1 mutants, and COI and homeostasis are compromised. We propose that RTEL-1 implements the second level of CO control by promoting noncrossovers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770885/" 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/PMC4770885/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Youds, Jillian L -- Mets, David G -- McIlwraith, Michael J -- Martin, Julie S -- Ward, Jordan D -- ONeil, Nigel J -- Rose, Ann M -- West, Stephen C -- Meyer, Barbara J -- Boulton, Simon J -- Canadian Institutes of Health Research/Canada -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1254-8. doi: 10.1126/science.1183112.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, EN6 3LD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Chromatids/genetics ; Chromosomal Proteins, Non-Histone/genetics/metabolism ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; DNA Helicases/genetics/*metabolism ; DNA Repair ; DNA, Helminth/genetics/metabolism ; Homeostasis ; *Meiosis ; Mutation ; Polymorphism, Single Nucleotide ; X Chromosome/genetics
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    Phosphatidic acid is a pH biosensor that links membrane biogenesis to metabolism (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: Recognition of lipids by proteins is important for their targeting and activation in many signaling pathways, but the mechanisms that regulate such interactions are largely unknown. Here, we found that binding of proteins to the ubiquitous signaling lipid phosphatidic acid (PA) depended on intracellular pH and the protonation state of its phosphate headgroup. In yeast, a rapid decrease in intracellular pH in response to glucose starvation regulated binding of PA to a transcription factor, Opi1, that coordinately repressed phospholipid metabolic genes. This enabled coupling of membrane biogenesis to nutrient availability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Barry P -- Shin, John J H -- Orij, Rick -- Chao, Jesse T -- Li, Shu Chen -- Guan, Xue Li -- Khong, Anthony -- Jan, Eric -- Wenk, Markus R -- Prinz, William A -- Smits, Gertien J -- Loewen, Christopher J R -- Canadian Institutes of Health Research/Canada -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1085-8. doi: 10.1126/science.1191026.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798321" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Cation Transport Proteins/genetics/metabolism ; Cell Membrane/*metabolism ; Cell Nucleus/metabolism ; Endoplasmic Reticulum/metabolism ; Gene Expression Regulation, Fungal ; Genes, Fungal ; Glucose/metabolism ; Hydrogen-Ion Concentration ; Inositol/genetics/metabolism ; Liposomes/metabolism ; Mutation ; Phosphatidic Acids/*metabolism ; Protein Binding ; Protein Phosphatase 1/genetics/metabolism ; Proton-Translocating ATPases/genetics/metabolism ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Saccharomyces cerevisiae/genetics/growth & development/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Signal Transduction ; Transcription, Genetic ; Vacuolar Proton-Translocating ATPases/genetics/metabolism
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    pH sensing by intracellular Salmonella induces effector translocation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-17
    Description: Salmonella enterica is an important intracellular bacterial pathogen of humans and animals. It replicates within host-cell vacuoles by delivering virulence (effector) proteins through a vacuolar membrane pore made by the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (T3SS). T3SS assembly follows vacuole acidification, but when bacteria are grown at low pH, effector secretion is negligible. We found that effector secretion was activated at low pH from mutant strains lacking a complex of SPI-2-encoded proteins SsaM, SpiC, and SsaL. Exposure of wild-type bacteria to pH 7.2 after growth at pH 5.0 caused dissociation and degradation of SsaM/SpiC/SsaL complexes and effector secretion. In infected cells, loss of the pH 7.2 signal through acidification of host-cell cytosol prevented complex degradation and effector translocation. Thus, intravacuolar Salmonella senses host cytosolic pH, resulting in the degradation of regulatory complex proteins and effector translocation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Xiu-Jun -- McGourty, Kieran -- Liu, Mei -- Unsworth, Kate E -- Holden, David W -- 074553/Z/04/Z/Wellcome Trust/United Kingdom -- G0800148/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 May 21;328(5981):1040-3. doi: 10.1126/science.1189000. Epub 2010 Apr 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbiology, Centre for Molecular Microbiology and Infection, Imperial College London, Armstrong Road, London SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20395475" target="_blank"〉PubMed〈/a〉
    Keywords: Bacterial Processes ; Bacterial Proteins/chemistry/genetics/*metabolism ; Cytosol/chemistry ; Genomic Islands ; HeLa Cells ; Humans ; Hydrogen-Ion Concentration ; Molecular Chaperones/metabolism ; Multiprotein Complexes/metabolism ; Mutation ; Salmonella typhimurium/genetics/growth & development/*metabolism/pathogenicity ; Vacuoles/metabolism/*microbiology ; Virulence Factors/*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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    Adaptive evolution of an sRNA that controls Myxococcus development (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-22
    Description: Small RNA (sRNA) molecules regulate a vast array of processes in biology, but evidence for adaptive evolution of sRNA sequences has been indirect. Here, we identify an sRNA, Pxr, that negatively regulates fruiting body development in Myxococcus xanthus. We further show that a spontaneous evolutionary mutation in Pxr abolished its regulatory function and thereby adaptively restored developmental proficiency to a socially defective M. xanthus cheater. In wild-type M. xanthus, development is initiated only upon starvation, but deletion of pxr allows development to proceed even while nutrients remain abundant. Thus, Pxr serves as a major checkpoint controlling the transition from growth to development in the myxobacteria. These findings show that an sRNA molecule governs a complex form of multicellular development in prokaryotes and directly demonstrate the ability of sRNA regulators to facilitate evolutionary adaptations of major phenotypic effect.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3027070/" 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/PMC3027070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Yuen-Tsu N -- Yuan, Xi -- Velicer, Gregory J -- GM079690/GM/NIGMS NIH HHS/ -- R01 GM079690/GM/NIGMS NIH HHS/ -- R01 GM079690-01/GM/NIGMS NIH HHS/ -- R01 GM079690-02/GM/NIGMS NIH HHS/ -- R01 GM079690-03/GM/NIGMS NIH HHS/ -- R01 GM079690-04/GM/NIGMS NIH HHS/ -- R01 GM079690-05/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 May 21;328(5981):993. doi: 10.1126/science.1187200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20489016" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Evolution, Molecular ; Gene Deletion ; Genes, Bacterial ; Microbial Interactions ; Mutation ; Myxococcus xanthus/*genetics/*growth & development/physiology ; Phenotype ; RNA, Bacterial/chemistry/genetics/*physiology ; RNA, Untranslated/chemistry/genetics/*physiology ; Spores, Bacterial/growth & development
    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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    Whole-exome sequencing identifies recessive WDR62 mutations in severe brain malformations (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-08-24
    Description: The development of the human cerebral cortex is an orchestrated process involving the generation of neural progenitors in the periventricular germinal zones, cell proliferation characterized by symmetric and asymmetric mitoses, followed by migration of post-mitotic neurons to their final destinations in six highly ordered, functionally specialized layers. An understanding of the molecular mechanisms guiding these intricate processes is in its infancy, substantially driven by the discovery of rare mutations that cause malformations of cortical development. Mapping of disease loci in putative Mendelian forms of malformations of cortical development has been hindered by marked locus heterogeneity, small kindred sizes and diagnostic classifications that may not reflect molecular pathogenesis. Here we demonstrate the use of whole-exome sequencing to overcome these obstacles by identifying recessive mutations in WD repeat domain 62 (WDR62) as the cause of a wide spectrum of severe cerebral cortical malformations including microcephaly, pachygyria with cortical thickening as well as hypoplasia of the corpus callosum. Some patients with mutations in WDR62 had evidence of additional abnormalities including lissencephaly, schizencephaly, polymicrogyria and, in one instance, cerebellar hypoplasia, all traits traditionally regarded as distinct entities. In mice and humans, WDR62 transcripts and protein are enriched in neural progenitors within the ventricular and subventricular zones. Expression of WDR62 in the neocortex is transient, spanning the period of embryonic neurogenesis. Unlike other known microcephaly genes, WDR62 does not apparently associate with centrosomes and is predominantly nuclear in localization. These findings unify previously disparate aspects of cerebral cortical development and highlight the use of whole-exome sequencing to identify disease loci in settings in which traditional methods have proved challenging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3129007/" 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/PMC3129007/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bilguvar, Kaya -- Ozturk, Ali Kemal -- Louvi, Angeliki -- Kwan, Kenneth Y -- Choi, Murim -- Tatli, Burak -- Yalnizoglu, Dilek -- Tuysuz, Beyhan -- Caglayan, Ahmet Okay -- Gokben, Sarenur -- Kaymakcalan, Hande -- Barak, Tanyeri -- Bakircioglu, Mehmet -- Yasuno, Katsuhito -- Ho, Winson -- Sanders, Stephan -- Zhu, Ying -- Yilmaz, Sanem -- Dincer, Alp -- Johnson, Michele H -- Bronen, Richard A -- Kocer, Naci -- Per, Huseyin -- Mane, Shrikant -- Pamir, Mehmet Necmettin -- Yalcinkaya, Cengiz -- Kumandas, Sefer -- Topcu, Meral -- Ozmen, Meral -- Sestan, Nenad -- Lifton, Richard P -- State, Matthew W -- Gunel, Murat -- RC2 NS070477/NS/NINDS NIH HHS/ -- RC2 NS070477-01/NS/NINDS NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U24 NS051869-02S1/NS/NINDS NIH HHS/ -- UL1 RR024139NIH/RR/NCRR NIH HHS/ -- UO1MH081896/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 9;467(7312):207-10. doi: 10.1038/nature09327. Epub 2010 Aug 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20729831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Brain/*abnormalities/growth & development/pathology ; Brain Diseases/*genetics/pathology ; DNA Mutational Analysis/*methods ; Female ; Genes, Recessive ; Humans ; Male ; Mice ; Microcephaly/genetics/pathology ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/*genetics/metabolism ; Pedigree
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    Subtypes of medulloblastoma have distinct developmental origins (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-15
    Description: Medulloblastoma encompasses a collection of clinically and molecularly diverse tumour subtypes that together comprise the most common malignant childhood brain tumour. These tumours are thought to arise within the cerebellum, with approximately 25% originating from granule neuron precursor cells (GNPCs) after aberrant activation of the Sonic Hedgehog pathway (hereafter, SHH subtype). The pathological processes that drive heterogeneity among the other medulloblastoma subtypes are not known, hindering the development of much needed new therapies. Here we provide evidence that a discrete subtype of medulloblastoma that contains activating mutations in the WNT pathway effector CTNNB1 (hereafter, WNT subtype) arises outside the cerebellum from cells of the dorsal brainstem. We found that genes marking human WNT-subtype medulloblastomas are more frequently expressed in the lower rhombic lip (LRL) and embryonic dorsal brainstem than in the upper rhombic lip (URL) and developing cerebellum. Magnetic resonance imaging (MRI) and intra-operative reports showed that human WNT-subtype tumours infiltrate the dorsal brainstem, whereas SHH-subtype tumours are located within the cerebellar hemispheres. Activating mutations in Ctnnb1 had little impact on progenitor cell populations in the cerebellum, but caused the abnormal accumulation of cells on the embryonic dorsal brainstem which included aberrantly proliferating Zic1(+) precursor cells. These lesions persisted in all mutant adult mice; moreover, in 15% of cases in which Tp53 was concurrently deleted, they progressed to form medulloblastomas that recapitulated the anatomy and gene expression profiles of human WNT-subtype medulloblastoma. We provide the first evidence, to our knowledge, that subtypes of medulloblastoma have distinct cellular origins. Our data provide an explanation for the marked molecular and clinical differences between SHH- and WNT-subtype medulloblastomas and have profound implications for future research and treatment of this important childhood cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059767/" 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/PMC3059767/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Paul -- Tong, Yiai -- Robinson, Giles -- Thompson, Margaret C -- Currle, D Spencer -- Eden, Christopher -- Kranenburg, Tanya A -- Hogg, Twala -- Poppleton, Helen -- Martin, Julie -- Finkelstein, David -- Pounds, Stanley -- Weiss, Aaron -- Patay, Zoltan -- Scoggins, Matthew -- Ogg, Robert -- Pei, Yanxin -- Yang, Zeng-Jie -- Brun, Sonja -- Lee, Youngsoo -- Zindy, Frederique -- Lindsey, Janet C -- Taketo, Makoto M -- Boop, Frederick A -- Sanford, Robert A -- Gajjar, Amar -- Clifford, Steven C -- Roussel, Martine F -- McKinnon, Peter J -- Gutmann, David H -- Ellison, David W -- Wechsler-Reya, Robert -- Gilbertson, Richard J -- 01CA96832/CA/NCI NIH HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-06A18120/CA/NCI NIH HHS/ -- P01 CA096832-078120/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-01/CA/NCI NIH HHS/ -- R01 CA129541-02/CA/NCI NIH HHS/ -- R01 CA129541-03/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- R01 CA129541-05/CA/NCI NIH HHS/ -- R01 NS037956/NS/NINDS NIH HHS/ -- R01 NS037956-13/NS/NINDS NIH HHS/ -- R01CA129541/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1095-9. doi: 10.1038/nature09587. Epub 2010 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21150899" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Stem/*pathology ; Cerebellar Neoplasms/*pathology ; Disease Models, Animal ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Medulloblastoma/*pathology ; Mice ; Mice, Transgenic ; Mutation ; beta Catenin/genetics
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    Hsp90 prevents phenotypic variation by suppressing the mutagenic activity of transposons (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-12
    Description: The canalization concept describes the resistance of a developmental process to phenotypic variation, regardless of genetic and environmental perturbations, owing to the existence of buffering mechanisms. Severe perturbations, which overcome such buffering mechanisms, produce altered phenotypes that can be heritable and can themselves be canalized by a genetic assimilation process. An important implication of this concept is that the buffering mechanism could be genetically controlled. Recent studies on Hsp90, a protein involved in several cellular processes and development pathways, indicate that it is a possible molecular mechanism for canalization and genetic assimilation. In both flies and plants, mutations in the Hsp90-encoding gene induce a wide range of phenotypic abnormalities, which have been interpreted as an increased sensitivity of different developmental pathways to hidden genetic variability. Thus, Hsp90 chaperone machinery may be an evolutionarily conserved buffering mechanism of phenotypic variance, which provides the genetic material for natural selection. Here we offer an additional, perhaps alternative, explanation for proposals of a concrete mechanism underlying canalization. We show that, in Drosophila, functional alterations of Hsp90 affect the Piwi-interacting RNA (piRNA; a class of germ-line-specific small RNAs) silencing mechanism leading to transposon activation and the induction of morphological mutants. This indicates that Hsp90 mutations can generate new variation by transposon-mediated 'canonical' mutagenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Specchia, Valeria -- Piacentini, Lucia -- Tritto, Patrizia -- Fanti, Laura -- D'Alessandro, Rosalba -- Palumbo, Gioacchino -- Pimpinelli, Sergio -- Bozzetti, Maria P -- England -- Nature. 2010 Feb 4;463(7281):662-5. doi: 10.1038/nature08739. Epub 2010 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali (DiSTeBA), University of Salento, 73100 Lecce, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20062045" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Benzoquinones/pharmacology ; Blotting, Southern ; DNA Transposable Elements/*genetics ; Drosophila Proteins/genetics/*metabolism ; Drosophila melanogaster/*genetics/*metabolism ; Female ; Gene Silencing/drug effects ; Genetic Variation/*genetics ; Genotype ; HSP90 Heat-Shock Proteins/genetics/*metabolism ; Heat-Shock Proteins/genetics/*metabolism ; Homozygote ; Lactams, Macrocyclic/pharmacology ; Male ; Molecular Sequence Data ; Mutagenesis/*genetics ; Mutant Proteins/genetics/metabolism ; Mutation ; Phenotype ; Protein Kinases/genetics ; RNA, Small Interfering/genetics/metabolism ; Transcription, Genetic/drug effects
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    A new DAF-16 isoform regulates longevity (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-09
    Description: The insulin/IGF-1 signalling (IIS) pathway has diverse roles from metabolism to longevity. In Caenorhabditis elegans, the single forkhead box O (FOXO) homologue, DAF-16, functions as the major target of the IIS pathway. One of two isoforms, DAF-16a, is known to regulate longevity, stress response and dauer diapause. However, it remains unclear how DAF-16 achieves its specificity in regulating these various biological processes. Here we identify a new isoform, DAF-16d/f, as an important isoform regulating longevity. We show that DAF-16 isoforms functionally cooperate to modulate IIS-mediated processes through differential tissue enrichment, preferential modulation by upstream kinases, and regulating distinct and overlapping target genes. Promoter-swapping experiments show both the promoter and the coding region of DAF-16 are important for its function. Importantly, in mammals, four FOXO genes have overlapping and different functions, and in C. elegans, a single FOXO/DAF-16 uses distinct isoforms to fine-tune the IIS-mediated processes in the context of a whole organism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109862/" 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/PMC3109862/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Eun-Soo -- Narasimhan, Sri Devi -- Yen, Kelvin -- Tissenbaum, Heidi A -- AG025891/AG/NIA NIH HHS/ -- AG03123/AG/NIA NIH HHS/ -- R01 AG025891/AG/NIA NIH HHS/ -- R01 AG025891-07/AG/NIA NIH HHS/ -- R01 AG031237/AG/NIA NIH HHS/ -- R01 AG031237-02/AG/NIA NIH HHS/ -- England -- Nature. 2010 Jul 22;466(7305):498-502. doi: 10.1038/nature09184. Epub 2010 Jul 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613724" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/enzymology/genetics/metabolism/*physiology ; Caenorhabditis elegans Proteins/chemistry/genetics/*metabolism ; Forkhead Transcription Factors ; Gene Expression Regulation ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; Longevity/genetics/*physiology ; Mutation ; Organ Specificity ; Phosphatidylinositol 3-Kinases/metabolism ; Promoter Regions, Genetic ; Protein Isoforms/chemistry/genetics/metabolism ; Proto-Oncogene Proteins c-akt/genetics/metabolism ; Signal Transduction ; Superoxide Dismutase/genetics ; Transcription Factors/chemistry/genetics/*metabolism ; Transgenes
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    The scaffold protein Ste5 directly controls a switch-like mating decision in yeast (2010)
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    Publication Date: 2010-04-20
    Description: Evolution has resulted in numerous innovations that allow organisms to increase their fitness by choosing particular mating partners, including secondary sexual characteristics, behavioural patterns, chemical attractants and corresponding sensory mechanisms. The haploid yeast Saccharomyces cerevisiae selects mating partners by interpreting the concentration gradient of pheromone secreted by potential mates through a network of mitogen-activated protein kinase (MAPK) signalling proteins. The mating decision in yeast is an all-or-none, or switch-like, response that allows cells to filter weak pheromone signals, thus avoiding inappropriate commitment to mating by responding only at or above critical concentrations when a mate is sufficiently close. The molecular mechanisms that govern the switch-like mating decision are poorly understood. Here we show that the switching mechanism arises from competition between the MAPK Fus3 and a phosphatase Ptc1 for control of the phosphorylation state of four sites on the scaffold protein Ste5. This competition results in a switch-like dissociation of Fus3 from Ste5 that is necessary to generate the switch-like mating response. Thus, the decision to mate is made at an early stage in the pheromone pathway and occurs rapidly, perhaps to prevent the loss of the potential mate to competitors. We argue that the architecture of the Fus3-Ste5-Ptc1 circuit generates a novel ultrasensitivity mechanism, which is robust to variations in the concentrations of these proteins. This robustness helps assure that mating can occur despite stochastic or genetic variation between individuals. The role of Ste5 as a direct modulator of a cell-fate decision expands the functional repertoire of scaffold proteins beyond providing specificity and efficiency of information processing. Similar mechanisms may govern cellular decisions in higher organisms and be disrupted in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malleshaiah, Mohan K -- Shahrezaei, Vahid -- Swain, Peter S -- Michnick, Stephen W -- MOP-GMX-152556/Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 May 6;465(7294):101-5. doi: 10.1038/nature08946. Epub 2010 Apr 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departement de Biochimie, Bio-Informatique et Genomique Universite de Montreal, C.P. 6128, Succursale centre-ville Montreal, Quebec H3C 3J7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20400943" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Models, Biological ; Mutation ; Phosphorylation ; Protein Binding ; Protein Phosphatase 2/metabolism ; Reproduction/physiology ; Saccharomyces cerevisiae/genetics/metabolism/*physiology ; Saccharomyces cerevisiae Proteins/genetics/*metabolism
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    Analysis of Drosophila TRPA1 reveals an ancient origin for human chemical nociception (2010)
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    Publication Date: 2010-03-20
    Description: Chemical nociception, the detection of tissue-damaging chemicals, is important for animal survival and causes human pain and inflammation, but its evolutionary origins are largely unknown. Reactive electrophiles are a class of noxious compounds humans find pungent and irritating, such as allyl isothiocyanate (in wasabi) and acrolein (in cigarette smoke). Diverse animals, from insects to humans, find reactive electrophiles aversive, but whether this reflects conservation of an ancient sensory modality has been unclear. Here we identify the molecular basis of reactive electrophile detection in flies. We demonstrate that Drosophila TRPA1 (Transient receptor potential A1), the Drosophila melanogaster orthologue of the human irritant sensor, acts in gustatory chemosensors to inhibit reactive electrophile ingestion. We show that fly and mosquito TRPA1 orthologues are molecular sensors of electrophiles, using a mechanism conserved with vertebrate TRPA1s. Phylogenetic analyses indicate that invertebrate and vertebrate TRPA1s share a common ancestor that possessed critical characteristics required for electrophile detection. These findings support emergence of TRPA1-based electrophile detection in a common bilaterian ancestor, with widespread conservation throughout vertebrate and invertebrate evolution. Such conservation contrasts with the evolutionary divergence of canonical olfactory and gustatory receptors and may relate to electrophile toxicity. We propose that human pain perception relies on an ancient chemical sensor conserved across approximately 500 million years of animal evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845738/" 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/PMC2845738/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Kyeongjin -- Pulver, Stefan R -- Panzano, Vincent C -- Chang, Elaine C -- Griffith, Leslie C -- Theobald, Douglas L -- Garrity, Paul A -- P01 NS044232/NS/NINDS NIH HHS/ -- P01 NS044232-060002/NS/NINDS NIH HHS/ -- P01 NS044232-070002/NS/NINDS NIH HHS/ -- P01 NS044232-080002/NS/NINDS NIH HHS/ -- R01 MH067284/MH/NIMH NIH HHS/ -- R01 MH067284-06A1/MH/NIMH NIH HHS/ -- R01 MH067284-07/MH/NIMH NIH HHS/ -- R21 MH080206/MH/NIMH NIH HHS/ -- R21 MH080206-01/MH/NIMH NIH HHS/ -- R21 MH080206-02/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Mar 25;464(7288):597-600. doi: 10.1038/nature08848. Epub 2010 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Behavioral Genomics, Waltham, Massachusetts 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237474" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Conserved Sequence ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/classification/genetics/*metabolism ; Evolution, Molecular ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Molecular Sequence Data ; Mutation ; Phylogeny ; Sensory Receptor Cells/*metabolism ; TRPC Cation Channels/chemistry/genetics/*metabolism ; Taste Perception/physiology
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    Polyreactivity increases the apparent affinity of anti-HIV antibodies by heteroligation (2010)
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    Details
    Publication Date: 2010-10-01
    Description: During immune responses, antibodies are selected for their ability to bind to foreign antigens with high affinity, in part by their ability to undergo homotypic bivalent binding. However, this type of binding is not always possible. For example, the small number of gp140 glycoprotein spikes displayed on the surface of the human immunodeficiency virus (HIV) disfavours homotypic bivalent antibody binding. Here we show that during the human antibody response to HIV, somatic mutations that increase antibody affinity also increase breadth and neutralizing potency. Surprisingly, the responding naive and memory B cells produce polyreactive antibodies, which are capable of bivalent heteroligation between one high-affinity anti-HIV-gp140 combining site and a second low-affinity site on another molecular structure on HIV. Although cross-reactivity to self-antigens or polyreactivity is strongly selected against during B-cell development, it is a common serologic feature of certain infections in humans, including HIV, Epstein-Barr virus and hepatitis C virus. Seventy-five per cent of the 134 monoclonal anti-HIV-gp140 antibodies cloned from six patients with high titres of neutralizing antibodies are polyreactive. Despite the low affinity of the polyreactive combining site, heteroligation demonstrably increases the apparent affinity of polyreactive antibodies to HIV.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699875/" 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/PMC3699875/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mouquet, Hugo -- Scheid, Johannes F -- Zoller, Markus J -- Krogsgaard, Michelle -- Ott, Rene G -- Shukair, Shetha -- Artyomov, Maxim N -- Pietzsch, John -- Connors, Mark -- Pereyra, Florencia -- Walker, Bruce D -- Ho, David D -- Wilson, Patrick C -- Seaman, Michael S -- Eisen, Herman N -- Chakraborty, Arup K -- Hope, Thomas J -- Ravetch, Jeffrey V -- Wardemann, Hedda -- Nussenzweig, Michel C -- 1 P01 AI081677/AI/NIAID NIH HHS/ -- P01 AI081677/AI/NIAID NIH HHS/ -- R01 AI047770/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Sep 30;467(7315):591-5. doi: 10.1038/nature09385.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20882016" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal/immunology ; Antibodies, Neutralizing/immunology ; Antibody Affinity/genetics/*immunology ; Antigen-Antibody Reactions/genetics/*immunology ; Cardiolipins/immunology ; Cell Line, Tumor ; Cross Reactions/genetics/immunology ; Enzyme-Linked Immunosorbent Assay ; Epitopes/*chemistry/*immunology ; HIV Antibodies/genetics/*immunology ; HIV Antigens/chemistry/*immunology ; HIV-1/chemistry/*immunology ; Humans ; Immunoglobulin Fab Fragments/genetics/immunology ; Immunoglobulin Heavy Chains/genetics/immunology ; Mutation ; Surface Plasmon Resonance ; env Gene Products, Human Immunodeficiency Virus/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Genetics. The DNA damage road map (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Friedman, Nir -- Schuldiner, Maya -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1327-8. doi: 10.1126/science.1199862.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Computer Science and Engineering, The Hebrew University of Jerusalem, Jerusalem, Israel. nir@cs.huji.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127235" target="_blank"〉PubMed〈/a〉
    Keywords: *DNA Damage ; DNA Repair/*genetics ; *Epistasis, Genetic ; *Gene Regulatory Networks ; Genes, Fungal ; Methyl Methanesulfonate/pharmacology ; Mutagens/pharmacology ; Mutation ; Protein Interaction Mapping ; Saccharomyces cerevisiae/*genetics/metabolism ; Saccharomyces cerevisiae Proteins/*metabolism ; Signal Transduction ; Transcription Factors/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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    Human genetics. Affordable 'exomes' fill gaps in a catalog of rare diseases (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):903. doi: 10.1126/science.330.6006.903.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071642" target="_blank"〉PubMed〈/a〉
    Keywords: *Exons ; Genetic Diseases, Inborn/*genetics ; *Genome, Human ; Humans ; Mutation ; Rare Diseases/*genetics ; *Sequence Analysis, DNA
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    Spiroindolones, a potent compound class for the treatment of malaria (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-09-04
    Description: Recent reports of increased tolerance to artemisinin derivatives--the most recently adopted class of antimalarials--have prompted a need for new treatments. The spirotetrahydro-beta-carbolines, or spiroindolones, are potent drugs that kill the blood stages of Plasmodium falciparum and Plasmodium vivax clinical isolates at low nanomolar concentration. Spiroindolones rapidly inhibit protein synthesis in P. falciparum, an effect that is ablated in parasites bearing nonsynonymous mutations in the gene encoding the P-type cation-transporter ATPase4 (PfATP4). The optimized spiroindolone NITD609 shows pharmacokinetic properties compatible with once-daily oral dosing and has single-dose efficacy in a rodent malaria model.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050001/" 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/PMC3050001/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rottmann, Matthias -- McNamara, Case -- Yeung, Bryan K S -- Lee, Marcus C S -- Zou, Bin -- Russell, Bruce -- Seitz, Patrick -- Plouffe, David M -- Dharia, Neekesh V -- Tan, Jocelyn -- Cohen, Steven B -- Spencer, Kathryn R -- Gonzalez-Paez, Gonzalo E -- Lakshminarayana, Suresh B -- Goh, Anne -- Suwanarusk, Rossarin -- Jegla, Timothy -- Schmitt, Esther K -- Beck, Hans-Peter -- Brun, Reto -- Nosten, Francois -- Renia, Laurent -- Dartois, Veronique -- Keller, Thomas H -- Fidock, David A -- Winzeler, Elizabeth A -- Diagana, Thierry T -- R01 AI059472/AI/NIAID NIH HHS/ -- R01 AI059472-04/AI/NIAID NIH HHS/ -- R01 AI059472-05/AI/NIAID NIH HHS/ -- R01AI059472/AI/NIAID NIH HHS/ -- WT078285/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Sep 3;329(5996):1175-80. doi: 10.1126/science.1193225.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Tropical and Public Health Institute, Parasite Chemotherapy, CH-4002 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813948" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/antagonists & inhibitors/chemistry/genetics/metabolism ; Animals ; Antimalarials/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Cell Line ; Drug Discovery ; Drug Resistance ; Erythrocytes/parasitology ; Female ; Genes, Protozoan ; Humans ; Indoles/administration & dosage/chemistry/pharmacokinetics/*pharmacology ; Malaria/*drug therapy/parasitology ; Male ; Mice ; Models, Molecular ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Mutation ; Parasitic Sensitivity Tests ; Plasmodium berghei/*drug effects ; Plasmodium falciparum/*drug effects/genetics/growth & development ; Plasmodium vivax/*drug effects/growth & development ; Protein Synthesis Inhibitors/administration & ; dosage/chemistry/pharmacokinetics/pharmacology ; Protozoan Proteins/biosynthesis/chemistry/genetics/metabolism ; Rats ; Rats, Wistar ; Spiro Compounds/administration & dosage/chemistry/pharmacokinetics/*pharmacology
    Print ISSN: 0036-8075
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    Granulosa cell ligand NPPC and its receptor NPR2 maintain meiotic arrest in mouse oocytes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: Granulosa cells of mammalian Graafian follicles maintain oocytes in meiotic arrest, which prevents their precocious maturation. We show that mouse mural granulosa cells, which line the follicle wall, express natriuretic peptide precursor type C (Nppc) messenger RNA (mRNA), whereas cumulus cells surrounding oocytes express mRNA of the NPPC receptor NPR2, a guanylyl cyclase. NPPC increased cGMP levels in cumulus cells and oocytes and inhibited meiotic resumption in vitro. Meiotic arrest was not sustained in most Graafian follicles of Nppc or Npr2 mutant mice, and meiosis resumed precociously. Oocyte-derived paracrine factors promoted cumulus cell expression of Npr2 mRNA. Therefore, the granulosa cell ligand NPPC and its receptor NPR2 in cumulus cells prevent precocious meiotic maturation, which is critical for maturation and ovulation synchrony and for normal female fertility.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056542/" 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/PMC3056542/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Meijia -- Su, You-Qiang -- Sugiura, Koji -- Xia, Guoliang -- Eppig, John J -- HD21970/HD/NICHD NIH HHS/ -- HD23839/HD/NICHD NIH HHS/ -- R01 HD023839/HD/NICHD NIH HHS/ -- R01 HD023839-22/HD/NICHD NIH HHS/ -- R37 HD021970/HD/NICHD NIH HHS/ -- R37 HD021970-25/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):366-9. doi: 10.1126/science.1193573.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory for Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, People's Republic of China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947764" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cumulus Cells/*metabolism ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; Female ; Granulosa Cells/*metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Ligands ; *Meiosis ; Mice ; Models, Biological ; Mutation ; Natriuretic Peptide, C-Type/genetics/*metabolism ; Oocytes/*physiology ; Ovarian Follicle/cytology ; Protein Precursors/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Receptors, Atrial Natriuretic Factor/genetics/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Toward extracting all phylogenetic information from matrices of evolutionary distances (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-13
    Description: The matrix of evolutionary distances is a model-based statistic, derived from molecular sequences, summarizing the pairwise phylogenetic relations between a collection of species. Phylogenetic tree reconstruction methods relying on this matrix are relatively fast and thus widely used in molecular systematics. However, because of their intrinsic reliance on summary statistics, distance-matrix methods are assumed to be less accurate than likelihood-based approaches. In this paper, pairwise sequence comparisons are shown to be more powerful than previously hypothesized. A statistical analysis of certain distance-based techniques indicates that their data requirement for large evolutionary trees essentially matches the conjectured performance of maximum likelihood methods--challenging the idea that summary statistics lead to suboptimal analyses. On the basis of a connection between ancestral state reconstruction and distance averaging, the critical role played by the covariances of the distance matrix is identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roch, Sebastien -- New York, N.Y. -- Science. 2010 Mar 12;327(5971):1376-9. doi: 10.1126/science.1182300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Mathematics, University of California at Los Angeles, 520 Portola Plaza, Los Angeles, CA 90095, USA. roch@math.ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20223986" target="_blank"〉PubMed〈/a〉
    Keywords: *Algorithms ; Base Sequence ; Biological Evolution ; *Computational Biology ; DNA/genetics ; *Evolution, Molecular ; Likelihood Functions ; Models, Statistical ; Mutation ; *Phylogeny ; Sequence Alignment ; Software
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    Direct exchange of electrons within aggregates of an evolved syntrophic coculture of anaerobic bacteria (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-04
    Description: Microbial consortia that cooperatively exchange electrons play a key role in the anaerobic processing of organic matter. Interspecies hydrogen transfer is a well-documented strategy for electron exchange in dispersed laboratory cultures, but cooperative partners in natural environments often form multispecies aggregates. We found that laboratory evolution of a coculture of Geobacter metallireducens and Geobacter sulfurreducens metabolizing ethanol favored the formation of aggregates that were electrically conductive. Sequencing aggregate DNA revealed selection for a mutation that enhances the production of a c-type cytochrome involved in extracellular electron transfer and accelerates the formation of aggregates. Aggregate formation was also much faster in mutants that were deficient in interspecies hydrogen transfer, further suggesting direct interspecies electron transfer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Summers, Zarath M -- Fogarty, Heather E -- Leang, Ching -- Franks, Ashley E -- Malvankar, Nikhil S -- Lovley, Derek R -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1413-5. doi: 10.1126/science.1196526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127257" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis ; Bacterial Proteins/chemistry/genetics/*metabolism ; Biological Evolution ; Culture Media ; Cytochrome c Group/chemistry/genetics/*metabolism ; Electron Transport ; *Electrons ; Ethanol/metabolism ; Fimbriae Proteins/genetics/metabolism ; Geobacter/genetics/growth & development/*metabolism ; Hydrogen/metabolism ; Microbial Consortia/*physiology ; *Microbial Interactions ; Mutation ; Oxidation-Reduction ; Selection, 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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    Arabidopsis type I metacaspases control cell death (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-26
    Description: Metacaspases are distant relatives of animal caspases found in protozoa, fungi, and plants. Limited experimental data exist defining their function(s), despite their discovery by homology modeling a decade ago. We demonstrated that two type I metacaspases, AtMC1 and AtMC2, antagonistically control programmed cell death in Arabidopsis. AtMC1 is a positive regulator of cell death and requires conserved caspase-like putative catalytic residues for its function. AtMC2 negatively regulates cell death. This function is independent of the putative catalytic residues. Manipulation of the Arabidopsis type I metacaspase regulatory module can nearly eliminate the hypersensitive cell death response (HR) activated by plant intracellular immune receptors. This does not lead to enhanced pathogen proliferation, decoupling HR from restriction of pathogen growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coll, Nuria S -- Vercammen, Dominique -- Smidler, Andrea -- Clover, Charles -- Van Breusegem, Frank -- Dangl, Jeffery L -- Epple, Petra -- R01 GM057171/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1393-7. doi: 10.1126/science.1194980. Epub 2010 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, 108 Coker Hall, University of North Carolina (UNC), CB 3280, Chapel Hill, NC 27599-3280, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21097903" target="_blank"〉PubMed〈/a〉
    Keywords: *Apoptosis ; Arabidopsis/*enzymology/immunology/microbiology/*physiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Caspases/chemistry/genetics/*metabolism ; DNA-Binding Proteins/chemistry/genetics/metabolism ; Mutation ; Oomycetes/physiology ; Plant Diseases/immunology/microbiology ; Plants, Genetically Modified ; Pseudomonas syringae/physiology ; Transcription Factors/chemistry/genetics/metabolism ; Zinc Fingers
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    Cell biology. Irremediable complexity? (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, Michael W -- Lukes, Julius -- Archibald, John M -- Keeling, Patrick J -- Doolittle, W Ford -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):920-1. doi: 10.1126/science.1198594.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071654" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Cell Physiological Processes ; Genome, Mitochondrial ; Introns ; Mitochondria/genetics/physiology ; Models, Biological ; Mutation ; RNA Editing ; RNA Splicing ; Ribosomes/physiology ; Selection, Genetic ; Spliceosomes/genetics/physiology
    Print ISSN: 0036-8075
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    Human Evolution. Tracing evolution's recent fingerprints (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):740-2. doi: 10.1126/science.329.5993.740.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705825" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; *Biological Evolution ; Gene Frequency ; Genetic Techniques ; Genetics, Population/*methods ; *Genome, Human ; Haplotypes ; Humans ; Models, Genetic ; Multifactorial Inheritance ; Mutation ; *Polymorphism, Single Nucleotide ; *Selection, Genetic
    Print ISSN: 0036-8075
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    Medicine. Prion strain mutation and selection (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collinge, John -- MC_U123192748/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 May 28;328(5982):1111-2. doi: 10.1126/science.1190815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Prion Unit, Institute of Neurology, University College London, London WC1N3BG, UK. j.collinge@prion.ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20508117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Deer ; Evolution, Molecular ; Mutation ; Polymorphism, Genetic ; PrPC Proteins/*chemistry/genetics ; PrPSc Proteins/*chemistry/genetics/pathogenicity ; Protein Conformation ; Protein Folding ; Selection, Genetic ; Species Specificity ; *Wasting Disease, Chronic/transmission
    Print ISSN: 0036-8075
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    Paleogenetics. Close encounters of the prehistoric kind (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2010 May 7;328(5979):680-4. doi: 10.1126/science.328.5979.680.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448163" target="_blank"〉PubMed〈/a〉
    Keywords: African Continental Ancestry Group/genetics ; Animals ; Asian Continental Ancestry Group/genetics ; European Continental Ancestry Group/genetics ; Extinction, Biological ; Female ; *Fossils ; Gene Flow ; *Genome ; *Genome, Human ; Hominidae/anatomy & histology/*genetics/physiology ; Humans ; Mutation ; Pan troglodytes/genetics ; Polymorphism, Single Nucleotide ; *Sequence Analysis, DNA
    Print ISSN: 0036-8075
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    Dysregulated humoral immunity to nontyphoidal Salmonella in HIV-infected African adults (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-24
    Description: Nontyphoidal Salmonellae are a major cause of life-threatening bacteremia among HIV-infected individuals. Although cell-mediated immunity controls intracellular infection, antibodies protect against Salmonella bacteremia. We report that high-titer antibodies specific for Salmonella lipopolysaccharide (LPS) are associated with a lack of Salmonella-killing in HIV-infected African adults. Killing was restored by genetically shortening LPS from the target Salmonella or removing LPS-specific antibodies from serum. Complement-mediated killing of Salmonella by healthy serum is shown to be induced specifically by antibodies against outer membrane proteins. This killing is lost when excess antibody against Salmonella LPS is added. Thus, our study indicates that impaired immunity against nontyphoidal Salmonella bacteremia in HIV infection results from excess inhibitory antibodies against Salmonella LPS, whereas serum killing of Salmonella is induced by antibodies against outer membrane proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772309/" 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/PMC3772309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacLennan, Calman A -- Gilchrist, James J -- Gordon, Melita A -- Cunningham, Adam F -- Cobbold, Mark -- Goodall, Margaret -- Kingsley, Robert A -- van Oosterhout, Joep J G -- Msefula, Chisomo L -- Mandala, Wilson L -- Leyton, Denisse L -- Marshall, Jennifer L -- Gondwe, Esther N -- Bobat, Saeeda -- Lopez-Macias, Constantino -- Doffinger, Rainer -- Henderson, Ian R -- Zijlstra, Eduard E -- Dougan, Gordon -- Drayson, Mark T -- MacLennan, Ian C M -- Molyneux, Malcolm E -- 067321/Wellcome Trust/United Kingdom -- BB/F022778/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0701275/Medical Research Council/United Kingdom -- G108/574/Medical Research Council/United Kingdom -- G8402371/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Apr 23;328(5977):508-12. doi: 10.1126/science.1180346.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Centre for Immune Regulation and Clinical Immunology Service, Institute of Biomedical Research, School of Immunity and Infection, University of Birmingham, Birmingham, UK. c.maclennan@bham.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20413503" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS-Related Opportunistic Infections/immunology ; Adult ; Animals ; Antibodies, Bacterial/blood/*immunology ; Antibodies, Blocking/blood/*immunology ; Bacteremia/immunology ; Bacterial Outer Membrane Proteins/*immunology ; Complement Activation ; Disease Susceptibility ; HIV Infections/complications/*immunology ; Humans ; Immunoglobulin G/blood/immunology ; Lipopolysaccharides/blood/*immunology ; Malawi ; Mice ; Mutation ; O Antigens/*immunology ; Salmonella Infections/*immunology ; Salmonella typhimurium/genetics/*immunology
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    Bacteria use type IV pili to walk upright and detach from surfaces (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: Bacterial biofilms are structured multicellular communities involved in a broad range of infections. Knowing how free-swimming bacteria adapt their motility mechanisms near surfaces is crucial for understanding the transition between planktonic and biofilm phenotypes. By translating microscopy movies into searchable databases of bacterial behavior, we identified fundamental type IV pili-driven mechanisms for Pseudomonas aeruginosa surface motility involved in distinct foraging strategies. Bacteria stood upright and "walked" with trajectories optimized for two-dimensional surface exploration. Vertical orientation facilitated surface detachment and could influence biofilm morphology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibiansky, Maxsim L -- Conrad, Jacinta C -- Jin, Fan -- Gordon, Vernita D -- Motto, Dominick A -- Mathewson, Margie A -- Stopka, Wiktor G -- Zelasko, Daria C -- Shrout, Joshua D -- Wong, Gerard C L -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):197. doi: 10.1126/science.1194238.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, California Nano Systems Institute,University of California, Los Angeles, CA 90024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929769" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Bacterial Adhesion ; *Biofilms ; Cell Division ; Databases, Factual ; Fimbriae, Bacterial/*physiology ; Microscopy ; Motion Pictures as Topic ; Movement ; Mutation ; Pseudomonas aeruginosa/genetics/*physiology/ultrastructure
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    Long noncoding RNA as modular scaffold of histone modification complexes (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-10
    Description: Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967777/" 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/PMC2967777/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Miao-Chih -- Manor, Ohad -- Wan, Yue -- Mosammaparast, Nima -- Wang, Jordon K -- Lan, Fei -- Shi, Yang -- Segal, Eran -- Chang, Howard Y -- R01 CA118750/CA/NCI NIH HHS/ -- R01 CA119176/CA/NCI NIH HHS/ -- R01 CA119176-05/CA/NCI NIH HHS/ -- R01-CA118487/CA/NCI NIH HHS/ -- R01-HG004361/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):689-93. doi: 10.1126/science.1192002. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616235" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Carrier Proteins/metabolism ; Cell Line ; Cells, Cultured ; Chromatin/*metabolism ; Chromatin Immunoprecipitation ; Co-Repressor Proteins ; DNA-Binding Proteins/*metabolism ; HeLa Cells ; Histone Demethylases/*metabolism ; Histones/*metabolism ; Humans ; Methylation ; Mutation ; Nerve Tissue Proteins/metabolism ; Nuclear Proteins/metabolism ; Nucleic Acid Conformation ; Polycomb Repressive Complex 2 ; Polycomb-Group Proteins ; Promoter Regions, Genetic ; Protein Binding ; RNA Interference ; RNA, Untranslated/chemistry/*metabolism ; Repressor Proteins/*metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    The fusogen EFF-1 controls sculpting of mechanosensory dendrites (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-05-08
    Description: The mechanisms controlling the formation and maintenance of neuronal trees are poorly understood. We examined the dynamic development of two arborized mechanoreceptor neurons (PVDs) required for reception of strong mechanical stimuli in Caenorhabditis elegans. The PVDs elaborated dendritic trees comprising structural units we call "menorahs." We studied how the number, structure, and function of menorahs were maintained. EFF-1, an essential protein mediating cell fusion, acted autonomously in the PVDs to trim developing menorahs. eff-1 mutants displayed hyperbranched, disorganized menorahs. Overexpression of EFF-1 in the PVD reduced branching. Neuronal pruning appeared to involve EFF-1-dependent branch retraction and neurite-neurite autofusion. Thus, EFF-1 activities may act as a quality control mechanism during the sculpting of dendritic trees.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057141/" 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/PMC3057141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oren-Suissa, Meital -- Hall, David H -- Treinin, Millet -- Shemer, Gidi -- Podbilewicz, Benjamin -- R24 RR012596/RR/NCRR NIH HHS/ -- R24 RR012596-14/RR/NCRR NIH HHS/ -- RR12596/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1285-8. doi: 10.1126/science.1189095. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Technion-Israel Institute of Technology, Haifa 32000, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans/growth & development/*metabolism/*ultrastructure ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Dendrites/metabolism/physiology/*ultrastructure ; Imaging, Three-Dimensional ; Mechanoreceptors/*metabolism/*ultrastructure ; Membrane Glycoproteins/genetics/*metabolism ; Microscopy, Confocal ; Models, Neurological ; Mutant Proteins/metabolism ; Mutation ; Neurites/physiology/*ultrastructure ; Temperature
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    Medicine. Sickle cell disease at 100 years (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orkin, Stuart H -- Higgs, Douglas R -- R01 HL032259/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jul 16;329(5989):291-2. doi: 10.1126/science.1194035.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Hospital Boston and Dana-Farber Cancer Institute, Harvard Medical School, Howard Hughes Medical Institute, Boston, MA 02115, USA. stuart_orkin@dfci.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647458" target="_blank"〉PubMed〈/a〉
    Keywords: *Anemia, Sickle Cell/blood/genetics/therapy ; Carrier Proteins/genetics ; Fetal Hemoglobin/analysis/biosynthesis/*genetics ; GTP-Binding Proteins/genetics ; Gene Expression Regulation ; Genes, myb ; Hemoglobin, Sickle/chemistry/genetics ; Humans ; Multigene Family ; Mutation ; Nuclear Proteins/genetics ; beta-Globins/genetics ; gamma-Globins/genetics
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    Reprogramming cellular behavior with RNA controllers responsive to endogenous proteins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-27
    Description: Synthetic genetic devices that interface with native cellular pathways can be used to change natural networks to implement new forms of control and behavior. The engineering of gene networks has been limited by an inability to interface with native components. We describe a class of RNA control devices that overcome these limitations by coupling increased abundance of particular proteins to targeted gene expression events through the regulation of alternative RNA splicing. We engineered RNA devices that detect signaling through the nuclear factor kappaB and Wnt signaling pathways in human cells and rewire these pathways to produce new behaviors, thereby linking disease markers to noninvasive sensing and reprogrammed cellular fates. Our work provides a genetic platform that can build programmable sensing-actuation devices enabling autonomous control over cellular behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171693/" 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/PMC3171693/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Culler, Stephanie J -- Hoff, Kevin G -- Smolke, Christina D -- RC1 GM091298/GM/NIGMS NIH HHS/ -- RC1 GM091298-01/GM/NIGMS NIH HHS/ -- RC1 GM091298-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1251-5. doi: 10.1126/science.1192128.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Chemistry and Chemical Engineering, 1200 East California Boulevard, MC 210-41, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109673" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Apoptosis ; Aptamers, Nucleotide/chemistry/genetics/*metabolism ; Capsid Proteins/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Exons ; Ganciclovir/pharmacology ; *Gene Expression Regulation ; Gene Regulatory Networks ; *Genetic Engineering ; Green Fluorescent Proteins/genetics ; Humans ; Introns ; Ligands ; Mutation ; NF-kappa B p50 Subunit/genetics/metabolism ; Protein Binding ; Signal Transduction ; Survival of Motor Neuron 1 Protein/genetics ; Transcription Factor RelA/genetics/metabolism ; Transfection ; Wnt Proteins/metabolism ; beta Catenin/genetics/metabolism
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    Conserved molecular components for pollen tube reception and fungal invasion (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-13
    Description: During sexual reproduction in flowering plants such as Arabidopsis, a tip-growing pollen tube (PT) is guided to the synergid cells of the female gametophyte, where it bursts and releases the two sperm. Here we show that PT reception and powdery mildew (PM) infection, which involves communication between a tip-growing hypha and a plant epidermal cell, share molecular components. NORTIA (NTA), a member of the MLO family originally discovered in the context of PM resistance, and FERONIA (FER), a receptor-like kinase, both control PT reception in synergids. Homozygous fer mutants also display PM resistance, revealing a new function for FER and suggesting that conserved components, such as FER and distinct MLO proteins, are involved in both PT reception and PM infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessler, Sharon A -- Shimosato-Asano, Hiroko -- Keinath, Nana F -- Wuest, Samuel E -- Ingram, Gwyneth -- Panstruga, Ralph -- Grossniklaus, Ueli -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):968-71. doi: 10.1126/science.1195211.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Plant Biology and Zurich Basel Plant Science Center, University of Zurich, Zollikerstrasse 107, CH-8008 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071669" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*microbiology/*physiology ; Arabidopsis Proteins/chemistry/genetics/*metabolism ; Ascomycota/*physiology ; Calmodulin-Binding Proteins/chemistry/genetics/*metabolism ; Fertility ; Flowers/genetics ; Gene Expression Profiling ; Genes, Plant ; Hyphae/physiology ; Mutation ; Phosphotransferases/genetics/*metabolism ; Plant Diseases/*microbiology ; Plant Leaves/microbiology ; Pollen/genetics ; Pollen Tube/*physiology ; Pollination ; Recombinant Fusion Proteins/metabolism ; Seeds/growth & development ; Signal Transduction ; Spores, Fungal/physiology ; Transformation, Genetic
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    Planar cell polarity acts through septins to control collective cell movement and ciliogenesis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-07-31
    Description: The planar cell polarity (PCP) signaling pathway governs collective cell movements during vertebrate embryogenesis, and certain PCP proteins are also implicated in the assembly of cilia. The septins are cytoskeletal proteins controlling behaviors such as cell division and migration. Here, we identified control of septin localization by the PCP protein Fritz as a crucial control point for both collective cell movement and ciliogenesis in Xenopus embryos. We also linked mutations in human Fritz to Bardet-Biedl and Meckel-Gruber syndromes, a notable link given that other genes mutated in these syndromes also influence collective cell movement and ciliogenesis. These findings shed light on the mechanisms by which fundamental cellular machinery, such as the cytoskeleton, is regulated during embryonic development and human disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509789/" 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/PMC3509789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Su Kyoung -- Shindo, Asako -- Park, Tae Joo -- Oh, Edwin C -- Ghosh, Srimoyee -- Gray, Ryan S -- Lewis, Richard A -- Johnson, Colin A -- Attie-Bittach, Tania -- Katsanis, Nicholas -- Wallingford, John B -- G0700073/Medical Research Council/United Kingdom -- P50 MH094268/MH/NIMH NIH HHS/ -- R01 DK072301/DK/NIDDK NIH HHS/ -- R01 DK075972/DK/NIDDK NIH HHS/ -- R01 GM074104/GM/NIGMS NIH HHS/ -- R01 HD042601/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 10;329(5997):1337-40. doi: 10.1126/science.1191184. Epub 2010 Jul 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Molecular Cell and Developmental Biology and Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671153" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/genetics ; Animals ; Bardet-Biedl Syndrome/*genetics ; Cell Membrane/metabolism/ultrastructure ; *Cell Movement ; *Cell Polarity ; Cell Shape ; Cilia/*metabolism/ultrastructure ; Cytoskeletal Proteins/genetics/*metabolism ; Cytoskeleton/*metabolism/ultrastructure ; Embryo, Nonmammalian/cytology/physiology ; Embryonic Development ; Female ; GTP-Binding Proteins/genetics/*metabolism ; Gastrula/cytology ; Genetic Association Studies ; Glycoproteins/genetics/*metabolism ; Hedgehog Proteins/metabolism ; Humans ; Morphogenesis ; Mutant Proteins/metabolism ; Mutation ; Septins ; Syndrome ; Xenopus Proteins/genetics/*metabolism ; Xenopus laevis
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    On getting there from here (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: Studies on a variety of interesting biological problems, ranging from circadian rhythm to cancer cell growth to longevity, have begun to give evidence that the physiological state of cells and tissues reflects both the cell's regulatory systems and its state of intermediary metabolism. It is appreciated that the regulatory state of a cell or tissue, as driven by transcription factors and signaling pathways, can impose itself upon the dynamics of metabolic state. It follows that the reciprocal must also be the case, that metabolic state will feed back to impose itself on regulatory state. An appreciation and understanding of this reciprocity may be required to crack open problems in biological research that have heretofore been insoluble.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKnight, Steven L -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1338-9. doi: 10.1126/science.1199908.〈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. steven.mcknight@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127243" target="_blank"〉PubMed〈/a〉
    Keywords: Enzymes/genetics/*metabolism ; Gene Expression Regulation, Neoplastic ; Glycolysis ; Humans ; *Metabolism ; Mutation ; Neoplasm Proteins/genetics/*metabolism ; Neoplasms/genetics/*metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Tumor Cells, Cultured
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    Plant science. Saving the bilayer (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Browse, John -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):185-6. doi: 10.1126/science.1196737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Biological Chemistry, Washington State University, Pullman, WA 99164, USA. jab@wsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929764" target="_blank"〉PubMed〈/a〉
    Keywords: *Acclimatization ; Arabidopsis/genetics/metabolism/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Chloroplasts/chemistry/*metabolism/ultrastructure ; *Freezing ; Galactolipids/chemistry/metabolism ; Gene Expression Regulation, Plant ; Genes, Plant ; Intracellular Membranes/chemistry/*metabolism/ultrastructure ; Lipid Bilayers/chemistry/*metabolism ; Membrane Lipids/chemistry/metabolism ; Mutation ; beta-Glucosidase/genetics/*metabolism
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    A nodule-specific protein secretory pathway required for nitrogen-fixing symbiosis (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-02-27
    Description: The nitrogen-fixing symbiosis between Sinorhizobium meliloti and its leguminous host plant Medicago truncatula occurs in a specialized root organ called the nodule. Bacteria that are released into plant cells are surrounded by a unique plant membrane compartment termed a symbiosome. We found that in the symbiosis-defective dnf1 mutant of M. truncatula, bacteroid and symbiosome development are blocked. We identified the DNF1 gene as encoding a subunit of a signal peptidase complex that is highly expressed in nodules. By analyzing data from whole-genome expression analysis, we propose that correct symbiosome development in M. truncatula requires the orderly secretion of protein constituents through coordinated up-regulation of a nodule-specific pathway exemplified by DNF1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Dong -- Griffitts, Joel -- Starker, Colby -- Fedorova, Elena -- Limpens, Erik -- Ivanov, Sergey -- Bisseling, Ton -- Long, Sharon -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1126-9. doi: 10.1126/science.1184096.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185723" target="_blank"〉PubMed〈/a〉
    Keywords: Endoplasmic Reticulum/metabolism ; Gene Expression ; Gene Expression Profiling ; Genes, Plant ; Medicago truncatula/genetics/*metabolism/*microbiology ; Membrane Proteins/genetics/*metabolism ; Mutation ; *Nitrogen Fixation ; Plant Proteins/genetics/metabolism ; Plants, Genetically Modified ; Protein Subunits/genetics/metabolism ; Root Nodules, Plant/metabolism/*microbiology ; *Secretory Pathway ; Serine Endopeptidases/genetics/*metabolism ; Sinorhizobium meliloti/*physiology ; *Symbiosis
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    Histone H3 Thr-3 phosphorylation by Haspin positions Aurora B at centromeres in mitosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Aurora B is a component of the chromosomal passenger complex (CPC) required for correct spindle-kinetochore attachments during chromosome segregation and for cytokinesis. The chromatin factors that recruit the CPC to centromeres are unknown, however. Here we show that phosphorylation of histone H3 threonine 3 (H3T3ph) by Haspin is necessary for CPC accumulation at centromeres and that the CPC subunit Survivin binds directly to H3T3ph. A nonbinding Survivin-D70A/D71A mutant does not support centromeric CPC concentration, and both Haspin depletion and Survivin-D70A/D71A mutation diminish centromere localization of the kinesin MCAK and the mitotic checkpoint response to taxol. Survivin-D70A/D71A mutation and microinjection of H3T3ph-specific antibody both compromise centromeric Aurora B functions but do not prevent cytokinesis. Therefore, H3T3ph generated by Haspin positions the CPC at centromeres to regulate selected targets of Aurora B during mitosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967368/" 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/PMC2967368/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fangwei -- Dai, Jun -- Daum, John R -- Niedzialkowska, Ewa -- Banerjee, Budhaditya -- Stukenberg, P Todd -- Gorbsky, Gary J -- Higgins, Jonathan M G -- R01 GM050412/GM/NIGMS NIH HHS/ -- R01 GM050412-16/GM/NIGMS NIH HHS/ -- R01 GM063045/GM/NIGMS NIH HHS/ -- R01 GM063045-10/GM/NIGMS NIH HHS/ -- R01 GM074210/GM/NIGMS NIH HHS/ -- R01 GM074210-04/GM/NIGMS NIH HHS/ -- R01-GM050412/GM/NIGMS NIH HHS/ -- R01-GM063045/GM/NIGMS NIH HHS/ -- R01-GM074210/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):231-5. doi: 10.1126/science.1189435. Epub 2010 Aug 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School, Smith Building, 1 Jimmy Fund Way, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aurora Kinase B ; Aurora Kinases ; Cell Cycle Proteins/metabolism ; Cell Line ; Cell Line, Tumor ; Centromere/*metabolism ; Chromatin/*metabolism ; HeLa Cells ; Histones/*metabolism ; Humans ; Inhibitor of Apoptosis Proteins ; Intracellular Signaling Peptides and Proteins/genetics/*metabolism ; Kinesin/metabolism ; Kinetochores/metabolism ; Microtubule-Associated Proteins/chemistry/genetics/*metabolism ; *Mitosis ; Mutation ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; RNA Interference ; Recombinant Proteins/metabolism ; Spindle Apparatus/metabolism ; Swine ; Threonine/metabolism ; Xenopus
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    Acetylation of metabolic enzymes coordinates carbon source utilization and metabolic flux (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: Lysine acetylation regulates many eukaryotic cellular processes, but its function in prokaryotes is largely unknown. We demonstrated that central metabolism enzymes in Salmonella were acetylated extensively and differentially in response to different carbon sources, concomitantly with changes in cell growth and metabolic flux. The relative activities of key enzymes controlling the direction of glycolysis versus gluconeogenesis and the branching between citrate cycle and glyoxylate bypass were all regulated by acetylation. This modulation is mainly controlled by a pair of lysine acetyltransferase and deacetylase, whose expressions are coordinated with growth status. Reversible acetylation of metabolic enzymes ensure that cells respond environmental changes via promptly sensing cellular energy status and flexibly altering reaction rates or directions. It represents a metabolic regulatory mechanism conserved from bacteria to mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4183141/" 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/PMC4183141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Qijun -- Zhang, Yakun -- Yang, Chen -- Xiong, Hui -- Lin, Yan -- Yao, Jun -- Li, Hong -- Xie, Lu -- Zhao, Wei -- Yao, Yufeng -- Ning, Zhi-Bin -- Zeng, Rong -- Xiong, Yue -- Guan, Kun-Liang -- Zhao, Shimin -- Zhao, Guo-Ping -- R01 CA068377/CA/NCI NIH HHS/ -- R01 CA163834/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):1004-7. doi: 10.1126/science.1179687.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Genetic Engineering, Department of Microbiology, School of Life Sciences and Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167787" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/chemistry/genetics/metabolism ; Amino Acid Sequence ; Bacterial Proteins/*metabolism ; Citric Acid/*metabolism ; Energy Metabolism ; Enzymes/*metabolism ; Gene Expression Regulation, Bacterial ; *Gluconeogenesis ; Glucose/*metabolism ; Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism ; *Glycolysis ; Group III Histone Deacetylases/genetics/metabolism ; Isocitrate Lyase/metabolism ; Lysine/metabolism ; Metabolic Networks and Pathways ; Multienzyme Complexes/metabolism ; Mutation ; Protein Processing, Post-Translational ; Protein-Serine-Threonine Kinases/metabolism ; Recombinant Proteins/metabolism ; Salmonella typhimurium/enzymology/genetics/growth & development/*metabolism
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    Evolution. RNA GPS (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kluwe, Christien -- Ellington, Andrew D -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):330-1. doi: 10.1126/science.1197667.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of Texas at Austin, Austin, TX 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947753" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Directed Molecular Evolution ; *Evolution, Molecular ; Genotype ; Mutation ; RNA/metabolism ; RNA, Catalytic/chemistry/*genetics/*metabolism ; Selection, Genetic ; Sequence Analysis, RNA
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    Peptidomimetic antibiotics target outer-membrane biogenesis in Pseudomonas aeruginosa (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-02-20
    Description: Antibiotics with new mechanisms of action are urgently required to combat the growing health threat posed by resistant pathogenic microorganisms. We synthesized a family of peptidomimetic antibiotics based on the antimicrobial peptide protegrin I. Several rounds of optimization gave a lead compound that was active in the nanomolar range against Gram-negative Pseudomonas spp., but was largely inactive against other Gram-negative and Gram-positive bacteria. Biochemical and genetic studies showed that the peptidomimetics had a non-membrane-lytic mechanism of action and identified a homolog of the beta-barrel protein LptD (Imp/OstA), which functions in outer-membrane biogenesis, as a cellular target. The peptidomimetic showed potent antimicrobial activity in a mouse septicemia infection model. Drug-resistant strains of Pseudomonas are a serious health problem, so this family of antibiotics may have important therapeutic applications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srinivas, Nityakalyani -- Jetter, Peter -- Ueberbacher, Bernhard J -- Werneburg, Martina -- Zerbe, Katja -- Steinmann, Jessica -- Van der Meijden, Benjamin -- Bernardini, Francesca -- Lederer, Alexander -- Dias, Ricardo L A -- Misson, Pauline E -- Henze, Heiko -- Zumbrunn, Jurg -- Gombert, Frank O -- Obrecht, Daniel -- Hunziker, Peter -- Schauer, Stefan -- Ziegler, Urs -- Kach, Andres -- Eberl, Leo -- Riedel, Kathrin -- DeMarco, Steven J -- Robinson, John A -- New York, N.Y. -- Science. 2010 Feb 19;327(5968):1010-3. doi: 10.1126/science.1182749.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chemistry Department, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20167788" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/chemical synthesis/metabolism/*pharmacology ; Antimicrobial Cationic Peptides/chemistry ; Bacterial Outer Membrane Proteins/chemistry/genetics/*metabolism ; Cell Membrane/*metabolism ; Drug Design ; Drug Resistance, Bacterial/genetics ; Genes, Bacterial ; Lipopolysaccharides/metabolism ; Mice ; Microbial Sensitivity Tests ; Molecular Mimicry ; Mutation ; Peptide Library ; Peptides/chemical synthesis/chemistry/metabolism/*pharmacology ; Protein Structure, Tertiary ; Pseudomonas Infections/drug therapy/microbiology ; Pseudomonas aeruginosa/*drug effects/growth & ; development/*metabolism/ultrastructure ; Sepsis/drug therapy/microbiology
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    Freezing tolerance in plants requires lipid remodeling at the outer chloroplast membrane (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-28
    Description: Plants show complex adaptations to freezing that prevent cell damage caused by cellular dehydration. Lipid remodeling of cell membranes during dehydration is one critical mechanism countering loss of membrane integrity and cell death. SENSITIVE TO FREEZING 2 (SFR2), a gene essential for freezing tolerance in Arabidopsis, encodes a galactolipid remodeling enzyme of the outer chloroplast envelope membrane. SFR2 processively transfers galactosyl residues from the abundant monogalactolipid to different galactolipid acceptors, forming oligogalactolipids and diacylglycerol, which is further converted to triacylglycerol. The combined activity of SFR2 and triacylglycerol-biosynthetic enzymes leads to the removal of monogalactolipids from the envelope membrane, changing the ratio of bilayer- to non-bilayer-forming membrane lipids. This SFR2-based mechanism compensates for changes in organelle volume and stabilizes membranes during freezing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moellering, Eric R -- Muthan, Bagyalakshmi -- Benning, Christoph -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):226-8. doi: 10.1126/science.1191803. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798281" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization ; Arabidopsis/genetics/metabolism/*physiology ; Arabidopsis Proteins/genetics/*metabolism ; Chloroplasts/chemistry/*metabolism/ultrastructure ; Diglycerides/metabolism ; *Freezing ; Galactolipids/chemistry/metabolism ; Gene Expression Regulation, Plant ; Genes, Plant ; Intracellular Membranes/chemistry/*metabolism ; Lipid Bilayers/chemistry/*metabolism ; Membrane Lipids/chemistry/*metabolism ; Mutation ; Triglycerides/metabolism ; beta-Glucosidase/genetics/*metabolism
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    Olfactory plasticity is regulated by pheromonal signaling in Caenorhabditis elegans (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-12
    Description: Population density-dependent dispersal is a well-characterized strategy of animal behavior in which dispersal rate increases when population density is higher. Caenorhabditis elegans shows positive chemotaxis to a set of odorants, but the chemotaxis switches from attraction to dispersal after prolonged exposure to the odorants. We show here that this plasticity of olfactory behavior is dependent on population density and that this regulation is mediated by pheromonal signaling. We show that a peptide, suppressor of NEP-2 (SNET-1), negatively regulates olfactory plasticity and that its expression is down-regulated by the pheromone. NEP-2, a homolog of the extracellular peptidase neprilysin, antagonizes SNET-1, and this function is essential for olfactory plasticity. These results suggest that population density information is transmitted through the external pheromone and endogenous peptide signaling to modulate chemotactic behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021133/" 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/PMC3021133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamada, Koji -- Hirotsu, Takaaki -- Matsuki, Masahiro -- Butcher, Rebecca A -- Tomioka, Masahiro -- Ishihara, Takeshi -- Clardy, Jon -- Kunitomo, Hirofumi -- Iino, Yuichi -- CA24487/CA/NCI NIH HHS/ -- GM087533/GM/NIGMS NIH HHS/ -- K99 GM087533/GM/NIGMS NIH HHS/ -- K99 GM087533-01/GM/NIGMS NIH HHS/ -- R00 GM087533/GM/NIGMS NIH HHS/ -- R00 GM087533-03/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1647-50. doi: 10.1126/science.1192020.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929849" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; *Chemotaxis ; Down-Regulation ; Gene Expression Regulation ; Mutation ; Neprilysin/genetics/*metabolism ; Neurites/metabolism ; Neurons/metabolism ; Odors ; Olfactory Pathways/cytology/physiology ; Pheromones/*metabolism ; Population Density ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; *Signal Transduction ; Smell/physiology
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    Two histone marks establish the inner centromere and chromosome bi-orientation (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-12
    Description: For proper partitioning of chromosomes in mitosis, the chromosomal passenger complex (CPC) including Aurora B and survivin must be localized at the center of paired kinetochores, at the site called the inner centromere. It is largely unknown what defines the inner centromere and how the CPC is targeted to this site. Here, we show that the phosphorylation of histone H3-threonine 3 (H3-pT3) mediated by Haspin cooperates with Bub1-mediated histone 2A-serine 121 (H2A-S121) phosphorylation in targeting the CPC to the inner centromere in fission yeast and human cells. H3-pT3 promotes nucleosome binding of survivin, whereas phosphorylated H2A-S121 facilitates the binding of shugoshin, the centromeric CPC adaptor. Haspin colocalizes with cohesin by associating with Pds5, whereas Bub1 localizes at kinetochores. Thus, the inner centromere is defined by intersection of two histone kinases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamagishi, Yuya -- Honda, Takashi -- Tanno, Yuji -- Watanabe, Yoshinori -- New York, N.Y. -- Science. 2010 Oct 8;330(6001):239-43. doi: 10.1126/science.1194498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromosome Dynamics, Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929775" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Aurora Kinase B ; Aurora Kinases ; Cell Cycle Proteins/metabolism ; Centromere/*metabolism ; Chromatin/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation ; Chromosomes, Fungal/*physiology ; Chromosomes, Human/*physiology ; HeLa Cells ; Heterochromatin/metabolism ; Histones/*metabolism ; Humans ; Inhibitor of Apoptosis Proteins ; Intracellular Signaling Peptides and Proteins/chemistry/genetics/*metabolism ; Kinetochores/metabolism ; Microtubule-Associated Proteins/metabolism ; Mitosis ; Molecular Sequence Data ; Mutation ; Nucleosomes/metabolism ; Phosphorylation ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; Schizosaccharomyces/*genetics/metabolism ; Schizosaccharomyces pombe Proteins/genetics/*metabolism ; Serine/metabolism ; Threonine/metabolism
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    Evolution. Variation catches a ride (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Charlesworth, Brian -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):326-7. doi: 10.1126/science.1197700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3JT, UK. brian.charlesworth@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics ; Chromosomes/*genetics ; Crosses, Genetic ; *Evolution, Molecular ; Gene Expression ; Gene Frequency ; Genes, Helminth ; Genetic Variation ; Mutation ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Recombination, Genetic ; Selection, Genetic
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    Evolution. Trees, fast and accurate (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allman, Elizabeth S -- Rhodes, John A -- New York, N.Y. -- Science. 2010 Mar 12;327(5971):1334-5. doi: 10.1126/science.1187797.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Mathematics and Statistics, University of Alaska, P.O. Box 756660, Fairbanks, AK 99775, USA. e.allman@alaska.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20223973" target="_blank"〉PubMed〈/a〉
    Keywords: *Algorithms ; Base Sequence ; Biological Evolution ; Computational Biology ; DNA/genetics ; *Evolution, Molecular ; Likelihood Functions ; Models, Statistical ; Mutation ; *Phylogeny ; Software
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    Asymmetrical distribution of the second messenger c-di-GMP upon bacterial cell division (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-05
    Description: The bacterial second messenger cyclic diguanosine monophosphate (c-di-GMP) regulates cellular motility and the synthesis of organelles and molecules that promote adhesion to a variety of biological and nonbiological surfaces. These properties likely require tight spatial and temporal regulation of c-di-GMP concentration. We have developed genetically encoded fluorescence resonance energy transfer (FRET)-based biosensors to monitor c-di-GMP concentrations within single bacterial cells by microscopy. Fluctuations of c-di-GMP were visualized in diverse Gram-negative bacterial species and observed to be cell cycle dependent. Asymmetrical distribution of c-di-GMP in the progeny correlated with the time of cell division and polarization for Caulobacter crescentus and Pseudomonas aeruginosa. Thus, asymmetrical distribution of c-di-GMP was observed as part of cell division, which may indicate an important regulatory step in extracellular organelle biosynthesis or function.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3906730/" 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/PMC3906730/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Christen, Matthias -- Kulasekara, Hemantha D -- Christen, Beat -- Kulasekara, Bridget R -- Hoffman, Lucas R -- Miller, Samuel I -- 1R21NS067579-01/NS/NINDS NIH HHS/ -- K02 HL105543/HL/NHLBI NIH HHS/ -- K08 AI066251/AI/NIAID NIH HHS/ -- K08AI066251/AI/NIAID NIH HHS/ -- R01 HL098084/HL/NHLBI NIH HHS/ -- U54AI057141/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1295-7. doi: 10.1126/science.1188658.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20522779" target="_blank"〉PubMed〈/a〉
    Keywords: Biosensing Techniques ; Caulobacter crescentus/*cytology/genetics/*metabolism ; *Cell Division ; Cyclic GMP/*analogs & derivatives/metabolism ; Escherichia coli Proteins ; Fluorescence Resonance Energy Transfer ; Klebsiella pneumoniae/cytology/metabolism ; Microscopy ; Movement ; Mutation ; Phosphorus-Oxygen Lyases/genetics/metabolism ; Pseudomonas aeruginosa/*cytology/genetics/*metabolism ; Salmonella typhimurium/cytology/metabolism ; *Second Messenger Systems
    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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    Analysis of genetic inheritance in a family quartet by whole-genome sequencing (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-12
    Description: We analyzed the whole-genome sequences of a family of four, consisting of two siblings and their parents. Family-based sequencing allowed us to delineate recombination sites precisely, identify 70% of the sequencing errors (resulting in 〉 99.999% accuracy), and identify very rare single-nucleotide polymorphisms. We also directly estimated a human intergeneration mutation rate of approximately 1.1 x 10(-8) per position per haploid genome. Both offspring in this family have two recessive disorders: Miller syndrome, for which the gene was concurrently identified, and primary ciliary dyskinesia, for which causative genes have been previously identified. Family-based genome analysis enabled us to narrow the candidate genes for both of these Mendelian disorders to only four. Our results demonstrate the value of complete genome sequencing in families.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037280/" 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/PMC3037280/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roach, Jared C -- Glusman, Gustavo -- Smit, Arian F A -- Huff, Chad D -- Hubley, Robert -- Shannon, Paul T -- Rowen, Lee -- Pant, Krishna P -- Goodman, Nathan -- Bamshad, Michael -- Shendure, Jay -- Drmanac, Radoje -- Jorde, Lynn B -- Hood, Leroy -- Galas, David J -- GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547/GM/NIGMS NIH HHS/ -- P50 GM076547-05/GM/NIGMS NIH HHS/ -- R01 HG002939/HG/NHGRI NIH HHS/ -- R01 HG002939-08/HG/NHGRI NIH HHS/ -- R01GM081083/GM/NIGMS NIH HHS/ -- R01HD048895/HD/NICHD NIH HHS/ -- R01HL094976/HL/NHLBI NIH HHS/ -- RC2HG005608/HG/NHGRI NIH HHS/ -- RZ1HG004749/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 30;328(5978):636-9. doi: 10.1126/science.1186802. Epub 2010 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Systems Biology, Seattle, WA 98103, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220176" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Multiple/*genetics ; Algorithms ; Alleles ; Axonemal Dyneins/genetics ; Ciliary Motility Disorders/*genetics ; Crossing Over, Genetic ; Female ; Genes, Dominant ; Genes, Recessive ; Genetic Association Studies ; *Genome, Human ; Humans ; *Inheritance Patterns ; Limb Deformities, Congenital/genetics ; Male ; Mandibulofacial Dysostosis/genetics ; Mutation ; *Nuclear Family ; Oxidoreductases Acting on CH-CH Group Donors/genetics ; Pedigree ; Polymorphism, Single Nucleotide ; *Sequence Analysis, DNA ; Syndrome
    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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    Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2 (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-09
    Description: TET2 is a close relative of TET1, an enzyme that converts 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in DNA. The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies. Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML). We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity. Bone marrow samples from patients with TET2 mutations displayed uniformly low levels of 5hmC in genomic DNA compared to bone marrow samples from healthy controls. Moreover, small hairpin RNA (shRNA)-mediated depletion of Tet2 in mouse haematopoietic precursors skewed their differentiation towards monocyte/macrophage lineages in culture. There was no significant difference in DNA methylation between bone marrow samples from patients with high 5hmC versus healthy controls, but samples from patients with low 5hmC showed hypomethylation relative to controls at the majority of differentially methylated CpG sites. Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis. Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003755/" 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/PMC3003755/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ko, Myunggon -- Huang, Yun -- Jankowska, Anna M -- Pape, Utz J -- Tahiliani, Mamta -- Bandukwala, Hozefa S -- An, Jungeun -- Lamperti, Edward D -- Koh, Kian Peng -- Ganetzky, Rebecca -- Liu, X Shirley -- Aravind, L -- Agarwal, Suneet -- Maciejewski, Jaroslaw P -- Rao, Anjana -- 1 UL1 RR 025758-02/RR/NCRR NIH HHS/ -- K08 HL089150/HL/NHLBI NIH HHS/ -- K24 HL077522/HL/NHLBI NIH HHS/ -- R01 AI044432/AI/NIAID NIH HHS/ -- R01 AI044432-12/AI/NIAID NIH HHS/ -- R01 AI044432-13/AI/NIAID NIH HHS/ -- R01 AI44432/AI/NIAID NIH HHS/ -- R01 HD065812/HD/NICHD NIH HHS/ -- R01 HG4069/HG/NHGRI NIH HHS/ -- R01 HL098522/HL/NHLBI NIH HHS/ -- R37 CA042471/CA/NCI NIH HHS/ -- R37 CA042471-20/CA/NCI NIH HHS/ -- R37 CA042471-21/CA/NCI NIH HHS/ -- RC1 DA028422/DA/NIDA NIH HHS/ -- RC1 DA028422-01/DA/NIDA NIH HHS/ -- RC1 DA028422-02/DA/NIDA NIH HHS/ -- UL1 RR025758/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Dec 9;468(7325):839-43. doi: 10.1038/nature09586.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Immune Disease Institute and Program in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21057493" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/*metabolism ; Animals ; Biocatalysis ; Cell Differentiation ; Cell Line ; CpG Islands/genetics ; DNA Methylation ; DNA, Neoplasm/chemistry/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Humans ; *Hydroxylation ; Leukemia, Myeloid, Acute/genetics/*metabolism/pathology ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/genetics/*metabolism ; Mutation ; Myelodysplastic Syndromes/genetics/*metabolism/pathology ; Proto-Oncogene Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Loren Rieseberg profile. No garden-variety biologist (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Kathryn -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1499.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645825" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; *Biological Evolution ; Desert Climate ; Ecosystem ; Environment ; Genes, Plant ; Helianthus/*genetics/growth & development/physiology ; History, 20th Century ; History, 21st Century ; *Hybridization, Genetic ; Mutation ; Phenotype ; Sodium Chloride/pharmacology ; United States
    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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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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  • 89
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    Aging and genome maintenance: lessons from the mouse? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasty, Paul -- Campisi, Judith -- Hoeijmakers, Jan -- van Steeg, Harry -- Vijg, Jan -- AG17242/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1355-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA. hastye@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610296" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging/genetics ; Aging, Premature/*genetics ; Animals ; Apoptosis ; Cell Aging ; *DNA Damage ; DNA Helicases/genetics/metabolism ; *DNA Repair/genetics ; Exodeoxyribonucleases ; *Genome ; Genome, Human ; Humans ; Longevity/genetics ; Mice ; Mutation ; Reactive Oxygen Species/metabolism ; RecQ Helicases ; Syndrome ; Telomere/physiology ; Transcription, 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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    Molecular pathways of neurodegeneration in Parkinson's disease (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-11-01
    Description: Parkinson's disease (PD) is a complex disorder with many different causes, yet they may intersect in common pathways, raising the possibility that neuroprotective agents may have broad applicability in the treatment of PD. Current evidence suggests that mitochondrial complex I inhibition may be the central cause of sporadic PD and that derangements in complex I cause alpha-synuclein aggregation, which contributes to the demise of dopamine neurons. Accumulation and aggregation of alpha-synuclein may further contribute to the death of dopamine neurons through impairments in protein handling and detoxification. Dysfunction of parkin (a ubiquitin E3 ligase) and DJ-1 could contribute to these deficits. Strategies aimed at restoring complex I activity, reducing oxidative stress and alpha-synuclein aggregation, and enhancing protein degradation may hold particular promise as powerful neuroprotective agents in the treatment of PD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawson, Ted M -- Dawson, Valina L -- NS38377/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):819-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. tdawson@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593166" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Brain/*metabolism/pathology ; Cysteine Endopeptidases/metabolism ; Dopamine/metabolism ; Electron Transport Complex I/antagonists & inhibitors/genetics/*metabolism ; Humans ; Mitochondria/enzymology ; Multienzyme Complexes/metabolism ; Mutation ; Nerve Degeneration ; Nerve Tissue Proteins/chemistry/genetics/metabolism ; Neurons/*metabolism/pathology ; Oxidative Stress ; Parkinson Disease/*etiology/genetics/metabolism/pathology ; Parkinsonian Disorders/genetics/metabolism/pathology ; Proteasome Endopeptidase Complex ; Synucleins ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/genetics/metabolism ; alpha-Synuclein
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    Ecology. New count of old whales adds up to big debate (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lubick, Naomi -- New York, N.Y. -- Science. 2003 Jul 25;301(5632):451.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12881542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlantic Ocean ; Conservation of Natural Resources ; DNA, Mitochondrial/genetics ; *Ecosystem ; Female ; Genetic Variation ; Genetics, Population ; Male ; Mutation ; Population Density ; Population Dynamics ; Time Factors ; *Whales/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Chromosomal instability and tumors promoted by DNA hypomethylation (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eden, Amir -- Gaudet, Francois -- Waghmare, Alpana -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/*genetics/physiology ; DNA (Cytosine-5-)-Methyltransferase/genetics/metabolism ; *DNA Methylation ; Fibroblasts/metabolism ; Genes, Neurofibromatosis 1 ; Genes, p53 ; Humans ; *Loss of Heterozygosity ; Mice ; Mutation ; Neoplasms/genetics ; Recombination, Genetic ; Sarcoma/*genetics ; Soft Tissue Neoplasms/*genetics
    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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    Biomedicine. Ataxin-1 regulators in the spotlight (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-07-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintz, Nathaniel -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):59-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Rockefeller University, New York, NY 10021, USA. heintz@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843383" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins ; Amino Acid Substitution ; Animals ; Ataxin-1 ; Ataxins ; Cell Nucleus/metabolism ; Disease Progression ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Nuclear Proteins/*chemistry/genetics/*metabolism ; Peptides ; Phosphorylation ; *Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Purkinje Cells/metabolism/ultrastructure ; Signal Transduction ; Spinocerebellar Ataxias/etiology/genetics/pathology/*physiopathology ; *Trinucleotide Repeat Expansion ; Tyrosine 3-Monooxygenase/*metabolism
    Print ISSN: 0036-8075
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    Genetic control of surface curvature (2003)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2003-03-01
    Description: Although curvature of biological surfaces has been considered from mathematical and biophysical perspectives, its molecular and developmental basis is unclear. We have studied the cin mutant of Antirrhinum, which has crinkly rather than flat leaves. Leaves of cin display excess growth in marginal regions, resulting in a gradual introduction of negative curvature during development. This reflects a change in the shape and the progression of a cell-cycle arrest front moving from the leaf tip toward the base. CIN encodes a TCP protein and is expressed downstream of the arrest front. We propose that CIN promotes zero curvature (flatness) by making cells more sensitive to an arrest signal, particularly in marginal regions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nath, Utpal -- Crawford, Brian C W -- Carpenter, Rosemary -- Coen, Enrico -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1404-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, John Innes Centre, Norwich Research Park, Norwich, NR4 7UH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610308" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antirrhinum/cytology/*genetics/*growth & development/metabolism ; Base Sequence ; Cell Cycle ; Cell Differentiation ; Cell Division ; Cell Size ; Cyclin D3 ; Cyclins/genetics/metabolism ; Gene Deletion ; *Gene Expression Regulation, Plant ; *Genes, Plant ; Histones/genetics/metabolism ; Molecular Sequence Data ; Mutagenesis, Insertional ; Mutation ; Plant Leaves/anatomy & histology/cytology/*growth & development/metabolism ; Plant Proteins/chemistry/genetics/metabolism ; Surface Properties ; Transcription Factors/chemistry/genetics/*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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    Lamin a truncation in Hutchinson-Gilford progeria (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Sandre-Giovannoli, Annachiara -- Bernard, Rafaelle -- Cau, Pierre -- Navarro, Claire -- Amiel, Jeanne -- Boccaccio, Irene -- Lyonnet, Stanislas -- Stewart, Colin L -- Munnich, Arnold -- Le Merrer, Martine -- Levy, Nicolas -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2055. Epub 2003 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inserm U491: Genetique Medicale et Developpement, Faculte de Medecine Timone, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702809" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Nucleus/ultrastructure ; Child ; Exons ; Female ; Humans ; Lamin Type A/analysis/*chemistry/*genetics ; Lymphocytes/chemistry/ultrastructure ; Mutation ; Polymorphism, Genetic ; Progeria/blood/*genetics ; RNA Splicing ; RNA, Messenger/genetics ; Sequence Deletion ; Transcription, Genetic
    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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  • 96
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    The origins of genome complexity (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-25
    Description: Complete genomic sequences from diverse phylogenetic lineages reveal notable increases in genome complexity from prokaryotes to multicellular eukaryotes. The changes include gradual increases in gene number, resulting from the retention of duplicate genes, and more abrupt increases in the abundance of spliceosomal introns and mobile genetic elements. We argue that many of these modifications emerged passively in response to the long-term population-size reductions that accompanied increases in organism size. According to this model, much of the restructuring of eukaryotic genomes was initiated by nonadaptive processes, and this in turn provided novel substrates for the secondary evolution of phenotypic complexity by natural selection. The enormous long-term effective population sizes of prokaryotes may impose a substantial barrier to the evolution of complex genomes and morphologies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, Michael -- Conery, John S -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1401-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Indiana University, Bloomington, IN 47405, USA. mlynch@bio.indiana.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631042" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Bacteria/genetics ; Body Constitution ; Eukaryota/genetics ; *Evolution, Molecular ; Fungi/genetics ; Gene Duplication ; Gene Silencing ; Genetic Drift ; Genetic Variation ; *Genome ; Humans ; Interspersed Repetitive Sequences ; Introns ; Invertebrates/genetics ; Mutation ; *Phylogeny ; Plants/genetics ; Population Density ; Recombination, Genetic ; Selection, Genetic ; Spliceosomes ; Vertebrates/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Evolution. Climb every mountain? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elena, Santiago F -- Sanjuan, Rafael -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2074-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Biologia Molecular y Celular de Plantas, Consejo Superior de Investigaciones Cientificas-UPV, 46022 Valencia, Spain. sfelena@ibmcp.upv.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14684807" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; *Biological Evolution ; Chlamydomonas/physiology ; Darkness ; *Ecosystem ; Environment ; *Genetic Variation ; Genotype ; Light ; Mutation ; Phenotype ; Pseudomonas fluorescens/genetics/*physiology ; RNA Viruses/physiology ; Selection, 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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  • 98
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    Loss of a callose synthase results in salicylic acid-dependent disease resistance (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-08-16
    Description: Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nishimura, Marc T -- Stein, Monica -- Hou, Bi-Huei -- Vogel, John P -- Edwards, Herb -- Somerville, Shauna C -- New York, N.Y. -- Science. 2003 Aug 15;301(5635):969-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Biology, Carnegie Institution, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12920300" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Arabidopsis/cytology/genetics/*metabolism/*microbiology ; Ascomycota/*physiology ; Cell Death ; Gene Expression Profiling ; Gene Expression Regulation, Plant ; Genes, Plant ; Glucans/metabolism ; Glucosyltransferases/*genetics/metabolism ; *Membrane Proteins ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; *Plant Diseases ; Plant Leaves/metabolism ; Salicylic Acid/*metabolism ; *Schizosaccharomyces pombe Proteins ; 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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  • 99
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    Plant Biology. Hormones and the green revolution (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: The success of the green revolution largely resulted from the creation of dwarf cultivars of wheat and rice, which had much higher yields than conventional crops. Characterization of these dwarf cultivars showed that the mutant genes were involved in either the synthesis or signaling of gibberellin, a plant growth hormone. In his Perspective, Salamini highlights new work (Multani et al.) that identifies the cause of dwarfism in agronomically important varieties of maize and sorghum. In these cases, dwarfism is caused by defective transport of another growth hormone called auxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salamini, Francesco -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):71-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Breeding Research, 50829 Koln, Germany. salamini@mpiz-koeln.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526071" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Arabidopsis/genetics/growth & development/metabolism ; Arabidopsis Proteins/genetics/metabolism ; Biological Transport ; Breeding ; *Genes, Plant ; Genetic Engineering ; Genome, Plant ; Indoleacetic Acids/*metabolism ; Light ; Mutation ; P-Glycoproteins/genetics/metabolism ; Phenotype ; Plant Proteins/genetics/metabolism ; Poaceae/genetics/growth & development/*metabolism ; Quantitative Trait Loci ; Zea mays/genetics/growth & development/*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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  • 100
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    Cell biology. Microtubule asymmetry (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gundersen, Gregg G -- Bretscher, Anthony -- New York, N.Y. -- Science. 2003 Jun 27;300(5628):2040-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology and Department of Pathology, Columbia University, New York, NY 10032, USA. ggg1@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12829769" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; CDC28 Protein Kinase, S cerevisiae/*metabolism ; Cell Cycle Proteins/metabolism ; Cell Division ; Cell Polarity ; Cyclins/metabolism ; Microtubule Proteins/metabolism ; Microtubule-Organizing Center/*metabolism/ultrastructure ; Microtubules/*metabolism/ultrastructure ; Models, Biological ; Mutation ; Myosin Heavy Chains/metabolism ; Myosin Type V/metabolism ; Nuclear Proteins/*metabolism ; Phosphorylation ; Protein Transport ; Saccharomyces cerevisiae/cytology/metabolism/ultrastructure ; Saccharomyces cerevisiae Proteins/metabolism ; Spindle Apparatus/*physiology/ultrastructure
    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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