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  • 1
    Publication Date: 2013-04-13
    Description: Successful integration of advanced semiconductor devices with biological systems will accelerate basic scientific discoveries and their translation into clinical technologies. In neuroscience generally, and in optogenetics in particular, the ability to insert light sources, detectors, sensors, and other components into precise locations of the deep brain yields versatile and important capabilities. Here, we introduce an injectable class of cellular-scale optoelectronics that offers such features, with examples of unmatched operational modes in optogenetics, including completely wireless and programmed complex behavioral control over freely moving animals. The ability of these ultrathin, mechanically compliant, biocompatible devices to afford minimally invasive operation in the soft tissues of the mammalian brain foreshadow applications in other organ systems, with potential for broad utility in biomedical science and engineering.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769938/" 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/PMC3769938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Tae-il -- McCall, Jordan G -- Jung, Yei Hwan -- Huang, Xian -- Siuda, Edward R -- Li, Yuhang -- Song, Jizhou -- Song, Young Min -- Pao, Hsuan An -- Kim, Rak-Hwan -- Lu, Chaofeng -- Lee, Sung Dan -- Song, Il-Sun -- Shin, Gunchul -- Al-Hasani, Ream -- Kim, Stanley -- Tan, Meng Peun -- Huang, Yonggang -- Omenetto, Fiorenzo G -- Rogers, John A -- Bruchas, Michael R -- R00 DA025182/DA/NIDA NIH HHS/ -- R00DA025182/DA/NIDA NIH HHS/ -- R01 NS081707/NS/NINDS NIH HHS/ -- R01NS081707/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Apr 12;340(6129):211-6. doi: 10.1126/science.1232437.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, Frederick Seitz Materials Research Laboratory, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23580530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Brain/*physiology ; *Brain Mapping/instrumentation/methods ; Electric Stimulation ; Electrophysiological Phenomena ; HEK293 Cells ; Humans ; Mice ; Microelectrodes ; Miniaturization ; Neurons/*physiology ; *Optogenetics ; Photic Stimulation ; *Semiconductors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-06-04
    Description: Rev-Erb-alpha and Rev-Erb-beta are nuclear receptors that regulate the expression of genes involved in the control of circadian rhythm, metabolism and inflammatory responses. Rev-Erbs function as transcriptional repressors by recruiting nuclear receptor co-repressor (NCoR)-HDAC3 complexes to Rev-Erb response elements in enhancers and promoters of target genes, but the molecular basis for cell-specific programs of repression is not known. Here we present evidence that in mouse macrophages Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage-lineage-determining factors, thereby establishing a macrophage-specific program of repression. Remarkably, the repressive functions of Rev-Erbs are associated with their ability to inhibit the transcription of enhancer-derived RNAs (eRNAs). Furthermore, targeted degradation of eRNAs at two enhancers subject to negative regulation by Rev-Erbs resulted in reduced expression of nearby messenger RNAs, suggesting a direct role of these eRNAs in enhancer function. By precisely defining eRNA start sites using a modified form of global run-on sequencing that quantifies nascent 5' ends, we show that transfer of full enhancer activity to a target promoter requires both the sequences mediating transcription-factor binding and the specific sequences encoding the eRNA transcript. These studies provide evidence for a direct role of eRNAs in contributing to enhancer functions and suggest that Rev-Erbs act to suppress gene expression at a distance by repressing eRNA transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839578/" 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/PMC3839578/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Michael T Y -- Cho, Han -- Lesch, Hanna P -- Gosselin, David -- Heinz, Sven -- Tanaka-Oishi, Yumiko -- Benner, Christopher -- Kaikkonen, Minna U -- Kim, Aneeza S -- Kosaka, Mika -- Lee, Cindy Y -- Watt, Andy -- Grossman, Tamar R -- Rosenfeld, Michael G -- Evans, Ronald M -- Glass, Christopher K -- CA014195/CA/NCI NIH HHS/ -- CA17390/CA/NCI NIH HHS/ -- CA52599/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK091183/DK/NIDDK NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- R01 CA052599/CA/NCI NIH HHS/ -- R01 CA173903/CA/NCI NIH HHS/ -- R01 DK018477/DK/NIDDK NIH HHS/ -- R01 DK091183/DK/NIDDK NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- T32 GM007198-37/GM/NIGMS NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19DK62434/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 27;498(7455):511-5. doi: 10.1038/nature12209. Epub 2013 Jun 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23728303" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Binding Sites ; Down-Regulation/*genetics ; Enhancer Elements, Genetic/*genetics ; Gene Knockdown Techniques ; Macrophages/*metabolism ; Mice ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Organ Specificity ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics/metabolism ; Response Elements/genetics ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2013-07-23
    Description: Fluorescent calcium sensors are widely used to image neural activity. Using structure-based mutagenesis and neuron-based screening, we developed a family of ultrasensitive protein calcium sensors (GCaMP6) that outperformed other sensors in cultured neurons and in zebrafish, flies and mice in vivo. In layer 2/3 pyramidal neurons of the mouse visual cortex, GCaMP6 reliably detected single action potentials in neuronal somata and orientation-tuned synaptic calcium transients in individual dendritic spines. The orientation tuning of structurally persistent spines was largely stable over timescales of weeks. Orientation tuning averaged across spine populations predicted the tuning of their parent cell. Although the somata of GABAergic neurons showed little orientation tuning, their dendrites included highly tuned dendritic segments (5-40-microm long). GCaMP6 sensors thus provide new windows into the organization and dynamics of neural circuits over multiple spatial and temporal scales.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777791/" 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/PMC3777791/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Tsai-Wen -- Wardill, Trevor J -- Sun, Yi -- Pulver, Stefan R -- Renninger, Sabine L -- Baohan, Amy -- Schreiter, Eric R -- Kerr, Rex A -- Orger, Michael B -- Jayaraman, Vivek -- Looger, Loren L -- Svoboda, Karel -- Kim, Douglas S -- T32 GM008042/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jul 18;499(7458):295-300. doi: 10.1038/nature12354.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868258" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Calcium/metabolism ; Calcium-Binding Proteins/*chemistry/genetics ; Cells, Cultured ; Dendritic Spines/metabolism ; Fluorescent Dyes/*chemistry ; GABAergic Neurons/metabolism ; Luminescent Proteins/*chemistry/genetics ; Mice ; Molecular Imaging ; Mutagenesis ; Protein Engineering ; Pyramidal Cells/metabolism/physiology ; Visual Cortex/cytology/physiology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2013-12-20
    Description: Plasmodium falciparum resistance to artemisinin derivatives in southeast Asia threatens malaria control and elimination activities worldwide. To monitor the spread of artemisinin resistance, a molecular marker is urgently needed. Here, using whole-genome sequencing of an artemisinin-resistant parasite line from Africa and clinical parasite isolates from Cambodia, we associate mutations in the PF3D7_1343700 kelch propeller domain ('K13-propeller') with artemisinin resistance in vitro and in vivo. Mutant K13-propeller alleles cluster in Cambodian provinces where resistance is prevalent, and the increasing frequency of a dominant mutant K13-propeller allele correlates with the recent spread of resistance in western Cambodia. Strong correlations between the presence of a mutant allele, in vitro parasite survival rates and in vivo parasite clearance rates indicate that K13-propeller mutations are important determinants of artemisinin resistance. K13-propeller polymorphism constitutes a useful molecular marker for large-scale surveillance efforts to contain artemisinin resistance in the Greater Mekong Subregion and prevent its global spread.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariey, Frederic -- Witkowski, Benoit -- Amaratunga, Chanaki -- Beghain, Johann -- Langlois, Anne-Claire -- Khim, Nimol -- Kim, Saorin -- Duru, Valentine -- Bouchier, Christiane -- Ma, Laurence -- Lim, Pharath -- Leang, Rithea -- Duong, Socheat -- Sreng, Sokunthea -- Suon, Seila -- Chuor, Char Meng -- Bout, Denis Mey -- Menard, Sandie -- Rogers, William O -- Genton, Blaise -- Fandeur, Thierry -- Miotto, Olivo -- Ringwald, Pascal -- Le Bras, Jacques -- Berry, Antoine -- Barale, Jean-Christophe -- Fairhurst, Rick M -- Benoit-Vical, Francoise -- Mercereau-Puijalon, Odile -- Menard, Didier -- 090770/Z/09/Z/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- G0600718/Medical Research Council/United Kingdom -- Intramural NIH HHS/ -- England -- Nature. 2014 Jan 2;505(7481):50-5. doi: 10.1038/nature12876. Epub 2013 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France [3] Institut Pasteur, Genetics and Genomics of Insect Vectors Unit, 75724 Paris Cedex 15, France (F.A.); Institut Pasteur, Functional Genetics of Infectious Diseases Unit, 75724 Paris Cedex 15, France (J.B.); Centre de Physiopathologie de Toulouse-Purpan, Institut National de la Sante et de la Recherche Medicale UMR1043, Centre National de la Recherche Scientifique UMR5282, Universite Toulouse III, 31024 Toulouse Cedex 3, France Institut Pasteur, Unite de Biologie et Genetique du Paludisme, Team Malaria Targets and Drug Development, 75724 Paris Cedex 15, France (J.-C.B.). ; Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France. ; Institut Pasteur, Plate-forme Genomique, Departement Genomes et Genetique, 75724 Paris Cedex 15, France. ; 1] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia [2] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [3] National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; SSA WHO, Drug Monitoring in Cambodia, National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; 1] Service de Parasitologie et Mycologie, Centre Hospitalier Universitaire de Toulouse, 31059 Toulouse Cedex 9, France [2] Institut Pasteur, Genetics and Genomics of Insect Vectors Unit, 75724 Paris Cedex 15, France (F.A.); Institut Pasteur, Functional Genetics of Infectious Diseases Unit, 75724 Paris Cedex 15, France (J.B.); Centre de Physiopathologie de Toulouse-Purpan, Institut National de la Sante et de la Recherche Medicale UMR1043, Centre National de la Recherche Scientifique UMR5282, Universite Toulouse III, 31024 Toulouse Cedex 3, France Institut Pasteur, Unite de Biologie et Genetique du Paludisme, Team Malaria Targets and Drug Development, 75724 Paris Cedex 15, France (J.-C.B.). ; Naval Medical Research Unit #2 Detachment, Phnom Penh, Cambodia. ; Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia. ; 1] MRC Centre for Genomics and Global Health, University of Oxford, Oxford OX3 7BN, UK [2] Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University, Bangkok 10400, Thailand [3] Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Global Malaria Program, World Health Organization, 1211 Geneva, Switzerland. ; Centre National de Reference du Paludisme, CHU Bichat-Claude Bernard, APHP, PRES Sorbonne Paris Cite, 75018 Paris, France. ; 1] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. ; 1] Centre National de la Recherche Scientifique, Laboratoire de Chimie de Coordination UPR8241, 31077 Toulouse Cedex 4, France [2] Universite de Toulouse, UPS, Institut National Polytechnique de Toulouse, 31077 Toulouse Cedex 4, France [3]. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France [3]. ; 1] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24352242" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Antimalarials/*pharmacology ; Artemisinins/*pharmacology ; Blood Cells/parasitology ; Cambodia ; Drug Resistance/drug effects/*genetics ; Genetic Markers/genetics ; Half-Life ; Humans ; Malaria, Falciparum/drug therapy/*parasitology ; Mutation/genetics ; Parasitic Sensitivity Tests ; Plasmodium falciparum/*drug effects/*genetics/growth & development/isolation & ; purification ; Polymorphism, Single Nucleotide/genetics ; Protein Structure, Tertiary/genetics ; Protozoan Proteins/chemistry/*genetics ; Time Factors
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2015-02-25
    Description: V(D)J recombination in the vertebrate immune system generates a highly diverse population of immunoglobulins and T-cell receptors by combinatorial joining of segments of coding DNA. The RAG1-RAG2 protein complex initiates this site-specific recombination by cutting DNA at specific sites flanking the coding segments. Here we report the crystal structure of the mouse RAG1-RAG2 complex at 3.2 A resolution. The 230-kilodalton RAG1-RAG2 heterotetramer is 'Y-shaped', with the amino-terminal domains of the two RAG1 chains forming an intertwined stalk. Each RAG1-RAG2 heterodimer composes one arm of the 'Y', with the active site in the middle and RAG2 at its tip. The RAG1-RAG2 structure rationalizes more than 60 mutations identified in immunodeficient patients, as well as a large body of genetic and biochemical data. The architectural similarity between RAG1 and the hairpin-forming transposases Hermes and Tn5 suggests the evolutionary conservation of these DNA rearrangements.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342785/" 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/PMC4342785/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Min-Sung -- Lapkouski, Mikalai -- Yang, Wei -- Gellert, Martin -- Z01 DK036147-01/Intramural NIH HHS/ -- Z01 DK036147-02/Intramural NIH HHS/ -- Z01 DK036167-01/Intramural NIH HHS/ -- Z01 DK036167-02/Intramural NIH HHS/ -- ZIA DK036147-03/Intramural NIH HHS/ -- ZIA DK036147-04/Intramural NIH HHS/ -- ZIA DK036147-05/Intramural NIH HHS/ -- ZIA DK036147-06/Intramural NIH HHS/ -- ZIA DK036147-07/Intramural NIH HHS/ -- ZIA DK036147-08/Intramural NIH HHS/ -- ZIA DK036167-03/Intramural NIH HHS/ -- ZIA DK036167-04/Intramural NIH HHS/ -- ZIA DK036167-05/Intramural NIH HHS/ -- ZIA DK036167-06/Intramural NIH HHS/ -- ZIA DK036167-07/Intramural NIH HHS/ -- England -- Nature. 2015 Feb 26;518(7540):507-11. doi: 10.1038/nature14174. Epub 2015 Feb 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Biology, NIDDK, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25707801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Crystallography, X-Ray ; DNA/chemistry/metabolism ; DNA-Binding Proteins/*chemistry/genetics/metabolism ; Homeodomain Proteins/*chemistry/genetics/metabolism ; Humans ; Mice ; Models, Molecular ; Mutation/genetics ; Protein Multimerization ; Protein Structure, Quaternary ; Severe Combined Immunodeficiency/genetics ; Transposases/chemistry ; VDJ Recombinases/*chemistry/metabolism ; X-Linked Combined Immunodeficiency Diseases/genetics
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2013-02-02
    Description: The conserved kinases Mps1 and Ipl1/Aurora B are critical for enabling chromosomes to attach to microtubules so that partner chromosomes will be segregated correctly from each other, but the precise roles of these kinases have been unclear. We imaged live yeast cells to elucidate the stages of chromosome-microtubule interactions and their regulation by Ipl1 and Mps1 through meiosis I. Ipl1 was found to release kinetochore-microtubule (kMT) associations after meiotic entry, liberating chromosomes to begin homologous pairing. Surprisingly, most chromosome pairs began their spindle interactions with incorrect kMT attachments. Ipl1 released these improper connections, whereas Mps1 triggered the formation of new force-generating microtubule attachments. This microtubule release and reattachment cycle could prevent catastrophic chromosome segregation errors in meiosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3604795/" 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/PMC3604795/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Regis E -- Kim, Seoyoung -- Obeso, David -- Straight, Paul D -- Winey, Mark -- Dawson, Dean S -- GM-07135/GM/NIGMS NIH HHS/ -- GM087377/GM/NIGMS NIH HHS/ -- R01 GM051312/GM/NIGMS NIH HHS/ -- R01 GM087377/GM/NIGMS NIH HHS/ -- T32 GM007135/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 1;339(6123):1071-4. doi: 10.1126/science.1232518. Epub 2013 Jan 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23371552" target="_blank"〉PubMed〈/a〉
    Keywords: Aurora Kinases ; Chromosome Segregation/genetics/*physiology ; Chromosomes, Fungal/*genetics ; Intracellular Signaling Peptides and Proteins/genetics/*physiology ; Kinetochores/enzymology ; Meiosis/genetics/*physiology ; Microtubules/enzymology ; Mutation ; Protein-Serine-Threonine Kinases/genetics/*physiology ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; Saccharomyces cerevisiae Proteins/genetics/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2015-02-14
    Description: The identification of active neurons and circuits in vivo is a fundamental challenge in understanding the neural basis of behavior. Genetically encoded calcium (Ca(2+)) indicators (GECIs) enable quantitative monitoring of cellular-resolution activity during behavior. However, such indicators require online monitoring within a limited field of view. Alternatively, post hoc staining of immediate early genes (IEGs) indicates highly active cells within the entire brain, albeit with poor temporal resolution. We designed a fluorescent sensor, CaMPARI, that combines the genetic targetability and quantitative link to neural activity of GECIs with the permanent, large-scale labeling of IEGs, allowing a temporally precise "activity snapshot" of a large tissue volume. CaMPARI undergoes efficient and irreversible green-to-red conversion only when elevated intracellular Ca(2+) and experimenter-controlled illumination coincide. We demonstrate the utility of CaMPARI in freely moving larvae of zebrafish and flies, and in head-fixed mice and adult flies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fosque, Benjamin F -- Sun, Yi -- Dana, Hod -- Yang, Chao-Tsung -- Ohyama, Tomoko -- Tadross, Michael R -- Patel, Ronak -- Zlatic, Marta -- Kim, Douglas S -- Ahrens, Misha B -- Jayaraman, Vivek -- Looger, Loren L -- Schreiter, Eric R -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 13;347(6223):755-60. doi: 10.1126/science.1260922.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, 19700 Helix Drive, Ashburn, VA 20147, USA. ; Howard Hughes Medical Institute, Janelia Farm Research Campus, 19700 Helix Drive, Ashburn, VA 20147, USA. schreitere@janelia.hhmi.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25678659" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biosensing Techniques ; Calcium/*analysis/metabolism ; Drosophila melanogaster ; Fluorescence ; *Genes, Immediate-Early ; Indicators and Reagents/analysis/metabolism ; Luminescent Proteins/genetics/*metabolism ; Mice ; Neural Pathways/*chemistry/cytology/physiology ; Neuronal Calcium-Sensor Proteins/genetics/*metabolism ; Protein Engineering ; Sensory Receptor Cells/*chemistry/physiology ; Staining and Labeling/*methods ; Zebrafish
    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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  • 8
    Publication Date: 2016-01-30
    Description: Dietary antigens are normally rendered nonimmunogenic through a poorly understood "oral tolerance" mechanism that involves immunosuppressive regulatory T (Treg) cells, especially Treg cells induced from conventional T cells in the periphery (pTreg cells). Although orally introducing nominal protein antigens is known to induce such pTreg cells, whether a typical diet induces a population of pTreg cells under normal conditions thus far has been unknown. By using germ-free mice raised and bred on an elemental diet devoid of dietary antigens, we demonstrated that under normal conditions, the vast majority of the small intestinal pTreg cells are induced by dietary antigens from solid foods. Moreover, these pTreg cells have a limited life span, are distinguishable from microbiota-induced pTreg cells, and repress underlying strong immunity to ingested protein antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Kwang Soon -- Hong, Sung-Wook -- Han, Daehee -- Yi, Jaeu -- Jung, Jisun -- Yang, Bo-Gie -- Lee, Jun Young -- Lee, Minji -- Surh, Charles D -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):858-63. doi: 10.1126/science.aac5560. Epub 2016 Jan 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Academy of Immunology and Microbiology, Institute for Basic Science, Pohang, Republic of Korea. Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea. ; Academy of Immunology and Microbiology, Institute for Basic Science, Pohang, Republic of Korea. Department of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea. Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26822607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Diet ; Dietary Proteins/*immunology ; Dyspepsia/*immunology ; Gastrointestinal Microbiome/*immunology ; Germ-Free Life ; Immune Tolerance ; Immunity, Mucosal ; Intestine, Small/*immunology/*microbiology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory/*immunology
    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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  • 9
    Publication Date: 2011-08-16
    Description: CD4(+) T-helper type 2 (T(H)2) cells, characterized by their expression of interleukin (IL)-4, IL-5, IL-9 and IL-13, are required for immunity to helminth parasites and promote the pathological inflammation associated with asthma and allergic diseases. Polymorphisms in the gene encoding the cytokine thymic stromal lymphopoietin (TSLP) are associated with the development of multiple allergic disorders in humans, indicating that TSLP is a critical regulator of T(H)2 cytokine-associated inflammatory diseases. In support of genetic analyses, exaggerated TSLP production is associated with asthma, atopic dermatitis and food allergies in patients, and studies in murine systems demonstrated that TSLP promotes T(H)2 cytokine-mediated immunity and inflammation. However, the mechanisms through which TSLP induces T(H)2 cytokine responses remain poorly defined. Here we demonstrate that TSLP promotes systemic basophilia, that disruption of TSLP-TSLPR interactions results in defective basophil responses, and that TSLPR-sufficient basophils can restore T(H)2-cell-dependent immunity in vivo. TSLP acted directly on bone-marrow-resident progenitors to promote basophil responses selectively. Critically, TSLP could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and genome-wide transcriptional profiling and functional analyses identified heterogeneity between TSLP-elicited versus IL-3-elicited basophils. Furthermore, activated human basophils expressed TSLPR, and basophils isolated from eosinophilic oesophagitis patients were distinct from classical basophils. Collectively, these studies identify previously unrecognized heterogeneity within the basophil cell lineage and indicate that expression of TSLP may influence susceptibility to multiple allergic diseases by regulating basophil haematopoiesis and eliciting a population of functionally distinct basophils that promote T(H)2 cytokine-mediated inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3263308/" 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/PMC3263308/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Siracusa, Mark C -- Saenz, Steven A -- Hill, David A -- Kim, Brian S -- Headley, Mark B -- Doering, Travis A -- Wherry, E John -- Jessup, Heidi K -- Siegel, Lori A -- Kambayashi, Taku -- Dudek, Emily C -- Kubo, Masato -- Cianferoni, Antonella -- Spergel, Jonathan M -- Ziegler, Steven F -- Comeau, Michael R -- Artis, David -- AI083480/AI/NIAID NIH HHS/ -- AI61570/AI/NIAID NIH HHS/ -- AI74878/AI/NIAID NIH HHS/ -- AI87990/AI/NIAID NIH HHS/ -- F31 GM082187/GM/NIGMS NIH HHS/ -- F32 AI085828/AI/NIAID NIH HHS/ -- R01 AI061570/AI/NIAID NIH HHS/ -- R01 AI061570-09/AI/NIAID NIH HHS/ -- R01 AI074878/AI/NIAID NIH HHS/ -- R01 AI074878-05/AI/NIAID NIH HHS/ -- R01 AI095466/AI/NIAID NIH HHS/ -- R01 AI095466-02/AI/NIAID NIH HHS/ -- R01 HL107589/HL/NHLBI NIH HHS/ -- R21 AI083480/AI/NIAID NIH HHS/ -- R21 AI083480-02/AI/NIAID NIH HHS/ -- T32 AI060516/AI/NIAID NIH HHS/ -- U01 AI095608/AI/NIAID NIH HHS/ -- U01 AI095608-02/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Aug 14;477(7363):229-33. doi: 10.1038/nature10329.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21841801" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology ; Basophils/*cytology/metabolism ; Cytokines/genetics/immunology/*metabolism ; Dermatitis, Atopic/immunology ; Food Hypersensitivity/immunology ; *Hematopoiesis ; Humans ; Hypersensitivity, Immediate/*immunology ; Inflammation/*immunology/*metabolism ; *Interleukin-3/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Phenotype ; Receptors, Cytokine/metabolism ; Receptors, Interleukin-3/deficiency/genetics/metabolism ; Th2 Cells/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2013-03-15
    Description: Centrosome duplication is critical for cell division, and genome instability can result if duplication is not restricted to a single round per cell cycle. Centrosome duplication is controlled in part by CP110, a centriolar protein that positively regulates centriole duplication while restricting centriole elongation and ciliogenesis. Maintenance of normal CP110 levels is essential, as excessive CP110 drives centrosome over-duplication and suppresses ciliogenesis, whereas its depletion inhibits centriole amplification and leads to highly elongated centrioles and aberrant assembly of cilia in growing cells. CP110 levels are tightly controlled, partly through ubiquitination by the ubiquitin ligase complex SCF(cyclin F) during G2 and M phases of the cell cycle. Here, using human cells, we report a new mechanism for the regulation of centrosome duplication that requires USP33, a deubiquitinating enzyme that is able to regulate CP110 levels. USP33 interacts with CP110 and localizes to centrioles primarily in S and G2/M phases, the periods during which centrioles duplicate and elongate. USP33 potently and specifically deubiquitinates CP110, but not other cyclin-F substrates. USP33 activity antagonizes SCF(cyclin F)-mediated ubiquitination and promotes the generation of supernumerary centriolar foci, whereas ablation of USP33 destabilizes CP110 and thereby inhibits centrosome amplification and mitotic defects. To our knowledge, we have identified the first centriolar deubiquitinating enzyme whose expression regulates centrosome homeostasis by countering cyclin-F-mediated destruction of a key substrate. Our results point towards potential therapeutic strategies for inhibiting tumorigenesis associated with centrosome amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815529/" 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/PMC3815529/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Ji -- D'Angiolella, Vincenzo -- Seeley, E Scott -- Kim, Sehyun -- Kobayashi, Tetsuo -- Fu, Wenxiang -- Campos, Eric I -- Pagano, Michele -- Dynlacht, Brian David -- 5R01HD069647-02/HD/NICHD NIH HHS/ -- R01 GM057587/GM/NIGMS NIH HHS/ -- R01 HD069647/HD/NICHD NIH HHS/ -- R37 CA076584/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 14;495(7440):255-9. doi: 10.1038/nature11941.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Cancer Institute, Smilow Research Center, New York University School of Medicine, 522 1st Avenue, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23486064" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Cycle Proteins/*metabolism ; Cell Line ; Centrioles/metabolism ; Centrosome/*metabolism ; Cyclins/metabolism ; Homeostasis ; Humans ; Microtubule-Associated Proteins/*metabolism ; Neoplasms/pathology/therapy ; Phosphoproteins/*metabolism ; Protein Stability ; SKP Cullin F-Box Protein Ligases/metabolism ; Ubiquitin Thiolesterase/*metabolism ; *Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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