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  • Time Factors  (895)
  • Mice, Inbred C57BL  (470)
  • Nature Publishing Group (NPG)  (1,336)
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  • 1
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    What it takes to nurse a nest egg (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, Karen -- England -- Nature. 2010 Sep 23;467(7314):489-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20963934" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Emigration and Immigration ; Europe ; European Union ; Faculty ; Income/statistics & numerical data ; Internationality ; *Pensions/statistics & numerical data ; Research Personnel/*economics/statistics & numerical data ; Retirement/*economics/statistics & numerical data ; Time Factors ; United States
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Single-molecule imaging reveals mechanisms of protein disruption by a DNA translocase (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-26
    Description: In physiological settings, nucleic-acid translocases must act on substrates occupied by other proteins, and an increasingly appreciated role of translocases is to catalyse protein displacement from RNA and DNA. However, little is known regarding the inevitable collisions that must occur, and the fate of protein obstacles and the mechanisms by which they are evicted from DNA remain unexplored. Here we sought to establish the mechanistic basis for protein displacement from DNA using RecBCD as a model system. Using nanofabricated curtains of DNA and multicolour single-molecule microscopy, we visualized collisions between a model translocase and different DNA-bound proteins in real time. We show that the DNA translocase RecBCD can disrupt core RNA polymerase, holoenzymes, stalled elongation complexes and transcribing RNA polymerases in either head-to-head or head-to-tail orientations, as well as EcoRI(E111Q), lac repressor and even nucleosomes. RecBCD did not pause during collisions and often pushed proteins thousands of base pairs before evicting them from DNA. We conclude that RecBCD overwhelms obstacles through direct transduction of chemomechanical force with no need for specific protein-protein interactions, and that proteins can be removed from DNA through active disruption mechanisms that act on a transition state intermediate as they are pushed from one nonspecific site to the next.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230117/" 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/PMC3230117/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finkelstein, Ilya J -- Visnapuu, Mari-Liis -- Greene, Eric C -- F32GM80864/GM/NIGMS NIH HHS/ -- GM074739/GM/NIGMS NIH HHS/ -- GM082848/GM/NIGMS NIH HHS/ -- R01 CA146940/CA/NCI NIH HHS/ -- R01 GM074739/GM/NIGMS NIH HHS/ -- R01 GM074739-01A1/GM/NIGMS NIH HHS/ -- R01 GM074739-05/GM/NIGMS NIH HHS/ -- R01 GM082848/GM/NIGMS NIH HHS/ -- R01 GM082848-01A1/GM/NIGMS NIH HHS/ -- R01 GM082848-04/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 16;468(7326):983-7. doi: 10.1038/nature09561. Epub 2010 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biophysics, Columbia University, New York, New York 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107319" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage lambda/genetics ; Biocatalysis ; DNA/genetics/*metabolism ; DNA, Viral/genetics/metabolism ; DNA-Binding Proteins/*metabolism ; DNA-Directed RNA Polymerases/chemistry/metabolism ; Deoxyribonuclease EcoRI/metabolism ; Escherichia coli/enzymology ; Exodeoxyribonuclease V/*metabolism ; Holoenzymes/chemistry/metabolism ; Lac Repressors/metabolism ; Microscopy, Fluorescence ; *Movement ; Nucleosomes/metabolism ; Promoter Regions, Genetic/genetics ; Protein Binding ; Quantum Dots ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Regulation of myeloid leukaemia by the cell-fate determinant Musashi (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-20
    Description: Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this transition remains poorly understood. Here we have used mouse models of CML to show that disease progression is regulated by the Musashi-Numb signalling axis. Specifically, we find that the chronic phase is marked by high levels of Numb expression whereas the blast crisis phase has low levels of Numb expression, and that ectopic expression of Numb promotes differentiation and impairs advanced-phase disease in vivo. As a possible explanation for the decreased levels of Numb in the blast crisis phase, we show that NUP98-HOXA9, an oncogene associated with blast crisis CML, can trigger expression of the RNA-binding protein Musashi2 (Msi2), which in turn represses Numb. Notably, loss of Msi2 restores Numb expression and significantly impairs the development and propagation of blast crisis CML in vitro and in vivo. Finally we show that Msi2 expression is not only highly upregulated during human CML progression but is also an early indicator of poorer prognosis. These data show that the Musashi-Numb pathway can control the differentiation of CML cells, and raise the possibility that targeting this pathway may provide a new strategy for the therapy of aggressive leukaemias.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918284/" 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/PMC2918284/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Takahiro -- Kwon, Hyog Young -- Zimdahl, Bryan -- Congdon, Kendra L -- Blum, Jordan -- Lento, William E -- Zhao, Chen -- Lagoo, Anand -- Gerrard, Gareth -- Foroni, Letizia -- Goldman, John -- Goh, Harriet -- Kim, Soo-Hyun -- Kim, Dong-Wook -- Chuah, Charles -- Oehler, Vivian G -- Radich, Jerald P -- Jordan, Craig T -- Reya, Tannishtha -- AI067798/AI/NIAID NIH HHS/ -- CA122206/CA/NCI NIH HHS/ -- CA140371/CA/NCI NIH HHS/ -- CA18029/CA/NCI NIH HHS/ -- DK072234/DK/NIDDK NIH HHS/ -- DK63031/DK/NIDDK NIH HHS/ -- DP1 CA174422/CA/NCI NIH HHS/ -- DP1 OD006430/OD/NIH HHS/ -- DP1 OD006430-01/OD/NIH HHS/ -- DP1 OD006430-02/OD/NIH HHS/ -- DP1OD006430/OD/NIH HHS/ -- HL097767/HL/NHLBI NIH HHS/ -- P01 CA018029/CA/NCI NIH HHS/ -- R01 CA140371/CA/NCI NIH HHS/ -- R01 DK063031/DK/NIDDK NIH HHS/ -- R01 DK063031-01/DK/NIDDK NIH HHS/ -- R01 DK063031-01S1/DK/NIDDK NIH HHS/ -- R01 DK063031-02/DK/NIDDK NIH HHS/ -- R01 DK063031-03/DK/NIDDK NIH HHS/ -- R01 DK063031-04/DK/NIDDK NIH HHS/ -- R01 DK063031-05/DK/NIDDK NIH HHS/ -- R01 DK063031-06/DK/NIDDK NIH HHS/ -- R01 DK063031-07/DK/NIDDK NIH HHS/ -- R01 DK063031-07S1/DK/NIDDK NIH HHS/ -- R01 DK063031-08/DK/NIDDK NIH HHS/ -- R01 DK072234/DK/NIDDK NIH HHS/ -- R01 DK072234-01A1/DK/NIDDK NIH HHS/ -- R01 DK072234-02/DK/NIDDK NIH HHS/ -- R01 DK072234-03/DK/NIDDK NIH HHS/ -- R01 DK072234-04/DK/NIDDK NIH HHS/ -- R01 HL097767/HL/NHLBI NIH HHS/ -- R01 HL097767-01/HL/NHLBI NIH HHS/ -- R01 HL097767-02/HL/NHLBI NIH HHS/ -- T32 GM007184-33/GM/NIGMS NIH HHS/ -- U19 AI067798/AI/NIAID NIH HHS/ -- U19 AI067798-010006/AI/NIAID NIH HHS/ -- U19 AI067798-020006/AI/NIAID NIH HHS/ -- U19 AI067798-030006/AI/NIAID NIH HHS/ -- U19 AI067798-040006/AI/NIAID NIH HHS/ -- U19 AI067798-050006/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):765-8. doi: 10.1038/nature09171. Epub 2010 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20639863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blast Crisis/genetics/metabolism/pathology ; *Cell Differentiation/genetics ; Disease Progression ; Fusion Proteins, bcr-abl/genetics/metabolism ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/genetics/metabolism ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics/*metabolism/*pathology ; Membrane Proteins/biosynthesis/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/biosynthesis/genetics/metabolism ; Nuclear Pore Complex Proteins/genetics/metabolism ; Oncogene Proteins, Fusion/genetics/metabolism ; Prognosis ; RNA-Binding Proteins/biosynthesis/genetics/*metabolism ; Receptor, Notch1/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cancer: Genomic evolution of metastasis (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luebeck, E Georg -- England -- Nature. 2010 Oct 28;467(7319):1053-5. doi: 10.1038/4671053a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981088" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Lineage/genetics ; Clone Cells/metabolism/pathology ; DNA Mutational Analysis ; Disease Progression ; Early Detection of Cancer ; *Evolution, Molecular ; Genomic Instability/*genetics ; Humans ; Models, Biological ; Mutagenesis/*genetics ; Neoplasm Metastasis/*genetics/pathology ; Pancreatic Neoplasms/classification/*genetics/*pathology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Induction of tumour immunity by targeted inhibition of nonsense-mediated mRNA decay (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-14
    Description: The main reason why tumours are not controlled by the immune system is that, unlike pathogens, they do not express potent tumour rejection antigens (TRAs). Tumour vaccination aims at stimulating a systemic immune response targeted to, mostly weak, antigens expressed in the disseminated tumour lesions. Main challenges in developing effective vaccination protocols are the identification of potent and broadly expressed TRAs and effective adjuvants to stimulate a robust and durable immune response. Here we describe an alternative approach in which the expression of new, and thereby potent, antigens are induced in tumour cells by inhibiting nonsense-mediated messenger RNA decay (NMD). Small interfering RNA (siRNA)-mediated inhibition of NMD in tumour cells led to the expression of new antigenic determinants and their immune-mediated rejection. In subcutaneous and metastatic tumour models, tumour-targeted delivery of NMD factor-specific siRNAs conjugated to oligonucleotide aptamer ligands led to significant inhibition of tumour growth that was superior to that of vaccination with granulocyte-macrophage colony-stimulating factor (GM-CSF)-expressing irradiated tumour cells, and could be further enhanced by co-stimulation. Tumour-targeted NMD inhibition forms the basis of a simple, broadly useful, and clinically feasible approach to enhance the antigenicity of disseminated tumours leading to their immune recognition and rejection. The cell-free chemically synthesized oligonucleotide backbone of aptamer-siRNAs reduces the risk of immunogenicity and enhances the feasibility of generating reagents suitable for clinical use.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3107067/" 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/PMC3107067/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastor, Fernando -- Kolonias, Despina -- Giangrande, Paloma H -- Gilboa, Eli -- R01 CA138503/CA/NCI NIH HHS/ -- R01 CA151857-02/CA/NCI NIH HHS/ -- England -- Nature. 2010 May 13;465(7295):227-30. doi: 10.1038/nature08999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology & Immunology, Dodson Interdisciplinary Immunotherapy Institute, University of Miami Miller School of Medicine Miami, Florida 33134, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20463739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*genetics/*immunology ; Aptamers, Nucleotide/genetics ; Cancer Vaccines/genetics/immunology/metabolism ; Carrier Proteins/genetics ; Cell Line, Tumor ; Chickens/genetics ; Colonic Neoplasms/*genetics/*immunology/pathology ; Gene Expression Regulation, Neoplastic ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Nude ; Neoplasm Transplantation ; RNA Interference ; RNA Stability/*genetics ; RNA, Small Interfering/*genetics/therapeutic use ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Lkb1 regulates quiescence and metabolic homeostasis of haematopoietic stem cells (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-03
    Description: The capacity to fine-tune cellular bioenergetics with the demands of stem-cell maintenance and regeneration is central to normal development and ageing, and to organismal survival during periods of acute stress. How energy metabolism and stem-cell homeostatic processes are coordinated is not well understood. Lkb1 acts as an evolutionarily conserved regulator of cellular energy metabolism in eukaryotic cells and functions as the major upstream kinase to phosphorylate AMP-activated protein kinase (AMPK) and 12 other AMPK-related kinases. Whether Lkb1 regulates stem-cell maintenance remains unknown. Here we show that Lkb1 has an essential role in haematopoietic stem cell (HSC) homeostasis. We demonstrate that ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality. Loss of Lkb1 leads to impaired survival and escape from quiescence of HSCs, resulting in exhaustion of the HSC pool and a marked reduction of HSC repopulating potential in vivo. Lkb1 deletion has an impact on cell proliferation in HSCs, but not on more committed compartments, pointing to context-specific functions for Lkb1 in haematopoiesis. The adverse impact of Lkb1 deletion on haematopoiesis was predominantly cell-autonomous and mTOR complex 1 (mTORC1)-independent, and involves multiple mechanisms converging on mitochondrial apoptosis and possibly downregulation of PGC-1 coactivators and their transcriptional network, which have critical roles in mitochondrial biogenesis and function. Thus, Lkb1 serves as an essential regulator of HSCs and haematopoiesis, and more generally, points to the critical importance of coupling energy metabolism and stem-cell homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058342/" 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/PMC3058342/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gan, Boyi -- Hu, Jian -- Jiang, Shan -- Liu, Yingchun -- Sahin, Ergun -- Zhuang, Li -- Fletcher-Sananikone, Eliot -- Colla, Simona -- Wang, Y Alan -- Chin, Lynda -- Depinho, Ronald A -- 01CA141508/CA/NCI NIH HHS/ -- R21 CA135057/CA/NCI NIH HHS/ -- R21 CA135057-01/CA/NCI NIH HHS/ -- R21CA135057/CA/NCI NIH HHS/ -- U01 CA141508/CA/NCI NIH HHS/ -- U01 CA141508-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):701-4. doi: 10.1038/nature09595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Cycle/*physiology ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Female ; Gene Deletion ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; *Homeostasis ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Pancytopenia/genetics ; Phenotype ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/metabolism ; Survival Analysis ; TOR Serine-Threonine Kinases ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
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    Genome-wide RNAi screen identifies human host factors crucial for influenza virus replication (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-19
    Description: Influenza A virus, being responsible for seasonal epidemics and reoccurring pandemics, represents a worldwide threat to public health. High mutation rates facilitate the generation of viral escape mutants, rendering vaccines and drugs directed against virus-encoded targets potentially ineffective. In contrast, targeting host cell determinants temporarily dispensable for the host but crucial for virus replication could prevent viral escape. Here we report the discovery of 287 human host cell genes influencing influenza A virus replication in a genome-wide RNA interference (RNAi) screen. Using an independent assay we confirmed 168 hits (59%) inhibiting either the endemic H1N1 (119 hits) or the current pandemic swine-origin (121 hits) influenza A virus strains, with an overlap of 60%. Notably, a subset of these common hits was also essential for replication of a highly pathogenic avian H5N1 strain. In-depth analyses of several factors provided insights into their infection stage relevance. Notably, SON DNA binding protein (SON) was found to be important for normal trafficking of influenza virions to late endosomes early in infection. We also show that a small molecule inhibitor of CDC-like kinase 1 (CLK1) reduces influenza virus replication by more than two orders of magnitude, an effect connected with impaired splicing of the viral M2 messenger RNA. Furthermore, influenza-virus-infected p27(-/-) (cyclin-dependent kinase inhibitor 1B; Cdkn1b) mice accumulated significantly lower viral titres in the lung, providing in vivo evidence for the importance of this gene. Thus, our results highlight the potency of genome-wide RNAi screening for the dissection of virus-host interactions and the identification of drug targets for a broad range of influenza viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karlas, Alexander -- Machuy, Nikolaus -- Shin, Yujin -- Pleissner, Klaus-Peter -- Artarini, Anita -- Heuer, Dagmar -- Becker, Daniel -- Khalil, Hany -- Ogilvie, Lesley A -- Hess, Simone -- Maurer, Andre P -- Muller, Elke -- Wolff, Thorsten -- Rudel, Thomas -- Meyer, Thomas F -- England -- Nature. 2010 Feb 11;463(7282):818-22. doi: 10.1038/nature08760. Epub 2010 Jan 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Department, Max Planck Institute for Infection Biology, Chariteplatz 1, 10117 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20081832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Factors/genetics/metabolism ; Cell Line ; Cells, Cultured ; Chick Embryo ; Cyclin-Dependent Kinase Inhibitor p27/deficiency/genetics/metabolism ; Epithelial Cells/virology ; Genome, Human/genetics ; *Host-Pathogen Interactions/genetics/physiology ; Humans ; Influenza A Virus, H1N1 Subtype/classification/*growth & development ; Influenza, Human/*genetics/*virology ; Lung/cytology ; Mice ; Mice, Inbred C57BL ; Protein-Serine-Threonine Kinases/genetics ; Protein-Tyrosine Kinases/genetics ; *RNA Interference ; Virus Replication/*physiology
    Print ISSN: 0028-0836
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    Real-time tRNA transit on single translating ribosomes at codon resolution (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-16
    Description: Translation by the ribosome occurs by a complex mechanism involving the coordinated interaction of multiple nucleic acid and protein ligands. Here we use zero-mode waveguides (ZMWs) and sophisticated detection instrumentation to allow real-time observation of translation at physiologically relevant micromolar ligand concentrations. Translation at each codon is monitored by stable binding of transfer RNAs (tRNAs)-labelled with distinct fluorophores-to translating ribosomes, which allows direct detection of the identity of tRNA molecules bound to the ribosome and therefore the underlying messenger RNA (mRNA) sequence. We observe the transit of tRNAs on single translating ribosomes and determine the number of tRNA molecules simultaneously bound to the ribosome, at each codon of an mRNA molecule. Our results show that ribosomes are only briefly occupied by two tRNA molecules and that release of deacylated tRNA from the exit (E) site is uncoupled from binding of aminoacyl-tRNA site (A-site) tRNA and occurs rapidly after translocation. The methods outlined here have broad application to the study of mRNA sequences, and the mechanism and regulation of translation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4466108/" 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/PMC4466108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uemura, Sotaro -- Aitken, Colin Echeverria -- Korlach, Jonas -- Flusberg, Benjamin A -- Turner, Stephen W -- Puglisi, Joseph D -- GM51266/GM/NIGMS NIH HHS/ -- R01 GM051266/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Apr 15;464(7291):1012-7. doi: 10.1038/nature08925.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Stanford University School of Medicine, Stanford, California 94305-5126, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393556" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Codon/*genetics ; Escherichia coli ; Fluorescence ; Kinetics ; Ligands ; Luminescent Measurements ; Optical Tweezers ; Protein Biosynthesis/genetics/*physiology ; RNA, Transfer/genetics/*metabolism ; Ribosomes/chemistry/genetics/*metabolism ; Time Factors
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    Chemical genetics strategy identifies an HCV NS5A inhibitor with a potent clinical effect (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-23
    Description: The worldwide prevalence of chronic hepatitis C virus (HCV) infection is estimated to be approaching 200 million people. Current therapy relies upon a combination of pegylated interferon-alpha and ribavirin, a poorly tolerated regimen typically associated with less than 50% sustained virological response rate in those infected with genotype 1 virus. The development of direct-acting antiviral agents to treat HCV has focused predominantly on inhibitors of the viral enzymes NS3 protease and the RNA-dependent RNA polymerase NS5B. Here we describe the profile of BMS-790052, a small molecule inhibitor of the HCV NS5A protein that exhibits picomolar half-maximum effective concentrations (EC(50)) towards replicons expressing a broad range of HCV genotypes and the JFH-1 genotype 2a infectious virus in cell culture. In a phase I clinical trial in patients chronically infected with HCV, administration of a single 100-mg dose of BMS-790052 was associated with a 3.3 log(10) reduction in mean viral load measured 24 h post-dose that was sustained for an additional 120 h in two patients infected with genotype 1b virus. Genotypic analysis of samples taken at baseline, 24 and 144 h post-dose revealed that the major HCV variants observed had substitutions at amino-acid positions identified using the in vitro replicon system. These results provide the first clinical validation of an inhibitor of HCV NS5A, a protein with no known enzymatic function, as an approach to the suppression of virus replication that offers potential as part of a therapeutic regimen based on combinations of HCV inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gao, Min -- Nettles, Richard E -- Belema, Makonen -- Snyder, Lawrence B -- Nguyen, Van N -- Fridell, Robert A -- Serrano-Wu, Michael H -- Langley, David R -- Sun, Jin-Hua -- O'Boyle, Donald R 2nd -- Lemm, Julie A -- Wang, Chunfu -- Knipe, Jay O -- Chien, Caly -- Colonno, Richard J -- Grasela, Dennis M -- Meanwell, Nicholas A -- Hamann, Lawrence G -- England -- Nature. 2010 May 6;465(7294):96-100. doi: 10.1038/nature08960. Epub 2010 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Bristol-Myers Squibb Research and Development, 5 Research Parkway, Wallingford, Connecticut 06492, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20410884" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antiviral Agents/blood/chemistry/*pharmacology/therapeutic use ; Cell Line ; Cercopithecus aethiops ; Drug Resistance, Viral ; Female ; Genotype ; HeLa Cells ; Hepacivirus/*drug effects ; Hepatitis C/drug therapy/virology ; Humans ; Imidazoles/blood/chemistry/*pharmacology ; Inhibitory Concentration 50 ; Male ; Middle Aged ; Time Factors ; Vero Cells ; Viral Load/drug effects ; Viral Nonstructural Proteins/*antagonists & inhibitors ; Young Adult
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    Questioning the timeline of H1N1 flu vaccination contracts (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Deborah -- Carter, Philip -- England -- Nature. 2010 Jul 15;466(7304):315. doi: 10.1038/466315a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631779" target="_blank"〉PubMed〈/a〉
    Keywords: *Conflict of Interest ; *Drug Industry ; Humans ; *Influenza A Virus, H1N1 Subtype ; Influenza Vaccines/*supply & distribution ; Influenza, Human/*epidemiology/prevention & control/virology ; Reproducibility of Results ; Time Factors ; *Vaccination ; *World Health Organization
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    Direct conversion of fibroblasts to functional neurons by defined factors (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-29
    Description: Cellular differentiation and lineage commitment are considered to be robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly induce other defined somatic cell fates, and not only an undifferentiated state. We hypothesized that combinatorial expression of neural-lineage-specific transcription factors could directly convert fibroblasts into neurons. Starting from a pool of nineteen candidate genes, we identified a combination of only three factors, Ascl1, Brn2 (also called Pou3f2) and Myt1l, that suffice to rapidly and efficiently convert mouse embryonic and postnatal fibroblasts into functional neurons in vitro. These induced neuronal (iN) cells express multiple neuron-specific proteins, generate action potentials and form functional synapses. Generation of iN cells from non-neural lineages could have important implications for studies of neural development, neurological disease modelling and regenerative medicine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829121/" 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/PMC2829121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vierbuchen, Thomas -- Ostermeier, Austin -- Pang, Zhiping P -- Kokubu, Yuko -- Sudhof, Thomas C -- Wernig, Marius -- 1018438-142-PABCA/PHS HHS/ -- 5T32NS007280/NS/NINDS NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 25;463(7284):1035-41. doi: 10.1038/nature08797. Epub 2010 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Biology and Regenerative Medicine, Department of Pathology, Stanford University School of Medicine, 1050 Arastradero Road, Palo Alto, California 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20107439" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Biomarkers/analysis ; Cell Line ; *Cell Lineage ; *Cell Transdifferentiation ; Cells, Cultured ; Embryo, Mammalian/cytology ; Fibroblasts/*cytology ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Neurons/*cytology/metabolism/*physiology ; POU Domain Factors/genetics/metabolism ; Regenerative Medicine ; Synapses/metabolism ; Tail/cytology ; Time Factors ; Transcription Factors/genetics/metabolism
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    The bridge between lab and clinic. Interview by Meredith Wadman (2010)
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    Publication Date: 2010-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, Francis -- England -- Nature. 2010 Dec 16;468(7326):877. doi: 10.1038/468877a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21164451" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Industry ; National Institutes of Health (U.S.)/economics/*organization & administration ; Time Factors ; Translational Medical Research/economics/*organization & administration/trends ; United States
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  • 13
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    Coots use hatch order to learn to recognize and reject conspecific brood parasitic chicks (2009)
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    Publication Date: 2009-12-18
    Description: Avian brood parasites and their hosts provide model systems for investigating links between recognition, learning, and their fitness consequences. One major evolutionary puzzle has continued to capture the attention of naturalists for centuries: why do hosts of brood parasites generally fail to recognize parasitic offspring after they have hatched from the egg, even when the host and parasitic chicks differ to almost comic degrees? One prominent theory to explain this pattern proposes that the costs of mistakenly learning to recognize the wrong offspring make recognition maladaptive. Here we show that American coots, Fulica americana, can recognize and reject parasitic chicks in their brood by using learned cues, despite the fact that the hosts and the brood parasites are of the same species. A series of chick cross-fostering experiments confirm that coots use first-hatched chicks in a brood as referents to learn to recognize their own chicks and then discriminate against later-hatched parasitic chicks in the same brood. When experimentally provided with the wrong reference chicks, coots can be induced to discriminate against their own offspring, confirming that the learning errors proposed by theory can exist. However, learning based on hatching order is reliable in naturally parasitized coot nests because host eggs hatch predictably ahead of parasite eggs. Conversely, a lack of reliable information may help to explain why the evolution of chick recognition is not more common in hosts of most interspecific brood parasites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shizuka, Daizaburo -- Lyon, Bruce E -- England -- Nature. 2010 Jan 14;463(7278):223-6. doi: 10.1038/nature08655. Epub 2009 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, California 95064, USA. shizuka@biology.ucsc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20016486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/*parasitology/*physiology ; British Columbia ; Cues ; Discrimination Learning/*physiology ; Feeding Behavior/physiology ; Genetic Fitness ; Nesting Behavior/*physiology ; Ovum/growth & development ; Pattern Recognition, Visual/physiology ; Survival Rate ; Time Factors ; Wetlands
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    RANK ligand mediates progestin-induced mammary epithelial proliferation and carcinogenesis (2010)
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    Publication Date: 2010-10-01
    Description: RANK ligand (RANKL), a TNF-related molecule, is essential for osteoclast formation, function and survival through interaction with its receptor RANK. Mammary glands of RANK- and RANKL-deficient mice develop normally during sexual maturation, but fail to form lobuloalveolar structures during pregnancy because of defective proliferation and increased apoptosis of mammary epithelium. It has been shown that RANKL is responsible for the major proliferative response of mouse mammary epithelium to progesterone during mammary lactational morphogenesis, and in mouse models, manipulated to induce activation of the RANK/RANKL pathway in the absence of strict hormonal control, inappropriate mammary proliferation is observed. However, there is no evidence so far of a functional contribution of RANKL to tumorigenesis. Here we show that RANK and RANKL are expressed within normal, pre-malignant and neoplastic mammary epithelium, and using complementary gain-of-function (mouse mammary tumour virus (MMTV)-RANK transgenic mice) and loss-of function (pharmacological inhibition of RANKL) approaches, define a direct contribution of this pathway in mammary tumorigenesis. Accelerated pre-neoplasias and increased mammary tumour formation were observed in MMTV-RANK transgenic mice after multiparity or treatment with carcinogen and hormone (progesterone). Reciprocally, selective pharmacological inhibition of RANKL attenuated mammary tumour development not only in hormone- and carcinogen-treated MMTV-RANK and wild-type mice, but also in the MMTV-neu transgenic spontaneous tumour model. The reduction in tumorigenesis upon RANKL inhibition was preceded by a reduction in pre-neoplasias as well as rapid and sustained reductions in hormone- and carcinogen-induced mammary epithelial proliferation and cyclin D1 levels. Collectively, our results indicate that RANKL inhibition is acting directly on hormone-induced mammary epithelium at early stages in tumorigenesis, and the permissive contribution of progesterone to increased mammary cancer incidence is due to RANKL-dependent proliferative changes in the mammary epithelium. The current study highlights a potential role for RANKL inhibition in the management of proliferative breast disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gonzalez-Suarez, Eva -- Jacob, Allison P -- Jones, Jon -- Miller, Robert -- Roudier-Meyer, Martine P -- Erwert, Ryan -- Pinkas, Jan -- Branstetter, Dan -- Dougall, William C -- England -- Nature. 2010 Nov 4;468(7320):103-7. doi: 10.1038/nature09495. Epub 2010 Sep 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hematology/Oncology Research, Amgen Inc, Seattle, Washington 98119, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20881963" target="_blank"〉PubMed〈/a〉
    Keywords: 9,10-Dimethyl-1,2-benzanthracene/administration & dosage/adverse effects ; Animals ; Breast Neoplasms/metabolism/pathology ; Cell Proliferation/drug effects ; Cell Transformation, Neoplastic/*chemically induced/*drug effects/pathology ; Disease Models, Animal ; Epithelial Cells/drug effects/metabolism/pathology ; Female ; Humans ; Lung Neoplasms/secondary ; Mammary Neoplasms, Experimental/*chemically ; induced/genetics/metabolism/*pathology ; Mammary Tumor Virus, Mouse/genetics/physiology ; Medroxyprogesterone Acetate/administration & dosage/adverse effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasm Invasiveness ; Precancerous Conditions/pathology/prevention & control ; Progesterone/administration & dosage/adverse effects ; Progestins/administration & dosage/*adverse effects ; RANK Ligand/antagonists & inhibitors/genetics/*metabolism ; Receptor Activator of Nuclear Factor-kappa B/genetics/metabolism
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    Neuroscience: Editing out fear (2010)
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    Publication Date: 2010-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quirk, Gregory J -- Milad, Mohammed R -- England -- Nature. 2010 Jan 7;463(7277):36-7. doi: 10.1038/463036a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054384" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical/*physiology ; Cues ; Electroshock ; Extinction, Psychological/*physiology ; Fear/*physiology/*psychology ; Humans ; Memory/*physiology ; Models, Neurological ; Models, Psychological ; Neuronal Plasticity/*physiology ; Photic Stimulation ; Rats ; Stress Disorders, Post-Traumatic/therapy ; Time Factors
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    Reprogramming towards pluripotency requires AID-dependent DNA demethylation (2009)
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    Publication Date: 2009-12-23
    Description: Reprogramming of somatic cell nuclei to yield induced pluripotent stem (iPS) cells makes possible derivation of patient-specific stem cells for regenerative medicine. However, iPS cell generation is asynchronous and slow (2-3 weeks), the frequency is low (〈0.1%), and DNA demethylation constitutes a bottleneck. To determine regulatory mechanisms involved in reprogramming, we generated interspecies heterokaryons (fused mouse embryonic stem (ES) cells and human fibroblasts) that induce reprogramming synchronously, frequently and fast. Here we show that reprogramming towards pluripotency in single heterokaryons is initiated without cell division or DNA replication, rapidly (1 day) and efficiently (70%). Short interfering RNA (siRNA)-mediated knockdown showed that activation-induced cytidine deaminase (AID, also known as AICDA) is required for promoter demethylation and induction of OCT4 (also known as POU5F1) and NANOG gene expression. AID protein bound silent methylated OCT4 and NANOG promoters in fibroblasts, but not active demethylated promoters in ES cells. These data provide new evidence that mammalian AID is required for active DNA demethylation and initiation of nuclear reprogramming towards pluripotency in human somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" 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/PMC2906123/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhutani, Nidhi -- Brady, Jennifer J -- Damian, Mara -- Sacco, Alessandra -- Corbel, Stephane Y -- Blau, Helen M -- AG009521/AG/NIA NIH HHS/ -- AG024987/AG/NIA NIH HHS/ -- AI007328/AI/NIAID NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG024987/AG/NIA NIH HHS/ -- R01 AG024987-05/AG/NIA NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1042-7. doi: 10.1038/nature08752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Fusion ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; Chromatin Immunoprecipitation ; Cytidine Deaminase/deficiency/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; *DNA Methylation ; DNA Replication ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Lung/cytology/embryology ; Mice ; Models, Biological ; Octamer Transcription Factor-3/genetics ; Promoter Regions, Genetic/genetics ; Time Factors
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    Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-12
    Description: Reciprocity of inflammation, oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression. Whereas the mechanism of hypoxia-driven angiogenesis is well understood, the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure. Here we show that the end products of lipid oxidation, omega-(2-carboxyethyl)pyrrole (CEP) and other related pyrroles, are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma. The molecular patterns of carboxyalkylpyrroles are recognized by Toll-like receptor 2 (TLR2), but not TLR4 or scavenger receptors on endothelial cells, leading to an angiogenic response that is independent of vascular endothelial growth factor. CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-dependent TLR2 signalling. Neutralization of endogenous carboxyalkylpyrroles impaired wound healing and tissue revascularization and diminished tumour angiogenesis. Both TLR2 and MyD88 are required for CEP-induced stimulation of Rac1 and endothelial migration. Taken together, these findings establish a new function of TLR2 as a sensor of oxidation-associated molecular patterns, providing a key link connecting inflammation, oxidative stress, innate immunity and angiogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990914/" 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/PMC2990914/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, Xiaoxia Z -- Malinin, Nikolay L -- Merkulova, Alona A -- Tischenko, Mira -- Kerr, Bethany A -- Borden, Ernest C -- Podrez, Eugene A -- Salomon, Robert G -- Byzova, Tatiana V -- CA126847/CA/NCI NIH HHS/ -- GM021249/GM/NIGMS NIH HHS/ -- HL071625/HL/NHLBI NIH HHS/ -- HL073311/HL/NHLBI NIH HHS/ -- HL077213/HL/NHLBI NIH HHS/ -- R01 HL071625/HL/NHLBI NIH HHS/ -- R01 HL071625-07/HL/NHLBI NIH HHS/ -- R01 HL071625-08/HL/NHLBI NIH HHS/ -- R01 HL077213/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):972-6. doi: 10.1038/nature09421. Epub 2010 Oct 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Cardiology, J. J. Jacobs Center for Thrombosis and Vascular Biology, NB50, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20927103" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/metabolism ; Animals ; Antigens, CD31/metabolism ; Aorta/cytology/drug effects ; Cell Line ; Cell Movement ; Endothelial Cells/metabolism ; Hindlimb/metabolism ; Humans ; Immunity, Innate/immunology ; Inflammation/metabolism ; Ischemia/metabolism ; Ligands ; Melanoma/blood supply/metabolism ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/metabolism ; Neovascularization, Pathologic/*metabolism ; *Neovascularization, Physiologic/drug effects ; Oxidation-Reduction ; Oxidative Stress/*physiology ; Propionates ; Pyrroles/chemistry/*metabolism/pharmacology ; Receptors, Scavenger/metabolism ; Signal Transduction/drug effects ; Toll-Like Receptor 2/agonists/*metabolism ; Toll-Like Receptor 4/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Wound Healing/drug effects/physiology ; rac1 GTP-Binding Protein/metabolism
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    Structural basis of semaphorin-plexin signalling (2010)
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    Publication Date: 2010-09-30
    Description: Cell-cell signalling of semaphorin ligands through interaction with plexin receptors is important for the homeostasis and morphogenesis of many tissues and is widely studied for its role in neural connectivity, cancer, cell migration and immune responses. SEMA4D and Sema6A exemplify two diverse vertebrate, membrane-spanning semaphorin classes (4 and 6) that are capable of direct signalling through members of the two largest plexin classes, B and A, respectively. In the absence of any structural information on the plexin ectodomain or its interaction with semaphorins the extracellular specificity and mechanism controlling plexin signalling has remained unresolved. Here we present crystal structures of cognate complexes of the semaphorin-binding regions of plexins B1 and A2 with semaphorin ectodomains (human PLXNB1(1-2)-SEMA4D(ecto) and murine PlxnA2(1-4)-Sema6A(ecto)), plus unliganded structures of PlxnA2(1-4) and Sema6A(ecto). These structures, together with biophysical and cellular assays of wild-type and mutant proteins, reveal that semaphorin dimers independently bind two plexin molecules and that signalling is critically dependent on the avidity of the resulting bivalent 2:2 complex (monomeric semaphorin binds plexin but fails to trigger signalling). In combination, our data favour a cell-cell signalling mechanism involving semaphorin-stabilized plexin dimerization, possibly followed by clustering, which is consistent with previous functional data. Furthermore, the shared generic architecture of the complexes, formed through conserved contacts of the amino-terminal seven-bladed beta-propeller (sema) domains of both semaphorin and plexin, suggests that a common mode of interaction triggers all semaphorin-plexin based signalling, while distinct insertions within or between blades of the sema domains determine binding specificity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587840/" 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/PMC3587840/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Janssen, Bert J C -- Robinson, Ross A -- Perez-Branguli, Francesc -- Bell, Christian H -- Mitchell, Kevin J -- Siebold, Christian -- Jones, E Yvonne -- 082301/Wellcome Trust/United Kingdom -- 083111/Wellcome Trust/United Kingdom -- 10976/Cancer Research UK/United Kingdom -- A10976/Cancer Research UK/United Kingdom -- A3964/Cancer Research UK/United Kingdom -- A5261/Cancer Research UK/United Kingdom -- G0700232/Medical Research Council/United Kingdom -- G0700232(82098)/Medical Research Council/United Kingdom -- G0900084/Medical Research Council/United Kingdom -- G9900061/Medical Research Council/United Kingdom -- G9900061(69203)/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Oct 28;467(7319):1118-22. doi: 10.1038/nature09468. Epub 2010 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Structural Biology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20877282" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/chemistry/genetics/metabolism ; Binding Sites ; Cell Adhesion Molecules/*chemistry/genetics/*metabolism ; Cell Communication ; Crystallography, X-Ray ; Humans ; Ligands ; Mice ; Mice, Inbred C57BL ; Models, Molecular ; NIH 3T3 Cells ; Nerve Tissue Proteins/*chemistry/genetics/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Cell Surface/chemistry/genetics/metabolism ; Semaphorins/*chemistry/genetics/*metabolism ; *Signal Transduction ; Structure-Activity Relationship
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    Subcapsular sinus macrophages prevent CNS invasion on peripheral infection with a neurotropic virus (2010)
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    Publication Date: 2010-06-26
    Description: Lymph nodes (LNs) capture microorganisms that breach the body's external barriers and enter draining lymphatics, limiting the systemic spread of pathogens. Recent work has shown that CD11b(+)CD169(+) macrophages, which populate the subcapsular sinus (SCS) of LNs, are critical for the clearance of viruses from the lymph and for initiating antiviral humoral immune responses. Here we show, using vesicular stomatitis virus (VSV), a relative of rabies virus transmitted by insect bites, that SCS macrophages perform a third vital function: they prevent lymph-borne neurotropic viruses from infecting the central nervous system (CNS). On local depletion of LN macrophages, about 60% of mice developed ascending paralysis and died 7-10 days after subcutaneous infection with a small dose of VSV, whereas macrophage-sufficient animals remained asymptomatic and cleared the virus. VSV gained access to the nervous system through peripheral nerves in macrophage-depleted LNs. In contrast, within macrophage-sufficient LNs VSV replicated preferentially in SCS macrophages but not in adjacent nerves. Removal of SCS macrophages did not compromise adaptive immune responses against VSV, but decreased type I interferon (IFN-I) production within infected LNs. VSV-infected macrophages recruited IFN-I-producing plasmacytoid dendritic cells to the SCS and in addition were a major source of IFN-I themselves. Experiments in bone marrow chimaeric mice revealed that IFN-I must act on both haematopoietic and stromal compartments, including the intranodal nerves, to prevent lethal infection with VSV. These results identify SCS macrophages as crucial gatekeepers to the CNS that prevent fatal viral invasion of the nervous system on peripheral infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892812/" 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/PMC2892812/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iannacone, Matteo -- Moseman, E Ashley -- Tonti, Elena -- Bosurgi, Lidia -- Junt, Tobias -- Henrickson, Sarah E -- Whelan, Sean P -- Guidotti, Luca G -- von Andrian, Ulrich H -- AI069259/AI/NIAID NIH HHS/ -- AI072252/AI/NIAID NIH HHS/ -- AI078897/AI/NIAID NIH HHS/ -- AR42689/AR/NIAMS NIH HHS/ -- P01 AI078897/AI/NIAID NIH HHS/ -- P01 AI078897-01/AI/NIAID NIH HHS/ -- P01 CA071932/CA/NCI NIH HHS/ -- P01 CA071932-12S29003/CA/NCI NIH HHS/ -- R01 AI069259/AI/NIAID NIH HHS/ -- R01 AI069259-06/AI/NIAID NIH HHS/ -- R01 AI072252/AI/NIAID NIH HHS/ -- R01 AI072252-04/AI/NIAID NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jun 24;465(7301):1079-83. doi: 10.1038/nature09118.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA. Matteo_Iannacone@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20577213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Central Nervous System/cytology/*immunology/*virology ; Dendritic Cells/immunology ; Injections ; Interferon Type I/immunology ; Lymph Nodes/cytology/*immunology/innervation/*virology ; Macrophages/*immunology/virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Paralysis/complications/virology ; Peripheral Nerves/virology ; Receptor, Interferon alpha-beta/deficiency ; Rhabdoviridae Infections/complications/*immunology/virology ; Survival Rate ; Vesicular stomatitis Indiana virus/immunology/pathogenicity/physiology ; Vesicular stomatitis New Jersey virus/immunology/pathogenicity/physiology ; Vesiculovirus/*immunology/pathogenicity/physiology
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    Ribosome dynamics and tRNA movement by time-resolved electron cryomicroscopy (2010)
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    Publication Date: 2010-07-16
    Description: The translocation step of protein synthesis entails large-scale rearrangements of the ribosome-transfer RNA (tRNA) complex. Here we have followed tRNA movement through the ribosome during translocation by time-resolved single-particle electron cryomicroscopy (cryo-EM). Unbiased computational sorting of cryo-EM images yielded 50 distinct three-dimensional reconstructions, showing the tRNAs in classical, hybrid and various novel intermediate states that provide trajectories and kinetic information about tRNA movement through the ribosome. The structures indicate how tRNA movement is coupled with global and local conformational changes of the ribosome, in particular of the head and body of the small ribosomal subunit, and show that dynamic interactions between tRNAs and ribosomal residues confine the path of the tRNAs through the ribosome. The temperature dependence of ribosome dynamics reveals a surprisingly flat energy landscape of conformational variations at physiological temperature. The ribosome functions as a Brownian machine that couples spontaneous conformational changes driven by thermal energy to directed movement.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fischer, Niels -- Konevega, Andrey L -- Wintermeyer, Wolfgang -- Rodnina, Marina V -- Stark, Holger -- England -- Nature. 2010 Jul 15;466(7304):329-33. doi: 10.1038/nature09206.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉3D Electron Cryomicroscopy Group, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631791" target="_blank"〉PubMed〈/a〉
    Keywords: Cryoelectron Microscopy ; Escherichia coli ; Kinetics ; Models, Molecular ; Molecular Conformation ; *Movement ; *Protein Biosynthesis ; RNA, Transfer/genetics/*metabolism ; Ribosome Subunits, Large, Bacterial/chemistry/metabolism ; Ribosome Subunits, Small, Bacterial/chemistry/metabolism ; Ribosomes/chemistry/*metabolism ; Temperature ; Thermodynamics ; Time Factors
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    Dendritic organization of sensory input to cortical neurons in vivo (2010)
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    Publication Date: 2010-04-30
    Description: In sensory cortex regions, neurons are tuned to specific stimulus features. For example, in the visual cortex, many neurons fire predominantly in response to moving objects of a preferred orientation. However, the characteristics of the synaptic input that cortical neurons receive to generate their output firing pattern remain unclear. Here we report a novel approach for the visualization and functional mapping of sensory inputs to the dendrites of cortical neurons in vivo. By combining high-speed two-photon imaging with electrophysiological recordings, we identify local subthreshold calcium signals that correspond to orientation-specific synaptic inputs. We find that even inputs that share the same orientation preference are widely distributed throughout the dendritic tree. At the same time, inputs of different orientation preference are interspersed, so that adjacent dendritic segments are tuned to distinct orientations. Thus, orientation-tuned neurons can compute their characteristic firing pattern by integrating spatially distributed synaptic inputs coding for multiple stimulus orientations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jia, Hongbo -- Rochefort, Nathalie L -- Chen, Xiaowei -- Konnerth, Arthur -- England -- Nature. 2010 Apr 29;464(7293):1307-12. doi: 10.1038/nature08947.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience and Center for Integrated Protein Science, Technical University Munich, Biedersteinerstrasse 29, 80802 Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20428163" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium Signaling ; Dendrites/*physiology ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Sensory Receptor Cells/cytology/*physiology ; Synapses/metabolism ; Visual Cortex/*cytology
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    Molecular robots guided by prescriptive landscapes (2010)
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    Publication Date: 2010-05-14
    Description: Traditional robots rely for their function on computing, to store internal representations of their goals and environment and to coordinate sensing and any actuation of components required in response. Moving robotics to the single-molecule level is possible in principle, but requires facing the limited ability of individual molecules to store complex information and programs. One strategy to overcome this problem is to use systems that can obtain complex behaviour from the interaction of simple robots with their environment. A first step in this direction was the development of DNA walkers, which have developed from being non-autonomous to being capable of directed but brief motion on one-dimensional tracks. Here we demonstrate that previously developed random walkers-so-called molecular spiders that comprise a streptavidin molecule as an inert 'body' and three deoxyribozymes as catalytic 'legs'-show elementary robotic behaviour when interacting with a precisely defined environment. Single-molecule microscopy observations confirm that such walkers achieve directional movement by sensing and modifying tracks of substrate molecules laid out on a two-dimensional DNA origami landscape. When using appropriately designed DNA origami, the molecular spiders autonomously carry out sequences of actions such as 'start', 'follow', 'turn' and 'stop'. We anticipate that this strategy will result in more complex robotic behaviour at the molecular level if additional control mechanisms are incorporated. One example might be interactions between multiple molecular robots leading to collective behaviour; another might be the ability to read and transform secondary cues on the DNA origami landscape as a means of implementing Turing-universal algorithmic behaviour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907518/" 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/PMC2907518/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lund, Kyle -- Manzo, Anthony J -- Dabby, Nadine -- Michelotti, Nicole -- Johnson-Buck, Alexander -- Nangreave, Jeanette -- Taylor, Steven -- Pei, Renjun -- Stojanovic, Milan N -- Walter, Nils G -- Winfree, Erik -- Yan, Hao -- P41 RR017573/RR/NCRR NIH HHS/ -- P41 RR017573-086704/RR/NCRR NIH HHS/ -- R01 GM062357/GM/NIGMS NIH HHS/ -- R01 GM062357-09/GM/NIGMS NIH HHS/ -- T32 EB005582/EB/NIBIB NIH HHS/ -- T32 EB005582-05/EB/NIBIB NIH HHS/ -- T32 GM008270/GM/NIGMS NIH HHS/ -- T32 GM008270-24/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 May 13;465(7295):206-10. doi: 10.1038/nature09012.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, Arizona State University, Tempe, Arizona 85287, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20463735" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Computers, Molecular ; DNA, Catalytic/*metabolism ; DNA, Single-Stranded/chemistry/*metabolism ; Microscopy, Atomic Force ; Microscopy, Fluorescence ; *Movement/drug effects ; Nanotechnology/*methods ; Robotics ; Streptavidin/*chemistry ; Surface Plasmon Resonance ; Time Factors ; Zinc/metabolism/pharmacology
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    Start/stop signals emerge in nigrostriatal circuits during sequence learning (2010)
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    Publication Date: 2010-07-24
    Description: Learning new action sequences subserves a plethora of different abilities such as escaping a predator, playing the piano, or producing fluent speech. Proper initiation and termination of each action sequence is critical for the organization of behaviour, and is compromised in nigrostriatal disorders like Parkinson's and Huntington's diseases. Using a self-paced operant task in which mice learn to perform a particular sequence of actions to obtain an outcome, we found neural activity in nigrostriatal circuits specifically signalling the initiation or the termination of each action sequence. This start/stop activity emerged during sequence learning, was specific for particular actions, and did not reflect interval timing, movement speed or action value. Furthermore, genetically altering the function of striatal circuits disrupted the development of start/stop activity and selectively impaired sequence learning. These results have important implications for understanding the functional organization of actions and the sequence initiation and termination impairments observed in basal ganglia disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477867/" 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/PMC3477867/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jin, Xin -- Costa, Rui M -- 243393/European Research Council/International -- Z01 AA000416-02/Intramural NIH HHS/ -- England -- Nature. 2010 Jul 22;466(7305):457-62. doi: 10.1038/nature09263.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Bethesda, Maryland 20892-9412, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651684" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal/physiology ; Dopamine/metabolism ; Glutamic Acid/metabolism ; Learning/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neostriatum/*physiology ; Neural Pathways/*physiology ; Receptors, N-Methyl-D-Aspartate/deficiency/genetics/metabolism ; Substantia Nigra/*physiology
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    Coupled dynamics of body mass and population growth in response to environmental change (2010)
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    Publication Date: 2010-07-24
    Description: Environmental change has altered the phenology, morphological traits and population dynamics of many species. However, the links underlying these joint responses remain largely unknown owing to a paucity of long-term data and the lack of an appropriate analytical framework. Here we investigate the link between phenotypic and demographic responses to environmental change using a new methodology and a long-term (1976-2008) data set from a hibernating mammal (the yellow-bellied marmot) inhabiting a dynamic subalpine habitat. We demonstrate how earlier emergence from hibernation and earlier weaning of young has led to a longer growing season and larger body masses before hibernation. The resulting shift in both the phenotype and the relationship between phenotype and fitness components led to a decline in adult mortality, which in turn triggered an abrupt increase in population size in recent years. Direct and trait-mediated effects of environmental change made comparable contributions to the observed marked increase in population growth. Our results help explain how a shift in phenology can cause simultaneous phenotypic and demographic changes, and highlight the need for a theory integrating ecological and evolutionary dynamics in stochastic environments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ozgul, Arpat -- Childs, Dylan Z -- Oli, Madan K -- Armitage, Kenneth B -- Blumstein, Daniel T -- Olson, Lucretia E -- Tuljapurkar, Shripad -- Coulson, Tim -- P01 AG022500/AG/NIA NIH HHS/ -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jul 22;466(7305):482-5. doi: 10.1038/nature09210.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Life Sciences, Imperial College London, Ascot, Berkshire SL5 7PY, UK. a.ozgul@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Body Weight/*physiology ; Colorado ; Female ; *Global Warming ; Hibernation/*physiology ; Marmota/*anatomy & histology/growth & development/*physiology ; Phenotype ; Population Dynamics ; Reproduction/physiology ; Survival Rate ; Time Factors ; Weaning
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    Climate-driven population divergence in sex-determining systems (2010)
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    Publication Date: 2010-10-29
    Description: Sex determination is a fundamental biological process, yet its mechanisms are remarkably diverse. In vertebrates, sex can be determined by inherited genetic factors or by the temperature experienced during embryonic development. However, the evolutionary causes of this diversity remain unknown. Here we show that live-bearing lizards at different climatic extremes of the species' distribution differ in their sex-determining mechanisms, with temperature-dependent sex determination in lowlands and genotypic sex determination in highlands. A theoretical model parameterized with field data accurately predicts this divergence in sex-determining systems and the consequence thereof for variation in cohort sex ratios among years. Furthermore, we show that divergent natural selection on sex determination across altitudes is caused by climatic effects on lizard life history and variation in the magnitude of between-year temperature fluctuations. Our results establish an adaptive explanation for intra-specific divergence in sex-determining systems driven by phenotypic plasticity and ecological selection, thereby providing a unifying framework for integrating the developmental, ecological and evolutionary basis for variation in vertebrate sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pen, Ido -- Uller, Tobias -- Feldmeyer, Barbara -- Harts, Anna -- While, Geoffrey M -- Wapstra, Erik -- England -- Nature. 2010 Nov 18;468(7322):436-8. doi: 10.1038/nature09512. Epub 2010 Oct 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Theoretical Biology Group, University of Groningen, PO Box 14, 9750 AA Haren, the Netherlands. i.r.pen@rug.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981009" target="_blank"〉PubMed〈/a〉
    Keywords: Altitude ; Animals ; Biological Evolution ; *Climate ; Female ; Genotype ; Lizards/*genetics/*physiology ; Male ; Models, Biological ; Phenotype ; Selection, Genetic ; Sex Chromosomes ; *Sex Determination Processes/genetics/physiology ; *Sex Differentiation/genetics/physiology ; Sex Ratio ; *Temperature ; Time Factors ; Viviparity, Nonmammalian/physiology
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    Human genome: Genomes by the thousand (2010)
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    Publication Date: 2010-10-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 Oct 28;467(7319):1026-7. doi: 10.1038/4671026a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20981067" target="_blank"〉PubMed〈/a〉
    Keywords: Americas ; Asia ; Europe ; Genetic Predisposition to Disease ; Genetics, Population ; *Genome, Human ; Genomics/economics/*statistics & numerical data/trends ; Humans ; Precision Medicine/trends ; Sequence Analysis, DNA/economics/*statistics & numerical data/trends ; Time Factors
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    Protein-protein interactions: Real-time analysis (2010)
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    Publication Date: 2010-12-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonetta, Laura -- England -- Nature. 2010 Dec 9;468(7325):854. doi: 10.1038/468854a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21151000" target="_blank"〉PubMed〈/a〉
    Keywords: California ; Protein Binding ; Protein Interaction Mapping/*methods ; RNA, Transfer/metabolism ; Ribosomes/metabolism ; Sequence Analysis, DNA/methods ; Time Factors
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    Archiving lessons from radiobiology (2010)
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    Publication Date: 2010-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schofield, Paul N -- Tapio, Soile -- Grosche, Bernd -- England -- Nature. 2010 Dec 2;468(7324):634. doi: 10.1038/468634a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124436" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archives/*history ; Databases, Factual/history ; Europe ; History, 20th Century ; Information Storage and Retrieval ; Japan ; Radiobiology/*history ; Time Factors ; United States
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    Hobbit origins pushed back (2010)
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    Publication Date: 2010-03-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalton, Rex -- England -- Nature. 2010 Mar 18;464(7287):335. doi: 10.1038/464335a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20237533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Geography ; Hominidae/*classification ; Indonesia ; Paleontology ; *Phylogeny ; Time Factors
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    Biomarkers: casting the net wide (2010)
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    Publication Date: 2010-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Rachel -- England -- Nature. 2010 Aug 26;466(7310):S11-2. doi: 10.1038/466S11a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20739930" target="_blank"〉PubMed〈/a〉
    Keywords: *Biomarkers ; Brain/pathology ; *Early Diagnosis ; Ethics, Medical ; Humans ; Parkinson Disease/*diagnosis/pathology ; Risk Factors ; Time Factors
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    Gene therapy: Targeting beta-thalassaemia (2010)
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    Publication Date: 2010-09-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persons, Derek A -- England -- Nature. 2010 Sep 16;467(7313):277-8. doi: 10.1038/467277a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844523" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Blood Cells/cytology/metabolism ; Blood Transfusion ; Clone Cells/metabolism ; *Genetic Therapy ; HMGA2 Protein/genetics/*metabolism ; Humans ; Male ; Time Factors ; Transcriptional Activation ; Young Adult ; beta-Globins/*genetics/*metabolism ; beta-Thalassemia/*genetics/metabolism/*therapy
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    Spatiotemporal regulation of cell-cycle genes by SHORTROOT links patterning and growth (2010)
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    Publication Date: 2010-07-03
    Description: The development of multicellular organisms relies on the coordinated control of cell divisions leading to proper patterning and growth. The molecular mechanisms underlying pattern formation, particularly the regulation of formative cell divisions, remain poorly understood. In Arabidopsis, formative divisions generating the root ground tissue are controlled by SHORTROOT (SHR) and SCARECROW (SCR). Here we show, using cell-type-specific transcriptional effects of SHR and SCR combined with data from chromatin immunoprecipitation-based microarray experiments, that SHR regulates the spatiotemporal activation of specific genes involved in cell division. Coincident with the onset of a specific formative division, SHR and SCR directly activate a D-type cyclin; furthermore, altering the expression of this cyclin resulted in formative division defects. Our results indicate that proper pattern formation is achieved through transcriptional regulation of specific cell-cycle genes in a cell-type- and developmental-stage-specific context. Taken together, we provide evidence for a direct link between developmental regulators, specific components of the cell-cycle machinery and organ patterning.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967763/" 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/PMC2967763/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sozzani, R -- Cui, H -- Moreno-Risueno, M A -- Busch, W -- Van Norman, J M -- Vernoux, T -- Brady, S M -- Dewitte, W -- Murray, J A H -- Benfey, P N -- BB/E022383/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E022383/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E022383/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- P50 GM081883/GM/NIGMS NIH HHS/ -- P50 GM081883-020003/GM/NIGMS NIH HHS/ -- P50 GM081883-030003/GM/NIGMS NIH HHS/ -- P50-GM081883/GM/NIGMS NIH HHS/ -- R01 GM043778/GM/NIGMS NIH HHS/ -- R01 GM043778-18/GM/NIGMS NIH HHS/ -- R01 GM043778-19/GM/NIGMS NIH HHS/ -- R01 GM043778-20/GM/NIGMS NIH HHS/ -- R01 GM043778-21/GM/NIGMS NIH HHS/ -- R01-GM043778/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Jul 1;466(7302):128-32. doi: 10.1038/nature09143.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and IGSP Center for Systems Biology, Duke University, Durham, North Carolina 27708, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20596025" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/cytology/embryology/*genetics/*growth & development ; Arabidopsis Proteins/genetics/*metabolism ; Body Patterning/*genetics/*physiology ; Cell Cycle/genetics/physiology ; Cell Division/genetics ; Cyclin D/genetics/metabolism ; Cyclin-Dependent Kinases/metabolism ; Gene Expression Regulation, Plant ; Genes, cdc/*physiology ; Organogenesis/genetics/physiology ; Plant Roots/cytology/embryology/genetics/growth & development ; Time Factors ; Transcription Factors/genetics/*metabolism
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    Role of conserved non-coding DNA elements in the Foxp3 gene in regulatory T-cell fate (2010)
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    Publication Date: 2010-01-15
    Description: Immune homeostasis is dependent on tight control over the size of a population of regulatory T (T(reg)) cells capable of suppressing over-exuberant immune responses. The T(reg) cell subset is comprised of cells that commit to the T(reg) lineage by upregulating the transcription factor Foxp3 either in the thymus (tT(reg)) or in the periphery (iT(reg)). Considering a central role for Foxp3 in T(reg) cell differentiation and function, we proposed that conserved non-coding DNA sequence (CNS) elements at the Foxp3 locus encode information defining the size, composition and stability of the T(reg) cell population. Here we describe the function of three Foxp3 CNS elements (CNS1-3) in T(reg) cell fate determination in mice. The pioneer element CNS3, which acts to potently increase the frequency of T(reg) cells generated in the thymus and the periphery, binds c-Rel in in vitro assays. In contrast, CNS1, which contains a TGF-beta-NFAT response element, is superfluous for tT(reg) cell differentiation, but has a prominent role in iT(reg) cell generation in gut-associated lymphoid tissues. CNS2, although dispensable for Foxp3 induction, is required for Foxp3 expression in the progeny of dividing T(reg) cells. Foxp3 binds to CNS2 in a Cbf-beta-Runx1 and CpG DNA demethylation-dependent manner, suggesting that Foxp3 recruitment to this 'cellular memory module' facilitates the heritable maintenance of the active state of the Foxp3 locus and, therefore, T(reg) lineage stability. Together, our studies demonstrate that the composition, size and maintenance of the T(reg) cell population are controlled by Foxp3 CNS elements engaged in response to distinct cell-extrinsic or -intrinsic cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884187/" 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/PMC2884187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Ye -- Josefowicz, Steven -- Chaudhry, Ashutosh -- Peng, Xiao P -- Forbush, Katherine -- Rudensky, Alexander Y -- R37 AI034206/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 11;463(7282):808-12. doi: 10.1038/nature08750. Epub 2010 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Immunology, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20072126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage/*genetics ; Chromatin Assembly and Disassembly ; Conserved Sequence/*genetics ; CpG Islands/genetics ; DNA Methylation ; Female ; Forkhead Transcription Factors/*genetics/metabolism ; Gene Expression Regulation ; Lymphocyte Count ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-rel/metabolism ; Regulatory Sequences, Nucleic Acid/*genetics ; Response Elements/genetics ; T-Lymphocytes, Regulatory/*cytology/immunology/*metabolism ; Thymus Gland/cytology/immunology/metabolism
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    Atmospheric science: A towering experiment (2010)
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    Publication Date: 2010-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tollefson, Jeff -- England -- Nature. 2010 Sep 23;467(7314):386-7. doi: 10.1038/467386a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20864970" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Brazil ; Carbon Dioxide/*analysis/metabolism ; *Ecosystem ; Environmental Monitoring/economics/*instrumentation ; Forestry ; Germany ; Global Warming ; *Greenhouse Effect ; Time Factors ; Trees/growth & development/*metabolism ; Tropical Climate
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    Preventing the return of fear in humans using reconsolidation update mechanisms (2009)
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    Publication Date: 2009-12-17
    Description: Recent research on changing fears has examined targeting reconsolidation. During reconsolidation, stored information is rendered labile after being retrieved. Pharmacological manipulations at this stage result in an inability to retrieve the memories at later times, suggesting that they are erased or persistently inhibited. Unfortunately, the use of these pharmacological manipulations in humans can be problematic. Here we introduce a non-invasive technique to target the reconsolidation of fear memories in humans. We provide evidence that old fear memories can be updated with non-fearful information provided during the reconsolidation window. As a consequence, fear responses are no longer expressed, an effect that lasted at least a year and was selective only to reactivated memories without affecting others. These findings demonstrate the adaptive role of reconsolidation as a window of opportunity to rewrite emotional memories, and suggest a non-invasive technique that can be used safely in humans to prevent the return of fear.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640262/" 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/PMC3640262/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schiller, Daniela -- Monfils, Marie-H -- Raio, Candace M -- Johnson, David C -- Ledoux, Joseph E -- Phelps, Elizabeth A -- K05 MH067048/MH/NIMH NIH HHS/ -- P50 MH058911/MH/NIMH NIH HHS/ -- R01 MH038774/MH/NIMH NIH HHS/ -- R01 MH046516/MH/NIMH NIH HHS/ -- R21 MH072279/MH/NIMH NIH HHS/ -- R37 MH038774/MH/NIMH NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Jan 7;463(7277):49-53. doi: 10.1038/nature08637. Epub 2009 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, New York University, New York, New York 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010606" target="_blank"〉PubMed〈/a〉
    Keywords: Conditioning, Classical/*physiology ; Cues ; Electrodes ; Electroshock ; Extinction, Psychological/*physiology ; Fear/*physiology/*psychology ; Humans ; Memory/*physiology ; Models, Neurological ; Models, Psychological ; Neuronal Plasticity/*physiology ; Photic Stimulation ; Time Factors
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    Damage-induced phosphorylation of Sld3 is important to block late origin firing (2010)
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    Publication Date: 2010-09-25
    Description: Origins of replication are activated throughout the S phase of the cell cycle such that some origins fire early and others fire late to ensure that each chromosome is completely replicated in a timely fashion. However, in response to DNA damage or replication fork stalling, eukaryotic cells block activation of unfired origins. Human cells derived from patients with ataxia telangiectasia are deficient in this process due to the lack of a functional ataxia telangiectasia mutated (ATM) kinase and elicit radioresistant DNA synthesis after gamma-irradiation(2). This effect is conserved in budding yeast, as yeast cells lacking the related kinase Mec1 (ATM and Rad3-related (ATR in humans)) also fail to inhibit DNA synthesis in the presence of DNA damage. This intra-S-phase checkpoint actively regulates DNA synthesis by inhibiting the firing of late replicating origins, and this inhibition requires both Mec1 and the downstream checkpoint kinase Rad53 (Chk2 in humans). However, the Rad53 substrate(s) whose phosphorylation is required to mediate this function has remained unknown. Here we show that the replication initiation protein Sld3 is phosphorylated by Rad53, and that this phosphorylation, along with phosphorylation of the Cdc7 kinase regulatory subunit Dbf4, blocks late origin firing in Saccharomyces cerevisiae. Upon exposure to DNA-damaging agents, cells expressing non-phosphorylatable alleles of SLD3 and DBF4 (SLD3-m25 and dbf4-m25, respectively) proceed through the S phase faster than wild-type cells by inappropriately firing late origins of replication. SLD3-m25 dbf4-m25 cells grow poorly in the presence of the replication inhibitor hydroxyurea and accumulate multiple Rad52 foci. Moreover, SLD3-m25 dbf4-m25 cells are delayed in recovering from transient blocks to replication and subsequently arrest at the DNA damage checkpoint. These data indicate that the intra-S-phase checkpoint functions to block late origin firing in adverse conditions to prevent genomic instability and maximize cell survival.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3393088/" 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/PMC3393088/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Mosqueda, Jaime -- Maas, Nancy L -- Jonsson, Zophonias O -- Defazio-Eli, Lisa G -- Wohlschlegel, James -- Toczyski, David P -- GM059691/GM/NIGMS NIH HHS/ -- R01 GM059691/GM/NIGMS NIH HHS/ -- R01 GM059691-09/GM/NIGMS NIH HHS/ -- R01 GM059691-10/GM/NIGMS NIH HHS/ -- R01 GM059691-11/GM/NIGMS NIH HHS/ -- R01 GM059691-12/GM/NIGMS NIH HHS/ -- R01 GM089778/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Sep 23;467(7314):479-83. doi: 10.1038/nature09377.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California 94158-9001, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20865002" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle Proteins/genetics/*metabolism ; Checkpoint Kinase 2 ; DNA Damage/*physiology ; DNA Replication/drug effects/*physiology ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Hydroxyurea/pharmacology ; Phosphorylation/drug effects ; Protein-Serine-Threonine Kinases ; Rad52 DNA Repair and Recombination Protein/metabolism ; Replication Origin/drug effects/*physiology ; *S Phase/drug effects/physiology ; Saccharomyces cerevisiae/cytology/drug effects/genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics/*metabolism ; Time Factors
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    Encoding of conditioned fear in central amygdala inhibitory circuits (2010)
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    Publication Date: 2010-11-12
    Description: The central amygdala (CEA), a nucleus predominantly composed of GABAergic inhibitory neurons, is essential for fear conditioning. How the acquisition and expression of conditioned fear are encoded within CEA inhibitory circuits is not understood. Using in vivo electrophysiological, optogenetic and pharmacological approaches in mice, we show that neuronal activity in the lateral subdivision of the central amygdala (CEl) is required for fear acquisition, whereas conditioned fear responses are driven by output neurons in the medial subdivision (CEm). Functional circuit analysis revealed that inhibitory CEA microcircuits are highly organized and that cell-type-specific plasticity of phasic and tonic activity in the CEl to CEm pathway may gate fear expression and regulate fear generalization. Our results define the functional architecture of CEA microcircuits and their role in the acquisition and regulation of conditioned fear behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciocchi, Stephane -- Herry, Cyril -- Grenier, Francois -- Wolff, Steffen B E -- Letzkus, Johannes J -- Vlachos, Ioannis -- Ehrlich, Ingrid -- Sprengel, Rolf -- Deisseroth, Karl -- Stadler, Michael B -- Muller, Christian -- Luthi, Andreas -- England -- Nature. 2010 Nov 11;468(7321):277-82. doi: 10.1038/nature09559.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068837" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Amygdala/anatomy & histology/cytology/*physiology ; Animals ; Conditioning, Classical/*physiology ; Fear/*physiology ; Freezing Reaction, Cataleptic ; Male ; Mice ; Mice, Inbred C57BL ; Neural Inhibition/*physiology ; Neural Pathways/cytology/*physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; gamma-Aminobutyric Acid/metabolism
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    mTORC1 controls fasting-induced ketogenesis and its modulation by ageing (2010)
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    Publication Date: 2010-12-24
    Description: The multi-component mechanistic target of rapamycin complex 1 (mTORC1) kinase is the central node of a mammalian pathway that coordinates cell growth with the availability of nutrients, energy and growth factors. Progress has been made in the identification of mTORC1 pathway components and in understanding their functions in cells, but there is relatively little known about the role of the pathway in vivo. Specifically, we have little knowledge regarding the role mTOCR1 has in liver physiology. In fasted animals, the liver performs numerous functions that maintain whole-body homeostasis, including the production of ketone bodies for peripheral tissues to use as energy sources. Here we show that mTORC1 controls ketogenesis in mice in response to fasting. We find that liver-specific loss of TSC1 (tuberous sclerosis 1), an mTORC1 inhibitor, leads to a fasting-resistant increase in liver size, and to a pronounced defect in ketone body production and ketogenic gene expression on fasting. The loss of raptor (regulatory associated protein of mTOR, complex 1) an essential mTORC1 component, has the opposite effects. In addition, we find that the inhibition of mTORC1 is required for the fasting-induced activation of PPARalpha (peroxisome proliferator activated receptor alpha), the master transcriptional activator of ketogenic genes, and that suppression of NCoR1 (nuclear receptor co-repressor 1), a co-repressor of PPARalpha, reactivates ketogenesis in cells and livers with hyperactive mTORC1 signalling. Like livers with activated mTORC1, livers from aged mice have a defect in ketogenesis, which correlates with an increase in mTORC1 signalling. Moreover, we show that the suppressive effects of mTORC1 activation and ageing on PPARalpha activity and ketone production are not additive, and that mTORC1 inhibition is sufficient to prevent the ageing-induced defect in ketogenesis. Thus, our findings reveal that mTORC1 is a key regulator of PPARalpha function and hepatic ketogenesis and suggest a role for mTORC1 activity in promoting the ageing of the liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sengupta, Shomit -- Peterson, Timothy R -- Laplante, Mathieu -- Oh, Stephanie -- Sabatini, David M -- CA103866/CA/NCI NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-04/CA/NCI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Dec 23;468(7327):1100-4. doi: 10.1038/nature09584.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179166" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Fasting/*metabolism ; *Gene Expression Regulation ; Humans ; Ketone Bodies/*biosynthesis/metabolism ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multiprotein Complexes ; Nuclear Receptor Co-Repressor 1/metabolism ; PPAR alpha/antagonists & inhibitors/metabolism ; Proteins/genetics/*metabolism ; TOR Serine-Threonine Kinases
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    Interdependence of behavioural variability and response to small stimuli in bacteria (2010)
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    Publication Date: 2010-11-16
    Description: The chemotaxis signalling network in Escherichia coli that controls the locomotion of bacteria is a classic model system for signal transduction. This pathway modulates the behaviour of flagellar motors to propel bacteria towards sources of chemical attractants. Although this system relaxes to a steady state in response to environmental changes, the signalling events within the chemotaxis network are noisy and cause large temporal variations of the motor behaviour even in the absence of stimulus. That the same signalling network governs both behavioural variability and cellular response raises the question of whether these two traits are independent. Here, we experimentally establish a fluctuation-response relationship in the chemotaxis system of living bacteria. Using this relationship, we demonstrate the possibility of inferring the cellular response from the behavioural variability measured before stimulus. In monitoring the pre- and post-stimulus switching behaviour of individual bacterial motors, we found that variability scales linearly with the response time for different functioning states of the cell. This study highlights that the fundamental relationship between fluctuation and response is not constrained to physical systems at thermodynamic equilibrium but is extensible to living cells. Such a relationship not only implies that behavioural variability and cellular response can be coupled traits, but it also provides a general framework within which we can examine how the selection of a network design shapes this interdependence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230254/" 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/PMC3230254/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Heungwon -- Pontius, William -- Guet, Calin C -- Marko, John F -- Emonet, Thierry -- Cluzel, Philippe -- 1U54CA143869-01/CA/NCI NIH HHS/ -- P50 GM081892/GM/NIGMS NIH HHS/ -- P50 GM081892-04/GM/NIGMS NIH HHS/ -- R01 AI059195-03/AI/NIAID NIH HHS/ -- R01AI059195-03/AI/NIAID NIH HHS/ -- U54 CA143869/CA/NCI NIH HHS/ -- U54 CA143869-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 9;468(7325):819-23. doi: 10.1038/nature09551. Epub 2010 Nov 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The James Franck Institute, The Institute for Biophysical Dynamics, and The Department of Physics, University of Chicago, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21076396" target="_blank"〉PubMed〈/a〉
    Keywords: Aspartic Acid/metabolism/pharmacology ; Calibration ; Chemotaxis/drug effects/*physiology ; Chromatography, High Pressure Liquid ; *Environment ; Escherichia coli/*cytology/drug effects/*physiology ; Flagella/drug effects/physiology ; Molecular Motor Proteins/metabolism ; Rotation ; *Signal Transduction/drug effects ; Stochastic Processes ; Time Factors
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    Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke (2010)
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    Publication Date: 2010-11-05
    Description: Stroke is a leading cause of disability, but no pharmacological therapy is currently available for promoting recovery. The brain region adjacent to stroke damage-the peri-infarct zone-is critical for rehabilitation, as it shows heightened neuroplasticity, allowing sensorimotor functions to re-map from damaged areas. Thus, understanding the neuronal properties constraining this plasticity is important for the development of new treatments. Here we show that after a stroke in mice, tonic neuronal inhibition is increased in the peri-infarct zone. This increased tonic inhibition is mediated by extrasynaptic GABA(A) receptors and is caused by an impairment in GABA (gamma-aminobutyric acid) transporter (GAT-3/GAT-4) function. To counteract the heightened inhibition, we administered in vivo a benzodiazepine inverse agonist specific for alpha5-subunit-containing extrasynaptic GABA(A) receptors at a delay after stroke. This treatment produced an early and sustained recovery of motor function. Genetically lowering the number of alpha5- or delta-subunit-containing GABA(A) receptors responsible for tonic inhibition also proved beneficial for recovery after stroke, consistent with the therapeutic potential of diminishing extrasynaptic GABA(A) receptor function. Together, our results identify new pharmacological targets and provide the rationale for a novel strategy to promote recovery after stroke and possibly other brain injuries.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058798/" 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/PMC3058798/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clarkson, Andrew N -- Huang, Ben S -- Macisaac, Sarah E -- Mody, Istvan -- Carmichael, S Thomas -- NS30549/NS/NINDS NIH HHS/ -- R01 NS030549/NS/NINDS NIH HHS/ -- R01 NS030549-18/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Nov 11;468(7321):305-9. doi: 10.1038/nature09511. Epub 2010 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21048709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/pharmacology ; Cerebral Infarction/metabolism/pathology/physiopathology ; Disease Models, Animal ; Drug Inverse Agonism ; GABA Antagonists/pharmacology ; GABA Plasma Membrane Transport Proteins/metabolism ; Imidazoles/pharmacology ; Male ; Membrane Potentials/drug effects ; Mice ; Mice, Inbred C57BL ; Motor Cortex/metabolism/pathology/*physiology/*physiopathology ; Neuronal Plasticity/physiology ; Receptors, GABA/deficiency/genetics/metabolism ; Recovery of Function/*physiology ; Stroke/drug therapy/*metabolism/pathology ; Synapses/metabolism ; Time Factors ; gamma-Aminobutyric Acid/*metabolism
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    Putting brain training to the test (2010)
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    Publication Date: 2010-04-22
    Description: 'Brain training', or the goal of improved cognitive function through the regular use of computerized tests, is a multimillion-pound industry, yet in our view scientific evidence to support its efficacy is lacking. Modest effects have been reported in some studies of older individuals and preschool children, and video-game players outperform non-players on some tests of visual attention. However, the widely held belief that commercially available computerized brain-training programs improve general cognitive function in the wider population in our opinion lacks empirical support. The central question is not whether performance on cognitive tests can be improved by training, but rather, whether those benefits transfer to other untrained tasks or lead to any general improvement in the level of cognitive functioning. Here we report the results of a six-week online study in which 11,430 participants trained several times each week on cognitive tasks designed to improve reasoning, memory, planning, visuospatial skills and attention. Although improvements were observed in every one of the cognitive tasks that were trained, no evidence was found for transfer effects to untrained tasks, even when those tasks were cognitively closely related.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884087/" 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/PMC2884087/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owen, Adrian M -- Hampshire, Adam -- Grahn, Jessica A -- Stenton, Robert -- Dajani, Said -- Burns, Alistair S -- Howard, Robert J -- Ballard, Clive G -- MC_U105559837/Medical Research Council/United Kingdom -- MC_U105559847/Medical Research Council/United Kingdom -- U.1055.01.002.00001.01/Medical Research Council/United Kingdom -- U.1055.01.002.00001.01(80449)/Medical Research Council/United Kingdom -- U.1055.01.003.00001.01/Medical Research Council/United Kingdom -- England -- Nature. 2010 Jun 10;465(7299):775-8. doi: 10.1038/nature09042.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Cognition and Brain Sciences Unit, 15 Chaucer Road, Cambridge CB2 7EF, UK. adrian.owen@mrc-cbu.cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20407435" target="_blank"〉PubMed〈/a〉
    Keywords: Attention/physiology ; Brain/*physiology ; Cognition/*physiology ; Computers ; Exercise/*physiology ; Humans ; Memory/physiology ; Task Performance and Analysis ; Thinking/physiology ; Time Factors
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    Ensemble reconstruction constraints on the global carbon cycle sensitivity to climate (2010)
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    Publication Date: 2010-01-30
    Description: The processes controlling the carbon flux and carbon storage of the atmosphere, ocean and terrestrial biosphere are temperature sensitive and are likely to provide a positive feedback leading to amplified anthropogenic warming. Owing to this feedback, at timescales ranging from interannual to the 20-100-kyr cycles of Earth's orbital variations, warming of the climate system causes a net release of CO(2) into the atmosphere; this in turn amplifies warming. But the magnitude of the climate sensitivity of the global carbon cycle (termed gamma), and thus of its positive feedback strength, is under debate, giving rise to large uncertainties in global warming projections. Here we quantify the median gamma as 7.7 p.p.m.v. CO(2) per degrees C warming, with a likely range of 1.7-21.4 p.p.m.v. CO(2) per degrees C. Sensitivity experiments exclude significant influence of pre-industrial land-use change on these estimates. Our results, based on the coupling of a probabilistic approach with an ensemble of proxy-based temperature reconstructions and pre-industrial CO(2) data from three ice cores, provide robust constraints for gamma on the policy-relevant multi-decadal to centennial timescales. By using an ensemble of 〉200,000 members, quantification of gamma is not only improved, but also likelihoods can be assigned, thereby providing a benchmark for future model simulations. Although uncertainties do not at present allow exclusion of gamma calculated from any of ten coupled carbon-climate models, we find that gamma is about twice as likely to fall in the lowermost than in the uppermost quartile of their range. Our results are incompatibly lower (P 〈 0.05) than recent pre-industrial empirical estimates of approximately 40 p.p.m.v. CO(2) per degrees C (refs 6, 7), and correspondingly suggest approximately 80% less potential amplification of ongoing global warming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, David C -- Esper, Jan -- Raible, Christoph C -- Buntgen, Ulf -- Trouet, Valerie -- Stocker, Benjamin -- Joos, Fortunat -- England -- Nature. 2010 Jan 28;463(7280):527-30. doi: 10.1038/nature08769.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Federal Research Institute WSL, Zurcherstrasse 111, CH-8903 Birmensdorf, Switzerland. david.frank@wsl.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20110999" target="_blank"〉PubMed〈/a〉
    Keywords: Carbon/*metabolism ; Carbon Dioxide/analysis ; *Climate Change ; Ice/analysis ; *Models, Theoretical ; Temperature ; Time Factors
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    The prion protein as a receptor for amyloid-beta (2010)
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    Publication Date: 2010-08-13
    Description: Increased levels of brain amyloid-beta, a secreted peptide cleavage product of amyloid precursor protein (APP), is believed to be critical in the aetiology of Alzheimer's disease. Increased amyloid-beta can cause synaptic depression, reduce the number of spine protrusions (that is, sites of synaptic contacts) and block long-term synaptic potentiation (LTP), a form of synaptic plasticity; however, the receptor through which amyloid-beta produces these synaptic perturbations has remained elusive. Lauren et al. suggested that binding between oligomeric amyloid-beta (a form of amyloid-beta thought to be most active) and the cellular prion protein (PrP(C)) is necessary for synaptic perturbations. Here we show that PrP(C) is not required for amyloid-beta-induced synaptic depression, reduction in spine density, or blockade of LTP; our results indicate that amyloid-beta-mediated synaptic defects do not require PrP(c).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057871/" 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/PMC3057871/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kessels, Helmut W -- Nguyen, Louis N -- Nabavi, Sadegh -- Malinow, Roberto -- R01 AG032132/AG/NIA NIH HHS/ -- R01 AG032132-14/AG/NIA NIH HHS/ -- R01 AG032132-15/AG/NIA NIH HHS/ -- R01 AG032132-17/AG/NIA NIH HHS/ -- R01 AG032132-18/AG/NIA NIH HHS/ -- R01 MH049159/MH/NIMH NIH HHS/ -- R01 MH049159-09/MH/NIMH NIH HHS/ -- R01 MH049159-21/MH/NIMH NIH HHS/ -- R01 MH049159-22/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Aug 12;466(7308):E3-4; discussion E4-5. doi: 10.1038/nature09217.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Circuits and Behavior, 9500 Gilman Drive 0634, University of California at San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703260" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amyloid beta-Peptides/chemistry/genetics/*metabolism ; Animals ; Learning/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; PrPC Proteins/deficiency/genetics/*metabolism ; Reproducibility of Results ; Serotonin/metabolism ; Synapses/*metabolism/*pathology ; Synaptic Transmission
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    The human genome at ten (2010)
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    Publication Date: 2010-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 Apr 1;464(7289):649-50. doi: 10.1038/464649a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360688" target="_blank"〉PubMed〈/a〉
    Keywords: Data Collection ; Genetic Testing/trends ; Genetics, Medical/*trends ; Genome, Human/*genetics ; Genomics/economics/*history/trends ; Haplotypes/genetics ; History, 20th Century ; History, 21st Century ; Human Genome Project/*history ; Humans ; Time Factors
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    Single-molecule analysis: A ribosome in action (2010)
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    Publication Date: 2010-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brakmann, Susanne -- England -- Nature. 2010 Apr 15;464(7291):987-8. doi: 10.1038/464987a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393548" target="_blank"〉PubMed〈/a〉
    Keywords: Codon/*genetics ; Fluorescence ; Ligands ; Protein Biosynthesis/genetics/*physiology ; RNA, Transfer/genetics/*metabolism ; Ribosomes/chemistry/genetics/*metabolism ; Time Factors
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    Scientists need a shorter path to research freedom (2010)
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    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, Francis -- England -- Nature. 2010 Oct 7;467(7316):635. doi: 10.1038/467635a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20930798" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aptitude ; Awards and Prizes ; *Career Mobility ; Creativity ; Financing, Organized/economics ; *Freedom ; Humans ; Laboratories/economics/manpower ; National Institutes of Health (U.S.) ; Pilot Projects ; *Research/education/manpower ; *Research Personnel/education ; Research Support as Topic/economics/organization & administration ; Time Factors ; United States
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    Climate change: Fatter marmots on the rise (2010)
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    Publication Date: 2010-07-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Visser, Marcel E -- England -- Nature. 2010 Jul 22;466(7305):445-7. doi: 10.1038/466445a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20651679" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Body Weight/*physiology ; Colorado ; *Global Warming ; Hibernation/*physiology ; Marmota/*anatomy & histology/growth & development/*physiology ; Population Dynamics ; Time Factors
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    Far-sighted vision (2010)
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    Publication Date: 2010-08-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 Aug 19;466(7309):903. doi: 10.1038/466903a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20724996" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/economics/instrumentation/trends ; Budgets/trends ; *Data Collection ; Program Evaluation ; Research/economics/trends ; Time Factors ; United States ; United States National Aeronautics and Space Administration/*economics/trends
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    No gain from brain training (2010)
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    Publication Date: 2010-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Katsnelson, Alla -- England -- Nature. 2010 Apr 22;464(7292):1111. doi: 10.1038/4641111a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414280" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Brain/*physiology ; Exercise/physiology ; Humans ; Mental Processes/*physiology ; Middle Aged ; Time Factors ; Treatment Failure ; *Video Games ; Young Adult
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    Step up aspirations to save biodiversity as 2010 begins (2010)
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    Publication Date: 2010-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Khosla, Ashok -- Marton-Lefevre, Julia -- England -- Nature. 2010 Jan 7;463(7277):25. doi: 10.1038/463025c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054377" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; Conservation of Natural Resources/*trends ; Extinction, Biological ; Politics ; Time Factors
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    Behavioural ecology: Learn to beat an identity cheat (2010)
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    Publication Date: 2010-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kilner, Rebecca -- England -- Nature. 2010 Jan 14;463(7278):165-7. doi: 10.1038/463165a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075907" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Birds/*parasitology/*physiology ; Cues ; Discrimination Learning/*physiology ; Models, Biological ; Nesting Behavior/*physiology ; Pattern Recognition, Visual/physiology ; Survival Rate ; Time Factors
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    Using temperature to analyse temporal dynamics in the songbird motor pathway (2008)
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    Publication Date: 2008-11-14
    Description: Many complex behaviours, like speech or music, have a hierarchical organization with structure on many timescales, but it is not known how the brain controls the timing of behavioural sequences, or whether different circuits control different timescales of the behaviour. Here we address these issues by using temperature to manipulate the biophysical dynamics in different regions of the songbird forebrain involved in song production. We find that cooling the premotor nucleus HVC (formerly known as the high vocal centre) slows song speed across all timescales by up to 45 per cent but only slightly alters the acoustic structure, whereas cooling the downstream motor nucleus RA (robust nucleus of the arcopallium) has no observable effect on song timing. Our observations suggest that dynamics within HVC are involved in the control of song timing, perhaps through a chain-like organization. Local manipulation of brain temperature should be broadly applicable to the identification of neural circuitry that controls the timing of behavioural sequences and, more generally, to the study of the origin and role of oscillatory and other forms of brain dynamics in neural systems.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723166/" 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/PMC2723166/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Michael A -- Fee, Michale S -- DC009280/DC/NIDCD NIH HHS/ -- K99 DC009280/DC/NIDCD NIH HHS/ -- K99 DC009280-02/DC/NIDCD NIH HHS/ -- MH067105/MH/NIMH NIH HHS/ -- R01 MH067105/MH/NIMH NIH HHS/ -- R01 MH067105-04/MH/NIMH NIH HHS/ -- England -- Nature. 2008 Nov 13;456(7219):189-94. doi: 10.1038/nature07448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19005546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cold Temperature ; Efferent Pathways/physiology ; Finches/*physiology ; High Vocal Center/*physiology ; Neurons/physiology ; Prosencephalon/*physiology/radiography ; Time Factors ; Vocalization, Animal/*physiology
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    James Watson's genome sequenced at high speed (2008)
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    Publication Date: 2008-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wadman, Meredith -- England -- Nature. 2008 Apr 17;452(7189):788. doi: 10.1038/452788b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18431822" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Counseling/trends ; *Genome, Human ; Genomics/economics/*trends ; History, 21st Century ; Humans ; Individuality ; Male ; Reference Standards ; Sequence Analysis, DNA/economics/*trends ; Time Factors
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    Orbital and millennial-scale features of atmospheric CH4 over the past 800,000 years (2008)
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    Details
    Publication Date: 2008-05-16
    Description: Atmospheric methane is an important greenhouse gas and a sensitive indicator of climate change and millennial-scale temperature variability. Its concentrations over the past 650,000 years have varied between approximately 350 and approximately 800 parts per 10(9) by volume (p.p.b.v.) during glacial and interglacial periods, respectively. In comparison, present-day methane levels of approximately 1,770 p.p.b.v. have been reported. Insights into the external forcing factors and internal feedbacks controlling atmospheric methane are essential for predicting the methane budget in a warmer world. Here we present a detailed atmospheric methane record from the EPICA Dome C ice core that extends the history of this greenhouse gas to 800,000 yr before present. The average time resolution of the new data is approximately 380 yr and permits the identification of orbital and millennial-scale features. Spectral analyses indicate that the long-term variability in atmospheric methane levels is dominated by approximately 100,000 yr glacial-interglacial cycles up to approximately 400,000 yr ago with an increasing contribution of the precessional component during the four more recent climatic cycles. We suggest that changes in the strength of tropical methane sources and sinks (wetlands, atmospheric oxidation), possibly influenced by changes in monsoon systems and the position of the intertropical convergence zone, controlled the atmospheric methane budget, with an additional source input during major terminations as the retreat of the northern ice sheet allowed higher methane emissions from extending periglacial wetlands. Millennial-scale changes in methane levels identified in our record as being associated with Antarctic isotope maxima events are indicative of ubiquitous millennial-scale temperature variability during the past eight glacial cycles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loulergue, Laetitia -- Schilt, Adrian -- Spahni, Renato -- Masson-Delmotte, Valerie -- Blunier, Thomas -- Lemieux, Benedicte -- Barnola, Jean-Marc -- Raynaud, Dominique -- Stocker, Thomas F -- Chappellaz, Jerome -- England -- Nature. 2008 May 15;453(7193):383-6. doi: 10.1038/nature06950.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Glaciologie et Geophysique de l'Environnement, CNRS-Universite Joseph Fourier Grenoble, 54 Rue Moliere, 38402 St Martin d'Heres, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18480822" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Greenhouse Effect ; History, Ancient ; Ice Cover ; Methane/*analysis ; Temperature ; Time Factors ; Tropical Climate ; Wetlands
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    Microbiology: metagenomics (2008)
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    Publication Date: 2008-09-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hugenholtz, Philip -- Tyson, Gene W -- England -- Nature. 2008 Sep 25;455(7212):481-3. doi: 10.1038/455481a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18818648" target="_blank"〉PubMed〈/a〉
    Keywords: Biodiversity ; Computational Biology/trends ; *Ecosystem ; *Environmental Microbiology ; Eukaryotic Cells/metabolism ; Evolution, Molecular ; *Genetics, Microbial/methods ; Genome/genetics ; *Genomics/economics/methods/trends ; Humans ; Marine Biology ; Prokaryotic Cells/metabolism ; Sequence Analysis, DNA/economics ; Time Factors ; Viruses/genetics
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    T-cell-expressed proprotein convertase furin is essential for maintenance of peripheral immune tolerance (2008)
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    Publication Date: 2008-08-15
    Description: Furin is one of seven proprotein convertase family members that promote proteolytic maturation of proproteins. It is induced in activated T cells and is reported to process a variety of substrates including the anti-inflammatory cytokine transforming growth factor (TGF)-beta1 (refs 2-4), but the non-redundant functions of furin versus other proprotein convertases in T cells are unclear. Here we show that conditional deletion of furin in T cells allowed for normal T-cell development but impaired the function of regulatory and effector T cells, which produced less TGF-beta1. Furin-deficient T regulatory (Treg) cells were less protective in a T-cell transfer colitis model and failed to induce Foxp3 in normal T cells. Additionally, furin-deficient effector cells were inherently over-active and were resistant to suppressive activity of wild-type Treg cells. Thus, our results indicate that furin is indispensable in maintaining peripheral tolerance, which is due, at least in part, to its non-redundant, essential function in regulating TGF-beta1 production. Targeting furin has emerged as a strategy in malignant and infectious disease. Our results suggest that inhibiting furin might activate immune responses, but may result in a breakdown in peripheral tolerance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758057/" 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/PMC2758057/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pesu, Marko -- Watford, Wendy T -- Wei, Lai -- Xu, Lili -- Fuss, Ivan -- Strober, Warren -- Andersson, John -- Shevach, Ethan M -- Quezado, Martha -- Bouladoux, Nicolas -- Roebroek, Anton -- Belkaid, Yasmine -- Creemers, John -- O'Shea, John J -- Z99 EY999999/Intramural NIH HHS/ -- England -- Nature. 2008 Sep 11;455(7210):246-50. doi: 10.1038/nature07210.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Immunology and Inflammation Branch, National Institute for Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. pesum@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18701887" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/immunology ; Antigens, CD4/immunology/metabolism ; Autoimmunity/immunology ; Colitis/immunology ; Furin/deficiency/genetics/*metabolism ; Gene Expression Profiling ; Immune Tolerance/*immunology ; Immunologic Memory/immunology ; Integrin alpha Chains/immunology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes/cytology/*enzymology/*immunology ; Thymus Gland/cytology/immunology ; Transforming Growth Factor beta1/biosynthesis/genetics/immunology
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    Loss of plant species after chronic low-level nitrogen deposition to prairie grasslands (2008)
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    Publication Date: 2008-02-08
    Description: Rates of atmospheric deposition of biologically active nitrogen (N) are two to seven times the pre-industrial rates in many developed nations because of combustion of fossil fuels and agricultural fertilization. They are expected to increase similarly over the next 50 years in industrializing nations of Asia and South America. Although the environmental impacts of high rates of nitrogen addition have been well studied, this is not so for the lower, chronic rates that characterize much of the globe. Here we present results of the first multi-decadal experiment to examine the impacts of chronic, experimental nitrogen addition as low as 10 kg N ha(-1) yr(-1) above ambient atmospheric nitrogen deposition (6 kg N ha(-1) yr(-1) at our site). This total input rate is comparable to terrestrial nitrogen deposition in many industrialized nations. We found that this chronic low-level nitrogen addition rate reduced plant species numbers by 17% relative to controls receiving ambient N deposition. Moreover, species numbers were reduced more per unit of added nitrogen at lower addition rates, suggesting that chronic but low-level nitrogen deposition may have a greater impact on diversity than previously thought. A second experiment showed that a decade after cessation of nitrogen addition, relative plant species number, although not species abundances, had recovered, demonstrating that some effects of nitrogen addition are reversible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Christopher M -- Tilman, David -- England -- Nature. 2008 Feb 7;451(7179):712-5. doi: 10.1038/nature06503.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology, Evolution and Behavior, 100 Ecology, 1987 Upper Buford Circle, University of Minnesota, St. Paul, Minnesota 55108, USA. clark134@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18256670" target="_blank"〉PubMed〈/a〉
    Keywords: *Biodiversity ; Biomass ; *Ecosystem ; Nitrogen/*metabolism ; Plants/classification/*metabolism ; *Poaceae/metabolism ; Random Allocation ; Time Factors
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    Palaeotemperature trend for Precambrian life inferred from resurrected proteins (2008)
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    Publication Date: 2008-02-08
    Description: Biosignatures and structures in the geological record indicate that microbial life has inhabited Earth for the past 3.5 billion years or so. Research in the physical sciences has been able to generate statements about the ancient environment that hosted this life. These include the chemical compositions and temperatures of the early ocean and atmosphere. Only recently have the natural sciences been able to provide experimental results describing the environments of ancient life. Our previous work with resurrected proteins indicated that ancient life lived in a hot environment. Here we expand the timescale of resurrected proteins to provide a palaeotemperature trend of the environments that hosted life from 3.5 to 0.5 billion years ago. The thermostability of more than 25 phylogenetically dispersed ancestral elongation factors suggest that the environment supporting ancient life cooled progressively by 30 degrees C during that period. Here we show that our results are robust to potential statistical bias associated with the posterior distribution of inferred character states, phylogenetic ambiguity, and uncertainties in the amino-acid equilibrium frequencies used by evolutionary models. Our results are further supported by a nearly identical cooling trend for the ancient ocean as inferred from the deposition of oxygen isotopes. The convergence of results from natural and physical sciences suggest that ancient life has continually adapted to changes in environmental temperatures throughout its evolutionary history.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaucher, Eric A -- Govindarajan, Sridhar -- Ganesh, Omjoy K -- England -- Nature. 2008 Feb 7;451(7179):704-7. doi: 10.1038/nature06510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Foundation for Applied Molecular Evolution, Gainesville, Florida 32601, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18256669" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Bacteria/classification/*metabolism ; Bacterial Proteins/analysis/*chemistry ; *Biological Evolution ; Enzyme Stability ; History, Ancient ; Hot Temperature ; Peptide Elongation Factor Tu/analysis/chemistry ; Phylogeny ; Seawater/*microbiology ; *Temperature ; Time Factors ; Uncertainty
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    Complex speciation of humans and chimpanzees (2008)
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    Publication Date: 2008-03-14
    Description: Genetic data from two or more species provide information about the process of speciation. In their analysis of DNA from humans, chimpanzees, gorillas, orangutans and macaques (HCGOM), Patterson et al. suggest that the apparently short divergence time between humans and chimpanzees on the X chromosome is explained by a massive interspecific hybridization event in the ancestry of these two species. However, Patterson et al. do not statistically test their own null model of simple speciation before concluding that speciation was complex, and--even if the null model could be rejected--they do not consider other explanations of a short divergence time on the X chromosome. These include natural selection on the X chromosome in the common ancestor of humans and chimpanzees, changes in the ratio of male-to-female mutation rates over time, and less extreme versions of divergence with gene flow (see ref. 2, for example). I therefore believe that their claim of hybridization is unwarranted.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakeley, John -- England -- Nature. 2008 Mar 13;452(7184):E3-4; discussion E4. doi: 10.1038/nature06805.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Organismic and Evolutionary Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA. wakeley@fas.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18337768" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/genetics ; Female ; *Genetic Speciation ; Humans ; Male ; *Models, Genetic ; Mutagenesis/genetics ; Pan troglodytes/*genetics ; Phylogeny ; Reproducibility of Results ; Selection, Genetic ; Sex Characteristics ; Time Factors ; X Chromosome/genetics
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    Late Pliocene Greenland glaciation controlled by a decline in atmospheric CO2 levels (2008)
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    Publication Date: 2008-08-30
    Description: It is thought that the Northern Hemisphere experienced only ephemeral glaciations from the Late Eocene to the Early Pliocene epochs (about 38 to 4 million years ago), and that the onset of extensive glaciations did not occur until about 3 million years ago. Several hypotheses have been proposed to explain this increase in Northern Hemisphere glaciation during the Late Pliocene. Here we use a fully coupled atmosphere-ocean general circulation model and an ice-sheet model to assess the impact of the proposed driving mechanisms for glaciation and the influence of orbital variations on the development of the Greenland ice sheet in particular. We find that Greenland glaciation is mainly controlled by a decrease in atmospheric carbon dioxide during the Late Pliocene. By contrast, our model results suggest that climatic shifts associated with the tectonically driven closure of the Panama seaway, with the termination of a permanent El Nino state or with tectonic uplift are not large enough to contribute significantly to the growth of the Greenland ice sheet; moreover, we find that none of these processes acted as a priming mechanism for glacial inception triggered by variations in the Earth's orbit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lunt, Daniel J -- Foster, Gavin L -- Haywood, Alan M -- Stone, Emma J -- England -- Nature. 2008 Aug 28;454(7208):1102-5. doi: 10.1038/nature07223.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BRIDGE, School of Geographical Sciences, University of Bristol, University Road, Bristol BS8 1SS, UK. d.j.lunt@bristol.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18756254" target="_blank"〉PubMed〈/a〉
    Keywords: Atmosphere/*chemistry ; Carbon Dioxide/analysis/*metabolism ; Climate ; Greenland ; History, Ancient ; *Ice Cover ; North America ; Rain ; Time Factors
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    Temporal identity in axonal target layer recognition (2008)
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    Publication Date: 2008-11-04
    Description: The segregation of axon and dendrite projections into distinct synaptic layers is a fundamental principle of nervous system organization and the structural basis for information processing in the brain. Layer-specific recognition molecules that allow projecting neurons to stabilize transient contacts and initiate synaptogenesis have been identified. However, most of the neuronal cell-surface molecules critical for layer organization are expressed broadly in the developing nervous system, raising the question of how these so-called permissive adhesion molecules support synaptic specificity. Here we show that the temporal expression dynamics of the zinc-finger protein sequoia is the major determinant of Drosophila photoreceptor connectivity into distinct synaptic layers. Neighbouring R8 and R7 photoreceptors show consecutive peaks of elevated sequoia expression, which correspond to their sequential target-layer innervation. Loss of sequoia in R7 leads to a projection switch into the R8 recipient layer, whereas a prolonged expression in R8 induces a redirection of their axons into the R7 layer. The sequoia-induced axon targeting is mediated through the ubiquitously expressed Cadherin-N cell adhesion molecule. Our data support a model in which recognition specificity during synaptic layer formation is generated through a temporally restricted axonal competence to respond to broadly expressed adhesion molecules. Because developing neurons innervating the same target area often project in a distinct, birth-order-dependent sequence, temporal identity seems to contain crucial information in generating not only cell type diversity during neuronal division but also connection diversity of projecting neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrovic, Milan -- Hummel, Thomas -- England -- Nature. 2008 Dec 11;456(7223):800-3. doi: 10.1038/nature07407. Epub 2008 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Neurobiologie, Universitat Munster, Badestrasse 9, D-48149 Munster, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18978776" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism/physiology ; Cadherins/metabolism ; Compound Eye, Arthropod/growth & development ; DNA-Binding Proteins/genetics/metabolism ; Drosophila Proteins/genetics/metabolism ; Drosophila melanogaster/genetics/*growth & development/*metabolism ; Gene Expression Regulation, Developmental ; Nerve Tissue Proteins/genetics/metabolism ; Photoreceptor Cells, Invertebrate/metabolism/physiology ; Protein Transport ; Time Factors
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    Suppression of Myc oncogenic activity by ribosomal protein haploinsufficiency (2008)
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    Publication Date: 2008-11-18
    Description: The Myc oncogene regulates the expression of several components of the protein synthetic machinery, including ribosomal proteins, initiation factors of translation, RNA polymerase III and ribosomal DNA. Whether and how increasing the cellular protein synthesis capacity affects the multistep process leading to cancer remains to be addressed. Here we use ribosomal protein heterozygote mice as a genetic tool to restore increased protein synthesis in Emu-Myc/+ transgenic mice to normal levels, and show that the oncogenic potential of Myc in this context is suppressed. Our findings demonstrate that the ability of Myc to increase protein synthesis directly augments cell size and is sufficient to accelerate cell cycle progression independently of known cell cycle targets transcriptionally regulated by Myc. In addition, when protein synthesis is restored to normal levels, Myc-overexpressing precancerous cells are more efficiently eliminated by programmed cell death. Our findings reveal a new mechanism that links increases in general protein synthesis rates downstream of an oncogenic signal to a specific molecular impairment in the modality of translation initiation used to regulate the expression of selective messenger RNAs. We show that an aberrant increase in cap-dependent translation downstream of Myc hyperactivation specifically impairs the translational switch to internal ribosomal entry site (IRES)-dependent translation that is required for accurate mitotic progression. Failure of this translational switch results in reduced mitotic-specific expression of the endogenous IRES-dependent form of Cdk11 (also known as Cdc2l and PITSLRE), which leads to cytokinesis defects and is associated with increased centrosome numbers and genome instability in Emu-Myc/+ mice. When accurate translational control is re-established in Emu-Myc/+ mice, genome instability is suppressed. Our findings demonstrate how perturbations in translational control provide a highly specific outcome for gene expression, genome stability and cancer initiation that have important implications for understanding the molecular mechanism of cancer formation at the post-genomic level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880952/" 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/PMC2880952/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barna, Maria -- Pusic, Aya -- Zollo, Ornella -- Costa, Maria -- Kondrashov, Nadya -- Rego, Eduardo -- Rao, Pulivarthi H -- Ruggero, Davide -- R01 HL085572/HL/NHLBI NIH HHS/ -- R01 HL085572-03/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):971-5. doi: 10.1038/nature07449. Epub 2008 Nov 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry & Biophysics, University of California San Francisco, Rock Hall Room 384C, 1550 Fourth Street, San Francisco, California 94158-2517, USA. maria.barna@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19011615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; B-Lymphocytes/cytology/metabolism/pathology ; Cell Division ; Cell Size ; Cells, Cultured ; Cytokinesis ; Gene Expression Regulation, Neoplastic ; Genes, myc/*genetics ; Genomic Instability ; Heterozygote ; Lymphoma/genetics/pathology ; Mice ; Mice, Inbred C57BL ; Mitosis ; Oncogene Protein p55(v-myc)/*genetics/*metabolism ; Precancerous Conditions/metabolism/pathology ; *Protein Biosynthesis ; Protein-Serine-Threonine Kinases/metabolism ; Ribosomal Proteins/*deficiency/*genetics
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    The coming acceleration of global population ageing (2008)
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    Publication Date: 2008-01-22
    Description: The future paths of population ageing result from specific combinations of declining fertility and increasing life expectancies in different parts of the world. Here we measure the speed of population ageing by using conventional measures and new ones that take changes in longevity into account for the world as a whole and for 13 major regions. We report on future levels of indicators of ageing and the speed at which they change. We show how these depend on whether changes in life expectancy are taken into account. We also show that the speed of ageing is likely to increase over the coming decades and to decelerate in most regions by mid-century. All our measures indicate a continuous ageing of the world's population throughout the century. The median age of the world's population increases from 26.6 years in 2000 to 37.3 years in 2050 and then to 45.6 years in 2100, when it is not adjusted for longevity increase. When increases in life expectancy are taken into account, the adjusted median age rises from 26.6 in 2000 to 31.1 in 2050 and only to 32.9 in 2100, slightly less than what it was in the China region in 2005. There are large differences in the regional patterns of ageing. In North America, the median age adjusted for life expectancy change falls throughout almost the entire century, whereas the conventional median age increases significantly. Our assessment of trends in ageing is based on new probabilistic population forecasts. The probability that growth in the world's population will end during this century is 88%, somewhat higher than previously assessed. After mid-century, lower rates of population growth are likely to coincide with slower rates of ageing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lutz, Wolfgang -- Sanderson, Warren -- Scherbov, Sergei -- England -- Nature. 2008 Feb 7;451(7179):716-9. doi: 10.1038/nature06516. Epub 2008 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉World Population Program, International Institute for Applied Systems Analysis, Schlossplatz 1, A-2361 Laxenburg, Austria. lutz@iiasa.ac.at〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18204438" target="_blank"〉PubMed〈/a〉
    Keywords: Age Distribution ; Aged ; Aged, 80 and over ; Aging/physiology ; Emigration and Immigration ; *Geography ; Humans ; *Internationality ; Life Expectancy/ethnology/*trends ; Longevity ; Middle Aged ; Mortality/trends ; Population Density ; Time Factors
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    Formation of accumbens GluR2-lacking AMPA receptors mediates incubation of cocaine craving (2008)
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    Publication Date: 2008-05-27
    Description: Relapse to cocaine use after prolonged abstinence is an important clinical problem. This relapse is often induced by exposure to cues associated with cocaine use. To account for the persistent propensity for relapse, it has been suggested that cue-induced cocaine craving increases over the first several weeks of abstinence and remains high for extended periods. We and others identified an analogous phenomenon in rats that was termed 'incubation of cocaine craving': time-dependent increases in cue-induced cocaine-seeking over the first months after withdrawal from self-administered cocaine. Cocaine-seeking requires the activation of glutamate projections that excite receptors for alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) in the nucleus accumbens. Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from cocaine self-administration by the addition of new AMPA receptors lacking glutamate receptor 2 (GluR2). Furthermore, we show that these new receptors mediate the incubation of cocaine craving. Our results indicate that GluR2-lacking AMPA receptors could be a new target for drug development for the treatment of cocaine addiction. We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of GluR2-lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine-related cues, leading to an intensification of drug craving and relapse.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574981/" 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/PMC2574981/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conrad, Kelly L -- Tseng, Kuei Y -- Uejima, Jamie L -- Reimers, Jeremy M -- Heng, Li-Jun -- Shaham, Yavin -- Marinelli, Michela -- Wolf, Marina E -- DA00453/DA/NIDA NIH HHS/ -- DA015835/DA/NIDA NIH HHS/ -- DA020654/DA/NIDA NIH HHS/ -- DA09621/DA/NIDA NIH HHS/ -- Z01 DA000434-08/Intramural NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):118-21. doi: 10.1038/nature06995. Epub 2008 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, Illinois 60064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18500330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cocaine ; Cocaine-Related Disorders/genetics/metabolism/*physiopathology ; Cues ; Gene Expression Regulation ; Male ; Nucleus Accumbens/*metabolism/physiopathology ; Rats ; Rats, Long-Evans ; Rats, Sprague-Dawley ; Receptors, AMPA/deficiency/genetics/*metabolism ; Self Administration ; Time Factors
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    Big data: How do your data grow? (2008)
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    Publication Date: 2008-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lynch, Clifford -- England -- Nature. 2008 Sep 4;455(7209):28-9. doi: 10.1038/455028a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Coalition for Networked Information, 21 Dupont Circle, Washington DC 20036, USA. cliff@cni.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18769419" target="_blank"〉PubMed〈/a〉
    Keywords: Archives ; Databases, Factual/economics/standards ; Humans ; Information Management/economics/*methods/organization & ; administration/*standards ; Information Storage and Retrieval/economics/methods/standards ; Research/economics/organization & administration/standards ; *Research Design ; Time Factors
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    Spatio-temporal correlations and visual signalling in a complete neuronal population (2008)
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    Publication Date: 2008-07-25
    Description: Statistical dependencies in the responses of sensory neurons govern both the amount of stimulus information conveyed and the means by which downstream neurons can extract it. Although a variety of measurements indicate the existence of such dependencies, their origin and importance for neural coding are poorly understood. Here we analyse the functional significance of correlated firing in a complete population of macaque parasol retinal ganglion cells using a model of multi-neuron spike responses. The model, with parameters fit directly to physiological data, simultaneously captures both the stimulus dependence and detailed spatio-temporal correlations in population responses, and provides two insights into the structure of the neural code. First, neural encoding at the population level is less noisy than one would expect from the variability of individual neurons: spike times are more precise, and can be predicted more accurately when the spiking of neighbouring neurons is taken into account. Second, correlations provide additional sensory information: optimal, model-based decoding that exploits the response correlation structure extracts 20% more information about the visual scene than decoding under the assumption of independence, and preserves 40% more visual information than optimal linear decoding. This model-based approach reveals the role of correlated activity in the retinal coding of visual stimuli, and provides a general framework for understanding the importance of correlated activity in populations of neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684455/" 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/PMC2684455/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pillow, Jonathan W -- Shlens, Jonathon -- Paninski, Liam -- Sher, Alexander -- Litke, Alan M -- Chichilnisky, E J -- Simoncelli, Eero P -- EY018003/EY/NEI NIH HHS/ -- R01 EY018003/EY/NEI NIH HHS/ -- R01 EY018003-01/EY/NEI NIH HHS/ -- R01 EY018003-02/EY/NEI NIH HHS/ -- R01 EY018003-03/EY/NEI NIH HHS/ -- England -- Nature. 2008 Aug 21;454(7207):995-9. doi: 10.1038/nature07140. Epub 2008 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gatsby Computational Neuroscience Unit, UCL, 17 Queen Square, London WC1N 3AR, UK. pillow@gatsby.ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18650810" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Macaca mulatta/*physiology ; *Models, Neurological ; Photic Stimulation ; Retinal Ganglion Cells/*physiology ; Time Factors ; Vision, Ocular/*physiology
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    GILT is a critical host factor for Listeria monocytogenes infection (2008)
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    Publication Date: 2008-09-26
    Description: Listeria monocytogenes is a gram-positive, intracellular, food-borne pathogen that can cause severe illness in humans and animals. On infection, it is actively phagocytosed by macrophages; it then escapes from the phagosome, replicates in the cytosol, and subsequently spreads from cell to cell by a non-lytic mechanism driven by actin polymerization. Penetration of the phagosomal membrane is initiated by the secreted haemolysin listeriolysin O (LLO), which is essential for vacuolar escape in vitro and for virulence in animal models of infection. Reduction is required to activate the lytic activity of LLO in vitro, and we show here that reduction by the enzyme gamma-interferon-inducible lysosomal thiol reductase (GILT, also called Ifi30) is responsible for the activation of LLO in vivo. GILT is a soluble thiol reductase expressed constitutively within the lysosomes of antigen-presenting cells, and it accumulates in macrophage phagosomes as they mature into phagolysosomes. The enzyme is delivered by a mannose-6-phosphate receptor-dependent mechanism to the endocytic pathway, where amino- and carboxy-terminal pro-peptides are cleaved to generate a 30-kDa mature enzyme. The active site of GILT contains two cysteine residues in a CXXC motif that catalyses the reduction of disulphide bonds. Mice lacking GILT are deficient in generating major histocompatibility complex class-II-restricted CD4(+) T-cell responses to protein antigens that contain disulphide bonds. Here we show that these mice are resistant to L. monocytogenes infection. Replication of the organism in GILT-negative macrophages, or macrophages expressing an enzymatically inactive GILT mutant, is impaired because of delayed escape from the phagosome. GILT activates LLO within the phagosome by the thiol reductase mechanism shared by members of the thioredoxin family. In addition, purified GILT activates recombinant LLO, facilitating membrane permeabilization and red blood cell lysis. The data show that GILT is a critical host factor that facilitates L. monocytogenes infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775488/" 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/PMC2775488/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Reshma -- Jamieson, Amanda -- Cresswell, Peter -- AI023081/AI/NIAID NIH HHS/ -- R37 AI023081/AI/NIAID NIH HHS/ -- R37 AI023081-24/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Oct 30;455(7217):1244-7. doi: 10.1038/nature07344. Epub 2008 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, 300 Cedar Street, New Haven, Connecticut 06250-8011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18815593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Toxins/metabolism ; Cell-Free System ; Heat-Shock Proteins/metabolism ; Hemolysin Proteins/metabolism ; Hemolysis ; Listeria monocytogenes/growth & development/*physiology ; Listeriosis/*metabolism/*microbiology ; Macrophages/cytology/metabolism/microbiology ; Mice ; Mice, Inbred C57BL ; Oxidation-Reduction ; Oxidoreductases/chemistry/deficiency/genetics/*metabolism ; Phagocytosis ; Phagosomes/microbiology ; Thioredoxins/metabolism ; Virulence Factors/metabolism
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    Old-growth forests as global carbon sinks (2008)
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    Publication Date: 2008-09-12
    Description: Old-growth forests remove carbon dioxide from the atmosphere at rates that vary with climate and nitrogen deposition. The sequestered carbon dioxide is stored in live woody tissues and slowly decomposing organic matter in litter and soil. Old-growth forests therefore serve as a global carbon dioxide sink, but they are not protected by international treaties, because it is generally thought that ageing forests cease to accumulate carbon. Here we report a search of literature and databases for forest carbon-flux estimates. We find that in forests between 15 and 800 years of age, net ecosystem productivity (the net carbon balance of the forest including soils) is usually positive. Our results demonstrate that old-growth forests can continue to accumulate carbon, contrary to the long-standing view that they are carbon neutral. Over 30 per cent of the global forest area is unmanaged primary forest, and this area contains the remaining old-growth forests. Half of the primary forests (6 x 10(8) hectares) are located in the boreal and temperate regions of the Northern Hemisphere. On the basis of our analysis, these forests alone sequester about 1.3 +/- 0.5 gigatonnes of carbon per year. Thus, our findings suggest that 15 per cent of the global forest area, which is currently not considered when offsetting increasing atmospheric carbon dioxide concentrations, provides at least 10 per cent of the global net ecosystem productivity. Old-growth forests accumulate carbon for centuries and contain large quantities of it. We expect, however, that much of this carbon, even soil carbon, will move back to the atmosphere if these forests are disturbed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luyssaert, Sebastiaan -- Schulze, E-Detlef -- Borner, Annett -- Knohl, Alexander -- Hessenmoller, Dominik -- Law, Beverly E -- Ciais, Philippe -- Grace, John -- England -- Nature. 2008 Sep 11;455(7210):213-5. doi: 10.1038/nature07276.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Antwerp, 2610 Wilrijk, Belgium. sebastiaan.luyssaert@ua.ac.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18784722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atmosphere/chemistry ; Biomass ; Carbon/*metabolism ; Carbon Dioxide/metabolism ; Databases, Factual ; Disasters ; *Ecosystem ; History, 15th Century ; History, 16th Century ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; History, 21st Century ; History, Ancient ; History, Medieval ; Human Activities ; Time Factors ; Trees/*metabolism
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    Open debate could slow flu vaccine production (2008)
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    Publication Date: 2008-08-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inglis, Stephen -- Wood, John -- Minor, Philip -- England -- Nature. 2008 Aug 21;454(7207):939. doi: 10.1038/454939c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719565" target="_blank"〉PubMed〈/a〉
    Keywords: Drug Industry/organization & administration/standards ; Humans ; Influenza Vaccines/classification/standards/*supply & distribution ; Orthomyxoviridae/physiology ; Orthomyxoviridae Infections/prevention & control ; Time Factors ; Virus Cultivation ; World Health Organization
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    REST maintains self-renewal and pluripotency of embryonic stem cells (2008)
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    Publication Date: 2008-03-26
    Description: The neuronal repressor REST (RE1-silencing transcription factor; also called NRSF) is expressed at high levels in mouse embryonic stem (ES) cells, but its role in these cells is unclear. Here we show that REST maintains self-renewal and pluripotency in mouse ES cells through suppression of the microRNA miR-21. We found that, as with known self-renewal markers, the level of REST expression is much higher in self-renewing mouse ES cells than in differentiating mouse ES (embryoid body, EB) cells. Heterozygous deletion of Rest (Rest+/-) and its short-interfering-RNA-mediated knockdown in mouse ES cells cause a loss of self-renewal-even when these cells are grown under self-renewal conditions-and lead to the expression of markers specific for multiple lineages. Conversely, exogenously added REST maintains self-renewal in mouse EB cells. Furthermore, Rest+/- mouse ES cells cultured under self-renewal conditions express substantially reduced levels of several self-renewal regulators, including Oct4 (also called Pou5f1), Nanog, Sox2 and c-Myc, and exogenously added REST in mouse EB cells maintains the self-renewal phenotypes and expression of these self-renewal regulators. We also show that in mouse ES cells, REST is bound to the gene chromatin of a set of miRNAs that potentially target self-renewal genes. Whereas mouse ES cells and mouse EB cells containing exogenously added REST express lower levels of these miRNAs, EB cells, Rest+/- ES cells and ES cells treated with short interfering RNA targeting Rest express higher levels of these miRNAs. At least one of these REST-regulated miRNAs, miR-21, specifically suppresses the self-renewal of mouse ES cells, corresponding to the decreased expression of Oct4, Nanog, Sox2 and c-Myc. Thus, REST is a newly discovered element of the interconnected regulatory network that maintains the self-renewal and pluripotency of mouse ES cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830094/" 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/PMC2830094/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Sanjay K -- Kagalwala, Mohamedi N -- Parker-Thornburg, Jan -- Adams, Henry -- Majumder, Sadhan -- CA81255/CA/NCI NIH HHS/ -- CA97124/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- R01 CA081255/CA/NCI NIH HHS/ -- R01 CA081255-10/CA/NCI NIH HHS/ -- R01 CA097124/CA/NCI NIH HHS/ -- R01 CA097124-07/CA/NCI NIH HHS/ -- England -- Nature. 2008 May 8;453(7192):223-7. doi: 10.1038/nature06863. Epub 2008 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Genetics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18362916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers ; Cell Differentiation ; Cell Line ; Cell Lineage ; Cell Proliferation ; Chromatin/genetics/metabolism ; Embryonic Stem Cells/*cytology/*metabolism ; Mice ; Mice, Inbred C57BL ; Pluripotent Stem Cells/*cytology/*metabolism ; Repressor Proteins/genetics/*metabolism ; Transcription Factors/deficiency/genetics/*metabolism
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    Beyond the notes (2008)
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    Publication Date: 2008-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, Nicholas -- England -- Nature. 2008 Jun 26;453(7199):1186-7. doi: 10.1038/4531186a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AHRC Research Centre for the History and Analysis of Recorded Music, Royal Holloway, University of London, Egham, Surrey TW20 0EX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18580933" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Humans ; Music/*psychology ; Time Factors
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    Polo-like kinase-1 is activated by aurora A to promote checkpoint recovery (2008)
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    Publication Date: 2008-07-11
    Description: Polo-like kinase-1 (PLK1) is an essential mitotic kinase regulating multiple aspects of the cell division process. Activation of PLK1 requires phosphorylation of a conserved threonine residue (Thr 210) in the T-loop of the PLK1 kinase domain, but the kinase responsible for this has not yet been affirmatively identified. Here we show that in human cells PLK1 activation occurs several hours before entry into mitosis, and requires aurora A (AURKA, also known as STK6)-dependent phosphorylation of Thr 210. We find that aurora A can directly phosphorylate PLK1 on Thr 210, and that activity of aurora A towards PLK1 is greatly enhanced by Bora (also known as C13orf34 and FLJ22624), a known cofactor for aurora A (ref. 7). We show that Bora/aurora-A-dependent phosphorylation is a prerequisite for PLK1 to promote mitotic entry after a checkpoint-dependent arrest. Importantly, expression of a PLK1-T210D phospho-mimicking mutant partially overcomes the requirement for aurora A in checkpoint recovery. Taken together, these data demonstrate that the initial activation of PLK1 is a primary function of aurora A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macurek, Libor -- Lindqvist, Arne -- Lim, Dan -- Lampson, Michael A -- Klompmaker, Rob -- Freire, Raimundo -- Clouin, Christophe -- Taylor, Stephen S -- Yaffe, Michael B -- Medema, Rene H -- CA112967/CA/NCI NIH HHS/ -- GM-60594/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Sep 4;455(7209):119-23. doi: 10.1038/nature07185. Epub 2008 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, University Medical Center Utrecht, Utrecht 3584CG, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18615013" target="_blank"〉PubMed〈/a〉
    Keywords: Aurora Kinase A ; Aurora Kinases ; Cell Cycle/*physiology ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; DNA Damage ; Enzyme Activation ; Humans ; Mitosis ; Molecular Sequence Data ; Phosphorylation ; Phosphothreonine/metabolism ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proto-Oncogene Proteins/genetics/*metabolism ; Time Factors
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    STING is an endoplasmic reticulum adaptor that facilitates innate immune signalling (2008)
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    Publication Date: 2008-08-30
    Description: The cellular innate immune system is essential for recognizing pathogen infection and for establishing effective host defence. But critical molecular determinants responsible for facilitating an appropriate immune response-following infection with DNA and RNA viruses, for example-remain to be identified. Here we report the identification, following expression cloning, of a molecule (STING; stimulator of interferon genes) that appears essential for effective innate immune signalling processes. It comprises five putative transmembrane regions, predominantly resides in the endoplasmic reticulum and is able to activate both NF-kappaB and IRF3 transcription pathways to induce expression of type I interferon (IFN-alpha and IFN-beta ) and exert a potent anti-viral state following expression. In contrast, loss of STING rendered murine embryonic fibroblasts extremely susceptible to negative-stranded virus infection, including vesicular stomatitis virus. Further, STING ablation abrogated the ability of intracellular B-form DNA, as well as members of the herpesvirus family, to induce IFN-beta, but did not significantly affect the Toll-like receptor (TLR) pathway. Yeast two-hybrid and co-immunoprecipitation studies indicated that STING interacts with RIG-I and with SSR2 (also known as TRAPbeta), which is a member of the translocon-associated protein (TRAP) complex required for protein translocation across the endoplasmic reticulum membrane following translation. Ablation by RNA interference of both TRAPbeta and translocon adaptor SEC61beta was subsequently found to inhibit STING's ability to stimulate expression of IFN-beta. Thus, as well as identifying a regulator of innate immune signalling, our results imply a potential role for the translocon in innate signalling pathways activated by select viruses as well as intracellular DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804933/" 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/PMC2804933/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ishikawa, Hiroki -- Barber, Glen N -- R01 AI079336/AI/NIAID NIH HHS/ -- R01 AI079336-01/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Oct 2;455(7213):674-8. doi: 10.1038/nature07317. Epub 2008 Aug 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, Florida 33136, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18724357" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Fibroblasts ; Humans ; Immunity, Innate/*immunology ; Interferons/biosynthesis/immunology ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Signal Transduction
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    Costa Rica's biotech project still on track for end of year (2008)
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    Publication Date: 2008-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corrales, Antonieta -- England -- Nature. 2008 May 29;453(7195):586. doi: 10.1038/453586b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509417" target="_blank"〉PubMed〈/a〉
    Keywords: Biotechnology/economics/organization & administration/standards/*trends ; Costa Rica ; European Union/economics ; Time Factors
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    PML targeting eradicates quiescent leukaemia-initiating cells (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-13
    Description: The existence of a small population of 'cancer-initiating cells' responsible for tumour maintenance has been firmly demonstrated in leukaemia. This concept is currently being tested in solid tumours. Leukaemia-initiating cells, particularly those that are in a quiescent state, are thought to be resistant to chemotherapy and targeted therapies, resulting in disease relapse. Chronic myeloid leukaemia is a paradigmatic haematopoietic stem cell disease in which the leukaemia-initiating-cell pool is not eradicated by current therapy, leading to disease relapse on drug discontinuation. Here we define the critical role of the promyelocytic leukaemia protein (PML) tumour suppressor in haematopoietic stem cell maintenance, and present a new therapeutic approach for targeting quiescent leukaemia-initiating cells and possibly cancer-initiating cells by pharmacological inhibition of PML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712082/" 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/PMC2712082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Keisuke -- Bernardi, Rosa -- Morotti, Alessandro -- Matsuoka, Sahoko -- Saglio, Giuseppe -- Ikeda, Yasuo -- Rosenblatt, Jacalyn -- Avigan, David E -- Teruya-Feldstein, Julie -- Pandolfi, Pier Paolo -- K99 CA139009/CA/NCI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R37 CA071692/CA/NCI NIH HHS/ -- R37 CA071692-12/CA/NCI NIH HHS/ -- England -- Nature. 2008 Jun 19;453(7198):1072-8. doi: 10.1038/nature07016. Epub 2008 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genetics Program, Beth Israel Deaconess Cancer Center, Department of Medicine, Harvard Medical School, New Research Building, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18469801" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arsenicals/pharmacology/therapeutic use ; Cell Line ; Coculture Techniques ; Female ; Gene Expression Regulation, Neoplastic ; Hematopoietic Stem Cells/pathology ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism/*pathology ; Male ; Mice ; Mice, Inbred C57BL ; Neoplastic Stem Cells/metabolism/*pathology ; Nuclear Proteins/antagonists & inhibitors/deficiency/genetics/*metabolism ; Oxides/pharmacology/therapeutic use ; Recurrence ; Regeneration ; Transcription Factors/antagonists & inhibitors/deficiency/genetics/*metabolism ; Tumor Suppressor Proteins/antagonists & ; inhibitors/deficiency/genetics/*metabolism
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    Glycogen synthase kinase 3 in MLL leukaemia maintenance and targeted therapy (2008)
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    Publication Date: 2008-09-23
    Description: Glycogen synthase kinase 3 (GSK3) is a multifunctional serine/threonine kinase that participates in numerous signalling pathways involved in diverse physiological processes. Several of these pathways are implicated in disease pathogenesis, which has prompted efforts to develop GSK3-specific inhibitors for therapeutic applications. However, before now, there has been no strong rationale for targeting GSK3 in malignancies. Here we report pharmacological, physiological and genetic studies that demonstrate an oncogenic requirement for GSK3 in the maintenance of a specific subtype of poor prognosis human leukaemia, genetically defined by mutations of the MLL proto-oncogene. In contrast to its previously characterized roles in suppression of neoplasia-associated signalling pathways, GSK3 paradoxically supports MLL leukaemia cell proliferation and transformation by a mechanism that ultimately involves destabilization of the cyclin-dependent kinase inhibitor p27(Kip1). Inhibition of GSK3 in a preclinical murine model of MLL leukaemia provides promising evidence of efficacy and earmarks GSK3 as a candidate cancer drug target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084721/" 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/PMC4084721/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Zhong -- Smith, Kevin S -- Murphy, Mark -- Piloto, Obdulio -- Somervaille, Tim C P -- Cleary, Michael L -- CA116606/CA/NCI NIH HHS/ -- CA55029/CA/NCI NIH HHS/ -- R01 CA055029/CA/NCI NIH HHS/ -- R01 CA116606/CA/NCI NIH HHS/ -- England -- Nature. 2008 Oct 30;455(7217):1205-9. doi: 10.1038/nature07284. Epub 2008 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806775" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Line, Transformed ; Cell Line, Tumor ; Cell Proliferation ; *Cell Transformation, Neoplastic ; Cyclin-Dependent Kinase Inhibitor p27 ; Disease Models, Animal ; G1 Phase ; Glycogen Synthase Kinase 3/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Histone-Lysine N-Methyltransferase ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors/metabolism ; Isoenzymes/metabolism ; Leukemia, Lymphoid/*drug therapy/enzymology/metabolism/*pathology ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Myeloid Progenitor Cells/enzymology/metabolism/pathology ; Myeloid-Lymphoid Leukemia Protein/*metabolism ; Precursor Cells, B-Lymphoid/enzymology/metabolism/pathology
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    Replication fork movement sets chromatin loop size and origin choice in mammalian cells (2008)
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    Publication Date: 2008-08-22
    Description: Genome stability requires one, and only one, DNA duplication at each S phase. The mechanisms preventing origin firing on newly replicated DNA are well documented, but much less is known about the mechanisms controlling the spacing of initiation events(2,3), namely the completion of DNA replication. Here we show that origin use in Chinese hamster cells depends on both the movement of the replication forks and the organization of chromatin loops. We found that slowing the replication speed triggers the recruitment of latent origins within minutes, allowing the completion of S phase in a timely fashion. When slowly replicating cells are shifted to conditions of fast fork progression, although the decrease in the overall number of active origins occurs within 2 h, the cells still have to go through a complete cell cycle before the efficiency specific to each origin is restored. We observed a strict correlation between replication speed during a given S phase and the size of chromatin loops in the next G1 phase. Furthermore, we found that origins located at or near sites of anchorage of chromatin loops in G1 are activated preferentially in the following S phase. These data suggest a mechanism of origin programming in which replication speed determines the spacing of anchorage regions of chromatin loops, that, in turn, controls the choice of initiation sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Courbet, Sylvain -- Gay, Sophie -- Arnoult, Nausica -- Wronka, Gerd -- Anglana, Mauro -- Brison, Olivier -- Debatisse, Michelle -- England -- Nature. 2008 Sep 25;455(7212):557-60. doi: 10.1038/nature07233. Epub 2008 Aug 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie, 26 rue d'Ulm, 75248 Paris, France; UPMC Univ. Paris 06, F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromatin/genetics/*metabolism ; Cricetinae ; Cricetulus ; DNA/biosynthesis/genetics ; DNA Replication/*physiology ; G1 Phase ; *Movement ; Nuclear Matrix/metabolism ; Replication Origin/*genetics ; S Phase ; Time Factors
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    Polar bear numbers set to fall (2008)
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    Publication Date: 2008-05-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Courtland, Rachel -- England -- Nature. 2008 May 22;453(7194):432-3. doi: 10.1038/453432a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497777" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arctic Regions ; Conservation of Natural Resources/*legislation & jurisprudence/trends ; *Greenhouse Effect ; *Ice Cover ; Internationality ; Population Density ; Time Factors ; United States ; Ursidae/*physiology
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    Neuroscience: Cool songs (2008)
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    Publication Date: 2008-11-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glaze, Chris M -- Troyer, Todd -- England -- Nature. 2008 Nov 13;456(7219):187-8. doi: 10.1038/456187a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19005545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cold Temperature ; Finches/*physiology ; High Vocal Center/physiology ; Time Factors ; Vocalization, Animal/*physiology
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    Internal brain state regulates membrane potential synchrony in barrel cortex of behaving mice (2008)
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    Publication Date: 2008-07-18
    Description: Internal brain states form key determinants for sensory perception, sensorimotor coordination and learning. A prominent reflection of different brain states in the mammalian central nervous system is the presence of distinct patterns of cortical synchrony, as revealed by extracellular recordings of the electroencephalogram, local field potential and action potentials. Such temporal correlations of cortical activity are thought to be fundamental mechanisms of neuronal computation. However, it is unknown how cortical synchrony is reflected in the intracellular membrane potential (V(m)) dynamics of behaving animals. Here we show, using dual whole-cell recordings from layer 2/3 primary somatosensory barrel cortex in behaving mice, that the V(m) of nearby neurons is highly correlated during quiet wakefulness. However, when the mouse is whisking, an internally generated state change reduces the V(m) correlation, resulting in a desynchronized local field potential and electroencephalogram. Action potential activity was sparse during both quiet wakefulness and active whisking. Single action potentials were driven by a large, brief and specific excitatory input that was not present in the V(m) of neighbouring cells. Action potential initiation occurs with a higher signal-to-noise ratio during active whisking than during quiet periods. Therefore, we show that an internal brain state dynamically regulates cortical membrane potential synchrony during behaviour and defines different modes of cortical processing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poulet, James F A -- Petersen, Carl C H -- England -- Nature. 2008 Aug 14;454(7206):881-5. doi: 10.1038/nature07150. Epub 2008 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Sensory Processing, Brain Mind Institute, Faculty of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18633351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electroencephalography ; Exploratory Behavior/*physiology ; Male ; Membrane Potentials/*physiology ; Mice ; Mice, Inbred C57BL ; Neurons/*physiology ; Somatosensory Cortex/*physiology ; Wakefulness/*physiology
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    Chaos in a long-term experiment with a plankton community (2008)
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    Publication Date: 2008-02-15
    Description: Mathematical models predict that species interactions such as competition and predation can generate chaos. However, experimental demonstrations of chaos in ecology are scarce, and have been limited to simple laboratory systems with a short duration and artificial species combinations. Here, we present the first experimental demonstration of chaos in a long-term experiment with a complex food web. Our food web was isolated from the Baltic Sea, and consisted of bacteria, several phytoplankton species, herbivorous and predatory zooplankton species, and detritivores. The food web was cultured in a laboratory mesocosm, and sampled twice a week for more than 2,300 days. Despite constant external conditions, the species abundances showed striking fluctuations over several orders of magnitude. These fluctuations displayed a variety of different periodicities, which could be attributed to different species interactions in the food web. The population dynamics were characterized by positive Lyapunov exponents of similar magnitude for each species. Predictability was limited to a time horizon of 15-30 days, only slightly longer than the local weather forecast. Hence, our results demonstrate that species interactions in food webs can generate chaos. This implies that stability is not required for the persistence of complex food webs, and that the long-term prediction of species abundances can be fundamentally impossible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beninca, Elisa -- Huisman, Jef -- Heerkloss, Reinhard -- Johnk, Klaus D -- Branco, Pedro -- Van Nes, Egbert H -- Scheffer, Marten -- Ellner, Stephen P -- England -- Nature. 2008 Feb 14;451(7180):822-5. doi: 10.1038/nature06512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aquatic Microbiology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, Nieuwe Achtergracht 127, 1018 WS Amsterdam, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18273017" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/metabolism ; *Food Chain ; Models, Biological ; *Nonlinear Dynamics ; Oceans and Seas ; Plankton/*metabolism ; Population Dynamics ; Species Specificity ; Time Factors
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    Endogenous siRNAs from naturally formed dsRNAs regulate transcripts in mouse oocytes (2008)
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    Publication Date: 2008-04-12
    Description: RNA interference (RNAi) is a mechanism by which double-stranded RNAs (dsRNAs) suppress specific transcripts in a sequence-dependent manner. dsRNAs are processed by Dicer to 21-24-nucleotide small interfering RNAs (siRNAs) and then incorporated into the argonaute (Ago) proteins. Gene regulation by endogenous siRNAs has been observed only in organisms possessing RNA-dependent RNA polymerase (RdRP). In mammals, where no RdRP activity has been found, biogenesis and function of endogenous siRNAs remain largely unknown. Here we show, using mouse oocytes, that endogenous siRNAs are derived from naturally occurring dsRNAs and have roles in the regulation of gene expression. By means of deep sequencing, we identify a large number of both approximately 25-27-nucleotide Piwi-interacting RNAs (piRNAs) and approximately 21-nucleotide siRNAs corresponding to messenger RNAs or retrotransposons in growing oocytes. piRNAs are bound to Mili and have a role in the regulation of retrotransposons. siRNAs are exclusively mapped to retrotransposons or other genomic regions that produce transcripts capable of forming dsRNA structures. Inverted repeat structures, bidirectional transcription and antisense transcripts from various loci are sources of the dsRNAs. Some precursor transcripts of siRNAs are derived from expressed pseudogenes, indicating that one role of pseudogenes is to adjust the level of the founding source mRNA through RNAi. Loss of Dicer or Ago2 results in decreased levels of siRNAs and increased levels of retrotransposon and protein-coding transcripts complementary to the siRNAs. Thus, the RNAi pathway regulates both protein-coding transcripts and retrotransposons in mouse oocytes. Our results reveal a role for endogenous siRNAs in mammalian oocytes and show that organisms lacking RdRP activity can produce functional endogenous siRNAs from naturally occurring dsRNAs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Totoki, Yasushi -- Toyoda, Atsushi -- Kaneda, Masahiro -- Kuramochi-Miyagawa, Satomi -- Obata, Yayoi -- Chiba, Hatsune -- Kohara, Yuji -- Kono, Tomohiro -- Nakano, Toru -- Surani, M Azim -- Sakaki, Yoshiyuki -- Sasaki, Hiroyuki -- England -- Nature. 2008 May 22;453(7194):539-43. doi: 10.1038/nature06908. Epub 2008 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima 411-8540, Japan. toshwata@lab.nig.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18404146" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Eukaryotic Initiation Factor-2/deficiency/genetics/metabolism ; Female ; Gene Expression Regulation, Developmental ; Gene Library ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Oocytes/growth & development/*metabolism ; Polymerase Chain Reaction ; Pseudogenes/genetics ; *RNA Interference ; RNA, Double-Stranded/*genetics/*metabolism ; RNA, Messenger/*genetics/metabolism ; RNA, Small Interfering/*genetics/*metabolism ; Retroelements/genetics ; Ribonuclease III/deficiency/genetics/metabolism
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    New York to police air monitoring (2008)
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    Publication Date: 2008-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Courtland, Rachel -- England -- Nature. 2008 Jan 31;451(7178):508. doi: 10.1038/451508a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18235463" target="_blank"〉PubMed〈/a〉
    Keywords: Environmental Monitoring/instrumentation/*legislation & jurisprudence ; *Law Enforcement ; New York City ; Police/*legislation & jurisprudence ; Security Measures/legislation & jurisprudence ; Terrorism/prevention & control ; Time Factors ; United States ; United States Department of Homeland Security/legislation & jurisprudence
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    Transient FTY720 treatment promotes immune-mediated clearance of a chronic viral infection (2008)
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    Publication Date: 2008-08-16
    Description: For a wide variety of microbial pathogens, the outcome of the infection is indeterminate. In some individuals the microbe is cleared, but in others it establishes a chronic infection, and the factors that tip this balance are often unknown. In a widely used model of chronic viral infection, C57BL/6 mice clear the Armstrong strain of lymphocytic choriomeningitis virus (LCMV), but the clone 13 strain persists. Here we show that the Armstrong strain induces a profound lymphopenia at days 1-3 after infection, but the clone 13 strain does not. If we transiently augment lymphopenia by treating the clone-13-infected mice with the drug FTY720 at days 0-2 after infection, the mice successfully clear the infection by day 30. Clearance does not occur when CD4 T cells are absent at the time of treatment, indicating that the drug is not exerting direct antiviral effects. Notably, FTY720 treatment of an already established persistent infection also leads to viral clearance. In both models, FTY720 treatment preserves or augments LCMV-specific CD4 and CD8 T-cell responses, a result that is counter-intuitive because FTY720 is generally regarded as a new immunosuppressive agent. Because FTY720 targets host pathways that are completely evolutionarily conserved, our results may be translatable into new immunotherapies for the treatment of chronic microbial infections in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Premenko-Lanier, Mary -- Moseley, Nelson B -- Pruett, Sarah T -- Romagnoli, Pablo A -- Altman, John D -- 5F32AI062002/AI/NIAID NIH HHS/ -- AI042373/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Aug 14;454(7206):894-8. doi: 10.1038/nature07199.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center and Department of Microbiology and Immunology, Yerkes National Primate Research Center and Emory University School of Medicine, 954 Gatewood Road, Atlanta, Georgia 30329, USA. mflanie@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18704087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chronic Disease ; Fingolimod Hydrochloride ; Lymphocytic Choriomeningitis/complications/*drug therapy/*immunology/prevention & ; control ; Lymphocytic choriomeningitis virus/*immunology/physiology ; Lymphopenia/etiology ; Mice ; Mice, Inbred C57BL ; Propylene Glycols/administration & dosage/*pharmacology/*therapeutic use ; Sphingosine/administration & dosage/*analogs & ; derivatives/pharmacology/therapeutic use ; T-Lymphocytes/drug effects/immunology ; Time Factors
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    Essential roles of PI(3)K-p110beta in cell growth, metabolism and tumorigenesis (2008)
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    Publication Date: 2008-07-03
    Description: On activation by receptors, the ubiquitously expressed class IA isoforms (p110alpha and p110beta) of phosphatidylinositol-3-OH kinase (PI(3)K) generate lipid second messengers, which initiate multiple signal transduction cascades. Recent studies have demonstrated specific functions for p110alpha in growth factor and insulin signalling. To probe for distinct functions of p110beta, we constructed conditional knockout mice. Here we show that ablation of p110beta in the livers of the resulting mice leads to impaired insulin sensitivity and glucose homeostasis, while having little effect on phosphorylation of Akt, suggesting the involvement of a kinase-independent role of p110beta in insulin metabolic action. Using established mouse embryonic fibroblasts, we found that removal of p110beta also had little effect on Akt phosphorylation in response to stimulation by insulin and epidermal growth factor, but resulted in retarded cell proliferation. Reconstitution of p110beta-null cells with a wild-type or kinase-dead allele of p110beta demonstrated that p110beta possesses kinase-independent functions in regulating cell proliferation and trafficking. However, the kinase activity of p110beta was required for G-protein-coupled receptor signalling triggered by lysophosphatidic acid and had a function in oncogenic transformation. Most strikingly, in an animal model of prostate tumour formation induced by Pten loss, ablation of p110beta (also known as Pik3cb), but not that of p110alpha (also known as Pik3ca), impeded tumorigenesis with a concomitant diminution of Akt phosphorylation. Taken together, our findings demonstrate both kinase-dependent and kinase-independent functions for p110beta, and strongly indicate the kinase-dependent functions of p110beta as a promising target in cancer therapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750091/" 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/PMC2750091/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jia, Shidong -- Liu, Zhenning -- Zhang, Sen -- Liu, Pixu -- Zhang, Lei -- Lee, Sang Hyun -- Zhang, Jing -- Signoretti, Sabina -- Loda, Massimo -- Roberts, Thomas M -- Zhao, Jean J -- P01 CA050661/CA/NCI NIH HHS/ -- P01 CA050661-200001/CA/NCI NIH HHS/ -- P01 CA089021/CA/NCI NIH HHS/ -- P01 CA089021-06A1/CA/NCI NIH HHS/ -- P50 CA089393/CA/NCI NIH HHS/ -- P50 CA089393-08S1/CA/NCI NIH HHS/ -- P50 CA090381/CA/NCI NIH HHS/ -- P50 CA090381-05/CA/NCI NIH HHS/ -- R01 CA030002/CA/NCI NIH HHS/ -- R01 CA030002-27/CA/NCI NIH HHS/ -- R01 CA134502/CA/NCI NIH HHS/ -- R01 CA134502-01/CA/NCI NIH HHS/ -- England -- Nature. 2008 Aug 7;454(7205):776-9. doi: 10.1038/nature07091. Epub 2008 Jun 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18594509" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Proliferation/drug effects ; *Cell Transformation, Neoplastic ; Epidermal Growth Factor/pharmacology ; Fibroblasts/cytology ; Glucose/*metabolism ; Glucose Intolerance/enzymology/genetics ; Homeostasis ; Humans ; Insulin/*metabolism/pharmacology ; Insulin Resistance/genetics ; Liver/enzymology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; PTEN Phosphohydrolase/deficiency/genetics ; Phosphatidylinositol 3-Kinases/deficiency/genetics/*metabolism ; Phosphorylation/drug effects ; Prostatic Neoplasms/enzymology/genetics/pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
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    Template-directed synthesis of a genetic polymer in a model protocell (2008)
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    Publication Date: 2008-06-06
    Description: Contemporary phospholipid-based cell membranes are formidable barriers to the uptake of polar and charged molecules ranging from metal ions to complex nutrients. Modern cells therefore require sophisticated protein channels and pumps to mediate the exchange of molecules with their environment. The strong barrier function of membranes has made it difficult to understand the origin of cellular life and has been thought to preclude a heterotrophic lifestyle for primitive cells. Although nucleotides can cross dimyristoyl phosphatidylcholine membranes through defects formed at the gel-to-liquid transition temperature, phospholipid membranes lack the dynamic properties required for membrane growth. Fatty acids and their corresponding alcohols and glycerol monoesters are attractive candidates for the components of protocell membranes because they are simple amphiphiles that form bilayer membrane vesicles that retain encapsulated oligonucleotides and are capable of growth and division. Here we show that such membranes allow the passage of charged molecules such as nucleotides, so that activated nucleotides added to the outside of a model protocell spontaneously cross the membrane and take part in efficient template copying in the protocell interior. The permeability properties of prebiotically plausible membranes suggest that primitive protocells could have acquired complex nutrients from their environment in the absence of any macromolecular transport machinery; that is, they could have been obligate heterotrophs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2743009/" 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/PMC2743009/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mansy, Sheref S -- Schrum, Jason P -- Krishnamurthy, Mathangi -- Tobe, Sylvia -- Treco, Douglas A -- Szostak, Jack W -- F32 GM074506-01/GM/NIGMS NIH HHS/ -- F32 GM07450601/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jul 3;454(7200):122-5. doi: 10.1038/nature07018. Epub 2008 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and the Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18528332" target="_blank"〉PubMed〈/a〉
    Keywords: Biological Transport ; Cell Membrane/chemistry/*metabolism ; Cell Membrane Permeability/physiology ; *Cell Physiological Phenomena ; Fatty Acids/metabolism ; Heterotrophic Processes ; *Models, Biological ; Nucleotides/metabolism ; Oligonucleotides/*metabolism ; Ribose/metabolism ; Templates, Genetic ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Financial planning (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldston, David -- England -- Nature. 2008 Aug 7;454(7205):680. doi: 10.1038/454680a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉House Committee on Science. partyofonecolumn@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18685673" target="_blank"〉PubMed〈/a〉
    Keywords: Budgets/*legislation & jurisprudence/*trends ; *Federal Government ; *Politics ; Research Support as Topic/economics/*legislation & jurisprudence ; Science/*economics/legislation & jurisprudence ; Time Factors ; United States
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    Evolutionary biology: a first for bats (2008)
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    Publication Date: 2008-02-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Speakman, John -- England -- Nature. 2008 Feb 14;451(7180):774-5. doi: 10.1038/451774a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18270540" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Chiroptera/anatomy & histology/*physiology ; Cochlea/anatomy & histology/physiology ; Darkness ; Echolocation/*physiology ; Extremities/anatomy & histology/physiology ; Flight, Animal/*physiology ; Fossils ; Models, Biological ; Time Factors ; Wyoming
    Print ISSN: 0028-0836
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    Following translation by single ribosomes one codon at a time (2008)
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    Publication Date: 2008-03-11
    Description: We have followed individual ribosomes as they translate single messenger RNA hairpins tethered by the ends to optical tweezers. Here we reveal that translation occurs through successive translocation--and-pause cycles. The distribution of pause lengths, with a median of 2.8 s, indicates that at least two rate-determining processes control each pause. Each translocation step measures three bases--one codon-and occurs in less than 0.1 s. Analysis of the times required for translocation reveals, surprisingly, that there are three substeps in each step. Pause lengths, and thus the overall rate of translation, depend on the secondary structure of the mRNA; the applied force destabilizes secondary structure and decreases pause durations, but does not affect translocation times. Translocation and RNA unwinding are strictly coupled ribosomal functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2556548/" 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/PMC2556548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wen, Jin-Der -- Lancaster, Laura -- Hodges, Courtney -- Zeri, Ana-Carolina -- Yoshimura, Shige H -- Noller, Harry F -- Bustamante, Carlos -- Tinoco, Ignacio -- R01 GM010840/GM/NIGMS NIH HHS/ -- R01 GM010840-49/GM/NIGMS NIH HHS/ -- R01 GM010840-50/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Apr 3;452(7187):598-603. doi: 10.1038/nature06716. Epub 2008 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, University of California, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18327250" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoacylation ; Base Pairing ; Codon/*genetics ; Kinetics ; *Optical Tweezers ; Protein Biosynthesis/*physiology ; RNA, Messenger/chemistry/genetics/metabolism ; RNA, Transfer/genetics/metabolism ; Ribosomes/*metabolism ; Time Factors
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    Innate immunity and intestinal microbiota in the development of Type 1 diabetes (2008)
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    Publication Date: 2008-09-23
    Description: Type 1 diabetes (T1D) is a debilitating autoimmune disease that results from T-cell-mediated destruction of insulin-producing beta-cells. Its incidence has increased during the past several decades in developed countries, suggesting that changes in the environment (including the human microbial environment) may influence disease pathogenesis. The incidence of spontaneous T1D in non-obese diabetic (NOD) mice can be affected by the microbial environment in the animal housing facility or by exposure to microbial stimuli, such as injection with mycobacteria or various microbial products. Here we show that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognize microbial stimuli) do not develop T1D. The effect is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabetes, whereas colonization of these germ-free MyD88-negative NOD mice with a defined microbial consortium (representing bacterial phyla normally present in human gut) attenuates T1D. We also find that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients. Together, these findings indicate that interaction of the intestinal microbes with the innate immune system is a critical epigenetic factor modifying T1D predisposition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574766/" 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/PMC2574766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wen, Li -- Ley, Ruth E -- Volchkov, Pavel Yu -- Stranges, Peter B -- Avanesyan, Lia -- Stonebraker, Austin C -- Hu, Changyun -- Wong, F Susan -- Szot, Gregory L -- Bluestone, Jeffrey A -- Gordon, Jeffrey I -- Chervonsky, Alexander V -- DK063452/DK/NIDDK NIH HHS/ -- DK30292/DK/NIDDK NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- DK45735/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- P30 DK042086/DK/NIDDK NIH HHS/ -- P30 DK042086-16/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-10/DK/NIDDK NIH HHS/ -- P30 DK045735-119006/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-07/DK/NIDDK NIH HHS/ -- P30 DK056341-08/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-01/DK/NIDDK NIH HHS/ -- P30 DK63720/DK/NIDDK NIH HHS/ -- R01 DK030292/DK/NIDDK NIH HHS/ -- R01 DK030292-24/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-04/DK/NIDDK NIH HHS/ -- R21 DK063452/DK/NIDDK NIH HHS/ -- R21 DK063452-02/DK/NIDDK NIH HHS/ -- R37 AI046643/AI/NIAID NIH HHS/ -- R37 AI046643-10/AI/NIAID NIH HHS/ -- R37 AI46643/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1109-13. doi: 10.1038/nature07336. Epub 2008 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/genetics/*immunology/isolation & purification ; CD8-Positive T-Lymphocytes/immunology ; Diabetes Mellitus, Type 1/genetics/*immunology/*microbiology ; Female ; Immunity, Innate/genetics/*immunology ; Interferon-gamma/immunology ; Intestines/*microbiology ; Islets of Langerhans/pathology ; Male ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Molecular Sequence Data ; Myeloid Differentiation Factor 88/genetics ; Phylogeny ; Specific Pathogen-Free Organisms ; Time Factors
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    Hazy reasoning behind clean air (2008)
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    Publication Date: 2008-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldston, David -- England -- Nature. 2008 Apr 3;452(7187):519. doi: 10.1038/452519a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard University's Center for the Environment. partyofonecolumn@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385707" target="_blank"〉PubMed〈/a〉
    Keywords: Air Pollution/analysis/*legislation & jurisprudence/prevention & control ; *Federal Government ; Humans ; Ozone/analysis/toxicity ; Plants/drug effects ; Smog/analysis/prevention & control ; Time Factors ; Uncertainty ; United States ; United States Environmental Protection Agency/*legislation & jurisprudence
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    The amphioxus genome and the evolution of the chordate karyotype (2008)
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    Publication Date: 2008-06-20
    Description: Lancelets ('amphioxus') are the modern survivors of an ancient chordate lineage, with a fossil record dating back to the Cambrian period. Here we describe the structure and gene content of the highly polymorphic approximately 520-megabase genome of the Florida lancelet Branchiostoma floridae, and analyse it in the context of chordate evolution. Whole-genome comparisons illuminate the murky relationships among the three chordate groups (tunicates, lancelets and vertebrates), and allow not only reconstruction of the gene complement of the last common chordate ancestor but also partial reconstruction of its genomic organization, as well as a description of two genome-wide duplications and subsequent reorganizations in the vertebrate lineage. These genome-scale events shaped the vertebrate genome and provided additional genetic variation for exploitation during vertebrate evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putnam, Nicholas H -- Butts, Thomas -- Ferrier, David E K -- Furlong, Rebecca F -- Hellsten, Uffe -- Kawashima, Takeshi -- Robinson-Rechavi, Marc -- Shoguchi, Eiichi -- Terry, Astrid -- Yu, Jr-Kai -- Benito-Gutierrez, E Lia -- Dubchak, Inna -- Garcia-Fernandez, Jordi -- Gibson-Brown, Jeremy J -- Grigoriev, Igor V -- Horton, Amy C -- de Jong, Pieter J -- Jurka, Jerzy -- Kapitonov, Vladimir V -- Kohara, Yuji -- Kuroki, Yoko -- Lindquist, Erika -- Lucas, Susan -- Osoegawa, Kazutoyo -- Pennacchio, Len A -- Salamov, Asaf A -- Satou, Yutaka -- Sauka-Spengler, Tatjana -- Schmutz, Jeremy -- Shin-I, Tadasu -- Toyoda, Atsushi -- Bronner-Fraser, Marianne -- Fujiyama, Asao -- Holland, Linda Z -- Holland, Peter W H -- Satoh, Nori -- Rokhsar, Daniel S -- BBS/B/12067/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/12067/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Jun 19;453(7198):1064-71. doi: 10.1038/nature06967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18563158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chordata/classification/*genetics ; Conserved Sequence ; DNA Transposable Elements/genetics ; *Evolution, Molecular ; Gene Duplication ; Genes/genetics ; Genetic Linkage ; Genome/*genetics ; Humans ; Introns/genetics ; Karyotyping ; Multigene Family ; Phylogeny ; Polymorphism, Genetic/genetics ; Proteins/genetics ; Synteny ; Time Factors ; Vertebrates/classification/genetics
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    Ecology: The heart of the wood (2008)
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    Publication Date: 2008-09-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marris, Emma -- England -- Nature. 2008 Sep 18;455(7211):277-80. doi: 10.1038/455277a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18800107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/methods ; *Ecosystem ; Human Activities ; Models, Biological ; Nature ; Poland ; Time Factors ; *Trees/physiology
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    Control of segment number in vertebrate embryos (2008)
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    Publication Date: 2008-06-20
    Description: The vertebrate body axis is subdivided into repeated segments, best exemplified by the vertebrae that derive from embryonic somites. The number of somites is precisely defined for any given species but varies widely from one species to another. To determine the mechanism controlling somite number, we have compared somitogenesis in zebrafish, chicken, mouse and corn snake embryos. Here we present evidence that in all of these species a similar 'clock-and-wavefront' mechanism operates to control somitogenesis; in all of them, somitogenesis is brought to an end through a process in which the presomitic mesoderm, having first increased in size, gradually shrinks until it is exhausted, terminating somite formation. In snake embryos, however, the segmentation clock rate is much faster relative to developmental rate than in other amniotes, leading to a greatly increased number of smaller-sized somites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez, Celine -- Ozbudak, Ertugrul M -- Wunderlich, Joshua -- Baumann, Diana -- Lewis, Julian -- Pourquie, Olivier -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jul 17;454(7202):335-9. doi: 10.1038/nature07020. Epub 2008 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18563087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Patterning/genetics ; Chick Embryo/*embryology ; Gene Expression Regulation, Developmental ; Mice/*embryology ; Molecular Sequence Data ; Snakes/*embryology ; Somites/*embryology ; Time Factors ; Zebrafish/*embryology
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    Slow shipping hobbles Chinese science (2008)
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    Publication Date: 2008-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2008 Dec 4;456(7222):550-1. doi: 10.1038/456550a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19052587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; China ; Commerce/economics ; Indicators and Reagents/*supply & distribution ; Mice ; *Postal Service/economics ; Science/economics/*instrumentation ; Time Factors
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    Imaging the biogenesis of individual HIV-1 virions in live cells (2008)
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    Publication Date: 2008-05-27
    Description: Observations of individual virions in live cells have led to the characterization of their attachment, entry and intracellular transport. However, the assembly of individual virions has never been observed in real time. Insights into this process have come primarily from biochemical analyses of populations of virions or from microscopic studies of fixed infected cells. Thus, some assembly properties, such as kinetics and location, are either unknown or controversial. Here we describe quantitatively the genesis of individual virions in real time, from initiation of assembly to budding and release. We studied fluorescently tagged derivatives of Gag, the major structural component of HIV-1-which is sufficient to drive the assembly of virus-like particles-with the use of fluorescence resonance energy transfer, fluorescence recovery after photobleaching and total-internal-reflection fluorescent microscopy in living cells. Virions appeared individually at the plasma membrane, their assembly rate accelerated as Gag protein accumulated in cells, and typically 5-6 min was required to complete the assembly of a single virion. These approaches allow a previously unobserved view of the genesis of individual virions and the determination of parameters of viral assembly that are inaccessible with conventional techniques.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2708942/" 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/PMC2708942/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jouvenet, Nolwenn -- Bieniasz, Paul D -- Simon, Sanford M -- P20 GM072015/GM/NIGMS NIH HHS/ -- P20 GM072015-01/GM/NIGMS NIH HHS/ -- P20 GM072015-02/GM/NIGMS NIH HHS/ -- P20 GM072015-02S1/GM/NIGMS NIH HHS/ -- P20 GM072015-03/GM/NIGMS NIH HHS/ -- P20 GM072015-04/GM/NIGMS NIH HHS/ -- P20 GM072015-04S1/GM/NIGMS NIH HHS/ -- R01 AI089844/AI/NIAID NIH HHS/ -- R01 GM087977/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Jul 10;454(7201):236-40. doi: 10.1038/nature06998. Epub 2008 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Aaron Diamond AIDS Research Center, 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/18500329" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Membrane/metabolism ; Cell Survival ; Fluorescence Recovery After Photobleaching ; Fluorescence Resonance Energy Transfer ; Fluorescent Dyes/*analysis ; HIV-1/genetics/*growth & development/metabolism ; HeLa Cells ; Humans ; Kinetics ; Microscopy, Fluorescence ; Time Factors ; Virion/*growth & development/metabolism ; *Virus Replication ; gag Gene Products, Human Immunodeficiency Virus/genetics/metabolism
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    Japan fast-tracks stem-cell patent (2008)
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    Publication Date: 2008-09-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2008 Sep 18;455(7211):269. doi: 10.1038/455269b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18800093" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/physiology ; Animals ; Humans ; Internationality ; Japan ; Mice ; Patents as Topic/*legislation & jurisprudence ; *Pluripotent Stem Cells/cytology ; Time Factors ; United States ; Universities
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    Ancient asexuals: darwinulids not exposed (2008)
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    Publication Date: 2008-05-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martens, Koen -- Schon, Isa -- England -- Nature. 2008 May 29;453(7195):587. doi: 10.1038/453587b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crustacea/anatomy & histology/*physiology ; Female ; History, 19th Century ; History, Ancient ; Male ; Reproduction, Asexual/*physiology ; Rotifera/*physiology ; Time Factors
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    Control of T(reg) and T(H)17 cell differentiation by the aryl hydrocarbon receptor (2008)
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    Details
    Publication Date: 2008-03-26
    Description: Regulatory T cells (T(reg)) expressing the transcription factor Foxp3 control the autoreactive components of the immune system. The development of T(reg) cells is reciprocally related to that of pro-inflammatory T cells producing interleukin-17 (T(H)17). Although T(reg) cell dysfunction and/or T(H)17 cell dysregulation are thought to contribute to the development of autoimmune disorders, little is known about the physiological pathways that control the generation of these cell lineages. Here we report the identification of the ligand-activated transcription factor aryl hydrocarbon receptor (AHR) as a regulator of T(reg) and T(H)17 cell differentiation in mice. AHR activation by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced functional T(reg) cells that suppressed experimental autoimmune encephalomyelitis. On the other hand, AHR activation by 6-formylindolo[3,2-b]carbazole interfered with T(reg) cell development, boosted T(H)17 cell differentiation and increased the severity of experimental autoimmune encephalomyelitis in mice. Thus, AHR regulates both T(reg) and T(H)17 cell differentiation in a ligand-specific fashion, constituting a unique target for therapeutic immunomodulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quintana, Francisco J -- Basso, Alexandre S -- Iglesias, Antonio H -- Korn, Thomas -- Farez, Mauricio F -- Bettelli, Estelle -- Caccamo, Mario -- Oukka, Mohamed -- Weiner, Howard L -- AI435801/AI/NIAID NIH HHS/ -- NS38037/NS/NINDS NIH HHS/ -- P01 NS038037/NS/NINDS NIH HHS/ -- R01 AI073542/AI/NIAID NIH HHS/ -- R01 AI073542-01/AI/NIAID NIH HHS/ -- R01 AI073542-02/AI/NIAID NIH HHS/ -- R01 NS059996/NS/NINDS NIH HHS/ -- R01AI073542-01/AI/NIAID NIH HHS/ -- England -- Nature. 2008 May 1;453(7191):65-71. doi: 10.1038/nature06880. Epub 2008 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18362915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbazoles/metabolism/pharmacology ; *Cell Differentiation ; Encephalomyelitis, Autoimmune, Experimental/chemically induced/immunology ; Forkhead Transcription Factors/genetics/metabolism ; Humans ; Indoles/metabolism/pharmacology ; Interleukin-17/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Receptors, Aryl Hydrocarbon/genetics/*metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/drug effects/*metabolism ; T-Lymphocytes, Regulatory/*cytology/drug effects/*metabolism ; Tetrachlorodibenzodioxin/metabolism/pharmacology ; Transforming Growth Factor beta1/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Neuropathology: Alzheimer's in real time (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-02-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masliah, Eliezer -- England -- Nature. 2008 Feb 7;451(7179):638-9. doi: 10.1038/451638a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18256653" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*metabolism/*pathology ; Amyloid beta-Peptides/*metabolism/toxicity ; Animals ; Axons/metabolism ; Dendrites/metabolism ; Disease Models, Animal ; Disease Progression ; Humans ; Mice ; Microglia/metabolism ; Plaque, Amyloid/*metabolism/*pathology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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