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  • Animals  (9,322)
  • 2010-2014  (7,118)
  • 1980-1984  (2,204)
  • 1925-1929
  • 1
    ISSN: 1432-1009
    Keywords: Animals ; Indicators ; Air pollution ; Ecosystem responses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract With existing and proposed air-quality regulations, ecological disasters resulting from air emissions such as those observed at Copperhill, Tennessee, and Sudbury, Ontario, are unlikely. Current air-quality standards, however, may not protect ecosystems from subacute and chronic exposure to air emissions. The encouragement of the use of coal for energy production and the development of the fossil-fuel industries, including oil shales, tar sands, and coal liquification, point to an increase and spread of fossil-fuel emissions and the potential to influence a number of natural ecosystems. This paper reviews the reported responses of ecosystems to air-borne pollutants and discusses the use of animals as indicators of ecosystem responses to these pollutants. Animal species and populations can act as important indicators of biotic and abiotic responses of aquatic and terrestrial ecosystems. These responses can indicate long-term trends in ecosystem health and productivity, chemical cycling, genetics, and regulation. For short-term trends, fish and wildlife also serve as monitors of changes in community structure, signaling food-web contamination, as well as providing a measure of ecosystem vitality. Information is presented to show not only the importance of animals as indicators of ecosystem responses to air-quality degradation, but also their value as air-pollution indices, that is, as air-quality-related values (AQRV), required in current air-pollution regulation.
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2010-04-02
    Description: Studies of post-mortem tissue have shown that the location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regions of massive neuronal death, severe cytological abnormalities, and markers of caspase activation and apoptosis, leading to the idea that tangles cause neurodegeneration in Alzheimer's disease and tau-related frontotemporal dementia. However, using in vivo multiphoton imaging to observe tangles and activation of executioner caspases in living tau transgenic mice (Tg4510 strain), we find the opposite: caspase activation occurs first, and precedes tangle formation by hours to days. New tangles form within a day. After a new tangle forms, the neuron remains alive and caspase activity seems to be suppressed. Similarly, introduction of wild-type 4-repeat tau (tau-4R) into wild-type animals triggered caspase activation, tau truncation and tau aggregation. Adeno-associated virus-mediated expression of a construct mimicking caspase-cleaved tau into wild-type mice led to the appearance of intracellular aggregates, tangle-related conformational- and phospho-epitopes, and the recruitment of full-length endogenous tau to the aggregates. On the basis of these data, we propose a new model in which caspase activation cleaves tau to initiate tangle formation, then truncated tau recruits normal tau to misfold and form tangles. Because tangle-bearing neurons are long-lived, we suggest that tangles are 'off pathway' to acute neuronal death. Soluble tau species, rather than fibrillar tau, may be the critical toxic moiety underlying neurodegeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091360/" 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/PMC3091360/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Calignon, Alix -- Fox, Leora M -- Pitstick, Rose -- Carlson, George A -- Bacskai, Brian J -- Spires-Jones, Tara L -- Hyman, Bradley T -- AG 026249/AG/NIA NIH HHS/ -- AG08487/AG/NIA NIH HHS/ -- K99 AG033670/AG/NIA NIH HHS/ -- K99 AG033670-01A1/AG/NIA NIH HHS/ -- R01 AG008487/AG/NIA NIH HHS/ -- R01 AG008487-18/AG/NIA NIH HHS/ -- R01 AG026249/AG/NIA NIH HHS/ -- R01 AG026249-01/AG/NIA NIH HHS/ -- England -- Nature. 2010 Apr 22;464(7292):1201-4. doi: 10.1038/nature08890. Epub 2010 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Alzheimer's Disease Research Laboratory, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20357768" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/metabolism/pathology ; Caspases/*metabolism ; Cell Death ; Enzyme Activation ; Humans ; Mice ; Mice, Transgenic ; Neurofibrillary Tangles/chemistry/enzymology/*metabolism/pathology ; Neurons/enzymology/metabolism/pathology ; Protein Processing, Post-Translational ; Solubility ; Time Factors ; tau Proteins/chemistry/genetics/*metabolism
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  • 3
    Publication Date: 2010-12-03
    Description: Haematopoietic stem cells (HSCs) can convert between growth states that have marked differences in bioenergetic needs. Although often quiescent in adults, these cells become proliferative upon physiological demand. Balancing HSC energetics in response to nutrient availability and growth state is poorly understood, yet essential for the dynamism of the haematopoietic system. Here we show that the Lkb1 tumour suppressor is critical for the maintenance of energy homeostasis in haematopoietic cells. Lkb1 inactivation in adult mice causes loss of HSC quiescence followed by rapid depletion of all haematopoietic subpopulations. Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP. The haematopoietic effects are largely independent of Lkb1 regulation of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling. Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037591/" 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/PMC3037591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurumurthy, Sushma -- Xie, Stephanie Z -- Alagesan, Brinda -- Kim, Judith -- Yusuf, Rushdia Z -- Saez, Borja -- Tzatsos, Alexandros -- Ozsolak, Fatih -- Milos, Patrice -- Ferrari, Francesco -- Park, Peter J -- Shirihai, Orian S -- Scadden, David T -- Bardeesy, Nabeel -- DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234-12/DK/NIDDK NIH HHS/ -- R01 DK050234-13/DK/NIDDK NIH HHS/ -- R01 HG005230/HG/NHGRI NIH HHS/ -- R01 HG005230-01/HG/NHGRI NIH HHS/ -- U01 CA141576-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):659-63. doi: 10.1038/nature09572.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center and Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124451" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Apoptosis ; Autophagy ; Bone Marrow/metabolism/pathology ; Cell Cycle ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Enzyme Activation ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; Homeostasis ; Lipid Metabolism ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/antagonists & inhibitors/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/metabolism
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  • 4
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    Nature Publishing Group (NPG)
    Publication Date: 2010-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koff, Wayne C -- England -- Nature. 2010 Mar 11;464(7286):161-2. doi: 10.1038/464161a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉International AIDS Vaccine Initiative, 110 William Street, 27th Floor, New York, New York 10038, USA. wkoff@iavi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220821" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Animals ; Antibodies, Neutralizing/immunology ; HIV/*immunology ; HIV Infections/*prevention & control ; Humans ; Immunity, Cellular/immunology ; Translational Medical Research/*economics/*standards/trends
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  • 5
    Publication Date: 2010-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kokko, Hanna -- Jennions, Michael -- England -- Nature. 2010 Apr 15;464(7291):990-1. doi: 10.1038/464990b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393552" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura/classification/*physiology ; *Ecosystem ; Female ; Food ; Fresh Water/*analysis ; Larva/physiology ; Male ; *Maternal Behavior/physiology ; *Paternal Behavior ; Phylogeny ; Survival Rate
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  • 6
    Publication Date: 2010-03-17
    Description: Demethylation at distinct lysine residues in histone H3 by lysine-specific demethylase 1 (LSD1) causes either gene repression or activation. As a component of co-repressor complexes, LSD1 contributes to target gene repression by removing mono- and dimethyl marks from lysine 4 of histone H3 (H3K4). In contrast, during androgen receptor (AR)-activated gene expression, LSD1 removes mono- and dimethyl marks from lysine 9 of histone H3 (H3K9). Yet, the mechanisms that control this dual specificity of demethylation are unknown. Here we show that phosphorylation of histone H3 at threonine 6 (H3T6) by protein kinase C beta I (PKCbeta(I), also known as PRKCbeta) is the key event that prevents LSD1 from demethylating H3K4 during AR-dependent gene activation. In vitro, histone H3 peptides methylated at lysine 4 and phosphorylated at threonine 6 are no longer LSD1 substrates. In vivo, PKCbeta(I) co-localizes with AR and LSD1 on target gene promoters and phosphorylates H3T6 after androgen-induced gene expression. RNA interference (RNAi)-mediated knockdown of PKCbeta(I) abrogates H3T6 phosphorylation, enhances demethylation at H3K4, and inhibits AR-dependent transcription. Activation of PKCbeta(I) requires androgen-dependent recruitment of the gatekeeper kinase protein kinase C (PKC)-related kinase 1 (PRK1). Notably, increased levels of PKCbeta(I) and phosphorylated H3T6 (H3T6ph) positively correlate with high Gleason scores of prostate carcinomas, and inhibition of PKCbeta(I) blocks AR-induced tumour cell proliferation in vitro and cancer progression of tumour xenografts in vivo. Together, our data establish that androgen-dependent kinase signalling leads to the writing of the new chromatin mark H3T6ph, which in consequence prevents removal of active methyl marks from H3K4 during AR-stimulated gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metzger, Eric -- Imhof, Axel -- Patel, Dharmeshkumar -- Kahl, Philip -- Hoffmeyer, Katrin -- Friedrichs, Nicolaus -- Muller, Judith M -- Greschik, Holger -- Kirfel, Jutta -- Ji, Sujuan -- Kunowska, Natalia -- Beisenherz-Huss, Christian -- Gunther, Thomas -- Buettner, Reinhard -- Schule, Roland -- England -- Nature. 2010 Apr 1;464(7289):792-6. doi: 10.1038/nature08839. Epub 2010 Mar 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Urologische Klinik/Frauenklinik und Zentrale Klinische Forschung, Klinikum der Universitat Freiburg, Breisacherstrasse 66, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20228790" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/metabolism/pharmacology ; Animals ; Cell Division/drug effects ; Cell Line, Tumor ; Chromatin/metabolism ; Gene Expression Regulation/drug effects ; Gene Knockdown Techniques ; Histone Demethylases/antagonists & inhibitors/*metabolism ; Histones/*chemistry/*metabolism ; Humans ; Lysine/chemistry/metabolism ; Male ; Methylation/drug effects ; Mice ; Mice, Nude ; Mice, SCID ; Phosphorylation/drug effects ; Phosphothreonine/metabolism ; Promoter Regions, Genetic/genetics ; Prostatic Neoplasms/enzymology/metabolism/pathology ; Protein Kinase C/antagonists & inhibitors/deficiency/genetics/*metabolism ; Protein Kinase C beta ; Signal Transduction/drug effects ; Xenograft Model Antitumor Assays
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  • 7
    Publication Date: 2010-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer-Lindenberg, Andreas -- England -- Nature. 2010 Aug 12;466(7308):827-8. doi: 10.1038/466827a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703297" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*metabolism ; Animals ; Anxiety/*genetics/*physiopathology ; Freezing Reaction, Cataleptic/physiology ; Genetic Predisposition to Disease/*genetics ; Glucose/metabolism ; Hippocampus/*metabolism ; Humans ; Macaca mulatta/genetics/physiology ; Stress, Psychological ; Temperament/*physiology
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  • 8
    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Demb, Jonathan B -- Brainard, David H -- England -- Nature. 2010 Oct 7;467(7316):670-1. doi: 10.1038/467670b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20930837" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Color ; Color Perception/*physiology ; Color Vision/*physiology ; Humans ; Light ; Macaca/*physiology ; Neural Pathways/*physiology ; Retinal Cone Photoreceptor Cells/*cytology/*physiology ; Retinal Ganglion Cells/cytology/physiology
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  • 9
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    Nature Publishing Group (NPG)
    Publication Date: 2010-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riley, Paul -- England -- Nature. 2010 Mar 25;464(7288):498-9. doi: 10.1038/464498a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Coronary Vessels/*cytology/*embryology ; Endothelial Cells/*cytology ; Humans
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  • 10
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    Nature Publishing Group (NPG)
    Publication Date: 2010-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2010 Mar 25;464(7288):478. doi: 10.1038/464478a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20336104" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biology/*legislation & jurisprudence/standards/trends ; *Legislation as Topic ; *Organisms, Genetically Modified ; Research/*legislation & jurisprudence/trends ; Turkey
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  • 11
    Publication Date: 2010-01-22
    Description: Grid cells in the entorhinal cortex of freely moving rats provide a strikingly periodic representation of self-location which is indicative of very specific computational mechanisms. However, the existence of grid cells in humans and their distribution throughout the brain are unknown. Here we show that the preferred firing directions of directionally modulated grid cells in rat entorhinal cortex are aligned with the grids, and that the spatial organization of grid-cell firing is more strongly apparent at faster than slower running speeds. Because the grids are also aligned with each other, we predicted a macroscopic signal visible to functional magnetic resonance imaging (fMRI) in humans. We then looked for this signal as participants explored a virtual reality environment, mimicking the rats' foraging task: fMRI activation and adaptation showing a speed-modulated six-fold rotational symmetry in running direction. The signal was found in a network of entorhinal/subicular, posterior and medial parietal, lateral temporal and medial prefrontal areas. The effect was strongest in right entorhinal cortex, and the coherence of the directional signal across entorhinal cortex correlated with spatial memory performance. Our study illustrates the potential power of combining single-unit electrophysiology with fMRI in systems neuroscience. Our results provide evidence for grid-cell-like representations in humans, and implicate a specific type of neural representation in a network of regions which supports spatial cognition and also autobiographical memory.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3173857/" 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/PMC3173857/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doeller, Christian F -- Barry, Caswell -- Burgess, Neil -- G0501672/Medical Research Council/United Kingdom -- G0501672(76328)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2010 Feb 4;463(7281):657-61. doi: 10.1038/nature08704. Epub 2010 Jan 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCL Institute of Cognitive Neuroscience, London WC1N 3AR, UK. c.doeller@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20090680" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adaptation, Physiological/physiology ; Adolescent ; Adult ; Animals ; Entorhinal Cortex/*cytology ; Humans ; Logic ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Neurons/*physiology ; Orientation/*physiology ; Rats ; Running ; Space Perception/*physiology ; User-Computer Interface ; Young Adult
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  • 12
    Publication Date: 2010-04-09
    Description: Cortical neurons form specific circuits, but the functional structure of this microarchitecture and its relation to behaviour are poorly understood. Two-photon calcium imaging can monitor activity of spatially defined neuronal ensembles in the mammalian cortex. Here we applied this technique to the motor cortex of mice performing a choice behaviour. Head-fixed mice were trained to lick in response to one of two odours, and to withhold licking for the other odour. Mice routinely showed significant learning within the first behavioural session and across sessions. Microstimulation and trans-synaptic tracing identified two non-overlapping candidate tongue motor cortical areas. Inactivating either area impaired voluntary licking. Imaging in layer 2/3 showed neurons with diverse response types in both areas. Activity in approximately half of the imaged neurons distinguished trial types associated with different actions. Many neurons showed modulation coinciding with or preceding the action, consistent with their involvement in motor control. Neurons with different response types were spatially intermingled. Nearby neurons (within approximately 150 mum) showed pronounced coincident activity. These temporal correlations increased with learning within and across behavioural sessions, specifically for neuron pairs with similar response types. We propose that correlated activity in specific ensembles of functionally related neurons is a signature of learning-related circuit plasticity. Our findings reveal a fine-scale and dynamic organization of the frontal cortex that probably underlies flexible behaviour.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Komiyama, Takaki -- Sato, Takashi R -- O'Connor, Daniel H -- Zhang, Ying-Xin -- Huber, Daniel -- Hooks, Bryan M -- Gabitto, Mariano -- Svoboda, Karel -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 22;464(7292):1182-6. doi: 10.1038/nature08897. Epub 2010 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, HHMI, Ashburn, Virginia 20147, USA. komiyamat@janelia.hhmi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20376005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Behavior, Animal/*physiology ; Choice Behavior/physiology ; Learning/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Cortex/*cytology/*physiology ; Motor Neurons/physiology ; Neural Pathways/*physiology ; Odors/analysis ; Pyramidal Cells/physiology ; Reward ; Stimulation, Chemical ; Time Factors ; Tongue/cytology/innervation/physiology
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  • 13
    Publication Date: 2010-08-13
    Description: Chaotic ecological dynamic systems defy conventional statistical analysis. Systems with near-chaotic dynamics are little better. Such systems are almost invariably driven by endogenous dynamic processes plus demographic and environmental process noise, and are only observable with error. Their sensitivity to history means that minute changes in the driving noise realization, or the system parameters, will cause drastic changes in the system trajectory. This sensitivity is inherited and amplified by the joint probability density of the observable data and the process noise, rendering it useless as the basis for obtaining measures of statistical fit. Because the joint density is the basis for the fit measures used by all conventional statistical methods, this is a major theoretical shortcoming. The inability to make well-founded statistical inferences about biological dynamic models in the chaotic and near-chaotic regimes, other than on an ad hoc basis, leaves dynamic theory without the methods of quantitative validation that are essential tools in the rest of biological science. Here I show that this impasse can be resolved in a simple and general manner, using a method that requires only the ability to simulate the observed data on a system from the dynamic model about which inferences are required. The raw data series are reduced to phase-insensitive summary statistics, quantifying local dynamic structure and the distribution of observations. Simulation is used to obtain the mean and the covariance matrix of the statistics, given model parameters, allowing the construction of a 'synthetic likelihood' that assesses model fit. This likelihood can be explored using a straightforward Markov chain Monte Carlo sampler, but one further post-processing step returns pure likelihood-based inference. I apply the method to establish the dynamic nature of the fluctuations in Nicholson's classic blowfly experiments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Simon N -- England -- Nature. 2010 Aug 26;466(7310):1102-4. doi: 10.1038/nature09319. Epub 2010 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mathematical Sciences, University of Bath, Bath BA2 7AY, UK. s.wood@bath.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20703226" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Computer Simulation ; *Data Interpretation, Statistical ; Diptera/physiology ; Ecology/methods ; *Models, Biological ; Population Density
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  • 14
    Publication Date: 2010-08-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lagier-Tourenne, Clotilde -- Cleveland, Don W -- 089701/Wellcome Trust/United Kingdom -- R37 NS027036/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Aug 26;466(7310):1052-3. doi: 10.1038/4661052a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20740002" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics/*physiopathology ; Animals ; Ataxins ; DNA-Binding Proteins/metabolism ; Humans ; Mutation/genetics ; Nerve Tissue Proteins/genetics/metabolism ; Peptides/metabolism ; Risk Factors ; Spinocerebellar Ataxias/genetics/physiopathology
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  • 15
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    Nature Publishing Group (NPG)
    Publication Date: 2010-04-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dolgin, Elie -- England -- Nature. 2010 Apr 1;464(7289):663. doi: 10.1038/464663a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360708" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Mammalian/genetics ; Embryo, Mammalian/cytology ; Embryonic Stem Cells/*cytology/*metabolism/transplantation ; Epigenesis, Genetic/genetics ; *Gene Expression Profiling ; Humans ; Induced Pluripotent Stem Cells/*cytology/*metabolism/transplantation ; Mice ; Neurons/cytology
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  • 16
    Publication Date: 2010-07-03
    Description: Cardiac hypertrophy and failure are characterized by transcriptional reprogramming of gene expression. Adult cardiomyocytes in mice primarily express alpha-myosin heavy chain (alpha-MHC, also known as Myh6), whereas embryonic cardiomyocytes express beta-MHC (also known as Myh7). Cardiac stress triggers adult hearts to undergo hypertrophy and a shift from alpha-MHC to fetal beta-MHC expression. Here we show that Brg1, a chromatin-remodelling protein, has a critical role in regulating cardiac growth, differentiation and gene expression. In embryos, Brg1 promotes myocyte proliferation by maintaining Bmp10 and suppressing p57(kip2) expression. It preserves fetal cardiac differentiation by interacting with histone deacetylase (HDAC) and poly (ADP ribose) polymerase (PARP) to repress alpha-MHC and activate beta-MHC. In adults, Brg1 (also known as Smarca4) is turned off in cardiomyocytes. It is reactivated by cardiac stresses and forms a complex with its embryonic partners, HDAC and PARP, to induce a pathological alpha-MHC to beta-MHC shift. Preventing Brg1 re-expression decreases hypertrophy and reverses this MHC switch. BRG1 is activated in certain patients with hypertrophic cardiomyopathy, its level correlating with disease severity and MHC changes. Our studies show that Brg1 maintains cardiomyocytes in an embryonic state, and demonstrate an epigenetic mechanism by which three classes of chromatin-modifying factors-Brg1, HDAC and PARP-cooperate to control developmental and pathological gene expression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898892/" 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/PMC2898892/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hang, Calvin T -- Yang, Jin -- Han, Pei -- Cheng, Hsiu-Ling -- Shang, Ching -- Ashley, Euan -- Zhou, Bin -- Chang, Ching-Pin -- R01 HL085345/HL/NHLBI NIH HHS/ -- R01 HL085345-03S1/HL/NHLBI NIH HHS/ -- R01 HL085345-04/HL/NHLBI NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- England -- Nature. 2010 Jul 1;466(7302):62-7. doi: 10.1038/nature09130.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cardiovascular Medicine, Department of Medicine, 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/20596014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomegaly/*genetics/*metabolism/pathology ; Cell Differentiation ; Cell Proliferation ; Chromatin/*genetics ; DNA Helicases/deficiency/genetics/*metabolism ; Embryo Loss/genetics ; Embryo, Mammalian/metabolism ; Gene Expression Regulation, Developmental ; Histone Deacetylases/metabolism ; Humans ; Mice ; Myocardium/cytology/*metabolism/pathology ; Myosin Heavy Chains/genetics/metabolism ; Nuclear Proteins/deficiency/genetics/*metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Transcription Factors/deficiency/genetics/*metabolism
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  • 17
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    Nature Publishing Group (NPG)
    Publication Date: 2010-05-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ren, Bing -- England -- Nature. 2010 May 13;465(7295):173-4. doi: 10.1038/465173a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20463730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/genetics ; Humans ; Mice ; Neurons/metabolism ; RNA, Untranslated/biosynthesis/*genetics ; Transcription, Genetic/*genetics
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  • 18
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    Nature Publishing Group (NPG)
    Publication Date: 2010-11-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2010 Nov 11;468(7321):158-9. doi: 10.1038/468158a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068804" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antipsychotic Agents/pharmacology/therapeutic use ; Clinical Trials as Topic ; Clozapine/adverse effects/pharmacology/therapeutic use ; Cognition/drug effects ; Dopamine D2 Receptor Antagonists ; Drug Evaluation, Preclinical/methods ; *Drug Industry/economics/trends ; Humans ; Perphenazine/therapeutic use ; Psychotic Disorders/complications/drug therapy ; Receptor, Serotonin, 5-HT2A/metabolism ; Receptors, Dopamine D2/metabolism ; Schizophrenia/complications/*drug therapy/epidemiology/physiopathology ; Serotonin 5-HT2 Receptor Antagonists/pharmacology/therapeutic use
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  • 19
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    Nature Publishing Group (NPG)
    Publication Date: 2010-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchen, Lizzie -- England -- Nature. 2010 Sep 9;467(7312):146-8. doi: 10.1038/467146a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829771" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Methylation ; *Epigenesis, Genetic ; Gene Expression Regulation ; *Genetics, Behavioral ; Humans ; Maternal Behavior ; Mice ; Parenting ; Rats ; Sexual Behavior, Animal ; Suicide
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  • 20
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    Nature Publishing Group (NPG)
    Publication Date: 2010-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchen, Lizzie -- England -- Nature. 2010 May 6;465(7294):26-8. doi: 10.1038/465026a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20445604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/physiology ; Brain/*physiology ; Humans ; Neurosciences/instrumentation/methods/*trends ; Systems Biology
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  • 21
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    Nature Publishing Group (NPG)
    Publication Date: 2010-07-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spinney, Laura -- England -- Nature. 2010 Jul 8;466(7303):174-5. doi: 10.1038/466174a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613815" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Biodiversity ; Cichlids/anatomy & histology/classification/genetics/*physiology ; Eutrophication/physiology ; Female ; *Fresh Water ; *Genetic Speciation ; Hybridization, Genetic/genetics ; Male ; Phylogeny ; Reproduction/physiology
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  • 22
    Publication Date: 2010-04-13
    Description: Mammalian cells require non-homologous end joining (NHEJ) for the efficient repair of chromosomal DNA double-strand breaks. A key feature of biological sources of strand breaks is associated nucleotide damage, including base loss (abasic or apurinic/apyrimidinic (AP) sites). At single-strand breaks, 5'-terminal abasic sites are excised by the 5'-deoxyribose-5-phosphate (5'-dRP) lyase activity of DNA polymerase beta (pol beta): here we show, in vitro and in cells, that accurate and efficient repair by NHEJ of double-strand breaks with such damage similarly requires 5'-dRP/AP lyase activity. Classically defined NHEJ is moreover uniquely effective at coupling this end-cleaning step to joining in cells, helping to distinguish this pathway from otherwise robust alternative NHEJ pathways. The NHEJ factor Ku can be identified as an effective 5'-dRP/AP lyase. In a similar manner to other lyases, Ku nicks DNA 3' of an abasic site by a mechanism involving a Schiff-base covalent intermediate with the abasic site. We show by using cell extracts that Ku is essential for the efficient removal of AP sites near double-strand breaks and, consistent with this result, that joining of such breaks is specifically decreased in cells complemented with a lyase-attenuated Ku mutant. Ku had previously been presumed only to recognize ends and recruit other factors that process ends; our data support an unexpected direct role for Ku in end-processing steps as well.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2859099/" 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/PMC2859099/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Steven A -- Strande, Natasha -- Burkhalter, Martin D -- Strom, Christina -- Havener, Jody M -- Hasty, Paul -- Ramsden, Dale A -- CA 84442/CA/NCI NIH HHS/ -- P01 AG17242/AG/NIA NIH HHS/ -- R01 CA084442/CA/NCI NIH HHS/ -- R01 CA084442-10/CA/NCI NIH HHS/ -- R01 CA76317-05A1/CA/NCI NIH HHS/ -- England -- Nature. 2010 Apr 22;464(7292):1214-7. doi: 10.1038/nature08926. Epub 2010 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, and Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20383123" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/genetics/*metabolism ; *Biocatalysis ; Cell Extracts ; Cell Line ; *DNA Breaks, Double-Stranded ; *DNA Damage ; *DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase/genetics/*metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Fibroblasts ; HeLa Cells ; Humans ; Mice ; Ribosemonophosphates/*metabolism ; Schiff Bases/chemistry
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  • 23
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    Nature Publishing Group (NPG)
    Publication Date: 2010-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buchen, Lizzie -- England -- Nature. 2010 Jan 14;463(7278):144-5. doi: 10.1038/463144a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075889" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Diseases/epidemiology/*mortality/therapy ; Animals ; Ascomycota/pathogenicity ; Chiroptera/*microbiology/physiology ; Europe/epidemiology ; Extinction, Biological ; Hibernation ; Mycoses/epidemiology/mortality/therapy/*veterinary ; United States/epidemiology
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  • 24
    Publication Date: 2010-08-06
    Description: Sponges are an ancient group of animals that diverged from other metazoans over 600 million years ago. Here we present the draft genome sequence of Amphimedon queenslandica, a demosponge from the Great Barrier Reef, and show that it is remarkably similar to other animal genomes in content, structure and organization. Comparative analysis enabled by the sequencing of the sponge genome reveals genomic events linked to the origin and early evolution of animals, including the appearance, expansion and diversification of pan-metazoan transcription factor, signalling pathway and structural genes. This diverse 'toolkit' of genes correlates with critical aspects of all metazoan body plans, and comprises cell cycle control and growth, development, somatic- and germ-cell specification, cell adhesion, innate immunity and allorecognition. Notably, many of the genes associated with the emergence of animals are also implicated in cancer, which arises from defects in basic processes associated with metazoan multicellularity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130542/" 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/PMC3130542/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srivastava, Mansi -- Simakov, Oleg -- Chapman, Jarrod -- Fahey, Bryony -- Gauthier, Marie E A -- Mitros, Therese -- Richards, Gemma S -- Conaco, Cecilia -- Dacre, Michael -- Hellsten, Uffe -- Larroux, Claire -- Putnam, Nicholas H -- Stanke, Mario -- Adamska, Maja -- Darling, Aaron -- Degnan, Sandie M -- Oakley, Todd H -- Plachetzki, David C -- Zhai, Yufeng -- Adamski, Marcin -- Calcino, Andrew -- Cummins, Scott F -- Goodstein, David M -- Harris, Christina -- Jackson, Daniel J -- Leys, Sally P -- Shu, Shengqiang -- Woodcroft, Ben J -- Vervoort, Michel -- Kosik, Kenneth S -- Manning, Gerard -- Degnan, Bernard M -- Rokhsar, Daniel S -- R01 HG004164/HG/NHGRI NIH HHS/ -- R01 HG004164-03/HG/NHGRI NIH HHS/ -- R01 HG004164-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Aug 5;466(7307):720-6. doi: 10.1038/nature09201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Integrative Genomics and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. mansi@wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20686567" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/genetics ; Cell Adhesion/genetics ; Cell Cycle/genetics ; Cell Polarity/genetics ; Cell Proliferation ; *Evolution, Molecular ; Genes/genetics ; Genome/*genetics ; Genomics ; Humans ; Immunity, Innate/genetics ; Models, Biological ; Neurons/metabolism ; Phosphotransferases/chemistry/genetics ; Phylogeny ; Porifera/anatomy & histology/cytology/*genetics/immunology ; Sequence Analysis, DNA ; Signal Transduction/genetics
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  • 25
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    Nature Publishing Group (NPG)
    Publication Date: 2010-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, Alison -- England -- Nature. 2010 Jul 15;466(7304):306-7. doi: 10.1038/466306a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631771" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology/*methods ; Color ; Coloring Agents/*analysis/chemistry ; Environmental Pollutants/*analysis/chemistry ; Hominidae ; Humans ; Italy ; *Museums ; *Natural History
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  • 26
    Publication Date: 2010-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harmon, Luke -- England -- Nature. 2010 Feb 25;463(7284):1003. doi: 10.1038/4631003e.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Idaho, Moscow.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20182473" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Finches/anatomy & histology/physiology ; Humans ; *Models, Biological ; Selection, Genetic ; Time Factors
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  • 27
    Publication Date: 2010-07-31
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3610560/" 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/PMC3610560/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Evans, Ronald M -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Jul 29;466(7306):571-2. doi: 10.1038/466571a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671699" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/genetics/*metabolism ; Animals ; Blood Glucose/metabolism ; CLOCK Proteins/genetics/*metabolism ; Circadian Rhythm/genetics/*physiology ; Diabetes Mellitus/genetics/*metabolism ; Insulin/*blood/metabolism/secretion ; Islets of Langerhans/*metabolism/pathology/secretion ; Mice
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  • 28
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    Nature Publishing Group (NPG)
    Publication Date: 2011-04-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, Robin R -- Sowden, Jane C -- G0700438/Medical Research Council/United Kingdom -- G0901550/Medical Research Council/United Kingdom -- England -- Nature. 2011 Apr 7;472(7341):42-3. doi: 10.1038/472042a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21475187" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques/methods ; Embryonic Stem Cells/*cytology ; Eye/*cytology/*embryology ; Humans ; Mice ; Morphogenesis ; Neural Stem Cells/cytology ; Organ Culture Techniques/methods ; *Organogenesis ; Regenerative Medicine/*methods ; Retinal Pigment Epithelium/cytology/embryology
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  • 29
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    Publication Date: 2011-07-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lerdau, Manuel -- Wickham, Jacob D -- England -- Nature. 2011 Jul 6;475(7354):36-7. doi: 10.1038/475036d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beetles/physiology ; China ; Ecology/*methods ; Food Chain ; *Introduced Species/statistics & numerical data ; North America ; Phylogeny ; Reproduction/physiology ; Risk Factors ; Trees/physiology
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  • 30
    Publication Date: 2011-03-25
    Description: Systematic annotation of gene regulatory elements is a major challenge in genome science. Direct mapping of chromatin modification marks and transcriptional factor binding sites genome-wide has successfully identified specific subtypes of regulatory elements. In Drosophila several pioneering studies have provided genome-wide identification of Polycomb response elements, chromatin states, transcription factor binding sites, RNA polymerase II regulation and insulator elements; however, comprehensive annotation of the regulatory genome remains a significant challenge. Here we describe results from the modENCODE cis-regulatory annotation project. We produced a map of the Drosophila melanogaster regulatory genome on the basis of more than 300 chromatin immunoprecipitation data sets for eight chromatin features, five histone deacetylases and thirty-eight site-specific transcription factors at different stages of development. Using these data we inferred more than 20,000 candidate regulatory elements and validated a subset of predictions for promoters, enhancers and insulators in vivo. We identified also nearly 2,000 genomic regions of dense transcription factor binding associated with chromatin activity and accessibility. We discovered hundreds of new transcription factor co-binding relationships and defined a transcription factor network with over 800 potential regulatory relationships.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179250/" 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/PMC3179250/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Negre, Nicolas -- Brown, Christopher D -- Ma, Lijia -- Bristow, Christopher Aaron -- Miller, Steven W -- Wagner, Ulrich -- Kheradpour, Pouya -- Eaton, Matthew L -- Loriaux, Paul -- Sealfon, Rachel -- Li, Zirong -- Ishii, Haruhiko -- Spokony, Rebecca F -- Chen, Jia -- Hwang, Lindsay -- Cheng, Chao -- Auburn, Richard P -- Davis, Melissa B -- Domanus, Marc -- Shah, Parantu K -- Morrison, Carolyn A -- Zieba, Jennifer -- Suchy, Sarah -- Senderowicz, Lionel -- Victorsen, Alec -- Bild, Nicholas A -- Grundstad, A Jason -- Hanley, David -- MacAlpine, David M -- Mannervik, Mattias -- Venken, Koen -- Bellen, Hugo -- White, Robert -- Gerstein, Mark -- Russell, Steven -- Grossman, Robert L -- Ren, Bing -- Posakony, James W -- Kellis, Manolis -- White, Kevin P -- F32 GM074364/GM/NIGMS NIH HHS/ -- F32 GM074364-01/GM/NIGMS NIH HHS/ -- F32 GM074364-02/GM/NIGMS NIH HHS/ -- P50 GM081892/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-04/HG/NHGRI NIH HHS/ -- RC2 HG005639/HG/NHGRI NIH HHS/ -- RC2 HG005639-02/HG/NHGRI NIH HHS/ -- U01 HG004264/HG/NHGRI NIH HHS/ -- U01 HG004279/HG/NHGRI NIH HHS/ -- U01HG004264/HG/NHGRI NIH HHS/ -- England -- Nature. 2011 Mar 24;471(7339):527-31. doi: 10.1038/nature09990.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomics and Systems Biology, Department of Human Genetics, The University of Chicago, 900 East 57th Street, Chicago, Illinois 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Chromatin Immunoprecipitation ; Drosophila melanogaster/*genetics ; Enhancer Elements, Genetic/genetics ; Genome, Insect/*genetics ; Histone Deacetylases/metabolism ; Insulator Elements/genetics ; *Molecular Sequence Annotation ; Promoter Regions, Genetic/genetics ; Regulatory Sequences, Nucleic Acid/*genetics ; Reproducibility of Results ; Silencer Elements, Transcriptional/genetics ; Transcription Factors/metabolism
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  • 31
    Publication Date: 2010-04-16
    Description: The four receptors of the Notch family are widely expressed transmembrane proteins that function as key conduits through which mammalian cells communicate to regulate cell fate and growth. Ligand binding triggers a conformational change in the receptor negative regulatory region (NRR) that enables ADAM protease cleavage at a juxtamembrane site that otherwise lies buried within the quiescent NRR. Subsequent intramembrane proteolysis catalysed by the gamma-secretase complex liberates the intracellular domain (ICD) to initiate the downstream Notch transcriptional program. Aberrant signalling through each receptor has been linked to numerous diseases, particularly cancer, making the Notch pathway a compelling target for new drugs. Although gamma-secretase inhibitors (GSIs) have progressed into the clinic, GSIs fail to distinguish individual Notch receptors, inhibit other signalling pathways and cause intestinal toxicity, attributed to dual inhibition of Notch1 and 2 (ref. 11). To elucidate the discrete functions of Notch1 and Notch2 and develop clinically relevant inhibitors that reduce intestinal toxicity, we used phage display technology to generate highly specialized antibodies that specifically antagonize each receptor paralogue and yet cross-react with the human and mouse sequences, enabling the discrimination of Notch1 versus Notch2 function in human patients and rodent models. Our co-crystal structure shows that the inhibitory mechanism relies on stabilizing NRR quiescence. Selective blocking of Notch1 inhibits tumour growth in pre-clinical models through two mechanisms: inhibition of cancer cell growth and deregulation of angiogenesis. Whereas inhibition of Notch1 plus Notch2 causes severe intestinal toxicity, inhibition of either receptor alone reduces or avoids this effect, demonstrating a clear advantage over pan-Notch inhibitors. Our studies emphasize the value of paralogue-specific antagonists in dissecting the contributions of distinct Notch receptors to differentiation and disease and reveal the therapeutic promise in targeting Notch1 and Notch2 independently.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Yan -- Cain-Hom, Carol -- Choy, Lisa -- Hagenbeek, Thijs J -- de Leon, Gladys P -- Chen, Yongmei -- Finkle, David -- Venook, Rayna -- Wu, Xiumin -- Ridgway, John -- Schahin-Reed, Dorreyah -- Dow, Graham J -- Shelton, Amy -- Stawicki, Scott -- Watts, Ryan J -- Zhang, Jeff -- Choy, Robert -- Howard, Peter -- Kadyk, Lisa -- Yan, Minhong -- Zha, Jiping -- Callahan, Christopher A -- Hymowitz, Sarah G -- Siebel, Christian W -- England -- Nature. 2010 Apr 15;464(7291):1052-7. doi: 10.1038/nature08878.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Antibody Engineering, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393564" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/immunology/pharmacology/therapeutic use ; Animals ; Antibodies/adverse effects/immunology/*pharmacology/*therapeutic use ; Antibody Specificity/immunology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Goblet Cells/drug effects/pathology ; Humans ; Mice ; Mice, Inbred BALB C ; NIH 3T3 Cells ; Neoplasms/blood supply/*drug therapy/*metabolism/pathology ; Neovascularization, Pathologic/drug therapy ; Peptide Library ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/metabolism/pathology ; Receptor, Notch1/antagonists & inhibitors/immunology ; Receptor, Notch2/antagonists & inhibitors/immunology ; Receptors, Notch/*antagonists & inhibitors/genetics/immunology/metabolism ; Signal Transduction/drug effects
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  • 32
    Publication Date: 2010-04-24
    Description: The cerebral cortex constructs a coherent representation of the world by integrating distinct features of the sensory environment. Although these features are processed vertically across cortical layers, horizontal projections interconnecting neighbouring cortical domains allow these features to be processed in a context-dependent manner. Despite the wealth of physiological and psychophysical studies addressing the function of horizontal projections, how they coordinate activity among cortical domains remains poorly understood. We addressed this question by selectively activating horizontal projection neurons in mouse somatosensory cortex, and determined how the resulting spatial pattern of excitation and inhibition affects cortical activity. We found that horizontal projections suppress superficial layers while simultaneously activating deeper cortical output layers. This layer-specific modulation does not result from a spatial separation of excitation and inhibition, but from a layer-specific ratio between these two opposing conductances. Through this mechanism, cortical domains exploit horizontal projections to compete for cortical space.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908490/" 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/PMC2908490/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adesnik, Hillel -- Scanziani, Massimo -- R01 MH070058/MH/NIMH NIH HHS/ -- R01 MH070058-05/MH/NIMH NIH HHS/ -- R01 MH70058/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 22;464(7292):1155-60. doi: 10.1038/nature08935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Neural Circuits and Behavior, Neurobiology Section and Department of Neurosciences, University of California San Diego, La Jolla, California 92093-0634, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414303" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Aging/physiology ; Animals ; Axons/metabolism ; Mice ; Models, Neurological ; Neural Inhibition/physiology ; Neural Pathways/*cytology/*physiology ; Pyramidal Cells/metabolism ; Rhodopsin/genetics/metabolism ; Somatosensory Cortex/anatomy & histology/*cytology/*physiology
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  • 33
    Publication Date: 2010-02-05
    Description: Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have broad therapeutic effects. Small molecule ATP-competitive RAF kinase inhibitors have potent antitumour effects on mutant BRAF(V600E) tumours but, in contrast to mitogen-activated protein kinase kinase (MEK) inhibitors, are not potent against RAS mutant tumour models, despite RAF functioning as a key effector downstream of RAS and upstream of MEK. Here we show that ATP-competitive RAF inhibitors have two opposing mechanisms of action depending on the cellular context. In BRAF(V600E) tumours, RAF inhibitors effectively block the mitogen-activated protein kinase (MAPK) signalling pathway and decrease tumour growth. Notably, in KRAS mutant and RAS/RAF wild-type tumours, RAF inhibitors activate the RAF-MEK-ERK pathway in a RAS-dependent manner, thus enhancing tumour growth in some xenograft models. Inhibitor binding activates wild-type RAF isoforms by inducing dimerization, membrane localization and interaction with RAS-GTP. These events occur independently of kinase inhibition and are, instead, linked to direct conformational effects of inhibitors on the RAF kinase domain. On the basis of these findings, we demonstrate that ATP-competitive kinase inhibitors can have opposing functions as inhibitors or activators of signalling pathways, depending on the cellular context. Furthermore, this work provides new insights into the therapeutic use of ATP-competitive RAF inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hatzivassiliou, Georgia -- Song, Kyung -- Yen, Ivana -- Brandhuber, Barbara J -- Anderson, Daniel J -- Alvarado, Ryan -- Ludlam, Mary J C -- Stokoe, David -- Gloor, Susan L -- Vigers, Guy -- Morales, Tony -- Aliagas, Ignacio -- Liu, Bonnie -- Sideris, Steve -- Hoeflich, Klaus P -- Jaiswal, Bijay S -- Seshagiri, Somasekar -- Koeppen, Hartmut -- Belvin, Marcia -- Friedman, Lori S -- Malek, Shiva -- England -- Nature. 2010 Mar 18;464(7287):431-5. doi: 10.1038/nature08833. Epub 2010 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech, South San Francisco, California 94080, USA. hatzivassiliou.georgia@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20130576" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Benzamides/pharmacology ; Cell Line ; Cell Membrane/drug effects/metabolism ; Cell Proliferation/drug effects ; Diphenylamine/analogs & derivatives/pharmacology ; Enzyme Activation/drug effects ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Indenes/pharmacology ; Indoles/pharmacology ; MAP Kinase Signaling System/*drug effects ; Mice ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Neoplasms/drug therapy/enzymology/metabolism/*pathology ; Protein Kinase Inhibitors/*pharmacology/therapeutic use ; Protein Multimerization ; Protein Structure, Tertiary ; Protein Transport/drug effects ; Proto-Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Proteins B-raf/antagonists & ; inhibitors/chemistry/genetics/metabolism ; Proto-Oncogene Proteins c-raf/deficiency/genetics/metabolism ; Pyrazoles/pharmacology ; Sulfonamides/pharmacology ; Xenograft Model Antitumor Assays ; raf Kinases/*antagonists & inhibitors/chemistry/genetics/*metabolism ; ras Proteins/genetics/metabolism
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  • 34
    Publication Date: 2011-08-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Legg, David A -- Ma, Xiaoya -- Wolfe, Joanna M -- Ortega-Hernandez, Javier -- Edgecombe, Gregory D -- Sutton, Mark D -- England -- Nature. 2011 Aug 10;476(7359):E2-3; discussion E3-4. doi: 10.1038/nature10267.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Science and Engineering, Imperial College London, London SW7 2AZ UK. d.legg10@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21833046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods/anatomy & histology/*classification ; Fossils ; *Phylogeny ; Pseudopodia/*classification ; Reproducibility of Results
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  • 35
    Publication Date: 2010-12-15
    Description: Individuals make choices and prioritize goals using complex processes that assign value to rewards and associated stimuli. During Pavlovian learning, previously neutral stimuli that predict rewards can acquire motivational properties, becoming attractive and desirable incentive stimuli. However, whether a cue acts solely as a predictor of reward, or also serves as an incentive stimulus, differs between individuals. Thus, individuals vary in the degree to which cues bias choice and potentially promote maladaptive behaviour. Here we use rats that differ in the incentive motivational properties they attribute to food cues to probe the role of the neurotransmitter dopamine in stimulus-reward learning. We show that intact dopamine transmission is not required for all forms of learning in which reward cues become effective predictors. Rather, dopamine acts selectively in a form of stimulus-reward learning in which incentive salience is assigned to reward cues. In individuals with a propensity for this form of learning, reward cues come to powerfully motivate and control behaviour. This work provides insight into the neurobiology of a form of stimulus-reward learning that confers increased susceptibility to disorders of impulse control.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058375/" 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/PMC3058375/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flagel, Shelly B -- Clark, Jeremy J -- Robinson, Terry E -- Mayo, Leah -- Czuj, Alayna -- Willuhn, Ingo -- Akers, Christina A -- Clinton, Sarah M -- Phillips, Paul E M -- Akil, Huda -- 5P01-DA021633-02/DA/NIDA NIH HHS/ -- F32-DA24540/DA/NIDA NIH HHS/ -- P01 DA021633/DA/NIDA NIH HHS/ -- P01 DA021633-02/DA/NIDA NIH HHS/ -- R00 MH085859/MH/NIMH NIH HHS/ -- R00 MH085859-02/MH/NIMH NIH HHS/ -- R01 DA027858/DA/NIDA NIH HHS/ -- R01 MH079292/MH/NIMH NIH HHS/ -- R01-DA027858/DA/NIDA NIH HHS/ -- R01-MH079292/MH/NIMH NIH HHS/ -- R37-DA04294/DA/NIDA NIH HHS/ -- T32-DA07278/DA/NIDA NIH HHS/ -- England -- Nature. 2011 Jan 6;469(7328):53-7. doi: 10.1038/nature09588. Epub 2010 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Behavioral Neuroscience Institute, University of Michigan, Michigan, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21150898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical/drug effects/physiology ; *Cues ; Disruptive, Impulse Control, and Conduct Disorders/physiopathology ; Dopamine/*metabolism ; Dopamine Antagonists/pharmacology ; Flupenthixol/pharmacology ; Food ; Learning/drug effects/*physiology ; Male ; Microelectrodes ; *Models, Neurological ; Motivation/drug effects ; Nucleus Accumbens/metabolism ; Phenotype ; Probability ; Rats ; Rats, Sprague-Dawley ; *Reward ; Signal Transduction ; Synaptic Transmission
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  • 36
    Publication Date: 2011-05-20
    Description: Blood vessels deliver oxygen and nutrients to every part of the body, but also nourish diseases such as cancer. Over the past decade, our understanding of the molecular mechanisms of angiogenesis (blood vessel growth) has increased at an explosive rate and has led to the approval of anti-angiogenic drugs for cancer and eye diseases. So far, hundreds of thousands of patients have benefited from blockers of the angiogenic protein vascular endothelial growth factor, but limited efficacy and resistance remain outstanding problems. Recent preclinical and clinical studies have shown new molecular targets and principles, which may provide avenues for improving the therapeutic benefit from anti-angiogenic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049445/" 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/PMC4049445/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmeliet, Peter -- Jain, Rakesh K -- P01 CA080124/CA/NCI NIH HHS/ -- P01-CA80124/CA/NCI NIH HHS/ -- R01 CA085140/CA/NCI NIH HHS/ -- R01 CA115767/CA/NCI NIH HHS/ -- R01 CA126642/CA/NCI NIH HHS/ -- R01 CA163815/CA/NCI NIH HHS/ -- R01-CA115767/CA/NCI NIH HHS/ -- R01-CA126642/CA/NCI NIH HHS/ -- R01-CA85140/CA/NCI NIH HHS/ -- England -- Nature. 2011 May 19;473(7347):298-307. doi: 10.1038/nature10144.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven B-3000, Belgium. peter.carmeliet@vib-kuleuven.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21593862" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/pharmacology/therapeutic use ; Animals ; Blood Vessels/growth & development/pathology/*physiology/physiopathology ; Fibroblast Growth Factors/metabolism ; Humans ; Neovascularization, Physiologic/*physiology ; Platelet-Derived Growth Factor/metabolism ; Transforming Growth Factor beta/metabolism ; Vascular Endothelial Growth Factor A/antagonists & inhibitors/metabolism ; Vesicular Transport Proteins/metabolism
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  • 37
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    Nature Publishing Group (NPG)
    Publication Date: 2011-12-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Samuel Reich, Eugenie -- England -- Nature. 2011 Dec 6;480(7376):160-1. doi: 10.1038/480160a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158217" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calibration ; Government Regulation ; Humans ; Nanostructures/*adverse effects/chemistry/*toxicity ; *Nanotechnology ; Nanotubes, Carbon/chemistry ; Particle Size ; Reference Standards ; Surface Properties ; Toxicity Tests ; Toxicology/*standards
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  • 38
    Publication Date: 2011-09-20
    Description: Dynamin-related proteins (DRPs) are multi-domain GTPases that function via oligomerization and GTP-dependent conformational changes to play central roles in regulating membrane structure across phylogenetic kingdoms. How DRPs harness self-assembly and GTP-dependent conformational changes to remodel membranes is not understood. Here we present the crystal structure of an assembly-deficient mammalian endocytic DRP, dynamin 1, lacking the proline-rich domain, in its nucleotide-free state. The dynamin 1 monomer is an extended structure with the GTPase domain and bundle signalling element positioned on top of a long helical stalk with the pleckstrin homology domain flexibly attached on its opposing end. Dynamin 1 dimer and higher order dimer multimers form via interfaces located in the stalk. Analysis of these interfaces provides insight into DRP family member specificity and regulation and provides a framework for understanding the biogenesis of higher order DRP structures and the mechanism of DRP-mediated membrane scission events.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075756/" 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/PMC4075756/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ford, Marijn G J -- Jenni, Simon -- Nunnari, Jodi -- DRG-2004-09/Howard Hughes Medical Institute/ -- R01 GM062942/GM/NIGMS NIH HHS/ -- R01 GM097432/GM/NIGMS NIH HHS/ -- R01GM062942S1/GM/NIGMS NIH HHS/ -- R01GM097432/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Sep 18;477(7366):561-6. doi: 10.1038/nature10441.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California, Davis, Davis, California 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21927001" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Crystallization ; Crystallography, X-Ray ; Dynamin I/*chemistry/genetics/metabolism ; Guanosine Triphosphate/metabolism ; Humans ; Models, Molecular ; Molecular Sequence Data ; Nucleotides ; Protein Binding ; Protein Conformation ; Protein Multimerization/genetics ; Protein Structure, Tertiary/genetics ; Rats
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  • 39
    Publication Date: 2011-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andelman, Sandy J -- England -- Nature. 2011 Jul 20;475(7356):290-1. doi: 10.1038/475290a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tropical Ecology, Assessment and Monitoring Network, Conservation International, Arlington, Virginia 22202, USA. s.andelman@conservation.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21776060" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Agriculture/methods/statistics & numerical data ; Animals ; Asia ; Biodiversity ; Climate Change/statistics & numerical data ; Conservation of Natural Resources/economics/*methods/*statistics & numerical ; data/trends ; Ecology/economics/*methods/trends ; Human Activities ; Latin America ; Pilot Projects ; *Policy Making ; Tanzania ; Time Factors ; Tropical Climate
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  • 40
    Publication Date: 2011-10-08
    Description: Spinal muscular atrophy (SMA) is a motor neuron disease and the leading genetic cause of infant mortality; it results from loss-of-function mutations in the survival motor neuron 1 (SMN1) gene. Humans have a paralogue, SMN2, whose exon 7 is predominantly skipped, but the limited amount of functional, full-length SMN protein expressed from SMN2 cannot fully compensate for a lack of SMN1. SMN is important for the biogenesis of spliceosomal small nuclear ribonucleoprotein particles, but downstream splicing targets involved in pathogenesis remain elusive. There is no effective SMA treatment, but SMN restoration in spinal cord motor neurons is thought to be necessary and sufficient. Non-central nervous system (CNS) pathologies, including cardiovascular defects, were recently reported in severe SMA mouse models and patients, reflecting autonomic dysfunction or direct effects in cardiac tissues. Here we compared systemic versus CNS restoration of SMN in a severe mouse model. We used an antisense oligonucleotide (ASO), ASO-10-27, that effectively corrects SMN2 splicing and restores SMN expression in motor neurons after intracerebroventricular injection. Systemic administration of ASO-10-27 to neonates robustly rescued severe SMA mice, much more effectively than intracerebroventricular administration; subcutaneous injections extended the median lifespan by 25 fold. Furthermore, neonatal SMA mice had decreased hepatic Igfals expression, leading to a pronounced reduction in circulating insulin-like growth factor 1 (IGF1), and ASO-10-27 treatment restored IGF1 to normal levels. These results suggest that the liver is important in SMA pathogenesis, underscoring the importance of SMN in peripheral tissues, and demonstrate the efficacy of a promising drug candidate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191865/" 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/PMC3191865/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hua, Yimin -- Sahashi, Kentaro -- Rigo, Frank -- Hung, Gene -- Horev, Guy -- Bennett, C Frank -- Krainer, Adrian R -- R01 GM042699/GM/NIGMS NIH HHS/ -- R01 GM042699-21/GM/NIGMS NIH HHS/ -- R37 GM042699/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Oct 5;478(7367):123-6. doi: 10.1038/nature10485.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, PO Box 100, Cold Spring Harbor, New York 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979052" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/drug effects/genetics ; Animals ; Animals, Newborn ; Carrier Proteins/metabolism ; *Disease Models, Animal ; Glycoproteins/deficiency/metabolism ; Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/deficiency/metabolism ; Kaplan-Meier Estimate ; Liver/metabolism ; Longevity/drug effects ; Mice ; Mice, Transgenic ; Motor Neurons/drug effects/metabolism/pathology ; Muscular Atrophy, Spinal/genetics/*metabolism/*pathology/physiopathology ; Oligonucleotides, Antisense/administration & dosage/genetics/pharmacology ; RNA Isoforms/analysis/genetics ; RNA, Messenger/analysis/genetics ; Rotarod Performance Test ; Spinal Cord/cytology/metabolism/pathology ; Survival of Motor Neuron 1 Protein/genetics ; Survival of Motor Neuron 2 Protein/genetics/metabolism ; Transgenes
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  • 41
    Publication Date: 2011-08-05
    Description: The role of African savannahs in the evolution of early hominins has been debated for nearly a century. Resolution of this issue has been hindered by difficulty in quantifying the fraction of woody cover in the fossil record. Here we show that the fraction of woody cover in tropical ecosystems can be quantified using stable carbon isotopes in soils. Furthermore, we use fossil soils from hominin sites in the Awash and Omo-Turkana basins in eastern Africa to reconstruct the fraction of woody cover since the Late Miocene epoch (about 7 million years ago). (13)C/(12)C ratio data from 1,300 palaeosols at or adjacent to hominin sites dating to at least 6 million years ago show that woody cover was predominantly less than approximately 40% at most sites. These data point to the prevalence of open environments at the majority of hominin fossil sites in eastern Africa over the past 6 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerling, Thure E -- Wynn, Jonathan G -- Andanje, Samuel A -- Bird, Michael I -- Korir, David Kimutai -- Levin, Naomi E -- Mace, William -- Macharia, Anthony N -- Quade, Jay -- Remien, Christopher H -- England -- Nature. 2011 Aug 3;476(7358):51-6. doi: 10.1038/nature10306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Utah, Salt Lake City, Utah 84112, USA. thure.cerling@utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814275" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Eastern ; Animals ; *Biological Evolution ; Calibration ; Carbon Isotopes/analysis ; *Ecosystem ; Fossils ; Gait/physiology ; Hominidae/anatomy & histology/*physiology ; Paleontology ; Plant Leaves/growth & development ; Poaceae/growth & development ; Population Dynamics ; Soil/chemistry ; *Trees/growth & development ; Tropical Climate ; Wilderness ; Wood
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  • 42
    Publication Date: 2011-06-21
    Description: High-dose intravenous immunoglobulin is a widely used therapeutic preparation of highly purified immunoglobulin G (IgG) antibodies. It is administered at high doses (1-2 grams per kilogram) for the suppression of autoantibody-triggered inflammation in a variety of clinical settings. This anti-inflammatory activity of intravenous immunoglobulin is triggered by a minor population of IgG crystallizable fragments (Fcs), with glycans terminating in alpha2,6 sialic acids (sFc) that target myeloid regulatory cells expressing the lectin dendritic-cell-specific ICAM-3 grabbing non-integrin (DC-SIGN; also known as CD209). Here, to characterize this response in detail, we generated humanized DC-SIGN mice (hDC-SIGN), and demonstrate that the anti-inflammatory activity of intravenous immunoglobulin can be recapitulated by the transfer of bone-marrow-derived sFc-treated hDC-SIGN(+) macrophages or dendritic cells into naive recipients. Furthermore, sFc administration results in the production of IL-33, which, in turn, induces expansion of IL-4-producing basophils that promote increased expression of the inhibitory Fc receptor FcgammaRIIB on effector macrophages. Systemic administration of the T(H)2 cytokines IL-33 or IL-4 upregulates FcgammaRIIB on macrophages, and suppresses serum-induced arthritis. Consistent with these results, transfer of IL-33-treated basophils suppressed induced arthritic inflammation. This novel DC-SIGN-T(H)2 pathway initiated by an endogenous ligand, sFc, provides an intrinsic mechanism for maintaining immune homeostasis that could be manipulated to provide therapeutic benefit in autoimmune diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694429/" 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/PMC3694429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anthony, Robert M -- Kobayashi, Toshihiko -- Wermeling, Fredrik -- Ravetch, Jeffrey V -- R01 AI035875/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Jun 19;475(7354):110-3. doi: 10.1038/nature10134.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Genetics and Immunology, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21685887" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/drug therapy/immunology/pathology ; Autoimmune Diseases/drug therapy/immunology ; Basophils/drug effects/immunology/metabolism ; Bone Marrow ; Cell Adhesion Molecules/genetics/immunology/metabolism ; Crystallization ; Dendritic Cells/cytology/immunology ; Humans ; Immunoglobulin G/chemistry/immunology/metabolism/pharmacology ; Immunoglobulins, Intravenous/chemistry/*immunology/metabolism/pharmacology ; Inflammation/drug therapy/*immunology ; Interleukin-33 ; Interleukin-4/immunology/metabolism ; Interleukins/immunology/metabolism/pharmacology ; Lectins, C-Type/genetics/immunology/metabolism ; Ligands ; Macrophages/cytology/immunology ; Mice ; Receptors, Cell Surface/genetics/immunology/metabolism ; Receptors, IgG/immunology/metabolism ; Th2 Cells/drug effects/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 43
    Publication Date: 2011-03-25
    Description: The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348545/" 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/PMC3348545/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ceol, Craig J -- Houvras, Yariv -- Jane-Valbuena, Judit -- Bilodeau, Steve -- Orlando, David A -- Battisti, Valentine -- Fritsch, Lauriane -- Lin, William M -- Hollmann, Travis J -- Ferre, Fabrizio -- Bourque, Caitlin -- Burke, Christopher J -- Turner, Laura -- Uong, Audrey -- Johnson, Laura A -- Beroukhim, Rameen -- Mermel, Craig H -- Loda, Massimo -- Ait-Si-Ali, Slimane -- Garraway, Levi A -- Young, Richard A -- Zon, Leonard I -- CA103846/CA/NCI NIH HHS/ -- CA146455/CA/NCI NIH HHS/ -- DK055381/DK/NIDDK NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- K08 DK075432/DK/NIDDK NIH HHS/ -- K08 DK075432-04/DK/NIDDK NIH HHS/ -- K08DK075432-04/DK/NIDDK NIH HHS/ -- K99AR056899-02/AR/NIAMS NIH HHS/ -- R00 AR056899/AR/NIAMS NIH HHS/ -- R00 AR056899-02/AR/NIAMS NIH HHS/ -- R01 CA103846/CA/NCI NIH HHS/ -- R01 CA103846-09/CA/NCI NIH HHS/ -- R01 CA146445/CA/NCI NIH HHS/ -- R01 CA146445-03/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-08/HG/NHGRI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):513-7. doi: 10.1038/nature09806.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430779" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Cell Transformation, Neoplastic/genetics ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 1/genetics ; DNA Copy Number Variations/*genetics ; Disease Models, Animal ; Gene Amplification/*genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Genes, Homeobox/genetics ; Histone-Lysine N-Methyltransferase/*genetics/metabolism ; Humans ; Melanocytes/cytology/enzymology/metabolism/pathology ; Melanoma/enzymology/*genetics/*pathology ; Nevus/enzymology ; Oncogenes/genetics ; Protein Methyltransferases/*genetics/*metabolism ; Proto-Oncogene Proteins B-raf/chemistry/genetics/metabolism ; Zebrafish/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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