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  • Mice, Inbred C57BL  (257)
  • Chemistry  (231)
  • Development
  • American Association for the Advancement of Science (AAAS)  (554)
  • Institute of Physics
  • 2015-2019  (346)
  • 2010-2014  (208)
  • 1
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    [Perspective] Molecular sieves for gas separation (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-07-08
    Description: Separation and purification are critical industrial processes for separating components of chemical mixtures, and these processes account for about half of industrial energy usage (1). Gas mixtures of compounds with very similar physical properties are particularly difficult to separate. On pages 137 and 141 of this issue, Cadiau et al. (2) and Cui et al. (3), respectively, show that microporous materials can be designed to have high adsorption capacity and selectivity for particular hydrocarbons, enabling energy-efficient separation. Author: Jerry Y. S. Lin
    Keywords: Chemistry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 2
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    [Perspective] How to break down crystalline cellulose (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-05-27
    Description: Biomass-degrading microorganisms use lytic polysaccharide monooxygenase (LPMO) enzymes to help digest cellulose, chitin, and starch. By cleaving otherwise inaccessible crystalline cellulose chains, these enzymes provide access to hydrolytic enzymes. LPMOs are of interest to biotechnology because efficient depolymerization of cellulose is a major bottleneck for the production of biologically based chemicals and fuels. On page 1098 of this issue, Kracher et al. (1) compare LPMO-reducing substrates in fungi from different taxonomic groups and lifestyles, based on both biochemical and genomic evidence. The results provide insights into reductive activation of LPMO that are important for developing more efficient industrial enzymes for lignocellulose biorefineries. Author: Angel T. Martínez
    Keywords: Chemistry
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  • 3
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    [Editors' Choice] Engineering open structures using DNA (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-03-25
    Description: Author: Marc S. Lavine
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    [This Week in Science] Altered fluid flow causes curved spine (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-06-10
    Description: Author: Beverly A. Purnell
    Keywords: Development
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  • 5
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    [In Depth] CRISPR views of embryos and cells (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-06-03
    Description: Two teams have developed innovative new applications of the popular genome-editing method CRISPR. One of the groups has used it to mark and trace cells in a developing animal. In the method's first test, described online today in Science, the researchers reveal that many tissues and organs in adult zebrafish form from just a few embryonic cells. Other researchers are already looking to adapt the method to mice, or to exploit it to trace the evolution of tumors. The second group found a way to use CRISPR-guided mutations to record a cell's history—for example, the environmental signals that influence it. Author: Kai Kupferschmidt
    Keywords: Development
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  • 6
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    [Editors' Choice] Microtubule sliding during Drosophila development (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-09-03
    Description: Author: Valda Vinson
    Keywords: Development
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Left- or right-handed C-H bond activation (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-02-16
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Comment on "Selective anaerobic oxidation of methane enables direct synthesis of methanol" (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-02-16
    Description: The comment and response concerning the report of oxidation of methane to methanol by water (Reports, 5 May 2017, p. 523) do not fully capture the implications of thermodynamic limitations. A nonisothermal process in which each cycle requires a large temperature swing and permits only substoichiometric methane conversion surely could not be carried out on any practical scale.
    Keywords: Chemistry
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  • 9
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    Response to Comment on "Selective anaerobic oxidation of methane enables direct synthesis of methanol" (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-02-16
    Description: Labinger argues that stepwise reaction of methane with water to produce methanol and hydrogen will never be commercially feasible because of its substoichiometric basis with respect to the active site and the requirement of a large temperature swing. This comment is not touching any new ground, beyond describing the thermodynamic feasibility, thermal cycling, and the role of water as discussed previously. Most important, it does not have a solid numerical basis.
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Silicon smooths the way to vinyl cations (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-07-27
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Teaching an old carbocation new tricks: Intermolecular C-H insertion reactions of vinyl cations (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-07-27
    Description: Vinyl carbocations have been the subject of extensive experimental and theoretical studies over the past five decades. Despite this long history in chemistry, the utility of vinyl cations in chemical synthesis has been limited, with most reactivity studies focusing on solvolysis reactions or intramolecular processes. Here we report synthetic and mechanistic studies of vinyl cations generated through silylium–weakly coordinating anion catalysis. We find that these reactive intermediates undergo mild intermolecular carbon-carbon bond–forming reactions, including carbon-hydrogen (C–H) insertion into unactivated sp 3 C–H bonds and reductive Friedel-Crafts reactions with arenes. Moreover, we conducted computational studies of these alkane C–H functionalization reactions and discovered that they proceed through nonclassical, ambimodal transition structures. This reaction manifold provides a framework for the catalytic functionalization of hydrocarbons using simple ketone derivatives.
    Keywords: Chemistry
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  • 12
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    Separation of enantiomers by their enantiospecific interaction with achiral magnetic substrates (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-06-22
    Description: It is commonly assumed that recognition and discrimination of chirality, both in nature and in artificial systems, depend solely on spatial effects. However, recent studies have suggested that charge redistribution in chiral molecules manifests an enantiospecific preference in electron spin orientation. We therefore reasoned that the induced spin polarization may affect enantiorecognition through exchange interactions. Here we show experimentally that the interaction of chiral molecules with a perpendicularly magnetized substrate is enantiospecific. Thus, one enantiomer adsorbs preferentially when the magnetic dipole is pointing up, whereas the other adsorbs faster for the opposite alignment of the magnetization. The interaction is not controlled by the magnetic field per se, but rather by the electron spin orientations, and opens prospects for a distinct approach to enantiomeric separations.
    Keywords: Chemistry
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  • 13
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    Inspiration from a vitamin (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-06-29
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Observation of the geometric phase effect in the H + HD -〉 H2 + D reaction (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-12-14
    Description: Theory has established the importance of geometric phase (GP) effects in the adiabatic dynamics of molecular systems with a conical intersection connecting the ground- and excited-state potential energy surfaces, but direct observation of their manifestation in chemical reactions remains a major challenge. Here, we report a high-resolution crossed molecular beams study of the H + HD -〉 H 2 + D reaction at a collision energy slightly above the conical intersection. Velocity map ion imaging revealed fast angular oscillations in product quantum state–resolved differential cross sections in the forward scattering direction for H 2 products at specific rovibrational levels. The experimental results agree with adiabatic quantum dynamical calculations only when the GP effect is included.
    Keywords: Chemistry
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  • 15
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    Fragile X mental retardation 1 gene enhances the translation of large autism-related proteins (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Description: Mutations in the fragile X mental retardation 1 gene ( FMR1 ) cause the most common inherited human autism spectrum disorder. FMR1 influences messenger RNA (mRNA) translation, but identifying functional targets has been difficult. We analyzed quiescent Drosophila oocytes, which, like neural synapses, depend heavily on translating stored mRNA. Ribosome profiling revealed that FMR1 enhances rather than represses the translation of mRNAs that overlap previously identified FMR1 targets, and acts preferentially on large proteins. Human homologs of at least 20 targets are associated with dominant intellectual disability, and 30 others with recessive neurodevelopmental dysfunction. Stored oocytes lacking FMR1 usually generate embryos with severe neural defects, unlike stored wild-type oocytes, which suggests that translation of multiple large proteins by stored mRNAs is defective in fragile X syndrome and possibly other autism spectrum disorders.
    Keywords: Development
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  • 16
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    Choosing the right input in cell signaling (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Development
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Photocatalytic upgrading of natural gas (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Radically transforming light hydrocarbons (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    Stereodivergent synthesis of 1,4-dicarbonyls by traceless charge-accelerated sulfonium rearrangement (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Description: The chemistry of the carbonyl group is essential to modern organic synthesis. The preparation of substituted, enantioenriched 1,3- or 1,5-dicarbonyls is well developed, as their disconnection naturally follows from the intrinsic polarity of the carbonyl group. By contrast, a general enantioselective access to quaternary stereocenters in acyclic 1,4-dicarbonyl systems remains an unresolved problem, despite the tremendous importance of 2,3-substituted 1,4-dicarbonyl motifs in natural products and drug scaffolds. Here we present a broad enantioselective and stereodivergent strategy to access acyclic, polysubstituted 1,4-dicarbonyls via acid-catalyzed [3,3]-sulfonium rearrangement starting from vinyl sulfoxides and ynamides. The stereochemistry at sulfur governs the absolute sense of chiral induction, whereas the double bond geometry dictates the relative configuration of the final products.
    Keywords: Chemistry
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  • 20
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    Four varieties of carbonyl sandwich (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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    Fragile X and fragile translation in flies (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Development
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 22
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    Selective functionalization of methane, ethane, and higher alkanes by cerium photocatalysis (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Description: With the recent soaring production of natural gas, the use of methane and other light hydrocarbon feedstocks as starting materials in synthetic transformations is becoming increasingly economically attractive, although it remains chemically challenging. We report the development of photocatalytic C–H amination, alkylation, and arylation of methane, ethane, and higher alkanes under visible light irradiation at ambient temperature. High catalytic efficiency (turnover numbers up to 2900 for methane and 9700 for ethane) and selectivity were achieved using abundant, inexpensive cerium salts as photocatalysts. Ligand-to-metal charge transfer excitation generated alkoxy radicals from simple alcohols that in turn acted as hydrogen atom transfer catalysts. The mixed-phase gas/liquid reaction was adapted to continuous flow, enabling the efficient use of gaseous feedstocks in scalable photocatalytic transformations.
    Keywords: Chemistry
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  • 23
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    Orchestrating cortical brain development (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-24
    Keywords: Development
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Hot lithium-oxygen batteries charge ahead (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-24
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 25
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    A preference for acids (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-24
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 26
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    18 electrons and counting (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-31
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    Directional control of a processive molecular hopper (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-31
    Description: Intrigued by the potential of nanoscale machines, scientists have long attempted to control molecular motion. We monitored the individual 0.7-nanometer steps of a single molecular hopper as it moved in an electric field along a track in a nanopore controlled by a chemical ratchet. The hopper demonstrated characteristics desired in a moving molecule: defined start and end points, processivity, no chemical fuel requirement, directional motion, and external control. The hopper was readily functionalized to carry cargos. For example, a DNA molecule could be ratcheted along the track in either direction, a prerequisite for nanopore sequencing.
    Keywords: Chemistry
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  • 28
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    Unlocking P(V): Reagents for chiral phosphorothioate synthesis (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-21
    Description: Phosphorothioate nucleotides have emerged as powerful pharmacological substitutes of their native phosphodiester analogs with important translational applications in antisense oligonucleotide (ASO) therapeutics and cyclic dinucleotide (CDN) synthesis. Stereocontrolled installation of this chiral motif has long been hampered by the systemic use of phosphorus(III) [P(III)]–based reagent systems as the sole practical means of oligonucleotide assembly. A fundamentally different approach is described herein: the invention of a P(V)-based reagent platform for programmable, traceless, diastereoselective phosphorus-sulfur incorporation. The power of this reagent system is demonstrated through the robust and stereocontrolled synthesis of various nucleotidic architectures, including ASOs and CDNs, via an efficient, inexpensive, and operationally simple protocol.
    Keywords: Chemistry
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  • 29
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    Self-assembly of lattices with high structural complexity from a geometrically simple molecule (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-21
    Description: Here we report an anomalous porous molecular crystal built of C–H···N-bonded double-layered roof-floor components and wall components of a segregatively interdigitated architecture. This complicated porous structure consists of only one type of fully aromatic multijoint molecule carrying three identical dipyridylphenyl wedges. Despite its high symmetry, this molecule accomplishes difficult tasks by using two of its three wedges for roof-floor formation and using its other wedge for wall formation. Although a C–H···N bond is extremely labile, the porous crystal maintains its porosity until thermal breakdown of the C–H···N bonds at 202°C occurs, affording a nonporous polymorph. Though this nonporous crystal survives even at 325°C, it can retrieve the parent porosity under acetonitrile vapor. These findings show how one can translate simplicity into ultrahigh complexity.
    Keywords: Chemistry
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  • 30
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    How birds change their stripes (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-09-21
    Keywords: Development
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 31
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    Hox genes and body segmentation (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-09-28
    Keywords: Development
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  • 32
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    Two ways out of an oxetane (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-09-28
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 33
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    Arenes and amides from a single source (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-09-28
    Keywords: Chemistry
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 34
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    Interrupted carbonyl-olefin metathesis via oxygen atom transfer (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-28
    Description: Some of the simplest and most powerful carbon-carbon bond forming strategies take advantage of readily accessible ubiquitous motifs: carbonyls and olefins. Here we report a fundamentally distinct mode of reactivity between carbonyls and olefins that differs from established acid-catalyzed carbonyl-ene, Prins, and carbonyl-olefin metathesis reaction paths. A range of epsilon, zeta-unsaturated ketones undergo Brønsted acid–catalyzed intramolecular cyclization to provide tetrahydrofluorene products via the formation of two new carbon-carbon bonds. Theoretical calculations and accompanying mechanistic studies suggest that this carbocyclization reaction proceeds through the intermediacy of a transient oxetane formed by oxygen atom transfer. The complex polycyclic frameworks in this product class appear as common substructures in organic materials, bioactive natural products, and recently developed pharmaceuticals.
    Keywords: Chemistry
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    Arylsulfonylacetamides as bifunctional reagents for alkene aminoarylation (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-28
    Description: Alkene aminoarylation with a single, bifunctional reagent is a concise synthetic strategy. We report a catalytic protocol for the addition of arylsulfonylacetamides across electron-rich alkenes with complete anti-Markovnikov regioselectivity and excellent diastereoselectivity to provide 2,2-diarylethylamines. In this process, single-electron alkene oxidation enables carbon-nitrogen bond formation to provide a key benzylic radical poised for a Smiles-Truce 1,5-aryl shift. This reaction is redox-neutral, exhibits broad functional group compatibility, and occurs at room temperature with loss of sulfur dioxide. As this process is driven by visible light, uses readily available starting materials, and demonstrates convergent synthesis, it is well suited for use in a variety of synthetic endeavors.
    Keywords: Chemistry
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    Activating plasmonic chemistry (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-05
    Keywords: Chemistry
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    Hot carriers reducing thermal barriers (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-05
    Keywords: Chemistry
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    Quantifying hot carrier and thermal contributions in plasmonic photocatalysis (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-05
    Description: Photocatalysis based on optically active, "plasmonic" metal nanoparticles has emerged as a promising approach to facilitate light-driven chemical conversions under far milder conditions than thermal catalysis. However, an understanding of the relation between thermal and electronic excitations has been lacking. We report the substantial light-induced reduction of the thermal activation barrier for ammonia decomposition on a plasmonic photocatalyst. We introduce the concept of a light-dependent activation barrier to account for the effect of light illumination on electronic and thermal excitations in a single unified picture. This framework provides insight into the specific role of hot carriers in plasmon-mediated photochemistry, which is critically important for designing energy-efficient plasmonic photocatalysts.
    Keywords: Chemistry
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    Thyroid hormone in color vision development (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-12
    Keywords: Development
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    An acid inaccessible to aldol products (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-10-12
    Keywords: Chemistry
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    Iodine smooths the way to ketyl radicals (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-10-12
    Keywords: Chemistry
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  • 42
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    Ketyl radical reactivity via atom transfer catalysis (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-12
    Description: Single-electron reduction of a carbonyl to a ketyl enables access to a polarity-reversed platform of reactivity for this cornerstone functional group. However, the synthetic utility of the ketyl radical is hindered by the strong reductants necessary for its generation, which also limit its reactivity to net reductive mechanisms. We report a strategy for net redox-neutral generation and reaction of ketyl radicals. The in situ conversion of aldehydes to α-acetoxy iodides lowers their reduction potential by more than 1 volt, allowing for milder access to the corresponding ketyl radicals and an oxidative termination event. Upon subjecting these iodides to a dimanganese decacarbonyl precatalyst and visible light irradiation, an atom transfer radical addition (ATRA) mechanism affords a broad scope of vinyl iodide products with high Z -selectivity.
    Keywords: Chemistry
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    Confined acids catalyze asymmetric single aldolizations of acetaldehyde enolates (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-10-12
    Description: Reactions that form a product with the same reactive functionality as that of one of the starting compounds frequently end in oligomerization. As a salient example, selective aldol coupling of the smallest, though arguably most useful, enolizable aldehyde, acetaldehyde, with just one partner substrate has proven to be extremely challenging. Here, we report a highly enantioselective Mukaiyama aldol reaction with the simple triethylsilyl (TES) and tert -butyldimethylsilyl (TBS) enolates of acetaldehyde and various aliphatic and aromatic acceptor aldehydes. The reaction is catalyzed by recently developed, strongly acidic imidodiphosphorimidates (IDPi), which, like enzymes, display a confined active site but, like small-molecule catalysts, have a broad substrate scope. The process is scalable, fast, efficient (0.5 to 1.5 mole % catalyst loading), and greatly simplifies access to highly valuable silylated acetaldehyde aldols.
    Keywords: Chemistry
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    Breaking through the nitrogen ceiling (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-12-21
    Keywords: Chemistry
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    Magnetic hysteresis up to 80 kelvin in a dysprosium metallocene single-molecule magnet (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-12-21
    Description: Single-molecule magnets (SMMs) containing only one metal center may represent the lower size limit for molecule-based magnetic information storage materials. Their current drawback is that all SMMs require liquid-helium cooling to show magnetic memory effects. We now report a chemical strategy to access the dysprosium metallocene cation [(Cp i Pr5 )Dy(Cp*)] + (Cp i Pr5 , penta-iso-propylcyclopentadienyl; Cp *, pentamethylcyclopentadienyl), which displays magnetic hysteresis above liquid-nitrogen temperatures. An effective energy barrier to reversal of the magnetization of U eff = 1541 wave number is also measured. The magnetic blocking temperature of T B = 80 kelvin for this cation overcomes an essential barrier toward the development of nanomagnet devices that function at practical temperatures.
    Keywords: Chemistry
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    PRDM9 is a major determinant of meiotic recombination hotspots in humans and mice (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-02
    Description: Meiotic recombination events cluster into narrow segments of the genome, defined as hotspots. Here, we demonstrate that a major player for hotspot specification is the Prdm9 gene. First, two mouse strains that differ in hotspot usage are polymorphic for the zinc finger DNA binding array of PRDM9. Second, the human consensus PRDM9 allele is predicted to recognize the 13-mer motif enriched at human hotspots; this DNA binding specificity is verified by in vitro studies. Third, allelic variants of PRDM9 zinc fingers are significantly associated with variability in genome-wide hotspot usage among humans. Our results provide a molecular basis for the distribution of meiotic recombination in mammals, in which the binding of PRDM9 to specific DNA sequences targets the initiation of recombination at specific locations in the genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295902/" 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/PMC4295902/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baudat, F -- Buard, J -- Grey, C -- Fledel-Alon, A -- Ober, C -- Przeworski, M -- Coop, G -- de Massy, B -- 03S1/PHS HHS/ -- GM83098/GM/NIGMS NIH HHS/ -- HD21244/HD/NICHD NIH HHS/ -- HL085197/HL/NHLBI NIH HHS/ -- R01 GM083098/GM/NIGMS NIH HHS/ -- R01 HD021244/HD/NICHD NIH HHS/ -- R01 HL085197/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):836-40. doi: 10.1126/science.1183439. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique Humaine, UPR1142, CNRS, Montpellier, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044539" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; DNA/chemistry/metabolism ; DNA Breaks, Double-Stranded ; DNA-Binding Proteins/chemistry/genetics/metabolism ; Genome ; Genome, Human ; Genotype ; Histone-Lysine N-Methyltransferase/chemistry/*genetics/*metabolism ; Humans ; Meiosis/*genetics ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Phenotype ; *Recombination, Genetic ; Zinc Fingers/genetics
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    The ligase PIAS1 restricts natural regulatory T cell differentiation by epigenetic repression (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: CD4(+)Foxp3(+) regulatory T (T(reg)) cells are important for maintaining immune tolerance. Understanding the molecular mechanism that regulates T(reg) differentiation will facilitate the development of effective therapeutic strategies against autoimmune diseases. We report here that the SUMO E3 ligase PIAS1 restricts the differentiation of natural T(reg) cells by maintaining a repressive chromatin state of the Foxp3 promoter. PIAS1 acts by binding to the Foxp3 promoter to recruit DNA methyltransferases and heterochromatin protein 1 for epigenetic modifications. Pias1 deletion caused promoter demethylation, reduced histone H3 methylation at Lys(9), and enhanced promoter accessibility. Consistently, Pias1(-/-) mice displayed an increased natural T(reg) cell population and were resistant to the development of experimental autoimmune encephalomyelitis. Our studies have identified an epigenetic mechanism that negatively regulates the differentiation of natural T(reg) cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3043201/" 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/PMC3043201/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Bin -- Tahk, Samuel -- Yee, Kathleen M -- Fan, Guoping -- Shuai, Ke -- K01 AR52717-01/AR/NIAMS NIH HHS/ -- R01 AI063286/AI/NIAID NIH HHS/ -- R01 AI063286-05/AI/NIAID NIH HHS/ -- R01 GM085797/GM/NIGMS NIH HHS/ -- R01 GM085797-03/GM/NIGMS NIH HHS/ -- R01AI063286/AI/NIAID NIH HHS/ -- R01GM085797/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):521-5. doi: 10.1126/science.1193787.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology-Oncology, Department of Medicine, 11-934 Factor Building, 10833 Le Conte Avenue, University of California, Los Angeles, Los Angeles, CA 90095, USA. bliu@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; CD4-Positive T-Lymphocytes/cytology ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/metabolism ; DNA Methylation ; Encephalomyelitis, Autoimmune, Experimental/immunology ; *Epigenesis, Genetic ; Female ; Forkhead Transcription Factors/genetics ; Histones/metabolism ; Lymphopoiesis/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Promoter Regions, Genetic ; Protein Inhibitors of Activated STAT/*physiology ; Repressor Proteins/*physiology ; T-Lymphocytes, Regulatory/*cytology/immunology ; Ubiquitin-Protein Ligases/*physiology
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    Identification of RACK1 and protein kinase Calpha as integral components of the mammalian circadian clock (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-23
    Description: At the core of the mammalian circadian clock is a negative feedback loop in which the dimeric transcription factor CLOCK-BMAL1 drives processes that in turn suppress its transcriptional activity. To gain insight into the mechanisms of circadian feedback, we analyzed mouse protein complexes containing BMAL1. Receptor for activated C kinase-1 (RACK1) and protein kinase C-alpha (PKCalpha) were recruited in a circadian manner into a nuclear BMAL1 complex during the negative feedback phase of the cycle. Overexpression of RACK1 and PKCalpha suppressed CLOCK-BMAL1 transcriptional activity, and RACK1 stimulated phosphorylation of BMAL1 by PKCalpha in vitro. Depletion of endogenous RACK1 or PKCalpha from fibroblasts shortened the circadian period, demonstrating that both molecules function in the clock oscillatory mechanism. Thus, the classical PKC signaling pathway is not limited to relaying external stimuli but is rhythmically activated by internal processes, forming an integral part of the circadian feedback loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robles, Maria S -- Boyault, Cyril -- Knutti, Darko -- Padmanabhan, Kiran -- Weitz, Charles J -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):463-6. doi: 10.1126/science.1180067.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093473" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/metabolism ; Animals ; CLOCK Proteins/metabolism ; Cell Nucleus/metabolism ; Circadian Rhythm/*physiology ; Feedback, Physiological ; Fibroblasts/metabolism/physiology ; Mice ; Mice, Inbred C57BL ; Neuropeptides/genetics/*metabolism ; Phosphorylation ; Protein Binding ; Protein Kinase C-alpha/*metabolism ; RNA Interference ; Signal Transduction ; Transcription, Genetic
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    Glucose and weight control in mice with a designed ghrelin O-acyltransferase inhibitor (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-11-26
    Description: Ghrelin is a gastric peptide hormone that stimulates weight gain in vertebrates. The biological activities of ghrelin require octanoylation of the peptide on Ser(3), an unusual posttranslational modification that is catalyzed by the enzyme ghrelin O-acyltransferase (GOAT). Here, we describe the design, synthesis, and characterization of GO-CoA-Tat, a peptide-based bisubstrate analog that antagonizes GOAT. GO-CoA-Tat potently inhibits GOAT in vitro, in cultured cells, and in mice. Intraperitoneal administration of GO-CoA-Tat improves glucose tolerance and reduces weight gain in wild-type mice but not in ghrelin-deficient mice, supporting the concept that its beneficial metabolic effects are due specifically to GOAT inhibition. In addition to serving as a research tool for mapping ghrelin actions, GO-CoA-Tat may help pave the way for clinical targeting of GOAT in metabolic diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068526/" 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/PMC3068526/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barnett, Brad P -- Hwang, Yousang -- Taylor, Martin S -- Kirchner, Henriette -- Pfluger, Paul T -- Bernard, Vincent -- Lin, Yu-yi -- Bowers, Erin M -- Mukherjee, Chandrani -- Song, Woo-Jin -- Longo, Patti A -- Leahy, Daniel J -- Hussain, Mehboob A -- Tschop, Matthias H -- Boeke, Jef D -- Cole, Philip A -- P01 CA016519/CA/NCI NIH HHS/ -- P01 CA016519-35/CA/NCI NIH HHS/ -- P30 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637/DK/NIDDK NIH HHS/ -- P60 DK079637-05/DK/NIDDK NIH HHS/ -- R01 DK081472/DK/NIDDK NIH HHS/ -- R01 DK081472-01A1/DK/NIDDK NIH HHS/ -- R01 DK081472-02/DK/NIDDK NIH HHS/ -- R01 DK081472-03/DK/NIDDK NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-04/GM/NIGMS NIH HHS/ -- R01 GM062437-11/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Dec 17;330(6011):1689-92. doi: 10.1126/science.1196154. Epub 2010 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21097901" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Acyltransferases/*antagonists & inhibitors ; Animals ; Cell Survival/drug effects ; Drug Design ; Enzyme Inhibitors/chemical synthesis/*pharmacology/toxicity ; Ghrelin/deficiency/genetics/*metabolism ; Glucose/*metabolism ; Glucose Tolerance Test ; HeLa Cells ; Homeostasis ; Humans ; Insulin/metabolism ; Ion Channels/metabolism ; Islets of Langerhans/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondrial Proteins/metabolism ; Peptides/chemical synthesis/*pharmacology/toxicity ; Weight Gain/*drug effects
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    Darwinian evolution of prions in cell culture (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-02
    Description: Prions are infectious proteins consisting mainly of PrP(Sc), a beta sheet-rich conformer of the normal host protein PrP(C), and occur in different strains. Strain identity is thought to be encoded by PrP(Sc) conformation. We found that biologically cloned prion populations gradually became heterogeneous by accumulating "mutants," and selective pressures resulted in the emergence of different mutants as major constituents of the evolving population. Thus, when transferred from brain to cultured cells, "cell-adapted" prions outcompeted their "brain-adapted" counterparts, and the opposite occurred when prions were returned from cells to brain. Similarly, the inhibitor swainsonine selected for a resistant substrain, whereas, in its absence, the susceptible substrain outgrew its resistant counterpart. Prions, albeit devoid of a nucleic acid genome, are thus subject to mutation and selective amplification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Jiali -- Browning, Shawn -- Mahal, Sukhvir P -- Oelschlegel, Anja M -- Weissmann, Charles -- NS059543/NS/NINDS NIH HHS/ -- R01 NS059543/NS/NINDS NIH HHS/ -- R01 NS059543-01/NS/NINDS NIH HHS/ -- R01 NS059543-02/NS/NINDS NIH HHS/ -- R01 NS067214/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):869-72. doi: 10.1126/science.1183218. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Infectology, Scripps Florida, 130 Scripps Way, Jupiter, FL 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cell Line ; Cell Line, Tumor ; Culture Media ; Culture Media, Conditioned ; *Evolution, Molecular ; Mice ; Mice, Inbred C57BL ; Mutation ; *PrPSc Proteins/chemistry/classification/pathogenicity ; Prion Diseases ; Prions/chemistry/classification/*pathogenicity/*physiology ; Protein Conformation ; Swainsonine/pharmacology
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    Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-14
    Description: Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3732486/" 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/PMC3732486/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manicassamy, Santhakumar -- Reizis, Boris -- Ravindran, Rajesh -- Nakaya, Helder -- Salazar-Gonzalez, Rosa Maria -- Wang, Yi-Chong -- Pulendran, Bali -- HHSN266 200700006C/PHS HHS/ -- N01 AI50019/AI/NIAID NIH HHS/ -- N01 AI50025/AI/NIAID NIH HHS/ -- R01 AI048638/AI/NIAID NIH HHS/ -- R01 AI056499/AI/NIAID NIH HHS/ -- R01 DK057665/DK/NIDDK NIH HHS/ -- R01DK057665,/DK/NIDDK NIH HHS/ -- R37 AI048638/AI/NIAID NIH HHS/ -- R37 DK057665/DK/NIDDK NIH HHS/ -- R37AI48638,/AI/NIAID NIH HHS/ -- U19 AI057266/AI/NIAID NIH HHS/ -- U19AI057266,/AI/NIAID NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- U54AI057157/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 13;329(5993):849-53. doi: 10.1126/science.1188510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20705860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytokines/metabolism ; Dendritic Cells/*immunology/metabolism ; Gene Expression Profiling ; *Inflammation ; Inflammatory Bowel Diseases/*immunology ; Intestinal Mucosa/cytology/*immunology/metabolism ; Macrophages/immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; *Self Tolerance ; Signal Transduction ; T-Lymphocytes, Helper-Inducer/cytology/*immunology ; T-Lymphocytes, Regulatory/*immunology ; Tretinoin/metabolism ; Wnt Proteins/metabolism ; beta Catenin/*metabolism
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    Cyclooxygenase-2 controls energy homeostasis in mice by de novo recruitment of brown adipocytes (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: Obesity results from chronic energy surplus and excess lipid storage in white adipose tissue (WAT). In contrast, brown adipose tissue (BAT) efficiently burns lipids through adaptive thermogenesis. Studying mouse models, we show that cyclooxygenase (COX)-2, a rate-limiting enzyme in prostaglandin (PG) synthesis, is a downstream effector of beta-adrenergic signaling in WAT and is required for the induction of BAT in WAT depots. PG shifted the differentiation of defined mesenchymal progenitors toward a brown adipocyte phenotype. Overexpression of COX-2 in WAT induced de novo BAT recruitment in WAT, increased systemic energy expenditure, and protected mice against high-fat diet-induced obesity. Thus, COX-2 appears integral to de novo BAT recruitment, which suggests that the PG pathway regulates systemic energy homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vegiopoulos, Alexandros -- Muller-Decker, Karin -- Strzoda, Daniela -- Schmitt, Iris -- Chichelnitskiy, Evgeny -- Ostertag, Anke -- Berriel Diaz, Mauricio -- Rozman, Jan -- Hrabe de Angelis, Martin -- Nusing, Rolf M -- Meyer, Carola W -- Wahli, Walter -- Klingenspor, Martin -- Herzig, Stephan -- New York, N.Y. -- Science. 2010 May 28;328(5982):1158-61. doi: 10.1126/science.1186034. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Emmy Noether and Marie Curie Research Group Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448152" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes, Brown/cytology/*physiology ; Adipogenesis ; Adipose Tissue ; Adipose Tissue, Brown/cytology/*physiology ; Adipose Tissue, White/enzymology/*physiology ; Adrenergic beta-3 Receptor Agonists ; Adrenergic beta-Agonists/pharmacology ; Animals ; Body Weight ; Cyclooxygenase 2/*genetics/*metabolism ; Dietary Fats/administration & dosage ; Dioxoles/pharmacology ; *Energy Metabolism ; Female ; Gene Expression Regulation, Enzymologic ; Homeostasis ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mice, Transgenic ; Norepinephrine/metabolism ; Obesity/etiology/prevention & control ; Oxygen Consumption ; Prostaglandins/*metabolism ; Receptors, Adrenergic, beta-3/metabolism ; Signal Transduction ; *Thermogenesis
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    G protein subunit Galpha13 binds to integrin alphaIIbbeta3 and mediates integrin "outside-in" signaling (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-16
    Description: Integrins mediate cell adhesion to the extracellular matrix and transmit signals within the cell that stimulate cell spreading, retraction, migration, and proliferation. The mechanism of integrin outside-in signaling has been unclear. We found that the heterotrimeric guanine nucleotide-binding protein (G protein) Galpha13 directly bound to the integrin beta3 cytoplasmic domain and that Galpha13-integrin interaction was promoted by ligand binding to the integrin alphaIIbbeta3 and by guanosine triphosphate (GTP) loading of Galpha13. Interference of Galpha13 expression or a myristoylated fragment of Galpha13 that inhibited interaction of alphaIIbbeta3 with Galpha13 diminished activation of protein kinase c-Src and stimulated the small guanosine triphosphatase RhoA, consequently inhibiting cell spreading and accelerating cell retraction. We conclude that integrins are noncanonical Galpha13-coupled receptors that provide a mechanism for dynamic regulation of RhoA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842917/" 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/PMC2842917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Haixia -- Shen, Bo -- Flevaris, Panagiotis -- Chow, Christina -- Lam, Stephen C-T -- Voyno-Yasenetskaya, Tatyana A -- Kozasa, Tohru -- Du, Xiaoping -- GM061454/GM/NIGMS NIH HHS/ -- GM074001/GM/NIGMS NIH HHS/ -- HL062350/HL/NHLBI NIH HHS/ -- HL068819/HL/NHLBI NIH HHS/ -- HL080264/HL/NHLBI NIH HHS/ -- R01 GM061454/GM/NIGMS NIH HHS/ -- R01 GM061454-09/GM/NIGMS NIH HHS/ -- R01 GM074001/GM/NIGMS NIH HHS/ -- R01 GM074001-02/GM/NIGMS NIH HHS/ -- R01 HL062350/HL/NHLBI NIH HHS/ -- R01 HL062350-09/HL/NHLBI NIH HHS/ -- R01 HL068819/HL/NHLBI NIH HHS/ -- R01 HL068819-08/HL/NHLBI NIH HHS/ -- R01 HL080264/HL/NHLBI NIH HHS/ -- R01 HL080264-04/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 15;327(5963):340-3. doi: 10.1126/science.1174779.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Illinois at Chicago, 835 South Wolcott Avenue, Room E403, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Blood Platelets/*physiology ; Clot Retraction ; Fibrinogen/metabolism ; GTP-Binding Protein alpha Subunits, G12-G13/genetics/*metabolism ; Humans ; Integrin beta3/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; Platelet Adhesiveness ; Platelet Glycoprotein GPIIb-IIIa Complex/*metabolism ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins pp60(c-src)/metabolism ; RNA, Small Interfering ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; rhoA GTP-Binding Protein/antagonists & inhibitors/metabolism
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    Mcl-1 is essential for germinal center formation and B cell memory (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-12
    Description: Lymphocyte survival during immune responses is controlled by the relative expression of pro- and anti-apoptotic molecules, regulating the magnitude, quality, and duration of the response. We investigated the consequences of deleting genes encoding the anti-apoptotic molecules Mcl1 and Bcl2l1 (Bcl-x(L)) from B cells using an inducible system synchronized with expression of activation-induced cytidine deaminase (Aicda) after immunization. This revealed Mcl1 and not Bcl2l1 to be indispensable for the formation and persistence of germinal centers (GCs). Limiting Mcl1 expression reduced the magnitude of the GC response with an equivalent, but not greater, effect on memory B cell formation and no effect on persistence. Our results identify Mcl1 as the main anti-apoptotic regulator of activated B cell survival and suggest distinct mechanisms controlling survival of GC and memory B cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991396/" 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/PMC2991396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vikstrom, Ingela -- Carotta, Sebastian -- Luthje, Katja -- Peperzak, Victor -- Jost, Philipp J -- Glaser, Stefan -- Busslinger, Meinrad -- Bouillet, Philippe -- Strasser, Andreas -- Nutt, Stephen L -- Tarlinton, David M -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-22/CA/NCI NIH HHS/ -- R01 CA080188-08/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 19;330(6007):1095-9. doi: 10.1126/science.1191793. Epub 2010 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Affinity ; B-Lymphocytes/*immunology ; Cell Survival ; Gene Deletion ; Germinal Center/cytology/*immunology ; *Immunologic Memory ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2/genetics/*immunology ; bcl-X Protein/genetics/immunology
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    Prdm9 controls activation of mammalian recombination hotspots (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-02
    Description: Mammalian meiotic recombination, which preferentially occurs at specialized sites called hotspots, ensures the orderly segregation of meiotic chromosomes and creates genetic variation among offspring. A locus on mouse chromosome 17, which controls activation of recombination at multiple distant hotspots, has been mapped within a 181-kilobase interval, three of whose genes can be eliminated as candidates. The remaining gene, Prdm9, codes for a zinc finger containing histone H3K4 trimethylase that is expressed in early meiosis and whose deficiency results in sterility in both sexes. Mus musculus exhibits five alleles of Prdm9; human populations exhibit two predominant alleles and multiple minor alleles. The identification of Prdm9 as a protein regulating mammalian recombination hotspots initiates molecular studies of this important biological control system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821451/" 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/PMC2821451/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parvanov, Emil D -- Petkov, Petko M -- Paigen, Kenneth -- 076468/PHS HHS/ -- 078452/PHS HHS/ -- 083408/PHS HHS/ -- CA 34196/CA/NCI NIH HHS/ -- GM 078643/GM/NIGMS NIH HHS/ -- P30 CA034196-26/CA/NCI NIH HHS/ -- P50 GM076468/GM/NIGMS NIH HHS/ -- P50 GM076468-030004/GM/NIGMS NIH HHS/ -- R01 GM078452/GM/NIGMS NIH HHS/ -- R01 GM078452-02/GM/NIGMS NIH HHS/ -- R01 GM078643/GM/NIGMS NIH HHS/ -- R01 GM078643-03/GM/NIGMS NIH HHS/ -- R01 GM083408/GM/NIGMS NIH HHS/ -- R01 GM083408-02/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 12;327(5967):835. doi: 10.1126/science.1181495. Epub 2009 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Jackson Laboratory, Bar Harbor, ME 04609, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044538" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Chromosome Mapping ; Female ; Histone-Lysine N-Methyltransferase/chemistry/*genetics/metabolism ; Humans ; Male ; Meiosis/*genetics ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; *Recombination, Genetic ; Sequence Analysis, DNA ; Testis/metabolism ; Zinc Fingers
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    Sex-specific parent-of-origin allelic expression in the mouse brain (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-10
    Description: Genomic imprinting results in preferential gene expression from paternally versus maternally inherited chromosomes. We used a genome-wide approach to uncover sex-specific parent-of-origin allelic effects in the adult mouse brain. Our study identified preferential selection of the maternally inherited X chromosome in glutamatergic neurons of the female cortex. Moreover, analysis of the cortex and hypothalamus identified 347 autosomal genes with sex-specific imprinting features. In the hypothalamus, sex-specific imprinted genes were mostly found in females, which suggests parental influence over the hypothalamic function of daughters. We show that interleukin-18, a gene linked to diseases with sex-specific prevalence, is subject to complex, regional, and sex-specific parental effects in the brain. Parent-of-origin effects thus provide new avenues for investigation of sexual dimorphism in brain function and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997643/" 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/PMC2997643/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- Zhang, Jiangwen -- Butler, James E -- Haig, David -- Dulac, Catherine -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):682-5. doi: 10.1126/science.1190831. Epub 2010 Jul 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20616234" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Crosses, Genetic ; Dioxygenases ; *Epigenesis, Genetic ; Female ; Gene Expression Profiling ; *Genes, X-Linked ; *Genomic Imprinting ; Glutamic Acid/metabolism ; Interleukin-18/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Neurons/metabolism ; Oxygenases/genetics ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/cytology/*metabolism ; Preoptic Area/cytology/*metabolism ; Ribosomal Proteins/genetics ; *Sex Characteristics ; Succinate Dehydrogenase/genetics ; X Chromosome Inactivation
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    Eppendorf winner. Parental control over the brain (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gregg, Christopher -- New York, N.Y. -- Science. 2010 Nov 5;330(6005):770-1. doi: 10.1126/science.1199054.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. cgregg@MCB.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21051625" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Awards and Prizes ; *Fathers ; *Gene Expression ; Gene Expression Profiling ; *Genomic Imprinting ; Humans ; Interleukin-18 ; Mice ; Mice, Inbred C57BL ; *Mothers ; Polymorphism, Single Nucleotide ; Prefrontal Cortex/embryology/growth & development/*metabolism ; Preoptic Area/embryology/growth & development/*metabolism ; Sex Characteristics
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    Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-22
    Description: Stem cells that naturally reside in adult tissues, such as muscle stem cells (MuSCs), exhibit robust regenerative capacity in vivo that is rapidly lost in culture. Using a bioengineered substrate to recapitulate key biophysical and biochemical niche features in conjunction with a highly automated single-cell tracking algorithm, we show that substrate elasticity is a potent regulator of MuSC fate in culture. Unlike MuSCs on rigid plastic dishes (approximately 10(6) kilopascals), MuSCs cultured on soft hydrogel substrates that mimic the elasticity of muscle (12 kilopascals) self-renew in vitro and contribute extensively to muscle regeneration when subsequently transplanted into mice and assayed histologically and quantitatively by noninvasive bioluminescence imaging. Our studies provide novel evidence that by recapitulating physiological tissue rigidity, propagation of adult muscle stem cells is possible, enabling future cell-based therapies for muscle-wasting diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929271/" 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/PMC2929271/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilbert, P M -- Havenstrite, K L -- Magnusson, K E G -- Sacco, A -- Leonardi, N A -- Kraft, P -- Nguyen, N K -- Thrun, S -- Lutolf, M P -- Blau, H M -- 2 T32 HD007249/HD/NICHD NIH HHS/ -- 52005886/Howard Hughes Medical Institute/ -- AG009521/AG/NIA NIH HHS/ -- AG020961/AG/NIA NIH HHS/ -- CA09151/CA/NCI NIH HHS/ -- HL096113/HL/NHLBI NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG020961/AG/NIA NIH HHS/ -- R01 AG020961-06A2/AG/NIA NIH HHS/ -- R01 AG020961-07/AG/NIA NIH HHS/ -- R01 HL096113/HL/NHLBI NIH HHS/ -- R01 HL096113-03/HL/NHLBI NIH HHS/ -- T32 CA009151/CA/NCI NIH HHS/ -- T32 CA009151-35/CA/NCI NIH HHS/ -- T32 HD007249/HD/NICHD NIH HHS/ -- T32 HD007249-25/HD/NICHD NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- U01 HL100397-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1078-81. doi: 10.1126/science.1191035. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647425" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Cell Count ; Cell Culture Techniques/*methods ; Cell Death ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cell Separation ; Cell Survival ; Cells, Cultured ; Elastic Modulus ; Hydrogels ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Muscle Fibers, Skeletal/*cytology/physiology ; Muscle, Skeletal/*cytology ; Polyethylene Glycols ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology ; Stem Cell Niche/*physiology ; Stem Cell Transplantation ; Stem Cells/cytology/*physiology
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    Loss of Rap1 induces telomere recombination in the absence of NHEJ or a DNA damage signal (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-27
    Description: Shelterin is an essential telomeric protein complex that prevents DNA damage signaling and DNA repair at mammalian chromosome ends. Here we report on the role of the TRF2-interacting factor Rap1, a conserved shelterin subunit of unknown function. We removed Rap1 from mouse telomeres either through gene deletion or by replacing TRF2 with a mutant that does not bind Rap1. Rap1 was dispensable for the essential functions of TRF2--repression of ATM kinase signaling and nonhomologous end joining (NHEJ)--and mice lacking telomeric Rap1 were viable and fertile. However, Rap1 was critical for the repression of homology-directed repair (HDR), which can alter telomere length. The data reveal that HDR at telomeres can take place in the absence of DNA damage foci and underscore the functional compartmentalization within shelterin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864730/" 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/PMC2864730/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- Kabir, Shaheen -- van Overbeek, Megan -- Celli, Giulia B -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM049046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 AG016642-01/AG/NIA NIH HHS/ -- R01 AG016642-02/AG/NIA NIH HHS/ -- R01 AG016642-03/AG/NIA NIH HHS/ -- R01 AG016642-04/AG/NIA NIH HHS/ -- R01 AG016642-05/AG/NIA NIH HHS/ -- R01 AG016642-06/AG/NIA NIH HHS/ -- R01 AG016642-07/AG/NIA NIH HHS/ -- R01 AG016642-08/AG/NIA NIH HHS/ -- R01 AG016642-09/AG/NIA NIH HHS/ -- R01 AG016642-10/AG/NIA NIH HHS/ -- R01 AG016642-11/AG/NIA NIH HHS/ -- R01 GM049046/GM/NIGMS NIH HHS/ -- R01 GM049046-07/GM/NIGMS NIH HHS/ -- R01 GM049046-08/GM/NIGMS NIH HHS/ -- R01 GM049046-09/GM/NIGMS NIH HHS/ -- R01 GM049046-10/GM/NIGMS NIH HHS/ -- R01 GM049046-11/GM/NIGMS NIH HHS/ -- R01 GM049046-12/GM/NIGMS NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- R37 GM049046-13/GM/NIGMS NIH HHS/ -- R37 GM049046-14/GM/NIGMS NIH HHS/ -- R37 GM049046-15/GM/NIGMS NIH HHS/ -- R37 GM049046-16/GM/NIGMS NIH HHS/ -- R37 GM049046-17/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1657-61. doi: 10.1126/science.1185100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339076" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Cells, Cultured ; Checkpoint Kinase 2 ; *DNA Damage ; *DNA Repair ; DNA-Binding Proteins/metabolism ; Gene Deletion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Protein-Serine-Threonine Kinases/metabolism ; Recombination, Genetic ; Signal Transduction ; Sister Chromatid Exchange ; Telomere/*genetics/metabolism ; Telomere-Binding Proteins/chemistry/*genetics/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
    Print ISSN: 0036-8075
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    Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-06-19
    Description: Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed in models of obesity and type 2 diabetes. Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the c-Jun N-terminal kinase signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132938/" 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/PMC3132938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouchi, Noriyuki -- Higuchi, Akiko -- Ohashi, Koji -- Oshima, Yuichi -- Gokce, Noyan -- Shibata, Rei -- Akasaki, Yuichi -- Shimono, Akihiko -- Walsh, Kenneth -- AG15052/AG/NIA NIH HHS/ -- AG34972/AG/NIA NIH HHS/ -- HL81587/HL/NHLBI NIH HHS/ -- HL86785/HL/NHLBI NIH HHS/ -- P01 HL081587/HL/NHLBI NIH HHS/ -- P01 HL081587-05/HL/NHLBI NIH HHS/ -- R01 AG015052/AG/NIA NIH HHS/ -- R01 AG015052-06/AG/NIA NIH HHS/ -- R01 AG034972/AG/NIA NIH HHS/ -- R01 AG034972-03/AG/NIA NIH HHS/ -- R01 HL086785/HL/NHLBI NIH HHS/ -- R01 HL086785-19/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):454-7. doi: 10.1126/science.1188280. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology and Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA. nouchi@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558665" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3-L1 Cells ; Adipocytes/*metabolism/pathology ; Adipokines/genetics/*metabolism ; Adipose Tissue/*metabolism/pathology ; Animals ; Dietary Fats/administration & dosage ; Dietary Sucrose/administration & dosage ; Fatty Liver/pathology/therapy ; Genetic Vectors ; Glucose/metabolism ; Humans ; Inflammation ; Insulin/metabolism ; Insulin Resistance ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Macrophages/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogen-Activated Protein Kinase 8/genetics/metabolism ; Obesity/*metabolism/pathology ; Phosphorylation ; Rats ; Rats, Zucker ; Signal Transduction ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
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    Essential role of the histone methyltransferase G9a in cocaine-induced plasticity (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-09
    Description: Cocaine-induced alterations in gene expression cause changes in neuronal morphology and behavior that may underlie cocaine addiction. In mice, we identified an essential role for histone 3 lysine 9 (H3K9) dimethylation and the lysine dimethyltransferase G9a in cocaine-induced structural and behavioral plasticity. Repeated cocaine administration reduced global levels of H3K9 dimethylation in the nucleus accumbens. This reduction in histone methylation was mediated through the repression of G9a in this brain region, which was regulated by the cocaine-induced transcription factor DeltaFosB. Using conditional mutagenesis and viral-mediated gene transfer, we found that G9a down-regulation increased the dendritic spine plasticity of nucleus accumbens neurons and enhanced the preference for cocaine, thereby establishing a crucial role for histone methylation in the long-term actions of cocaine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820240/" 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/PMC2820240/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maze, Ian -- Covington, Herbert E 3rd -- Dietz, David M -- LaPlant, Quincey -- Renthal, William -- Russo, Scott J -- Mechanic, Max -- Mouzon, Ezekiell -- Neve, Rachael L -- Haggarty, Stephen J -- Ren, Yanhua -- Sampath, Srihari C -- Hurd, Yasmin L -- Greengard, Paul -- Tarakhovsky, Alexander -- Schaefer, Anne -- Nestler, Eric J -- P01 DA008227/DA/NIDA NIH HHS/ -- P01 DA008227-120001/DA/NIDA NIH HHS/ -- P01 DA008227-129001/DA/NIDA NIH HHS/ -- P01 DA008227-13/DA/NIDA NIH HHS/ -- P01 DA008227-14/DA/NIDA NIH HHS/ -- P01 DA008227-15/DA/NIDA NIH HHS/ -- P01 DA008227-16/DA/NIDA NIH HHS/ -- P01 DA008227-170003/DA/NIDA NIH HHS/ -- P01 DA008227-180003/DA/NIDA NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P01 DA010044-15/DA/NIDA NIH HHS/ -- P01 DA010044-150005/DA/NIDA NIH HHS/ -- P01 DA010044-159002/DA/NIDA NIH HHS/ -- P01 DA08227/DA/NIDA NIH HHS/ -- P0110044/PHS HHS/ -- R01 DA007359/DA/NIDA NIH HHS/ -- R01 DA007359-02/DA/NIDA NIH HHS/ -- R01 DA007359-17/DA/NIDA NIH HHS/ -- R01 DA007359-18/DA/NIDA NIH HHS/ -- R01 DA007359-19/DA/NIDA NIH HHS/ -- R01 DA007359-20/DA/NIDA NIH HHS/ -- R01 DA007359-21/DA/NIDA NIH HHS/ -- R01 DA007359-22/DA/NIDA NIH HHS/ -- R01 DA014133/DA/NIDA NIH HHS/ -- R01 DA07359/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):213-6. doi: 10.1126/science.1179438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056891" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Cocaine/*administration & dosage/pharmacology ; Cocaine-Related Disorders/etiology/metabolism ; Dendritic Spines/physiology ; Down-Regulation ; Enzyme Repression ; Gene Expression Profiling ; Gene Expression Regulation ; Histone-Lysine N-Methyltransferase/genetics/*metabolism ; Histones/*metabolism ; Lysine/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred C57BL ; *Neuronal Plasticity ; Neurons/drug effects/*metabolism ; Nucleus Accumbens/cytology/drug effects/*metabolism ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Reward ; Self Administration ; Transcription, Genetic
    Print ISSN: 0036-8075
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    Induction of lymphoidlike stroma and immune escape by tumors that express the chemokine CCL21 (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-27
    Description: Tumor manipulation of host immunity is important for tumor survival and invasion. Many cancers secrete CCL21, a chemoattractant for various leukocytes and lymphoid tissue inducer cells, which drive lymphoid neogenesis. CCL21 expression by melanoma tumors in mice was associated with an immunotolerant microenvironment, which included the induction of lymphoid-like reticular stromal networks, an altered cytokine milieu, and the recruitment of regulatory leukocyte populations. In contrast, CCL21-deficient tumors induced antigen-specific immunity. CCL21-mediated immune tolerance was dependent on host rather than tumor expression of the CCL21 receptor, CCR7, and could protect distant, coimplanted CCL21-deficient tumors and even nonsyngeneic allografts from rejection. We suggest that by altering the tumor microenvironment, CCL21-secreting tumors shift the host immune response from immunogenic to tolerogenic, which facilitates tumor progression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shields, Jacqueline D -- Kourtis, Iraklis C -- Tomei, Alice A -- Roberts, Joanna M -- Swartz, Melody A -- New York, N.Y. -- Science. 2010 May 7;328(5979):749-52. doi: 10.1126/science.1185837. Epub 2010 Mar 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Chemokine CCL21/*metabolism ; Cytokines/metabolism ; Disease Progression ; Female ; Immune Tolerance ; Lymph Nodes/immunology ; Lymphoid Tissue/*immunology/pathology ; Melanoma, Experimental/*immunology/*pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; RNA Interference ; Receptors, CCR7/metabolism ; Signal Transduction ; Stromal Cells/*immunology/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/immunology ; *Tumor Escape
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A critical role for LTA4H in limiting chronic pulmonary neutrophilic inflammation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-09-04
    Description: Leukotriene A(4) hydrolase (LTA(4)H) is a proinflammatory enzyme that generates the inflammatory mediator leukotriene B(4) (LTB(4)). LTA(4)H also possesses aminopeptidase activity with unknown substrate and physiological importance; we identified the neutrophil chemoattractant proline-glycine-proline (PGP) as this physiological substrate. PGP is a biomarker for chronic obstructive pulmonary disease (COPD) and is implicated in neutrophil persistence in the lung. In acute neutrophil-driven inflammation, PGP was degraded by LTA(4)H, which facilitated the resolution of inflammation. In contrast, cigarette smoke, a major risk factor for the development of COPD, selectively inhibited LTA(4)H aminopeptidase activity, which led to the accumulation of PGP and neutrophils. These studies imply that therapeutic strategies inhibiting LTA(4)H to prevent LTB(4) generation may not reduce neutrophil recruitment because of elevated levels of PGP.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072752/" 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/PMC3072752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Snelgrove, Robert J -- Jackson, Patricia L -- Hardison, Matthew T -- Noerager, Brett D -- Kinloch, Andrew -- Gaggar, Amit -- Shastry, Suresh -- Rowe, Steven M -- Shim, Yun M -- Hussell, Tracy -- Blalock, J Edwin -- 082727/Z/07/Z/Wellcome Trust/United Kingdom -- 1K23DK075788/DK/NIDDK NIH HHS/ -- 1R03DK084110-01/DK/NIDDK NIH HHS/ -- G0400795/Medical Research Council/United Kingdom -- G0802752/Medical Research Council/United Kingdom -- HL07783/HL/NHLBI NIH HHS/ -- HL087824/HL/NHLBI NIH HHS/ -- HL090999/HL/NHLBI NIH HHS/ -- HL102371-A1/HL/NHLBI NIH HHS/ -- K08HL091127/HL/NHLBI NIH HHS/ -- P171/03/C1/048/Medical Research Council/United Kingdom -- P30 DK079337/DK/NIDDK NIH HHS/ -- P30AR050948/AR/NIAMS NIH HHS/ -- P30CA13148/CA/NCI NIH HHS/ -- P50 AT00477/AT/NCCIH NIH HHS/ -- R01 HL077783/HL/NHLBI NIH HHS/ -- R01 HL077783-05/HL/NHLBI NIH HHS/ -- R01 HL087824/HL/NHLBI NIH HHS/ -- R01 HL087824-02/HL/NHLBI NIH HHS/ -- R01 HL090999/HL/NHLBI NIH HHS/ -- R01 HL090999-02S1/HL/NHLBI NIH HHS/ -- R01 HL090999-04/HL/NHLBI NIH HHS/ -- R01 HL102371/HL/NHLBI NIH HHS/ -- RR19231/RR/NCRR NIH HHS/ -- U54CA100949/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):90-4. doi: 10.1126/science.1190594. Epub 2010 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham Lung Health Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA. rjs198@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20813919" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Cells, Cultured ; Chemokines, CXC/metabolism ; Chemotaxis, Leukocyte ; Epoxide Hydrolases/antagonists & inhibitors/isolation & purification/*metabolism ; Female ; Humans ; Inflammation ; Leukotriene B4/metabolism ; Lung/*immunology/metabolism/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/enzymology/immunology/*physiology ; Oligopeptides/*metabolism ; Orthomyxoviridae Infections/immunology/metabolism/pathology ; Pneumococcal Infections/immunology/metabolism/pathology ; Pneumonia/*immunology/metabolism/pathology/therapy ; Proline/*analogs & derivatives/metabolism ; Pulmonary Disease, Chronic Obstructive/immunology/metabolism/pathology ; *Smoke ; Tobacco
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    The Wnt/beta-catenin pathway is required for the development of leukemia stem cells in AML (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-27
    Description: Leukemia stem cells (LSCs) are capable of limitless self-renewal and are responsible for the maintenance of leukemia. Because selective eradication of LSCs could offer substantial therapeutic benefit, there is interest in identifying the signaling pathways that control their development. We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpression of the Hoxa9 and Meis1a oncogenes or by the fusion oncoprotein MLL-AF9. We show that the Wnt/beta-catenin signaling pathway is required for self-renewal of LSCs that are derived from either hematopoietic stem cells (HSC) or more differentiated granulocyte-macrophage progenitors (GMP). Because the Wnt/beta-catenin pathway is normally active in HSCs but not in GMP, these results suggest that reactivation of beta-catenin signaling is required for the transformation of progenitor cells by certain oncogenes. beta-catenin is not absolutely required for self-renewal of adult HSCs; thus, targeting the Wnt/beta-catenin pathway may represent a new therapeutic opportunity in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084586/" 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/PMC3084586/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yingzi -- Krivtsov, Andrei V -- Sinha, Amit U -- North, Trista E -- Goessling, Wolfram -- Feng, Zhaohui -- Zon, Leonard I -- Armstrong, Scott A -- 5P01CA66996/CA/NCI NIH HHS/ -- 5R01HL048801/HL/NHLBI NIH HHS/ -- P01 CA066996/CA/NCI NIH HHS/ -- P01 CA066996-11A1/CA/NCI NIH HHS/ -- R01 HL048801/HL/NHLBI NIH HHS/ -- R01 HL048801-16/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1650-3. doi: 10.1126/science.1186624.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339075" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Transformation, Neoplastic ; Genes, Homeobox ; Granulocyte-Macrophage Progenitor Cells/metabolism/pathology ; Hematopoietic Stem Cells/*metabolism/pathology ; Homeodomain Proteins/genetics ; Indomethacin/pharmacology ; Leukemia, Myeloid, Acute/*metabolism/*pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Proteins/genetics ; Neoplastic Stem Cells/*pathology ; *Signal Transduction ; Transduction, Genetic ; Wnt Proteins/*metabolism ; beta Catenin/*metabolism
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    Cortical plasticity induced by inhibitory neuron transplantation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-02-27
    Description: Critical periods are times of pronounced brain plasticity. During a critical period in the postnatal development of the visual cortex, the occlusion of one eye triggers a rapid reorganization of neuronal responses, a process known as ocular dominance plasticity. We have shown that the transplantation of inhibitory neurons induces ocular dominance plasticity after the critical period. Transplanted inhibitory neurons receive excitatory synapses, make inhibitory synapses onto host cortical neurons, and promote plasticity when they reach a cellular age equivalent to that of endogenous inhibitory neurons during the normal critical period. These findings suggest that ocular dominance plasticity is regulated by the execution of a maturational program intrinsic to inhibitory neurons. By inducing plasticity, inhibitory neuron transplantation may facilitate brain repair.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164148/" 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/PMC3164148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Froemke, Robert C -- Alvarez-Buylla, Arturo -- Stryker, Michael P -- Gandhi, Sunil P -- EY016317/EY/NEI NIH HHS/ -- F32 EY016317/EY/NEI NIH HHS/ -- F32 EY016317-03/EY/NEI NIH HHS/ -- P50 MH077972/MH/NIMH NIH HHS/ -- P50 MH077972-05/MH/NIMH NIH HHS/ -- R01 NS048528/NS/NINDS NIH HHS/ -- R01 NS048528-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Feb 26;327(5969):1145-8. doi: 10.1126/science.1183962.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185728" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Aging ; *Dominance, Ocular ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; *Neuronal Plasticity ; Neurons/*transplantation ; Prosencephalon/cytology/embryology ; Sensory Deprivation ; Synapses/physiology ; Visual Cortex/growth & development/*physiology
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    Hippocampal short- and long-term plasticity are not modulated by astrocyte Ca2+ signaling (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-03-06
    Description: The concept that astrocytes release neuroactive molecules (gliotransmitters) to affect synaptic transmission has been a paradigm shift in neuroscience research over the past decade. This concept suggests that astrocytes, together with pre- and postsynaptic neuronal elements, make up a functional synapse. Astrocyte release of gliotransmitters (for example, glutamate and adenosine triphosphate) is generally accepted to be a Ca2+-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic Gq G protein-coupled receptor Ca2+ signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca2+ fluxes affects spontaneous and evoked excitatory synaptic transmission or synaptic plasticity. Our findings suggest that, at least in the hippocampus, the mechanisms of gliotransmission need to be reconsidered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Agulhon, Cendra -- Fiacco, Todd A -- McCarthy, Ken D -- NS020212/NS/NINDS NIH HHS/ -- NS033938/NS/NINDS NIH HHS/ -- R01 NS020212/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 5;327(5970):1250-4. doi: 10.1126/science.1184821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of North Carolina at Chapel Hill, Genetic Medicine Building, CB 7365, Chapel Hill, NC 27599, USA. cendra_agulhon@med.unc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; CA1 Region, Hippocampal/cytology/*physiology ; Calcium/*metabolism ; *Calcium Signaling ; Excitatory Postsynaptic Potentials ; GTP-Binding Protein alpha Subunits, Gq-G11/metabolism ; In Vitro Techniques ; *Long-Term Potentiation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; N-Methylaspartate/metabolism ; *Neuronal Plasticity ; Neurons/physiology ; Neurotransmitter Agents/metabolism ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-02
    Description: Alpha-dystroglycan (alpha-DG) is a cell-surface glycoprotein that acts as a receptor for both extracellular matrix proteins containing laminin-G domains and certain arenaviruses. Receptor binding is thought to be mediated by a posttranslational modification, and defective binding with laminin underlies a subclass of congenital muscular dystrophy. Using mass spectrometry- and nuclear magnetic resonance (NMR)-based structural analyses, we identified a phosphorylated O-mannosyl glycan on the mucin-like domain of recombinant alpha-DG, which was required for laminin binding. We demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy, as well as mice with myodystrophy, commonly have defects in a postphosphoryl modification of this phosphorylated O-linked mannose, and that this modification is mediated by the like-acetylglucosaminyltransferase (LARGE) protein. These findings expand our understanding of the mechanisms that underlie congenital muscular dystrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978000/" 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/PMC2978000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoshida-Moriguchi, Takako -- Yu, Liping -- Stalnaker, Stephanie H -- Davis, Sarah -- Kunz, Stefan -- Madson, Michael -- Oldstone, Michael B A -- Schachter, Harry -- Wells, Lance -- Campbell, Kevin P -- 1U54NS053672/NS/NINDS NIH HHS/ -- AI55540/AI/NIAID NIH HHS/ -- P30 DK 54759/DK/NIDDK NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P41 RR018502/RR/NCRR NIH HHS/ -- R01 AI009484/AI/NIAID NIH HHS/ -- R01 AI009484-40/AI/NIAID NIH HHS/ -- R01 AI009484-41/AI/NIAID NIH HHS/ -- R01 AI045927/AI/NIAID NIH HHS/ -- R01 AI045927-08/AI/NIAID NIH HHS/ -- R01 AI045927-09/AI/NIAID NIH HHS/ -- R01 AI045927-10/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):88-92. doi: 10.1126/science.1180512.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Iowa Roy J. and Lucille A. Carver College of Medicine, 4283 Carver Biomedical Research Building, 285 Newton Road, Iowa City, IA 52242-1101, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20044576" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbohydrate Conformation ; Cell Line ; Dystroglycans/chemistry/*metabolism ; Glycosylation ; Humans ; Laminin/*metabolism ; Magnetic Resonance Spectroscopy ; Mannose/*metabolism ; Mass Spectrometry ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/metabolism ; Muscular Dystrophies/metabolism ; Muscular Dystrophy, Animal/metabolism ; N-Acetylglucosaminyltransferases/genetics/metabolism ; Phosphorylation ; Protein Binding ; Recombinant Proteins/chemistry/metabolism
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    Lynx1, a cholinergic brake, limits plasticity in adult visual cortex (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-13
    Description: Experience-dependent brain plasticity typically declines after an early critical period during which circuits are established. Loss of plasticity with closure of the critical period limits improvement of function in adulthood, but the mechanisms that change the brain's plasticity remain poorly understood. Here, we identified an increase in expression of Lynx1 protein in mice that prevented plasticity in the primary visual cortex late in life. Removal of this molecular brake enhanced nicotinic acetylcholine receptor signaling. Lynx1 expression thus maintains stability of mature cortical networks in the presence of cholinergic innervation. The results suggest that modulating the balance between excitatory and inhibitory circuits reactivates visual plasticity and may present a therapeutic target.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387538/" 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/PMC3387538/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morishita, Hirofumi -- Miwa, Julie M -- Heintz, Nathaniel -- Hensch, Takao K -- 1 DP1 OD003699-01/OD/NIH HHS/ -- DA-17279/DA/NIDA NIH HHS/ -- DP1 OD003699/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1238-40. doi: 10.1126/science.1195320. Epub 2010 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉FM Kirby Neurobiology Center, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21071629" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amblyopia/metabolism ; Animals ; Cholinesterase Inhibitors/pharmacology ; Dominance, Ocular ; Evoked Potentials, Visual ; Mecamylamine/pharmacology ; Membrane Glycoproteins/*genetics/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neural Inhibition ; *Neuronal Plasticity ; Neuropeptides/*genetics/metabolism/*physiology ; Nicotinic Antagonists/pharmacology ; Physostigmine/pharmacology ; Receptors, Nicotinic/genetics/*metabolism ; Sensory Deprivation ; Signal Transduction ; *Vision, Ocular ; Visual Cortex/*physiology ; Visual Pathways
    Print ISSN: 0036-8075
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    Predicting a human gut microbiota's response to diet in gnotobiotic mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-21
    Description: The interrelationships between our diets and the structure and operations of our gut microbial communities are poorly understood. A model community of 10 sequenced human gut bacteria was introduced into gnotobiotic mice, and changes in species abundance and microbial gene expression were measured in response to randomized perturbations of four defined ingredients in the host diet. From the responses, we developed a statistical model that predicted over 60% of the variation in species abundance evoked by diet perturbations, and we were able to identify which factors in the diet best explained changes seen for each community member. The approach is generally applicable, as shown by a follow-up study involving diets containing various mixtures of pureed human baby foods.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303606/" 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/PMC3303606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faith, Jeremiah J -- McNulty, Nathan P -- Rey, Federico E -- Gordon, Jeffrey I -- DK30292/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-08/DK/NIDDK NIH HHS/ -- R37 DK030292/DK/NIDDK NIH HHS/ -- R37 DK030292-31/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):101-4. doi: 10.1126/science.1206025. Epub 2011 May 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21596954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/genetics/physiology ; Biomass ; Caseins/administration & dosage ; Desulfovibrio/genetics/physiology ; *Diet ; Dietary Carbohydrates/administration & dosage ; Dietary Fats, Unsaturated/administration & dosage ; Dietary Proteins/administration & dosage ; Dietary Sucrose/administration & dosage ; Escherichia coli/genetics/physiology ; Feces/*microbiology ; Gastrointestinal Tract/*microbiology ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; *Germ-Free Life ; Gram-Negative Bacteria/*physiology ; Gram-Positive Bacteria/genetics/*physiology ; Humans ; Infant ; Infant Food ; Linear Models ; Male ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Animal
    Print ISSN: 0036-8075
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    Cerebellum shapes hippocampal spatial code (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Spatial representation is an active process that requires complex multimodal integration from a large interacting network of cortical and subcortical structures. We sought to determine the role of cerebellar protein kinase C (PKC)-dependent plasticity in spatial navigation by recording the activity of hippocampal place cells in transgenic L7PKCI mice with selective disruption of PKC-dependent plasticity at parallel fiber-Purkinje cell synapses. Place cell properties were exclusively impaired when L7PKCI mice had to rely on self-motion cues. The behavioral consequence of such a deficit is evidenced here by selectively impaired navigation capabilities during a path integration task. Together, these results suggest that cerebellar PKC-dependent mechanisms are involved in processing self-motion signals essential to the shaping of hippocampal spatial representation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rochefort, Christelle -- Arabo, Arnaud -- Andre, Marion -- Poucet, Bruno -- Save, Etienne -- Rondi-Reig, Laure -- New York, N.Y. -- Science. 2011 Oct 21;334(6054):385-9. doi: 10.1126/science.1207403.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiologie des Processus Adaptatifs (UMR 7102), Navigation, Memory, and Aging (ENMVI) Team, Universite Pierre et Marie Curie-Centre National de la Recherche Scientifique (CNRS), F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021859" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/cytology/*physiology ; Cerebellum/enzymology/*physiology ; Cues ; Darkness ; *Long-Term Synaptic Depression ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; *Motor Activity ; *Orientation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Purkinje Cells/physiology ; Pyramidal Cells/*physiology ; *Space Perception
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    A circadian rhythm orchestrated by histone deacetylase 3 controls hepatic lipid metabolism (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: Disruption of the circadian clock exacerbates metabolic diseases, including obesity and diabetes. We show that histone deacetylase 3 (HDAC3) recruitment to the genome displays a circadian rhythm in mouse liver. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Although amounts of HDAC3 are constant, its genomic recruitment in liver corresponds to the expression pattern of the circadian nuclear receptor Rev-erbalpha. Rev-erbalpha colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbalpha in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by Rev-erbalpha directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389392/" 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/PMC3389392/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng, Dan -- Liu, Tao -- Sun, Zheng -- Bugge, Anne -- Mullican, Shannon E -- Alenghat, Theresa -- Liu, X Shirley -- Lazar, Mitchell A -- DK19525/DK/NIDDK NIH HHS/ -- DK43806/DK/NIDDK NIH HHS/ -- DK45586/DK/NIDDK NIH HHS/ -- DK49210/DK/NIDDK NIH HHS/ -- HG4069/HG/NHGRI NIH HHS/ -- P30 DK019525/DK/NIDDK NIH HHS/ -- R01 DK045586/DK/NIDDK NIH HHS/ -- R37 DK043806/DK/NIDDK NIH HHS/ -- R37 DK043806-20/DK/NIDDK NIH HHS/ -- RC1 DK086239/DK/NIDDK NIH HHS/ -- RC1DK08623/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 11;331(6022):1315-9. doi: 10.1126/science.1198125.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393543" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Chromatin Immunoprecipitation ; Chronobiology Disorders/genetics/metabolism ; *Circadian Clocks ; *Circadian Rhythm ; DNA/metabolism ; Epigenesis, Genetic ; Fatty Liver/*metabolism ; Gene Expression Regulation ; *Genome ; Histone Deacetylases/*metabolism ; Histones/metabolism ; Homeostasis ; *Lipid Metabolism ; Lipogenesis/genetics ; Liver/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Nuclear Receptor Co-Repressor 1/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics/metabolism ; RNA Polymerase II/metabolism ; Up-Regulation
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    Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-12
    Description: Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus-1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253482/" 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/PMC3253482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ives, Annette -- Ronet, Catherine -- Prevel, Florence -- Ruzzante, Giulia -- Fuertes-Marraco, Silvia -- Schutz, Frederic -- Zangger, Haroun -- Revaz-Breton, Melanie -- Lye, Lon-Fye -- Hickerson, Suzanne M -- Beverley, Stephen M -- Acha-Orbea, Hans -- Launois, Pascal -- Fasel, Nicolas -- Masina, Slavica -- A129646/PHS HHS/ -- R01 AI029646/AI/NIAID NIH HHS/ -- R01 AI029646-23/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):775-8. doi: 10.1126/science.1199326.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311023" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemokines/*metabolism ; Cytokines/*metabolism ; Inflammation Mediators/metabolism ; Leishmania guyanensis/*pathogenicity/*virology ; Leishmaniasis, Mucocutaneous/*immunology/parasitology ; Leishmaniavirus/*immunology/physiology ; Macrophages/immunology/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Parasitemia ; Phagosomes/parasitology ; RNA, Double-Stranded/immunology ; RNA, Viral/immunology ; Toll-Like Receptor 3/*immunology ; Toll-Like Receptors/immunology
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    A gustotopic map of taste qualities in the mammalian brain (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: The taste system is one of our fundamental senses, responsible for detecting and responding to sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated by separate classes of taste receptor cells each finely tuned to a single taste quality. We explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty qualities are represented in the primary taste cortex of mice. We used in vivo two-photon calcium imaging to demonstrate topographic segregation in the functional architecture of the gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the existence of a gustotopic map in the brain. These results expose the basic logic for the central representation of taste.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523322/" 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/PMC3523322/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Xiaoke -- Gabitto, Mariano -- Peng, Yueqing -- Ryba, Nicholas J P -- Zuker, Charles S -- Z01 DE000561-15/Intramural NIH HHS/ -- Z01 DE000561-16/Intramural NIH HHS/ -- ZIA DE000561-17/Intramural NIH HHS/ -- ZIA DE000561-18/Intramural NIH HHS/ -- ZIA DE000561-19/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1262-6. doi: 10.1126/science.1204076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885776" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; *Brain Mapping ; Cerebral Cortex/cytology/*physiology ; Cycloheximide ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Imaging ; Neurons/*physiology ; Sodium Chloride ; Sodium Glutamate ; Sweetening Agents ; Taste/*physiology ; Taste Buds/physiology
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    The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-23
    Description: Mucosal surfaces constantly encounter microbes. Toll-like receptors (TLRs) mediate recognition of microbial patterns to eliminate pathogens. By contrast, we demonstrate that the prominent gut commensal Bacteroides fragilis activates the TLR pathway to establish host-microbial symbiosis. TLR2 on CD4(+) T cells is required for B. fragilis colonization of a unique mucosal niche in mice during homeostasis. A symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) regulatory T cells to promote immunologic tolerance. B. fragilis lacking PSA is unable to restrain T helper 17 cell responses and is defective in niche-specific mucosal colonization. Therefore, commensal bacteria exploit the TLR pathway to actively suppress immunity. We propose that the immune system can discriminate between pathogens and the microbiota through recognition of symbiotic bacterial molecules in a process that engenders commensal colonization.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164325/" 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/PMC3164325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Round, June L -- Lee, S Melanie -- Li, Jennifer -- Tran, Gloria -- Jabri, Bana -- Chatila, Talal A -- Mazmanian, Sarkis K -- AI 080002/AI/NIAID NIH HHS/ -- AI 088626/AI/NIAID NIH HHS/ -- DK 078938/DK/NIDDK NIH HHS/ -- DK 083633/DK/NIDDK NIH HHS/ -- R01 AI085090/AI/NIAID NIH HHS/ -- R01 AI085090-01/AI/NIAID NIH HHS/ -- R01 AI085090-01S1/AI/NIAID NIH HHS/ -- R01 AI085090-02/AI/NIAID NIH HHS/ -- R01 AI085090-03/AI/NIAID NIH HHS/ -- R01 DK078938/DK/NIDDK NIH HHS/ -- R01 DK078938-01A2/DK/NIDDK NIH HHS/ -- R01 DK078938-02/DK/NIDDK NIH HHS/ -- R01 DK078938-03/DK/NIDDK NIH HHS/ -- R01 DK078938-04/DK/NIDDK NIH HHS/ -- R21 AI080002/AI/NIAID NIH HHS/ -- R21 AI080002-01/AI/NIAID NIH HHS/ -- R21 AI080002-02/AI/NIAID NIH HHS/ -- R21 AI088626/AI/NIAID NIH HHS/ -- R21 AI088626-01/AI/NIAID NIH HHS/ -- R21 AI088626-02/AI/NIAID NIH HHS/ -- R21 DK083633/DK/NIDDK NIH HHS/ -- R21 DK083633-01A1/DK/NIDDK NIH HHS/ -- R21 DK083633-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2011 May 20;332(6032):974-7. doi: 10.1126/science.1206095. Epub 2011 Apr 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. jround@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21512004" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides fragilis/*growth & development/*immunology ; Colon/immunology/microbiology ; Germ-Free Life ; Homeostasis ; Humans ; *Immune Tolerance ; Immunity, Mucosal ; Interleukin-10/metabolism ; Intestinal Mucosa/*immunology/*microbiology ; Metagenome ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Polysaccharides, Bacterial/immunology/*metabolism ; Signal Transduction ; Specific Pathogen-Free Organisms ; Symbiosis ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Toll-Like Receptor 2/immunology/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Endocannabinoid hydrolysis generates brain prostaglandins that promote neuroinflammation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Phospholipase A(2)(PLA(2)) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol to generate a major arachidonate precursor pool for neuroinflammatory prostaglandins. MAGL-disrupted animals show neuroprotection in a parkinsonian mouse model. These animals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are instead regulated by cytosolic PLA(2). These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" 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/PMC3249428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nomura, Daniel K -- Morrison, Bradley E -- Blankman, Jacqueline L -- Long, Jonathan Z -- Kinsey, Steven G -- Marcondes, Maria Cecilia G -- Ward, Anna M -- Hahn, Yun Kyung -- Lichtman, Aron H -- Conti, Bruno -- Cravatt, Benjamin F -- 5P01DA009789/DA/NIDA NIH HHS/ -- AG028040/AG/NIA NIH HHS/ -- DA017259/DA/NIDA NIH HHS/ -- DA026261/DA/NIDA NIH HHS/ -- F31 DA026261-03/DA/NIDA NIH HHS/ -- K99 DA030908/DA/NIDA NIH HHS/ -- K99 DA030908-01/DA/NIDA NIH HHS/ -- K99DA030908/DA/NIDA NIH HHS/ -- P01 DA009789/DA/NIDA NIH HHS/ -- P01 DA009789-14/DA/NIDA NIH HHS/ -- P01 DA017259/DA/NIDA NIH HHS/ -- P01 DA017259-08/DA/NIDA NIH HHS/ -- P01DA01725/DA/NIDA NIH HHS/ -- R00 DA030908/DA/NIDA NIH HHS/ -- R00 DA030908-02/DA/NIDA NIH HHS/ -- R00DA030908/DA/NIDA NIH HHS/ -- R01 AG028040/AG/NIA NIH HHS/ -- R01 AG028040-04/AG/NIA NIH HHS/ -- R03 DA027936/DA/NIDA NIH HHS/ -- R03 DA027936-02/DA/NIDA NIH HHS/ -- R03DA027936/DA/NIDA NIH HHS/ -- T32 DA007027/DA/NIDA NIH HHS/ -- T32 DA007027-33/DA/NIDA NIH HHS/ -- T32DA007027/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):809-13. doi: 10.1126/science.1209200. Epub 2011 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. dnomura@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021672" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acid/metabolism ; Arachidonic Acids/*metabolism ; Benzodioxoles/pharmacology ; Brain/drug effects/*metabolism/pathology ; Cannabinoid Receptor Modulators/*metabolism ; Cyclooxygenase 1/metabolism ; Cytokines/metabolism ; Eicosanoids/metabolism ; *Endocannabinoids ; Enzyme Inhibitors/pharmacology ; Glycerides/*metabolism ; Hydrolysis ; Inflammation/*metabolism/pathology ; Inflammation Mediators/pharmacology ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Lung/metabolism ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/antagonists & inhibitors/genetics/*metabolism ; Neuroprotective Agents/pharmacology ; Parkinsonian Disorders/metabolism/pathology ; Phospholipases A2/genetics/metabolism ; Piperidines/pharmacology ; Prostaglandins/biosynthesis/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
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    Different B cell populations mediate early and late memory during an endogenous immune response (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-02-12
    Description: Memory B cells formed in response to microbial antigens provide immunity to later infections; however, the inability to detect rare endogenous antigen-specific cells limits current understanding of this process. Using an antigen-based technique to enrich these cells, we found that immunization with a model protein generated B memory cells that expressed isotype-switched immunoglobulins (swIg) or retained IgM. The more numerous IgM(+) cells were longer lived than the swIg(+) cells. However, swIg(+) memory cells dominated the secondary response because of the capacity to become activated in the presence of neutralizing serum immunoglobulin. Thus, we propose that memory relies on swIg(+) cells until they disappear and serum immunoglobulin falls to a low level, in which case memory resides with durable IgM(+) reserves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" 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/PMC3993090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pape, Kathryn A -- Taylor, Justin J -- Maul, Robert W -- Gearhart, Patricia J -- Jenkins, Marc K -- F32 AI091033/AI/NIAID NIH HHS/ -- R01 AI036914/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R37 AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1203-7. doi: 10.1126/science.1201730. Epub 2011 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD38/analysis ; B-Lymphocyte Subsets/*immunology ; Cell Survival ; Female ; Germinal Center/cytology/immunology ; Immunization ; *Immunoglobulin Class Switching ; Immunoglobulin M/genetics/*immunology ; *Immunologic Memory ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phycocyanin/immunology ; Phycoerythrin/immunology ; Spleen/cytology/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" 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/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
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    GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-10-01
    Description: Lymphocytes egress from lymphoid organs in response to sphingosine-1-phosphate (S1P); minutes later they migrate from blood into tissue against the S1P gradient. The mechanisms facilitating cell movement against the gradient have not been defined. Here, we show that heterotrimeric guanine nucleotide-binding protein-coupled receptor kinase-2 (GRK2) functions in down-regulation of S1P receptor-1 (S1PR1) on blood-exposed lymphocytes. T and B cell movement from blood into lymph nodes is reduced in the absence of GRK2 but is restored in S1P-deficient mice. In the spleen, B cell movement between the blood-rich marginal zone and follicles is disrupted by GRK2 deficiency and by mutation of an S1PR1 desensitization motif. Moreover, delivery of systemic antigen into follicles is impaired. Thus, GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate into lymphoid tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267326/" 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/PMC3267326/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arnon, Tal I -- Xu, Ying -- Lo, Charles -- Pham, Trung -- An, Jinping -- Coughlin, Shaun -- Dorn, Gerald W -- Cyster, Jason G -- AI74847/AI/NIAID NIH HHS/ -- R01 AI074847/AI/NIAID NIH HHS/ -- R01 AI074847-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 30;333(6051):1898-903. doi: 10.1126/science.1208248.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21960637" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/immunology ; B-Lymphocytes/immunology/*physiology ; Blood ; Cell Movement ; Chemokines/physiology ; Chemotaxis, Leukocyte ; Down-Regulation ; G-Protein-Coupled Receptor Kinase 2/*metabolism ; Ligands ; Lymph Nodes/cytology ; Lysophospholipids/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Receptors, Lysosphingolipid/genetics/*metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives/metabolism ; Spleen/cytology/immunology ; T-Lymphocytes/immunology/*physiology
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    Activation of visual pigments by light and heat (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-06-11
    Description: Vision begins with photoisomerization of visual pigments. Thermal energy can complement photon energy to drive photoisomerization, but it also triggers spontaneous pigment activation as noise that interferes with light detection. For half a century, the mechanism underlying this dark noise has remained controversial. We report here a quantitative relation between a pigment's photoactivation energy and its peak-absorption wavelength, lambda(max). Using this relation and assuming that pigment activations by light and heat go through the same ground-state isomerization energy barrier, we can predict the relative noise of diverse pigments with multi-vibrational-mode thermal statistics. The agreement between predictions and our measurements strongly suggests that pigment noise arises from canonical isomerization. The predicted high noise for pigments with lambda(max) in the infrared presumably explains why they apparently do not exist in nature.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4349410/" 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/PMC4349410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luo, Dong-Gen -- Yue, Wendy W S -- Ala-Laurila, Petri -- Yau, King-Wai -- EY06837/EY/NEI NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R37 EY006837/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jun 10;332(6035):1307-12. doi: 10.1126/science.1200172.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dgluo@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21659602" target="_blank"〉PubMed〈/a〉
    Keywords: Ambystoma ; Animals ; Bufo marinus ; Goldfish ; Hot Temperature ; In Vitro Techniques ; Light ; *Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Photons ; Retinal Cone Photoreceptor Cells/physiology ; Retinal Pigments/chemistry/*physiology/radiation effects ; Rhodopsin/physiology
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    The antibacterial lectin RegIIIgamma promotes the spatial segregation of microbiota and host in the intestine (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. The proximity of vast numbers of bacteria to host intestinal tissues raises the question of how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show that RegIIIgamma, a secreted antibacterial lectin, is essential for maintaining a ~50-micrometer zone that physically separates the microbiota from the small intestinal epithelial surface. Loss of host-bacterial segregation in RegIIIgamma(-/-) mice was coupled to increased bacterial colonization of the intestinal epithelial surface and enhanced activation of intestinal adaptive immune responses by the microbiota. Together, our findings reveal that RegIIIgamma is a fundamental immune mechanism that promotes host-bacterial mutualism by regulating the spatial relationships between microbiota and host.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321924/" 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/PMC3321924/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaishnava, Shipra -- Yamamoto, Miwako -- Severson, Kari M -- Ruhn, Kelly A -- Yu, Xiaofei -- Koren, Omry -- Ley, Ruth -- Wakeland, Edward K -- Hooper, Lora V -- R01 DK070855/DK/NIDDK NIH HHS/ -- R01 DK070855-06/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):255-8. doi: 10.1126/science.1209791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998396" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Anti-Bacterial Agents/pharmacology ; Bacterial Load ; Gram-Negative Bacteria/immunology/*physiology ; Gram-Positive Bacteria/immunology/*physiology ; Homeostasis ; Immunoglobulin A/analysis ; Intestinal Mucosa/immunology/*microbiology ; Intestine, Small/immunology/*microbiology ; Lectins, C-Type/physiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics/metabolism ; Proteins/*metabolism ; Symbiosis ; T-Lymphocytes, Helper-Inducer/immunology
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    Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-04-02
    Description: Waves of cyclin synthesis and degradation regulate the activity of Cdc2 protein kinase during the cell cycle. Cdc2 inactivation by Wee1B-mediated phosphorylation is necessary for arrest of the oocyte at G2-prophase, but it is unclear whether this regulation functions later during the metaphase-to-anaphase transition. We show that reactivation of a Wee1B pathway triggers the decrease in Cdc2 activity during egg activation. When Wee1B is down-regulated, oocytes fail to form a pronucleus in response to Ca(2+) signals. Calcium-calmodulin-dependent kinase II (CaMKII) activates Wee1B, and CaMKII-driven exit from metaphase II is inhibited by Wee1B down-regulation, demonstrating that exit from metaphase requires not only a proteolytic degradation of cyclin B but also the inhibitory phosphorylation of Cdc2 by Wee1B.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104668/" 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/PMC4104668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, Jeong Su -- Susor, Andrej -- Conti, Marco -- GM080527-05/GM/NIGMS NIH HHS/ -- HD052909/HD/NICHD NIH HHS/ -- R01 GM080527/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):462-5. doi: 10.1126/science.1199211. Epub 2011 Mar 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA 94143-0556, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21454751" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CDC2 Protein Kinase/antagonists & inhibitors/metabolism ; Calcium/metabolism ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Cell Cycle Proteins/genetics/*metabolism ; Cyclin B/genetics/metabolism ; Down-Regulation ; Female ; Gene Knockdown Techniques ; Maturation-Promoting Factor/metabolism ; *Meiosis ; *Metaphase ; Mice ; Mice, Inbred C57BL ; Oocytes/*physiology ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; RNA, Messenger/genetics/metabolism
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    Successful transmission of a retrovirus depends on the commensal microbiota (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-15
    Description: To establish chronic infections, viruses must develop strategies to evade the host's immune responses. Many retroviruses, including mouse mammary tumor virus (MMTV), are transmitted most efficiently through mucosal surfaces rich in microbiota. We found that MMTV, when ingested by newborn mice, stimulates a state of unresponsiveness toward viral antigens. This process required the intestinal microbiota, as antibiotic-treated mice or germ-free mice did not transmit infectious virus to their offspring. MMTV-bound bacterial lipopolysaccharide triggered Toll-like receptor 4 and subsequent interleukin-6 (IL-6)-dependent induction of the inhibitory cytokine IL-10. Thus, MMTV has evolved to rely on the interaction with the microbiota to induce an immune evasion pathway. Together, these findings reveal the fundamental importance of commensal microbiota in viral infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3519937/" 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/PMC3519937/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kane, Melissa -- Case, Laure K -- Kopaskie, Karyl -- Kozlova, Alena -- MacDearmid, Cameron -- Chervonsky, Alexander V -- Golovkina, Tatyana V -- AI082418/AI/NIAID NIH HHS/ -- AI090084/AI/NIAID NIH HHS/ -- CA100383/CA/NCI NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- P30 CA014599/CA/NCI NIH HHS/ -- R01 AI090084/AI/NIAID NIH HHS/ -- R01 CA134667/CA/NCI NIH HHS/ -- R56 AI090084/AI/NIAID NIH HHS/ -- T32 AI065382-01/AI/NIAID NIH HHS/ -- T32GM007183/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):245-9. doi: 10.1126/science.1210718.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, The University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21998394" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Anti-Bacterial Agents/pharmacology ; Antibodies, Viral/biosynthesis ; Antigens, Viral/immunology ; *Bacterial Physiological Phenomena ; Female ; Germ-Free Life ; *Immune Evasion ; Interleukin-10/genetics/metabolism ; Intestinal Mucosa/*virology ; Intestines/*microbiology ; Lipopolysaccharides/immunology/metabolism ; Mammary Tumor Virus, Mouse/*immunology/*pathogenicity ; *Metagenome ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Pregnancy ; Pregnancy Complications, Infectious/virology ; Retroviridae Infections/immunology/*transmission/virology ; Specific Pathogen-Free Organisms ; Toll-Like Receptor 4/immunology/metabolism ; Tumor Virus Infections/immunology/transmission/virology ; Virus Replication
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Role for the membrane receptor guanylyl cyclase-C in attention deficiency and hyperactive behavior (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-13
    Description: Midbrain dopamine neurons regulate many important behavioral processes, and their dysfunctions are associated with several human neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD) and schizophrenia. Here, we report that these neurons in mice selectively express guanylyl cyclase-C (GC-C), a membrane receptor previously thought to be expressed mainly in the intestine. GC-C activation potentiates the excitatory responses mediated by glutamate and acetylcholine receptors via the activity of guanosine 3',5'-monophosphate-dependent protein kinase (PKG). Mice in which GC-C has been knocked out exhibit hyperactivity and attention deficits. Moreover, their behavioral phenotypes are reversed by ADHD therapeutics and a PKG activator. These results indicate important behavioral and physiological functions for the GC-C/PKG signaling pathway within the brain and suggest new therapeutic targets for neuropsychiatric disorders related to the malfunctions of midbrain dopamine neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Rong -- Ding, Cheng -- Hu, Ji -- Lu, Yao -- Liu, Fei -- Mann, Elizabeth -- Xu, Fuqiang -- Cohen, Mitchell B -- Luo, Minmin -- New York, N.Y. -- Science. 2011 Sep 16;333(6049):1642-6. doi: 10.1126/science.1207675. Epub 2011 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21835979" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/administration & dosage ; Animals ; Attention ; Attention Deficit Disorder with Hyperactivity/genetics/*metabolism ; Behavior, Animal/drug effects ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/*metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Enzyme Activation ; Gastrointestinal Hormones/metabolism/pharmacology ; Glycine/analogs & derivatives/metabolism/pharmacology ; Impulsive Behavior ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Natriuretic Peptides/metabolism/pharmacology ; Neurons/*metabolism ; Patch-Clamp Techniques ; Receptors, Glutamate/metabolism ; Receptors, Guanylate Cyclase-Coupled/genetics/*metabolism ; Receptors, Muscarinic/metabolism ; Receptors, Peptide/genetics/*metabolism ; Resorcinols/metabolism/pharmacology ; Signal Transduction ; Substantia Nigra/cytology/*metabolism ; Ventral Tegmental Area/cytology/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Chemical and genetic engineering of selective ion channel-ligand interactions (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: Ionic flux mediates essential physiological and behavioral functions in defined cell populations. Cell type-specific activators of diverse ionic conductances are needed for probing these effects. We combined chemistry and protein engineering to enable the systematic creation of a toolbox of ligand-gated ion channels (LGICs) with orthogonal pharmacologic selectivity and divergent functional properties. The LGICs and their small-molecule effectors were able to activate a range of ionic conductances in genetically specified cell types. LGICs constructed for neuronal perturbation could be used to selectively manipulate neuron activity in mammalian brains in vivo. The diversity of ion channel tools accessible from this approach will be useful for examining the relationship between neuronal activity and animal behavior, as well as for cell biological and physiological applications requiring chemical control of ion conductance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210548/" 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/PMC3210548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnus, Christopher J -- Lee, Peter H -- Atasoy, Deniz -- Su, Helen H -- Looger, Loren L -- Sternson, Scott M -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1292-6. doi: 10.1126/science.1206606.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885782" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides/chemistry/metabolism/pharmacology ; Bicyclo Compounds/chemistry/metabolism/pharmacology ; Brain/cytology/physiology ; Feeding Behavior ; Female ; HEK293 Cells ; Humans ; Ion Channel Gating ; Ligand-Gated Ion Channels/chemistry/*genetics/*metabolism ; Ligands ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; Neurons/*physiology ; Patch-Clamp Techniques ; Protein Binding ; *Protein Engineering ; Protein Structure, Tertiary ; Quinuclidines/chemistry/metabolism/pharmacology ; Receptors, Glycine/genetics/metabolism ; Receptors, Nicotinic/chemistry/genetics/metabolism ; Receptors, Serotonin, 5-HT3/genetics/metabolism ; Recombinant Fusion Proteins/chemistry/metabolism ; Small Molecule Libraries ; Stereoisomerism ; alpha7 Nicotinic Acetylcholine Receptor
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    Distinct properties of the XY pseudoautosomal region crucial for male meiosis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-02-19
    Description: Meiosis requires that each chromosome find its homologous partner and undergo at least one crossover. X-Y chromosome segregation hinges on efficient crossing-over in a very small region of homology, the pseudoautosomal region (PAR). We find that mouse PAR DNA occupies unusually long chromosome axes, potentially as shorter chromatin loops, predicted to promote double-strand break (DSB) formation. Most PARs show delayed appearance of RAD51/DMC1 foci, which mark DSB ends, and all PARs undergo delayed DSB-mediated homologous pairing. Analysis of Spo11beta isoform-specific transgenic mice revealed that late RAD51/DMC1 foci in the PAR are genetically distinct from both early PAR foci and global foci and that late PAR foci promote efficient X-Y pairing, recombination, and male fertility. Our findings uncover specific mechanisms that surmount the unique challenges of X-Y recombination.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151169/" 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/PMC3151169/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kauppi, Liisa -- Barchi, Marco -- Baudat, Frederic -- Romanienko, Peter J -- Keeney, Scott -- Jasin, Maria -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-01/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 18;331(6019):916-20. doi: 10.1126/science.1195774.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21330546" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Cycle Proteins/metabolism ; Chromatin/chemistry/metabolism ; *Chromosome Pairing ; Chromosome Segregation ; *Crossing Over, Genetic ; DNA Breaks, Double-Stranded ; Endodeoxyribonucleases/genetics/*metabolism ; Female ; In Situ Hybridization, Fluorescence ; Male ; *Meiosis ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Nuclear Proteins/metabolism ; Protein Isoforms ; Rad51 Recombinase/metabolism ; X Chromosome/*physiology ; Y Chromosome/*physiology
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    The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-19
    Description: The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isolated from t(8;21) AML patients, and that this acetylation is essential for its self-renewal-promoting effects in human cord blood CD34(+) cells and its leukemogenicity in mouse models. Inhibition of p300 abrogates the acetylation of AML1-ETO and impairs its ability to promote leukemic transformation. Thus, lysine acetyltransferases represent a potential therapeutic target in AML.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251012/" 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/PMC3251012/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Lan -- Gural, Alexander -- Sun, Xiao-Jian -- Zhao, Xinyang -- Perna, Fabiana -- Huang, Gang -- Hatlen, Megan A -- Vu, Ly -- Liu, Fan -- Xu, Haiming -- Asai, Takashi -- Xu, Hao -- Deblasio, Tony -- Menendez, Silvia -- Voza, Francesca -- Jiang, Yanwen -- Cole, Philip A -- Zhang, Jinsong -- Melnick, Ari -- Roeder, Robert G -- Nimer, Stephen D -- GM62437/GM/NIGMS NIH HHS/ -- R01 GM062437/GM/NIGMS NIH HHS/ -- R01 GM062437-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Aug 5;333(6043):765-9. doi: 10.1126/science.1201662. Epub 2011 Jul 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21764752" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/chemistry/*metabolism ; E1A-Associated p300 Protein/antagonists & inhibitors/*metabolism ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoietic Stem Cells/*cytology/physiology ; Humans ; Leukemia, Myeloid, Acute/*metabolism/pathology ; Lysine/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutant Proteins/metabolism ; Oncogene Proteins, Fusion/chemistry/*metabolism ; Preleukemia/metabolism/pathology ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Processing, Post-Translational ; Transcriptional Activation ; Tumor Cells, Cultured
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    Role for piRNAs and noncoding RNA in de novo DNA methylation of the imprinted mouse Rasgrf1 locus (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-05-14
    Description: Genomic imprinting causes parental origin-specific monoallelic gene expression through differential DNA methylation established in the parental germ line. However, the mechanisms underlying how specific sequences are selectively methylated are not fully understood. We have found that the components of the PIWI-interacting RNA (piRNA) pathway are required for de novo methylation of the differentially methylated region (DMR) of the imprinted mouse Rasgrf1 locus, but not other paternally imprinted loci. A retrotransposon sequence within a noncoding RNA spanning the DMR was targeted by piRNAs generated from a different locus. A direct repeat in the DMR, which is required for the methylation and imprinting of Rasgrf1, served as a promoter for this RNA. We propose a model in which piRNAs and a target RNA direct the sequence-specific methylation of Rasgrf1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368507/" 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/PMC3368507/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watanabe, Toshiaki -- Tomizawa, Shin-ichi -- Mitsuya, Kohzoh -- Totoki, Yasushi -- Yamamoto, Yasuhiro -- Kuramochi-Miyagawa, Satomi -- Iida, Naoko -- Hoki, Yuko -- Murphy, Patrick J -- Toyoda, Atsushi -- Gotoh, Kengo -- Hiura, Hitoshi -- Arima, Takahiro -- Fujiyama, Asao -- Sado, Takashi -- Shibata, Tatsuhiro -- Nakano, Toru -- Lin, Haifan -- Ichiyanagi, Kenji -- Soloway, Paul D -- Sasaki, Hiroyuki -- R01 CA098597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 May 13;332(6031):848-52. doi: 10.1126/science.1203919.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Human Genetics and Department of Integrated Genetics, National Institute of Genetics, Research Organization of Information and Systems, Mishima, Shizuoka, 411-8540, Japan. toshwatatoshiakiwatanabe@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21566194" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; *DNA Methylation ; *Genomic Imprinting ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Proteins/genetics/metabolism ; Models, Genetic ; Mutation ; Phospholipase D/genetics/metabolism ; Proteins/genetics/metabolism ; RNA, Small Interfering/*genetics/metabolism ; RNA, Untranslated/*genetics/metabolism ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Spermatogonia/metabolism ; Testis/embryology/metabolism ; Transcription, Genetic ; ras-GRF1/*genetics
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    Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: Eosinophils are associated with helminth immunity and allergy, often in conjunction with alternatively activated macrophages (AAMs). Adipose tissue AAMs are necessary to maintain glucose homeostasis and are induced by the cytokine interleukin-4 (IL-4). Here, we show that eosinophils are the major IL-4-expressing cells in white adipose tissues of mice, and, in their absence, AAMs are greatly attenuated. Eosinophils migrate into adipose tissue by an integrin-dependent process and reconstitute AAMs through an IL-4- or IL-13-dependent process. Mice fed a high-fat diet develop increased body fat, impaired glucose tolerance, and insulin resistance in the absence of eosinophils, and helminth-induced adipose tissue eosinophilia enhances glucose tolerance. Our results suggest that eosinophils play an unexpected role in metabolic homeostasis through maintenance of adipose AAMs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144160/" 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/PMC3144160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Davina -- Molofsky, Ari B -- Liang, Hong-Erh -- Ricardo-Gonzalez, Roberto R -- Jouihan, Hani A -- Bando, Jennifer K -- Chawla, Ajay -- Locksley, Richard M -- 5F30DK083194-02/DK/NIDDK NIH HHS/ -- AI026918/AI/NIAID NIH HHS/ -- DK063720/DK/NIDDK NIH HHS/ -- DP1 OD006415/OD/NIH HHS/ -- F30 DK083194-03/DK/NIDDK NIH HHS/ -- R01 AI030663/AI/NIAID NIH HHS/ -- R01 DK076760/DK/NIDDK NIH HHS/ -- R01 DK081405/DK/NIDDK NIH HHS/ -- R01 HL076746/HL/NHLBI NIH HHS/ -- R37 AI026918/AI/NIAID NIH HHS/ -- R37 AI026918-24/AI/NIAID NIH HHS/ -- T32 AI007290/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Apr 8;332(6026):243-7. doi: 10.1126/science.1201475. Epub 2011 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436399" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Adipose Tissue, White/cytology/*immunology/*metabolism ; Animals ; Blood Glucose/*metabolism ; Cell Movement ; Dietary Fats/administration & dosage ; Eosinophilia/immunology ; Eosinophils/immunology/*physiology ; Glucose Intolerance ; Homeostasis ; Insulin/metabolism ; Insulin Resistance ; Interleukin-13/genetics/metabolism ; Interleukin-4/genetics/metabolism ; *Macrophage Activation ; Macrophages/*immunology/*metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Nippostrongylus ; Strongylida Infections/immunology/metabolism
    Print ISSN: 0036-8075
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    Trim28 is required for epigenetic stability during mouse oocyte to embryo transition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Phenotypic variability in genetic disease is usually attributed to genetic background variation or environmental influence. Here, we show that deletion of a single gene, Trim28 (Kap1 or Tif1beta), from the maternal germ line alone, on an otherwise identical genetic background, results in severe phenotypic and epigenetic variability that leads to embryonic lethality. We identify early and minute epigenetic variations in blastomeres of the preimplantation embryo of these animals, suggesting that the embryonic lethality may result from the misregulation of genomic imprinting in mice lacking maternal Trim28. Our results reveal the long-range effects of a maternal gene deletion on epigenetic memory and illustrate the delicate equilibrium of maternal and zygotic factors during nuclear reprogramming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Messerschmidt, Daniel M -- de Vries, Wilhelmine -- Ito, Mitsuteru -- Solter, Davor -- Ferguson-Smith, Anne -- Knowles, Barbara B -- 079249/Wellcome Trust/United Kingdom -- 095606/Wellcome Trust/United Kingdom -- MR/J001597/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1499-502. doi: 10.1126/science.1216154.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Development Group, Institute of Medical Biology, Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/physiology ; DNA Methylation ; Down-Regulation ; *Embryo Loss ; Embryo, Mammalian/*physiology ; Embryonic Development ; *Epigenesis, Genetic ; Female ; Gene Expression Regulation, Developmental ; *Genomic Imprinting ; Insulin-Like Growth Factor II/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*genetics/*physiology ; Oligonucleotide Array Sequence Analysis ; Oocytes/*physiology ; Phenotype ; RNA, Long Noncoding ; RNA, Untranslated/genetics/metabolism ; Repressor Proteins/*genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" 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/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A single progenitor population switches behavior to maintain and repair esophageal epithelium (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" 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/PMC3527005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doupe, David P -- Alcolea, Maria P -- Roshan, Amit -- Zhang, Gen -- Klein, Allon M -- Simons, Benjamin D -- Jones, Philip H -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0601740/Medical Research Council/United Kingdom -- G0700600/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U105370181/Medical Research Council/United Kingdom -- U.1053.00.010(70181)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1091-3. doi: 10.1126/science.1218835. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Doxycycline/pharmacology ; Epithelial Cells/*physiology ; Epithelium/drug effects/metabolism/*physiology ; Esophagus/*cytology/*physiology ; Green Fluorescent Proteins/biosynthesis ; Histones/biosynthesis ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/biosynthesis ; *Regeneration ; Stem Cells/metabolism/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Locally synchronized synaptic inputs (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-24
    Description: Synaptic inputs on dendrites are nonlinearly converted to action potential outputs, yet the spatiotemporal patterns of dendritic activation remain to be elucidated at single-synapse resolution. In rodents, we optically imaged synaptic activities from hundreds of dendritic spines in hippocampal and neocortical pyramidal neurons ex vivo and in vivo. Adjacent spines were frequently synchronized in spontaneously active networks, thereby forming dendritic foci that received locally convergent inputs from presynaptic cell assemblies. This precise subcellular geometry manifested itself during N-methyl-D-aspartate receptor-dependent circuit remodeling. Thus, clustered synaptic plasticity is innately programmed to compartmentalize correlated inputs along dendrites and may reify nonlinear synaptic integration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takahashi, Naoya -- Kitamura, Kazuo -- Matsuo, Naoki -- Mayford, Mark -- Kano, Masanobu -- Matsuki, Norio -- Ikegaya, Yuji -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):353-6. doi: 10.1126/science.1210362.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22267814" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; CA3 Region, Hippocampal/cytology/physiology ; Calcium/metabolism ; Dendritic Spines/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Net/*physiology ; Neuronal Plasticity ; Organ Culture Techniques ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Somatosensory Cortex/cytology/physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interleukin-22 drives endogenous thymic regeneration in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-03
    Description: Endogenous thymic regeneration is a crucial function that allows for renewal of immune competence after stress, infection, or immunodepletion. However, the mechanisms governing this regeneration remain poorly understood. We detail such a mechanism, centered on interleukin-22 (IL-22) and triggered by the depletion of CD4(+)CD8(+) double-positive thymocytes. Intrathymic levels of IL-22 were increased after thymic insult, and thymic recovery was impaired in IL-22-deficient mice. IL-22, which signaled through thymic epithelial cells and promoted their proliferation and survival, was up-regulated by radio-resistant RORgamma(t)(+)CCR6(+)NKp46(-) lymphoid tissue inducer cells after thymic injury in an IL-23-dependent manner. Administration of IL-22 enhanced thymic recovery after total body irradiation. These studies reveal mechanisms of endogenous thymic repair and offer innovative regenerative strategies for improving immune competence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616391/" 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/PMC3616391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudakov, Jarrod A -- Hanash, Alan M -- Jenq, Robert R -- Young, Lauren F -- Ghosh, Arnab -- Singer, Natalie V -- West, Mallory L -- Smith, Odette M -- Holland, Amanda M -- Tsai, Jennifer J -- Boyd, Richard L -- van den Brink, Marcel R M -- AI080455/AI/NIAID NIH HHS/ -- CA107096/CA/NCI NIH HHS/ -- HL069929/HL/NHLBI NIH HHS/ -- HL095075/HL/NHLBI NIH HHS/ -- R01 AI080455/AI/NIAID NIH HHS/ -- R01 CA107096/CA/NCI NIH HHS/ -- R01 HL069929/HL/NHLBI NIH HHS/ -- R01 HL095075/HL/NHLBI NIH HHS/ -- T32 CA009207/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 6;336(6077):91-5. doi: 10.1126/science.1218004. Epub 2012 Mar 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. dudakovj@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22383805" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Proliferation ; Cell Survival ; Dendritic Cells/physiology ; Epithelial Cells/cytology/physiology ; Interleukin-23/metabolism ; Interleukins/administration & dosage/deficiency/genetics/*metabolism ; Lymphocytes/cytology/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics/metabolism ; Radiation Dosage ; Receptors, Interleukin/metabolism ; Recombinant Proteins/administration & dosage ; *Regeneration ; Signal Transduction ; Thymocytes/*physiology ; Thymus Gland/cytology/immunology/*physiology/radiation effects ; Up-Regulation ; Whole-Body Irradiation
    Print ISSN: 0036-8075
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    Asymmetric segregation of polarized antigen on B cell division shapes presentation capacity (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-01-28
    Description: During the activation of humoral immune responses, B cells acquire antigen for subsequent presentation to cognate T cells. Here we show that after mouse B cells accumulate antigen, it is maintained in a polarized distribution for extended periods in vivo. Using high-throughput imaging flow cytometry, we observed that this polarization is preserved during B cell division, promoting asymmetric antigen segregation among progeny. Antigen inheritance correlates with the ability of progeny to activate T cells: Daughter cells receiving larger antigen stores exhibit a prolonged capacity to present antigen, which renders them more effective in competing for T cell help. The generation of progeny with differential capacities for antigen presentation may have implications for somatic hypermutation and class switching during affinity maturation and as B cells commit to effector cell fates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thaunat, Olivier -- Granja, Aitor G -- Barral, Patricia -- Filby, Andrew -- Montaner, Beatriz -- Collinson, Lucy -- Martinez-Martin, Nuria -- Harwood, Naomi E -- Bruckbauer, Andreas -- Batista, Facundo D -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 27;335(6067):475-9. doi: 10.1126/science.1214100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens/*analysis/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Computer Simulation ; Flow Cytometry ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Muramidase/analysis/immunology ; T-Lymphocytes/*immunology
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    Pheromonal induction of spatial learning in mice (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-12-15
    Description: Many mammals use scent marking for sexual and competitive advertisement, but little is known about the mechanism by which scents are used to locate mates and competitors. We show that darcin, an involatile protein sex pheromone in male mouse urine, can rapidly condition preference for its remembered location among females and competitor males so that animals prefer to spend time in the site even when scent is absent. Learned spatial preference is conditioned through contact with darcin in a single trial and remembered for approximately 14 days. This pheromone-induced learning allows animals to relocate sites of particular social relevance and provides proof that pheromones such as darcin can be highly potent stimuli for social learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, Sarah A -- Davidson, Amanda J -- McLean, Lynn -- Beynon, Robert J -- Hurst, Jane L -- BB/J002631/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBC503897/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1462-5. doi: 10.1126/science.1225638.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Behaviour and Evolution Group, Institute of Integrative Biology, University of Liverpool, Leahurst Campus, Neston CH64 7TE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Competitive Behavior/drug effects/*physiology ; Conditioning (Psychology)/drug effects/physiology ; Female ; Male ; Maze Learning/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Proteins/pharmacology/*physiology ; Sex Attractants/pharmacology/*physiology/urine ; Smell/drug effects/physiology ; Spatial Behavior/drug effects/*physiology
    Print ISSN: 0036-8075
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    Gap junctions compensate for sublinear dendritic integration in an inhibitory network (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-03-10
    Description: Electrically coupled inhibitory interneurons dynamically control network excitability, yet little is known about how chemical and electrical synapses regulate their activity. Using two-photon glutamate uncaging and dendritic patch-clamp recordings, we found that the dendrites of cerebellar Golgi interneurons acted as passive cables. They conferred distance-dependent sublinear synaptic integration and weakened distal excitatory inputs. Gap junctions were present at a higher density on distal dendrites and contributed substantially to membrane conductance. Depolarization of one Golgi cell increased firing in its neighbors, and inclusion of dendritic gap junctions in interneuron network models enabled distal excitatory synapses to drive network activity more effectively. Our results suggest that dendritic gap junctions counteract sublinear dendritic integration by enabling excitatory synaptic charge to spread into the dendrites of neighboring inhibitory interneurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3587282/" 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/PMC3587282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vervaeke, Koen -- Lorincz, Andrea -- Nusser, Zoltan -- Silver, R Angus -- 064413/Wellcome Trust/United Kingdom -- 090197/Wellcome Trust/United Kingdom -- 095667/Wellcome Trust/United Kingdom -- 293681/European Research Council/International -- 294667/European Research Council/International -- BB/F005490/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- F005490/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400598/Medical Research Council/United Kingdom -- G0400598(71261)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1624-8. doi: 10.1126/science.1215101. Epub 2012 Mar 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology and Pharmacology, University College London, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22403180" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Cerebellar Cortex/cytology ; Computer Simulation ; Dendrites/*physiology/*ultrastructure ; Electrical Synapses/*physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; Interneurons/*physiology ; Ion Channels/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Neurological ; Nerve Net/*physiology/ultrastructure ; *Neural Inhibition ; Patch-Clamp Techniques ; Synapses/physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
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    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/physiology
    Print ISSN: 0036-8075
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    Regulated virulence controls the ability of a pathogen to compete with the gut microbiota (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-15
    Description: The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439148/" 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/PMC3439148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamada, Nobuhiko -- Kim, Yun-Gi -- Sham, Ho Pan -- Vallance, Bruce A -- Puente, Jose L -- Martens, Eric C -- Nunez, Gabriel -- DK091191/DK/NIDDK NIH HHS/ -- DK61707/DK/NIDDK NIH HHS/ -- R01 DK061707/DK/NIDDK NIH HHS/ -- R01 DK091191/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1325-9. doi: 10.1126/science.1222195. Epub 2012 May 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Comprehensive Cancer Center, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22582016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Load ; Bacterial Proteins/genetics/metabolism ; Bacteroides/*growth & development ; Citrobacter rodentium/genetics/growth & development/immunology/*pathogenicity ; Enterobacteriaceae Infections/immunology/*microbiology ; Escherichia coli/*growth & development ; Feces/microbiology ; Gene Expression Regulation, Bacterial ; Germ-Free Life ; Intestinal Mucosa/*microbiology ; Intestines/*microbiology ; *Metagenome ; Mice ; Mice, Inbred C57BL ; *Microbial Interactions ; Specific Pathogen-Free Organisms ; Virulence Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Glucocorticoids can induce PTSD-like memory impairments in mice (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-01
    Description: Posttraumatic stress disorder (PTSD) is characterized by a hypermnesia of the trauma and by a memory impairment that decreases the ability to restrict fear to the appropriate context. Infusion of glucocorticoids in the hippocampus after fear conditioning induces PTSD-like memory impairments and an altered pattern of neural activation in the hippocampal-amygdalar circuit. Mice become unable to identify the context as the correct predictor of the threat and show fear responses to a discrete cue not predicting the threat in normal conditions. These data demonstrate PTSD-like memory impairments in rodents and identify a potential pathophysiological mechanism of this condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaouane, Nadia -- Porte, Yves -- Vallee, Monique -- Brayda-Bruno, Laurent -- Mons, Nicole -- Calandreau, Ludovic -- Marighetto, Aline -- Piazza, Pier Vincenzo -- Desmedt, Aline -- New York, N.Y. -- Science. 2012 Mar 23;335(6075):1510-3. doi: 10.1126/science.1207615. Epub 2012 Feb 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS UMR 5228, Centre de Neurosciences Integratives et Cognitives, Talence, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22362879" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiopathology ; Animals ; Conditioning (Psychology) ; Corticosterone/*administration & dosage/blood/metabolism/pharmacology ; Cues ; Electroshock ; *Fear ; Hippocampus/*physiopathology ; Male ; Memory Disorders/chemically induced/*physiopathology ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-fos/metabolism ; Restraint, Physical ; Stress Disorders, Post-Traumatic/*physiopathology ; Stress, Psychological
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Microbial exposure during early life has persistent effects on natural killer T cell function (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-24
    Description: Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal-but not adult-GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437652/" 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/PMC3437652/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olszak, Torsten -- An, Dingding -- Zeissig, Sebastian -- Vera, Miguel Pinilla -- Richter, Julia -- Franke, Andre -- Glickman, Jonathan N -- Siebert, Reiner -- Baron, Rebecca M -- Kasper, Dennis L -- Blumberg, Richard S -- AI090102/AI/NIAID NIH HHS/ -- DK034854/DK/NIDDK NIH HHS/ -- DK44319/DK/NIDDK NIH HHS/ -- DK51362/DK/NIDDK NIH HHS/ -- DK53056/DK/NIDDK NIH HHS/ -- DK88199/DK/NIDDK NIH HHS/ -- P30 DK034854/DK/NIDDK NIH HHS/ -- R01 DK044319/DK/NIDDK NIH HHS/ -- R01 DK088199/DK/NIDDK NIH HHS/ -- R37 DK044319/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):489-93. doi: 10.1126/science.1219328. Epub 2012 Mar 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22442383" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; Antigens, CD1d/immunology ; Asthma/*immunology ; Bacteria/*growth & development ; Chemokine CXCL6/genetics/metabolism ; Colitis, Ulcerative/chemically induced/*immunology ; Colon/immunology/microbiology ; DNA Methylation ; Disease Models, Animal ; Disease Susceptibility ; Germ-Free Life ; Intestinal Mucosa/*immunology ; Intestines/immunology/*microbiology ; Lung/*immunology ; Mice ; Mice, Inbred C57BL ; Natural Killer T-Cells/*immunology ; Oxazolone ; Receptors, CXCR/genetics/metabolism ; Specific Pathogen-Free Organisms
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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