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  • Cells, Cultured  (359)
  • American Association for the Advancement of Science (AAAS)  (359)
  • Annual Reviews
  • 2005-2009  (154)
  • 1980-1984  (205)
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  • 1
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    American Society for Cell Biology. Sprayed-on growth factors guide stem cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-12-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2006 Dec 22;314(5807):1865.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17185579" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/*pharmacology ; Bone and Bones/*cytology ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Extracellular Matrix ; Myoblasts/cytology ; Rats ; Stem Cells/*cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    A regulatory SNP causes a human genetic disease by creating a new transcriptional promoter (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: We describe a pathogenetic mechanism underlying a variant form of the inherited blood disorder alpha thalassemia. Association studies of affected individuals from Melanesia localized the disease trait to the telomeric region of human chromosome 16, which includes the alpha-globin gene cluster, but no molecular defects were detected by conventional approaches. After resequencing and using a combination of chromatin immunoprecipitation and expression analysis on a tiled oligonucleotide array, we identified a gain-of-function regulatory single-nucleotide polymorphism (rSNP) in a nongenic region between the alpha-globin genes and their upstream regulatory elements. The rSNP creates a new promoterlike element that interferes with normal activation of all downstream alpha-like globin genes. Thus, our work illustrates a strategy for distinguishing between neutral and functionally important rSNPs, and it also identifies a pathogenetic mechanism that could potentially underlie other genetic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Gobbi, Marco -- Viprakasit, Vip -- Hughes, Jim R -- Fisher, Chris -- Buckle, Veronica J -- Ayyub, Helena -- Gibbons, Richard J -- Vernimmen, Douglas -- Yoshinaga, Yuko -- de Jong, Pieter -- Cheng, Jan-Fang -- Rubin, Edward M -- Wood, William G -- Bowden, Don -- Higgs, Douglas R -- MC_U137961143/Medical Research Council/United Kingdom -- MC_U137961145/Medical Research Council/United Kingdom -- MC_U137961147/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 May 26;312(5777):1215-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728641" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Cells, Cultured ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 16/*genetics ; Erythroblasts ; GATA1 Transcription Factor/metabolism ; Gene Expression ; Gene Expression Profiling ; Globins/*genetics ; Haplotypes ; Humans ; Melanesia ; Minisatellite Repeats ; Multigene Family ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, Single Nucleotide ; *Promoter Regions, Genetic ; Regulatory Elements, Transcriptional ; Transcription, Genetic ; alpha-Thalassemia/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Role of iNOS in human host defense (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathan, Carl -- New York, N.Y. -- Science. 2006 Jun 30;312(5782):1874-5; author reply 1874-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/enzymology/*immunology ; Cell Culture Techniques ; Cell Differentiation ; Cells, Cultured ; Humans ; Macrophages/cytology/*enzymology ; Mice ; Nitric Oxide Synthase Type II/biosynthesis/*metabolism ; Tuberculosis/enzymology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Ca2+ entry through plasma membrane IP3 receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-15
    Description: Inositol 1,4,5-trisphosphate receptors (IP3Rs) release calcium ions, Ca2+, from intracellular stores, but their roles in mediating Ca2+ entry are unclear. IP3 stimulated opening of very few (1.9 +/- 0.2 per cell) Ca2+-permeable channels in whole-cell patch-clamp recording of DT40 chicken or mouse B cells. Activation of the B cell receptor (BCR) in perforated-patch recordings evoked the same response. IP3 failed to stimulate intracellular or plasma membrane (PM) channels in cells lacking IP3R. Expression of IP3R restored both responses. Mutations within the pore affected the conductances of IP3-activated PM and intracellular channels similarly. An impermeant pore mutant abolished BCR-evoked Ca2+ signals, and PM IP3Rs were undetectable. After introduction of an alpha-bungarotoxin binding site near the pore, PM IP3Rs were modulated by extracellular alpha-bungarotoxin. IP(3)Rs are unusual among endoplasmic reticulum proteins in being also functionally expressed at the PM, where very few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dellis, Olivier -- Dedos, Skarlatos G -- Tovey, Stephen C -- Taufiq-Ur-Rahman -- Dubel, Stefan J -- Taylor, Colin W -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Jul 14;313(5784):229-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1PD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16840702" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism ; Bungarotoxins/metabolism/pharmacology ; Calcium/*metabolism ; Calcium Channels/genetics/*metabolism ; *Calcium Signaling ; Cell Membrane/*metabolism ; Cells, Cultured ; Chickens ; Electric Conductivity ; Endoplasmic Reticulum/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism ; Inositol 1,4,5-Trisphosphate Receptors ; *Ion Channel Gating ; Mice ; Nuclear Envelope/metabolism ; Patch-Clamp Techniques ; Point Mutation ; Rats ; Receptors, Antigen, B-Cell/metabolism ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors/genetics/*metabolism ; Transfection
    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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  • 5
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    Microbiology. Breaking the barrier between commensalism and pathogenicity (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hayashi, Tetsuya -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):772-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Bioenvironmental Science, Frontier Science Research Center, University of Miyazaki, 5200 Kiyotake, Miyazaki 889-1692, Japan. thayash@med.miyazaki-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cell Death ; Cells, Cultured ; Colon/cytology/microbiology ; *DNA Damage ; Escherichia coli/classification/genetics/*pathogenicity/*physiology ; *Genomic Islands ; Humans ; Intestinal Mucosa/cytology/microbiology ; Mutagens/*metabolism ; Peptides/*metabolism ; Polyketide Synthases/genetics/metabolism ; Virulence Factors/*biosynthesis
    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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  • 6
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    Activity-dependent regulation of MEF2 transcription factors suppresses excitatory synapse number (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: In the mammalian nervous system, neuronal activity regulates the strength and number of synapses formed. The genetic program that coordinates this process is poorly understood. We show that myocyte enhancer factor 2 (MEF2) transcription factors suppressed excitatory synapse number in a neuronal activity- and calcineurin-dependent manner as hippocampal neurons formed synapses. In response to increased neuronal activity, calcium influx into neurons induced the activation of the calcium/calmodulin-regulated phosphatase calcineurin, which dephosphorylated and activated MEF2. When activated, MEF2 promoted the transcription of a set of genes, including arc and synGAP, that restrict synapse number. These findings define an activity-dependent transcriptional program that may control synapse number during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flavell, Steven W -- Cowan, Christopher W -- Kim, Tae-Kyung -- Greer, Paul L -- Lin, Yingxi -- Paradis, Suzanne -- Griffith, Eric C -- Hu, Linda S -- Chen, Chinfei -- Greenberg, Michael E -- AG05870/AG/NIA NIH HHS/ -- HD18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- R01 EY013613/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1008-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Program, Children's Hospital, and Departments of Neurology and Neurobiology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484497" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; Calcium/metabolism ; Cells, Cultured ; Cytoskeletal Proteins/genetics ; Dendrites/physiology/ultrastructure ; Excitatory Postsynaptic Potentials ; GTPase-Activating Proteins/genetics ; Gene Expression Regulation ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; MEF2 Transcription Factors ; Mutation ; Myogenic Regulatory Factors/genetics/*physiology ; Nerve Tissue Proteins/genetics ; Neurons/*physiology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; RNA Interference ; Rats ; Rats, Long-Evans ; Recombinant Fusion Proteins/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Transcription, Genetic ; Transfection
    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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  • 7
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    Muscular thin films for building actuators and powering devices (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-08
    Description: We demonstrate the assembly of biohybrid materials from engineered tissues and synthetic polymer thin films. The constructs were built by culturing neonatal rat ventricular cardiomyocytes on polydimethylsiloxane thin films micropatterned with extracellular matrix proteins to promote spatially ordered, two-dimensional myogenesis. The constructs, termed muscular thin films, adopted functional, three-dimensional conformations when released from a thermally sensitive polymer substrate and were designed to perform biomimetic tasks by varying tissue architecture, thin-film shape, and electrical-pacing protocol. These centimeter-scale constructs perform functions as diverse as gripping, pumping, walking, and swimming with fine spatial and temporal control and generating specific forces as high as 4 millinewtons per square millimeter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feinberg, Adam W -- Feigel, Alex -- Shevkoplyas, Sergey S -- Sheehy, Sean -- Whitesides, George M -- Parker, Kevin Kit -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Disease Biophysics Group, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17823347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisotropy ; Cell Culture Techniques ; Cells, Cultured ; Dimethylpolysiloxanes ; Microscopy, Fluorescence ; Motion ; Muscle Contraction ; *Myocardium ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley ; Robotics ; Silicones ; *Tissue Engineering
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    JETLAG resets the Drosophila circadian clock by promoting light-induced degradation of TIMELESS (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: Organisms ranging from bacteria to humans synchronize their internal clocks to daily cycles of light and dark. Photic entrainment of the Drosophila clock is mediated by proteasomal degradation of the clock protein TIMELESS (TIM). We have identified mutations in jetlag-a gene coding for an F-box protein with leucine-rich repeats-that result in reduced light sensitivity of the circadian clock. Mutant flies show rhythmic behavior in constant light, reduced phase shifts in response to light pulses, and reduced light-dependent degradation of TIM. Expression of JET along with the circadian photoreceptor cryptochrome (CRY) in cultured S2R cells confers light-dependent degradation onto TIM, thereby reconstituting the acute response + of the circadian clock to light in a cell culture system. Our results suggest that JET is essential for resetting the clock by transmitting light signals from CRY to TIM.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2767177/" 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/PMC2767177/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, Kyunghee -- Zheng, Xiangzhong -- Sehgal, Amita -- NS048471/NS/NINDS NIH HHS/ -- R01 NS048471/NS/NINDS NIH HHS/ -- R01 NS048471-02/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2006 Jun 23;312(5781):1809-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Neuroscience, 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/16794082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; *Circadian Rhythm ; Cryptochromes ; Drosophila/chemistry/genetics/physiology ; Drosophila Proteins/chemistry/*genetics/*metabolism/*physiology ; Drosophila melanogaster/chemistry/*genetics/*physiology ; Eye Proteins/metabolism ; F-Box Proteins/chemistry/*genetics/*physiology ; Female ; *Light ; Male ; Models, Biological ; Molecular Sequence Data ; Mutation ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/metabolism ; Transgenes ; Ubiquitin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Regulation of hepatic stellate cell differentiation by the neurotrophin receptor p75NTR (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-31
    Description: Differentiation of hepatic stellate cells (HSCs) to extracellular matrix- and growth factor-producing cells supports liver regeneration through promotion of hepatocyte proliferation. We show that the neurotrophin receptor p75NTR, a tumor necrosis factor receptor superfamily member expressed in HSCs after fibrotic and cirrhotic liver injury in humans, is a regulator of liver repair. In mice, depletion of p75NTR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo. p75NTR-/- HSCs failed to differentiate to myofibroblasts and did not support hepatocyte proliferation. Moreover, inhibition of p75NTR signaling to the small guanosine triphosphatase Rho resulted in impaired HSC differentiation. Our results identify signaling from p75NTR to Rho as a mechanism for the regulation of HSC differentiation to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Passino, Melissa A -- Adams, Ryan A -- Sikorski, Shoana L -- Akassoglou, Katerina -- 5T32-GM07752/GM/NIGMS NIH HHS/ -- NS051470/NS/NINDS NIH HHS/ -- P30-NS047101/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 30;315(5820):1853-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Diego (UCSD), La Jolla, CA 92093-0636, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17395831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Progression ; Extracellular Matrix/metabolism ; Fibroblasts/*cytology ; Hepatocyte Growth Factor/metabolism ; Hepatocytes/*cytology ; Liver/*cytology/metabolism/pathology/physiology ; Liver Diseases/metabolism/*pathology ; *Liver Regeneration ; Mice ; Nerve Growth Factor/pharmacology ; Receptors, Nerve Growth Factor/genetics/*metabolism ; Signal Transduction ; rho GTP-Binding Proteins/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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  • 10
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    Mosaic organization of neural stem cells in the adult brain (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-07
    Description: The in vivo potential of neural stem cells in the postnatal mouse brain is not known, but because they produce many different types of neurons, they must be either very versatile or very diverse. By specifically targeting stem cells and following their progeny in vivo, we showed that postnatal stem cells in different regions produce different types of neurons, even when heterotopically grafted or grown in culture. This suggests that rather than being plastic and homogeneous, neural stem cells are a restricted and diverse population of progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Merkle, Florian T -- Mirzadeh, Zaman -- Alvarez-Buylla, Arturo -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):381-4. Epub 2007 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery and Developmental and Stem Cell Biology Program, University of California, San Francisco, San Francisco, CA 94143-0525, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615304" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology ; Animals ; Animals, Newborn ; Astrocytes/cytology ; Brain/*cytology ; Cell Differentiation ; Cells, Cultured ; Interneurons/cytology ; Lateral Ventricles/cytology ; Mice ; Neuroglia/cytology ; Neurons/*cytology ; Olfactory Bulb/cytology ; Stem Cell Transplantation ; Transplantation, Heterotopic
    Print ISSN: 0036-8075
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  • 11
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    Molecular basis for the nerve dependence of limb regeneration in an adult vertebrate (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-03
    Description: The limb blastemal cells of an adult salamander regenerate the structures distal to the level of amputation, and the surface protein Prod 1 is a critical determinant of their proximodistal identity. The anterior gradient protein family member nAG is a secreted ligand for Prod 1 and a growth factor for cultured newt blastemal cells. nAG is sequentially expressed after amputation in the regenerating nerve and the wound epidermis-the key tissues of the stem cell niche-and its expression in both locations is abrogated by denervation. The local expression of nAG after electroporation is sufficient to rescue a denervated blastema and regenerate the distal structures. Our analysis brings together the positional identity of the blastema and the classical nerve dependence of limb regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696928/" 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/PMC2696928/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Anoop -- Godwin, James W -- Gates, Phillip B -- Garza-Garcia, A Acely -- Brockes, Jeremy P -- G0600229/Medical Research Council/United Kingdom -- G0600229(77696)/Medical Research Council/United Kingdom -- G9537983/Medical Research Council/United Kingdom -- G9537983(56733)/Medical Research Council/United Kingdom -- MC_U117574559/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):772-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17975060" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD59/*physiology ; COS Cells ; Cells, Cultured ; Cercopithecus aethiops ; Denervation ; Extremities/innervation ; Glycosylphosphatidylinositols/physiology ; Growth Substances ; Intercellular Signaling Peptides and Proteins/isolation & ; purification/*physiology/secretion ; Ligands ; Mice ; Notophthalmus viridescens ; Peripheral Nerves/*physiology ; Regeneration/*physiology ; Stem Cells/*cytology ; Two-Hybrid System Techniques
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  • 12
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    Protein kinase C beta and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66Shc (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: The 66-kilodalton isoform of the growth factor adapter Shc (p66Shc) translates oxidative damage into cell death by acting as reactive oxygen species (ROS) producer within mitochondria. However, the signaling link between cellular stress and mitochondrial proapoptotic activity of p66Shc was not known. We demonstrate that protein kinase C beta, activated by oxidative conditions in the cell, induces phosphorylation of p66Shc and triggers mitochondrial accumulation of the protein after it is recognized by the prolyl isomerase Pin1. Once imported, p66Shc causes alterations of mitochondrial Ca2+ responses and three-dimensional structure, thus inducing apoptosis. These data identify a signaling route that activates an apoptotic inducer shortening the life span and could be a potential target of pharmacological approaches to inhibit aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pinton, Paolo -- Rimessi, Alessandro -- Marchi, Saverio -- Orsini, Francesca -- Migliaccio, Enrica -- Giorgio, Marco -- Contursi, Cristina -- Minucci, Saverio -- Mantovani, Fiamma -- Wieckowski, Mariusz R -- Del Sal, Giannino -- Pelicci, Pier Giuseppe -- Rizzuto, Rosario -- GGP05284/Telethon/Italy -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):659-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental and Diagnostic Medicine, Section of General Pathology and Interdisciplinary Center for the Study of Inflammation (ICSI), University of Ferrara, Ferrera, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272725" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*metabolism ; Adenosine Triphosphate/metabolism/pharmacology ; Animals ; *Apoptosis ; Calcium/metabolism ; Calcium Signaling ; *Cell Aging ; Cell Survival ; Cells, Cultured ; Cyclosporine/pharmacology ; Hydrogen Peroxide/metabolism/pharmacology ; Mice ; Mitochondria/*metabolism/ultrastructure ; Mutation ; Oxidative Stress ; Peptidylprolyl Isomerase/*metabolism ; Permeability ; Phosphorylation ; Protein Kinase C/antagonists & inhibitors/genetics/*metabolism ; Protein Kinase C beta ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/metabolism ; Shc Signaling Adaptor Proteins ; *Signal Transduction
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  • 13
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    Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/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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  • 14
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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/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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  • 15
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    Dynamic visualization of thrombopoiesis within bone marrow (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-22
    Description: Platelets are generated from megakaryocytes (MKs) in mammalian bone marrow (BM) by mechanisms that remain poorly understood. Here we describe the use of multiphoton intravital microscopy in intact BM to visualize platelet generation in mice. MKs were observed as sessile cells that extended dynamic proplatelet-like protrusions into microvessels. These intravascular extensions appeared to be sheared from their transendothelial stems by flowing blood, resulting in the appearance of proplatelets in peripheral blood. In vitro, proplatelet production from differentiating MKs was enhanced by fluid shear. These results confirm the concept of proplatelet formation in vivo and are consistent with the possibility that blood flow-induced hydrodynamic shear stress is a biophysical determinant of thrombopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junt, Tobias -- Schulze, Harald -- Chen, Zhao -- Massberg, Steffen -- Goerge, Tobias -- Krueger, Andreas -- Wagner, Denisa D -- Graf, Thomas -- Italiano, Joseph E Jr -- Shivdasani, Ramesh A -- von Andrian, Ulrich H -- HL068130/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL63143/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2007 Sep 21;317(5845):1767-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17885137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins ; Blood Platelets/*cytology ; Bone Marrow/*physiology ; Cells, Cultured ; Luminescent Proteins ; Megakaryocytes/*cytology ; Mice ; Microscopy, Fluorescence, Multiphoton ; Platelet Membrane Glycoprotein IIb ; Shear Strength ; Thrombopoiesis/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
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    Cell signaling. mTOR, unleashed (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Proud, Christopher G -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):926-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, British Columbia V6T 1Z3, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Cells, Cultured ; Guanosine Triphosphate/metabolism ; Humans ; Insulin/metabolism ; Models, Biological ; Monomeric GTP-Binding Proteins/*metabolism ; Multiprotein Complexes ; Neuropeptides/*metabolism ; Protein Binding ; Protein Kinases/*metabolism ; Proteins ; *Signal Transduction ; Sirolimus/metabolism/pharmacology ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Protein 1A/metabolism ; Tacrolimus Binding Proteins/antagonists & inhibitors/*metabolism ; Transcription Factors/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Host immune system gene targeting by a viral miRNA (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-21
    Description: Virally encoded microRNAs (miRNAs) have recently been discovered in herpesviruses. However, their biological roles are mostly unknown. We developed an algorithm for the prediction of miRNA targets and applied it to human cytomegalovirus miRNAs, resulting in the identification of the major histocompatibility complex class I-related chain B (MICB) gene as a top candidate target of hcmv-miR-UL112. MICB is a stress-induced ligand of the natural killer (NK) cell activating receptor NKG2D and is critical for the NK cell killing of virus-infected cells and tumor cells. We show that hcmv-miR-UL112 specifically down-regulates MICB expression during viral infection, leading to decreased binding of NKG2D and reduced killing by NK cells. Our results reveal a miRNA-based immunoevasion mechanism that appears to be exploited by human cytomegalovirus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283197/" 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/PMC4283197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stern-Ginossar, Noam -- Elefant, Naama -- Zimmermann, Albert -- Wolf, Dana G -- Saleh, Nivin -- Biton, Moshe -- Horwitz, Elad -- Prokocimer, Zafnat -- Prichard, Mark -- Hahn, Gabriele -- Goldman-Wohl, Debra -- Greenfield, Caryn -- Yagel, Simcha -- Hengel, Hartmut -- Altuvia, Yael -- Margalit, Hanah -- Mandelboim, Ofer -- N01 AI030049/AI/NIAID NIH HHS/ -- N01 AI30049/AI/NIAID NIH HHS/ -- N01-30049/PHS HHS/ -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):376-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lautenberg Center for General and Tumor Immunology, Hebrew University Hadassah Medical School, Jerusalem, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641203" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Algorithms ; Binding Sites ; Cell Line, Tumor ; Cells, Cultured ; Cytomegalovirus/genetics/*immunology/*pathogenicity ; Cytotoxicity, Immunologic ; Down-Regulation ; Histocompatibility Antigens Class I/*genetics/metabolism ; Humans ; Killer Cells, Natural/immunology ; Ligands ; MicroRNAs/genetics/*metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; RNA, Viral/*metabolism ; Receptors, Immunologic/metabolism ; Receptors, Natural Killer Cell ; Transduction, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Multiple functions of the IKK-related kinase IKKepsilon in interferon-mediated antiviral immunity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: IKKepsilon is an IKK (inhibitor of nuclear factor kappaBkinase)-related kinase implicated in virus induction of interferon-beta (IFNbeta). We report that, although mice lacking IKKepsilon produce normal amounts of IFNbeta, they are hypersusceptible to viral infection because of a defect in the IFN signaling pathway. Specifically, a subset of type I IFN-stimulated genes are not activated in the absence of IKKepsilon because the interferon-stimulated gene factor 3 complex (ISGF3) does not bind to promoter elements of the affected genes. We demonstrate that IKKepsilon is activated by IFNbeta and that IKKepsilon directly phosphorylates signal transducer and activator of transcription 1 (STAT1), a component of ISGF3. We conclude that IKKepsilon plays a critical role in the IFN-inducible antiviral transcriptional response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tenoever, Benjamin R -- Ng, Sze-Ling -- Chua, Mark A -- McWhirter, Sarah M -- Garcia-Sastre, Adolfo -- Maniatis, Tom -- F31 AI056678/AI/NIAID NIH HHS/ -- P01AI058113/AI/NIAID NIH HHS/ -- R01AI46954/AI/NIAID NIH HHS/ -- U19AI62623/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1274-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332413" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/genetics/metabolism ; Animals ; Cells, Cultured ; Dimerization ; *Gene Expression Regulation ; I-kappa B Kinase/genetics/*metabolism ; *Influenza A Virus, H1N1 Subtype/immunology/physiology ; Interferon-Stimulated Gene Factor 3/metabolism ; Interferon-beta/*immunology/metabolism ; Lung/pathology/virology ; Mice ; Mice, Knockout ; Orthomyxoviridae Infections/*immunology/metabolism/pathology/virology ; Phosphorylation ; Promoter Regions, Genetic ; RNA-Binding Proteins ; STAT1 Transcription Factor/metabolism ; STAT2 Transcription Factor/metabolism ; Signal Transduction ; Transcription, Genetic ; Viral Load ; Virus Replication
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  • 19
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    Treatment of sickle cell anemia mouse model with iPS cells generated from autologous skin (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-08
    Description: It has recently been demonstrated that mouse and human fibroblasts can be reprogrammed into an embryonic stem cell-like state by introducing combinations of four transcription factors. However, the therapeutic potential of such induced pluripotent stem (iPS) cells remained undefined. By using a humanized sickle cell anemia mouse model, we show that mice can be rescued after transplantation with hematopoietic progenitors obtained in vitro from autologous iPS cells. This was achieved after correction of the human sickle hemoglobin allele by gene-specific targeting. Our results provide proof of principle for using transcription factor-induced reprogramming combined with gene and cell therapy for disease treatment in mice. The problems associated with using retroviruses and oncogenes for reprogramming need to be resolved before iPS cells can be considered for human therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanna, Jacob -- Wernig, Marius -- Markoulaki, Styliani -- Sun, Chiao-Wang -- Meissner, Alexander -- Cassady, John P -- Beard, Caroline -- Brambrink, Tobias -- Wu, Li-Chen -- Townes, Tim M -- Jaenisch, Rudolf -- 2-R01-HL057619/HL/NHLBI NIH HHS/ -- 5-R37-CA084198/CA/NCI NIH HHS/ -- 5-RO1-CA087869/CA/NCI NIH HHS/ -- 5-RO1-HDO45022/PHS HHS/ -- New York, N.Y. -- Science. 2007 Dec 21;318(5858):1920-3. Epub 2007 Dec 6.〈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/18063756" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/physiopathology/*therapy ; Animals ; Cell Differentiation ; Cells, Cultured ; *Cellular Reprogramming ; DNA-Binding Proteins/genetics ; Disease Models, Animal ; Embryonic Stem Cells/cytology ; Erythrocyte Count ; Fibroblasts/*cytology ; Genes, myc ; Globins/genetics ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology ; Hemoglobin A/analysis ; Hemoglobin, Sickle/analysis ; Humans ; Kidney Concentrating Ability ; Kruppel-Like Transcription Factors/genetics ; Male ; Mice ; Octamer Transcription Factor-3/genetics ; Pluripotent Stem Cells/*cytology ; SOXB1 Transcription Factors ; Trans-Activators/genetics ; Transduction, Genetic
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Regulation of the germinal center response by microRNA-155 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: MicroRNAs are small RNA species involved in biological control at multiple levels. Using genetic deletion and transgenic approaches, we show that the evolutionarily conserved microRNA-155 (miR-155) has an important role in the mammalian immune system, specifically in regulating T helper cell differentiation and the germinal center reaction to produce an optimal T cell-dependent antibody response. miR-155 exerts this control, at least in part, by regulating cytokine production. These results also suggest that individual microRNAs can exert critical control over mammalian differentiation processes in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thai, To-Ha -- Calado, Dinis Pedro -- Casola, Stefano -- Ansel, K Mark -- Xiao, Changchun -- Xue, Yingzi -- Murphy, Andrew -- Frendewey, David -- Valenzuela, David -- Kutok, Jeffery L -- Schmidt-Supprian, Marc -- Rajewsky, Nikolaus -- Yancopoulos, George -- Rao, Anjana -- Rajewsky, Klaus -- AI064345/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):604-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CBR Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Cell Differentiation ; Cells, Cultured ; Cytokines/biosynthesis ; Germinal Center/*immunology ; Immunoglobulin G/analysis ; Lymphocyte Activation ; Lymphotoxin-alpha/biosynthesis ; Lymphotoxin-beta/biosynthesis ; Mice ; Mice, Knockout ; Mice, Transgenic ; MicroRNAs/genetics/*physiology ; Nitrophenols/immunology ; Peyer's Patches/immunology ; Phenylacetates ; Somatic Hypermutation, Immunoglobulin ; Spleen/immunology ; T-Lymphocytes/cytology/*immunology/metabolism ; Th1 Cells/cytology/immunology ; Th2 Cells/cytology/immunology ; Tumor Necrosis Factor-alpha/biosynthesis
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  • 21
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    SCFFbxl3 controls the oscillation of the circadian clock by directing the degradation of cryptochrome proteins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: One component of the circadian clock in mammals is the Clock-Bmal1 heterodimeric transcription factor. Among its downstream targets, two genes, Cry1 and Cry2, encode inhibitors of the Clock-Bmal1 complex that establish a negative-feedback loop. We found that both Cry1 and Cry2 proteins are ubiquitinated and degraded via the SCF(Fbxl3) ubiquitin ligase complex. This regulation by SCF(Fbxl3) is a prerequisite for the efficient and timely reactivation of Clock-Bmal1 and the consequent expression of Per1 and Per2, two regulators of the circadian clock that display tumor suppressor activity. Silencing of Fbxl3 produced no effect in Cry1-/-;Cry2-/- cells, which shows that Fbxl3 controls clock oscillations by mediating the degradation of CRY proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Busino, Luca -- Bassermann, Florian -- Maiolica, Alessio -- Lee, Choogon -- Nolan, Patrick M -- Godinho, Sofia I H -- Draetta, Giulio F -- Pagano, Michele -- MC_U142684172/Medical Research Council/United Kingdom -- MC_U142684173/Medical Research Council/United Kingdom -- MC_U142684175/Medical Research Council/United Kingdom -- R01-GM57587/GM/NIGMS NIH HHS/ -- R21-CA125173/CA/NCI NIH HHS/ -- R37-CA76584/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):900-4. Epub 2007 Apr 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, NYU Cancer Institute, New York University School of Medicine, 550 First Avenue, MSB 599, New York, NY 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463251" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; CLOCK Proteins ; Cell Cycle Proteins/genetics/metabolism ; Cells, Cultured ; *Circadian Rhythm/genetics ; Cryptochromes ; F-Box Proteins/genetics/*metabolism ; Flavoproteins/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; NIH 3T3 Cells ; Nuclear Proteins/genetics/metabolism ; Period Circadian Proteins ; Promoter Regions, Genetic ; RNA Interference ; SKP Cullin F-Box Protein Ligases/*metabolism ; Trans-Activators/metabolism ; Transcription Factors/genetics/metabolism ; Transfection ; Ubiquitin/metabolism
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  • 22
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    Materials science. Printing cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Calvert, Paul -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):208-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials and Textiles, University of Massachusetts Dartmouth, North Dartmouth, MA 02747 USA. pcalvert@umassd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932278" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria ; *Cell Communication ; Cell Survival ; Cells, Cultured ; Computer Peripherals ; *Cytological Techniques/instrumentation ; Humans ; *Microbiological Techniques/instrumentation ; Printing/*instrumentation ; *Tissue Engineering ; Yeasts
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  • 23
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    Molecular biology. Do Watson and Crick motor from X to Z? (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-01-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapienza, Carmen -- New York, N.Y. -- Science. 2007 Jan 5;315(5808):46-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fels Institute for Cancer Research and Department of Pathology, Temple University Medical School, 3307 North Broad Street, Philadelphia, PA 19140, USA. sapienza@temple.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17204629" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonemal Dyneins ; Body Patterning ; Cell Line ; Cells, Cultured ; Chromatids/*physiology ; *Chromosome Segregation ; DNA Replication ; Dyneins/*genetics/*physiology ; Ectoderm/*cytology ; Embryonic Stem Cells/*cytology ; Endoderm/*cytology ; Interphase ; Mice ; Mitosis ; Recombination, Genetic ; Spindle Apparatus/physiology/ultrastructure
    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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  • 24
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    Regulation of B versus T lymphoid lineage fate decision by the proto-oncogene LRF (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-15
    Description: Hematopoietic stem cells in the bone marrow give rise to lymphoid progenitors, which subsequently differentiate into B and T lymphocytes. Here we show that the proto-oncogene LRF plays an essential role in the B versus T lymphoid cell-fate decision. We demonstrate that LRF is key for instructing early lymphoid progenitors in mice to develop into B lineage cells by repressing T cell-instructive signals produced by the cell-fate signal protein, Notch. We propose a new model for lymphoid lineage commitment, in which LRF acts as a master regulator of the cell's determination of B versus T lineage.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2978506/" 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/PMC2978506/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Takahiro -- Merghoub, Taha -- Hobbs, Robin M -- Dong, Lin -- Maeda, Manami -- Zakrzewski, Johannes -- van den Brink, Marcel R M -- Zelent, Arthur -- Shigematsu, Hirokazu -- Akashi, Koichi -- Teruya-Feldstein, Julie -- Cattoretti, Giorgio -- Pandolfi, Pier Paolo -- CA-102142/CA/NCI NIH HHS/ -- R01 CA102142/CA/NCI NIH HHS/ -- R01 CA102142-06A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 May 11;316(5826):860-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17495164" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/physiology ; Bone Marrow Cells/cytology ; Cell Lineage ; Cells, Cultured ; DNA-Binding Proteins/*genetics/physiology ; Gene Deletion ; Hematopoietic Stem Cells/*cytology/physiology ; *Lymphopoiesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Biological ; *Proto-Oncogenes ; Receptors, Notch/*metabolism ; Signal Transduction ; T-Lymphocytes/*cytology/physiology ; Thymus Gland/cytology ; Transcription Factors/*genetics/physiology
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    A MicroRNA feedback circuit in midbrain dopamine neurons (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" 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/PMC2782470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongpil -- Inoue, Keiichi -- Ishii, Jennifer -- Vanti, William B -- Voronov, Sergey V -- Murchison, Elizabeth -- Hannon, Gregory -- Abeliovich, Asa -- R01 NS064433/NS/NINDS NIH HHS/ -- R01 NS064433-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Neurology, Center for Neurobiology and Behavior, and Taub Institute, Columbia University, College of Physicians and Surgeons 15-403, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Dopamine/*metabolism ; Embryonic Stem Cells ; *Feedback, Physiological ; Female ; Gene Expression Regulation ; Homeodomain Proteins/*metabolism ; Humans ; Locomotion ; Male ; Mesencephalon/cytology/*metabolism ; Mice ; MicroRNAs/*metabolism ; Middle Aged ; Models, Biological ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Rats ; Ribonuclease III/genetics/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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    Molecular biology. miRNAs in neurodegeneration (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hebert, Sebastien S -- De Strooper, Bart -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1179-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Human Genetics, VIB and KULeuven, Herestraat 49, Leuven, Belgium. bart.destrooper@med.kuleuven.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761871" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Animals ; Brain/physiology/*physiopathology ; Cell Death ; Cell Differentiation ; Cells, Cultured ; Dopamine/*metabolism ; Feedback, Physiological ; Humans ; Mice ; MicroRNAs/genetics/*metabolism ; Neurodegenerative Diseases/genetics/*physiopathology ; Neurons/cytology/metabolism/*physiology ; Parkinson Disease/genetics/*physiopathology ; RNA, Messenger/genetics/metabolism ; Ribonuclease III/metabolism ; Transcription Factors/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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    Negative regulation of toll-like receptor signaling by NF-kappaB p50 ubiquitination blockade (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-04
    Description: Toll-like receptors (TLRs) trigger the production of inflammatory cytokines and shape adaptive and innate immunity to pathogens. We report the identification of B cell leukemia (Bcl)-3 as an essential negative regulator of TLR signaling. By blocking ubiquitination of p50, a member of the nuclear factor (NF)-kappaB family, Bcl-3 stabilizes a p50 complex that inhibits gene transcription. As a consequence, Bcl-3-deficient mice and cells were found to be hypersensitive to TLR activation and unable to control responses to lipopolysaccharides. Thus, p50 ubiquitination blockade by Bcl-3 limits the strength of TLR responses and maintains innate immune homeostasis. These findings indicate that the p50 ubiquitination pathway can be selectively targeted to control deleterious inflammatory diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carmody, Ruaidhri J -- Ruan, Qingguo -- Palmer, Scott -- Hilliard, Brendan -- Chen, Youhai H -- AI069289/AI/NIAID NIH HHS/ -- AI50059/AI/NIAID NIH HHS/ -- DK070691/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 3;317(5838):675-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory 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/17673665" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; DNA/metabolism ; Female ; Half-Life ; Immune Tolerance ; Immunity, Innate ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages, Peritoneal/*immunology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit/*metabolism ; Promoter Regions, Genetic ; Proto-Oncogene Proteins/genetics/*metabolism ; *Signal Transduction ; Toll-Like Receptors/*metabolism ; Transcription Factor RelA/metabolism ; Transcription Factors/genetics/*metabolism ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/genetics/metabolism ; Ubiquitin/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Telomeric repeat containing RNA and RNA surveillance factors at mammalian chromosome ends (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-06
    Description: Telomeres, the DNA-protein complexes located at the end of linear eukaryotic chromosomes, are essential for chromosome stability. Until now, telomeres have been considered to be transcriptionally silent. We demonstrate that mammalian telomeres are transcribed into telomeric repeat-containing RNA (TERRA). TERRA molecules are heterogeneous in length, are transcribed from several subtelomeric loci toward chromosome ends, and localize to telomeres. We also show that suppressors with morphogenetic defects in genitalia (SMG) proteins, which are effectors of nonsense-mediated messenger RNA decay, are enriched at telomeres in vivo, negatively regulate TERRA association with chromatin, and protect chromosome ends from telomere loss. Thus, telomeres are actively transcribed into TERRA, and SMG factors represent a molecular link between TERRA regulation and the maintenance of telomere integrity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Azzalin, Claus M -- Reichenbach, Patrick -- Khoriauli, Lela -- Giulotto, Elena -- Lingner, Joachim -- New York, N.Y. -- Science. 2007 Nov 2;318(5851):798-801. Epub 2007 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research (ISREC), CH-1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17916692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Cells, Cultured ; Chromosomes, Human ; Chromosomes, Mammalian ; HeLa Cells ; Humans ; In Situ Hybridization, Fluorescence ; Mice ; Molecular Sequence Data ; Proteins/metabolism ; RNA/*genetics ; Repetitive Sequences, Nucleic Acid ; Telomerase/physiology ; Telomere/*genetics ; Transcription, Genetic ; Tumor Cells, Cultured
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    Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-01
    Description: Long-term potentiation (LTP) at glutamatergic synapses is considered to underlie learning and memory and is associated with the enlargement of dendritic spines. Because the consolidation of memory and LTP require protein synthesis, it is important to clarify how protein synthesis affects spine enlargement. In rat brain slices, the repetitive pairing of postsynaptic spikes and two-photon uncaging of glutamate at single spines (a spike-timing protocol) produced both immediate and gradual phases of spine enlargement in CA1 pyramidal neurons. The gradual enlargement was strongly dependent on protein synthesis and brain-derived neurotrophic factor (BDNF) action, often associated with spine twitching, and was induced specifically at the spines that were immediately enlarged by the synaptic stimulation. Thus, this spike-timing protocol is an efficient trigger for BDNF secretion and induces protein synthesis-dependent long-term enlargement at the level of single spines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4218863/" 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/PMC4218863/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, Jun-Ichi -- Horiike, Yoshihiro -- Matsuzaki, Masanori -- Miyazaki, Takashi -- Ellis-Davies, Graham C R -- Kasai, Haruo -- R01 GM053395/GM/NIGMS NIH HHS/ -- R01 GM053395-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1683-7. doi: 10.1126/science.1152864. Epub 2008 Feb 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Structural Physiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309046" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain-Derived Neurotrophic Factor/*metabolism/pharmacology ; Cells, Cultured ; Dendritic Spines/*physiology/*ultrastructure ; Glutamic Acid/metabolism ; *Neuronal Plasticity ; Patch-Clamp Techniques ; *Protein Biosynthesis ; Protein Synthesis Inhibitors/pharmacology ; Pyramidal Cells/physiology/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Receptor, trkB/metabolism ; Synapses/*physiology
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    Design logic of a cannabinoid receptor signaling network that triggers neurite outgrowth (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: Cannabinoid receptor 1 (CB1R) regulates neuronal differentiation. To understand the logic underlying decision-making in the signaling network controlling CB1R-induced neurite outgrowth, we profiled the activation of several hundred transcription factors after cell stimulation. We assembled an in silico signaling network by connecting CB1R to 23 activated transcription factors. Statistical analyses of this network predicted a role for the breast cancer 1 protein BRCA1 in neuronal differentiation and a new pathway from CB1R through phosphoinositol 3-kinase to the transcription factor paired box 6 (PAX6). Both predictions were experimentally confirmed. Results of transcription factor activation experiments that used pharmacological inhibitors of kinases revealed a network organization of partial OR gates regulating kinases stacked above AND gates that control transcription factors, which together allow for distributed decision-making in CB1R-induced neurite outgrowth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776723/" 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/PMC2776723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bromberg, Kenneth D -- Ma'ayan, Avi -- Neves, Susana R -- Iyengar, Ravi -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- GM072853/GM/NIGMS NIH HHS/ -- GM54508/GM/NIGMS NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A2/GM/NIGMS NIH HHS/ -- P50 GM071558-01A20007/GM/NIGMS NIH HHS/ -- P50 GM071558-02/GM/NIGMS NIH HHS/ -- P50 GM071558-020007/GM/NIGMS NIH HHS/ -- P50 GM071558-030007/GM/NIGMS NIH HHS/ -- P50-071558/PHS HHS/ -- R01 GM054508/GM/NIGMS NIH HHS/ -- R01 GM054508-21/GM/NIGMS NIH HHS/ -- R01 GM072853/GM/NIGMS NIH HHS/ -- R01 GM072853-04/GM/NIGMS NIH HHS/ -- T32 CA88796/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):903-9. doi: 10.1126/science.1152662.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Cells, Cultured ; Computational Biology ; Computer Simulation ; Eye Proteins/metabolism ; Hippocampus/cytology ; Homeodomain Proteins/metabolism ; Metabolic Networks and Pathways ; Mice ; Neurites/*physiology ; Neurons/*cytology/metabolism ; Paired Box Transcription Factors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Interaction Mapping ; Rats ; Receptor, Cannabinoid, CB1/*metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Transcription Factors/antagonists & inhibitors/*metabolism
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    Intersection of the RNA interference and X-inactivation pathways (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-07
    Description: In mammals, dosage compensation is achieved by X-chromosome inactivation (XCI) in the female. The noncoding Xist gene initiates silencing of the X chromosome, whereas its antisense partner Tsix blocks silencing. The complementarity of Xist and Tsix RNAs has long suggested a role for RNA interference (RNAi). Here, we report that murine Xist and Tsix form duplexes in vivo. During XCI, the duplexes are processed to small RNAs (sRNAs), most likely on the active X (Xa) in a Dicer-dependent manner. Deleting Dicer compromises sRNA production and derepresses Xist. Furthermore, without Dicer, Xist RNA cannot accumulate and histone 3 lysine 27 trimethylation is blocked on the inactive X (Xi). The defects are partially rescued by truncating Tsix. Thus, XCI and RNAi intersect, down-regulating Xist on Xa and spreading silencing on Xi.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584363/" 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/PMC2584363/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Yuya -- Sun, Bryan K -- Lee, Jeannie T -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 6;320(5881):1336-41. doi: 10.1126/science.1157676.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Massachusetts General Hospital and Howard Hughes Medical Institute, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18535243" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cells, Cultured ; DEAD-box RNA Helicases/genetics/metabolism ; Embryonic Stem Cells ; Endoribonucleases/genetics/metabolism ; Female ; Histones/metabolism ; Male ; Methylation ; Mice ; *RNA Interference ; RNA, Double-Stranded/metabolism ; RNA, Long Noncoding ; RNA, Small Nuclear/metabolism ; RNA, Untranslated/genetics/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonuclease III ; X Chromosome/*genetics/metabolism ; *X Chromosome Inactivation
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    Hepatic glucose sensing via the CREB coactivator CRTC2 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-08
    Description: Chronic hyperglycemia contributes to the development of diabetes-associated complications. Increases in the concentration of circulating glucose activate the hexosamine biosynthetic pathway (HBP) and promote the O-glycosylation of proteins by O-glycosyl transferase (OGT). We show that OGT triggered hepatic gluconeogenesis through the O-glycosylation of the transducer of regulated cyclic adenosine monophosphate response element-binding protein (CREB) 2 (TORC2 or CRTC2). CRTC2 was O-glycosylated at sites that normally sequester CRTC2 in the cytoplasm through a phosphorylation-dependent mechanism. Decreasing amounts of O-glycosylated CRTC2 by expression of the deglycosylating enzyme O-GlcNAcase blocked effects of glucose on gluconeogenesis, demonstrating the importance of the HBP in the development of glucose intolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dentin, Renaud -- Hedrick, Susan -- Xie, Jianxin -- Yates, John 3rd -- Montminy, Marc -- R01 GM037828/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 7;319(5868):1402-5. doi: 10.1126/science.1151363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323454" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Blood Glucose/metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cytoplasm/metabolism ; Diabetes Mellitus/metabolism ; *Gluconeogenesis ; Glucose/*metabolism ; Glycosylation ; Glycosyltransferases/metabolism ; Hepatocytes/metabolism ; Humans ; Insulin/metabolism ; Liver/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; RNA Interference ; Signal Transduction ; Trans-Activators/genetics/*metabolism ; Transcription Factors ; beta-N-Acetylhexosaminidases/metabolism
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    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-08
    Description: We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its own receptor TrkA in mouse and rat neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain-derived neurotrophic factor and neurotrophin-4, which, through the receptor p75, can kill neighboring neurons with low retrograde NGF-TrkA signaling whereas neurons with high NGF-TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" 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/PMC3612357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deppmann, Christopher D -- Mihalas, Stefan -- Sharma, Nikhil -- Lonze, Bonnie E -- Niebur, Ernst -- Ginty, David D -- EY016281/EY/NEI NIH HHS/ -- F32 NS053187/NS/NINDS NIH HHS/ -- NS053187/NS/NINDS NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):369-73. doi: 10.1126/science.1152677. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon Snyder Department of Neuroscience, 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/18323418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Survival ; Cells, Cultured ; Computer Simulation ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Mathematics ; Mice ; *Models, Neurological ; Nerve Growth Factor/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/cytology/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Receptor, trkA/genetics/*metabolism ; Receptors, Nerve Growth Factor/genetics/metabolism ; Signal Transduction ; Superior Cervical Ganglion/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Ankyrin repeat proteins comprise a diverse family of bacterial type IV effectors (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-21
    Description: Specialized secretion systems are used by many bacteria to deliver effector proteins into host cells that can either mimic or disrupt the function of eukaryotic factors. We found that the intracellular pathogens Legionella pneumophila and Coxiella burnetii use a type IV secretion system to deliver into eukaryotic cells a large number of different bacterial proteins containing ankyrin repeat homology domains called Anks. The L. pneumophila AnkX protein prevented microtubule-dependent vesicular transport to interfere with fusion of the L. pneumophila-containing vacuole with late endosomes after infection of macrophages, which demonstrates that Ank proteins have effector functions important for bacterial infection of eukaryotic host cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2514061/" 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/PMC2514061/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Xiaoxiao -- Luhrmann, Anja -- Satoh, Ayano -- Laskowski-Arce, Michelle A -- Roy, Craig R -- AG030101/AG/NIA NIH HHS/ -- AI041699/AI/NIAID NIH HHS/ -- AI064559/AI/NIAID NIH HHS/ -- GM060919/GM/NIGMS NIH HHS/ -- R01 AI041699/AI/NIAID NIH HHS/ -- R01 AI041699-12/AI/NIAID NIH HHS/ -- R01 AI064559/AI/NIAID NIH HHS/ -- R01 AI064559-03/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2008 Jun 20;320(5883):1651-4. doi: 10.1126/science.1158160.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18566289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ankyrin Repeat ; Bacterial Proteins/*chemistry/genetics/*metabolism ; CHO Cells ; Cells, Cultured ; Coxiella burnetii/*metabolism/pathogenicity ; Cricetinae ; Cricetulus ; Cyclic AMP/metabolism ; Cytoplasmic Vesicles/metabolism/ultrastructure ; Cytosol/metabolism ; Golgi Apparatus/metabolism ; Humans ; Intracellular Membranes/metabolism ; Legionella pneumophila/*metabolism/pathogenicity ; Microtubules/metabolism ; Protein Transport ; Recombinant Fusion Proteins/metabolism ; Vacuoles/microbiology
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    Traction dynamics of filopodia on compliant substrates (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-17
    Description: Cells sense the environment's mechanical stiffness to control their own shape, migration, and fate. To better understand stiffness sensing, we constructed a stochastic model of the "motor-clutch" force transmission system, where molecular clutches link F-actin to the substrate and mechanically resist myosin-driven F-actin retrograde flow. The model predicts two distinct regimes: (i) "frictional slippage," with fast retrograde flow and low traction forces on stiff substrates and (ii) oscillatory "load-and-fail" dynamics, with slower retrograde flow and higher traction forces on soft substrates. We experimentally confirmed these model predictions in embryonic chick forebrain neurons by measuring the nanoscale dynamics of single-growth-cone filopodia. Furthermore, we experimentally observed a model-predicted switch in F-actin dynamics around an elastic modulus of 1 kilopascal. Thus, a motor-clutch system inherently senses and responds to the mechanical stiffness of the local environment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Clarence E -- Odde, David J -- R01-GM-76177/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 12;322(5908):1687-91. doi: 10.1126/science.1163595.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19074349" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*physiology ; Actins/*physiology ; Animals ; Biomechanical Phenomena ; Cell Adhesion ; Cells, Cultured ; Chick Embryo ; Compliance ; Computer Simulation ; Elastic Modulus ; Elasticity ; Growth Cones/*physiology/ultrastructure ; Models, Biological ; Myosin Type II/physiology ; Neurons/physiology ; Pseudopodia/*physiology ; Surface Tension
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    Neuroscience. Refreshing connections (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silver, R Angus -- Kanichay, Roby T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):183-4. doi: 10.1126/science.1157589.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK. a.silver@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Diffusion ; *Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; *Neuronal Plasticity ; Rats ; Receptors, AMPA/*metabolism ; Synapses/*physiology ; *Synaptic Transmission ; Synaptic Vesicles/metabolism
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    Adenovirus small e1a alters global patterns of histone modification (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-23
    Description: Adenovirus small early region 1a (e1a) protein drives cells into S phase by binding RB family proteins and the closely related histone acetyl transferases p300 and CBP. The interaction with RB proteins displaces them from DNA-bound E2F transcription factors, reversing their repression of cell cycle genes. However, it has been unclear how the e1a interaction with p300 and CBP promotes passage through the cell cycle. We show that this interaction causes a threefold reduction in total cellular histone H3 lysine 18 acetylation (H3K18ac). CBP and p300 are required for acetylation at this site because their knockdown causes specific hypoacetylation at H3K18. SV40 T antigen also induces H3K18 hypoacetylation. Because global hypoacetylation at this site is observed in prostate carcinomas with poor prognosis, this suggests that processes resulting in global H3K18 hypoacetylation may be linked to oncogenic transformation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2756290/" 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/PMC2756290/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horwitz, Gregory A -- Zhang, Kangling -- McBrian, Matthew A -- Grunstein, Michael -- Kurdistani, Siavash K -- Berk, Arnold J -- CA25235/CA/NCI NIH HHS/ -- R37 CA025235/CA/NCI NIH HHS/ -- R37 CA025235-30/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Aug 22;321(5892):1084-5. doi: 10.1126/science.1155544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719283" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/*metabolism ; Adenoviruses, Human/*metabolism ; Antigens, Polyomavirus Transforming/metabolism ; CREB-Binding Protein/metabolism ; *Cell Cycle ; Cell Line ; Cell Transformation, Viral ; Cells, Cultured ; HeLa Cells ; Histones/*metabolism ; Humans ; Lysine/metabolism ; Mutation ; p300-CBP Transcription Factors/metabolism
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    Absence of the SRC-2 coactivator results in a glycogenopathy resembling Von Gierke's disease (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-29
    Description: Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2668604/" 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/PMC2668604/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chopra, Atul R -- Louet, Jean-Francois -- Saha, Pradip -- An, Jie -- Demayo, Franco -- Xu, Jianming -- York, Brian -- Karpen, Saul -- Finegold, Milton -- Moore, David -- Chan, Lawrence -- Newgard, Christopher B -- O'Malley, Bert W -- DK58242/DK/NIDDK NIH HHS/ -- HL51586/HL/NHLBI NIH HHS/ -- P01 DK059820/DK/NIDDK NIH HHS/ -- P01 DK059820-08/DK/NIDDK NIH HHS/ -- P01 DK58398/DK/NIDDK NIH HHS/ -- P01 DK59820/DK/NIDDK NIH HHS/ -- R01 DK056239/DK/NIDDK NIH HHS/ -- R01 DK056239-08/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-07/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 28;322(5906):1395-9. doi: 10.1126/science.1164847.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19039140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Fasting ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Enzymologic ; Glucose/*metabolism ; Glucose-6-Phosphatase/*genetics/metabolism ; Glycogen Storage Disease Type I/*genetics/metabolism ; Hepatocytes/metabolism ; Kidney/metabolism ; Liver/*metabolism ; Liver Glycogen/metabolism ; Male ; Mice ; Mice, Knockout ; Nuclear Receptor Coactivator 2/genetics/*metabolism ; RNA Interference ; Receptors, Retinoic Acid/metabolism ; Response Elements ; Transcription, Genetic ; Triglycerides/metabolism
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    Leiomodin is an actin filament nucleator in muscle cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: Initiation of actin polymerization in cells requires nucleation factors. Here we describe an actin-binding protein, leiomodin, that acted as a strong filament nucleator in muscle cells. Leiomodin shared two actin-binding sites with the filament pointed end-capping protein tropomodulin: a flexible N-terminal region and a leucine-rich repeat domain. Leiomodin also contained a C-terminal extension of 150 residues. The smallest fragment with strong nucleation activity included the leucine-rich repeat and C-terminal extension. The N-terminal region enhanced the nucleation activity threefold and recruited tropomyosin, which weakly stimulated nucleation and mediated localization of leiomodin to the middle of muscle sarcomeres. Knocking down leiomodin severely compromised sarcomere assembly in cultured muscle cells, which suggests a role for leiomodin in the nucleation of tropomyosin-decorated filaments in muscles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845909/" 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/PMC2845909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chereau, David -- Boczkowska, Malgorzata -- Skwarek-Maruszewska, Aneta -- Fujiwara, Ikuko -- Hayes, David B -- Rebowski, Grzegorz -- Lappalainen, Pekka -- Pollard, Thomas D -- Dominguez, Roberto -- GM026338/GM/NIGMS NIH HHS/ -- GM073791/GM/NIGMS NIH HHS/ -- HL086655/HL/NHLBI NIH HHS/ -- P01 HL086655/HL/NHLBI NIH HHS/ -- P01 HL086655-01A10004/HL/NHLBI NIH HHS/ -- R01 GM073791/GM/NIGMS NIH HHS/ -- R01 GM073791-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):239-43. doi: 10.1126/science.1155313.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boston Biomedical Research Institute, Watertown, MA 02472, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403713" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actins/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Cells, Cultured ; Cytoskeletal Proteins/chemistry/*metabolism ; Humans ; Microfilament Proteins/chemistry/*metabolism ; Molecular Sequence Data ; Muscle Proteins/chemistry/*metabolism ; Myocytes, Cardiac/*metabolism ; Protein Structure, Tertiary ; RNA Interference ; Rabbits ; Rats ; Sarcomeres/*metabolism ; Tropomodulin/chemistry ; Tropomyosin/chemistry/metabolism
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    DNA oxidation as triggered by H3K9me2 demethylation drives estrogen-induced gene expression (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-01-12
    Description: Modifications at the N-terminal tails of nucleosomal histones are required for efficient transcription in vivo. We analyzed how H3 histone methylation and demethylation control expression of estrogen-responsive genes and show that a DNA-bound estrogen receptor directs transcription by participating in bending chromatin to contact the RNA polymerase II recruited to the promoter. This process is driven by receptor-targeted demethylation of H3 lysine 9 at both enhancer and promoter sites and is achieved by activation of resident LSD1 demethylase. Localized demethylation produces hydrogen peroxide, which modifies the surrounding DNA and recruits 8-oxoguanine-DNA glycosylase 1 and topoisomeraseIIbeta, triggering chromatin and DNA conformational changes that are essential for estrogen-induced transcription. Our data show a strategy that uses controlled DNA damage and repair to guide productive transcription.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perillo, Bruno -- Ombra, Maria Neve -- Bertoni, Alessandra -- Cuozzo, Concetta -- Sacchetti, Silvana -- Sasso, Annarita -- Chiariotti, Lorenzo -- Malorni, Antonio -- Abbondanza, Ciro -- Avvedimento, Enrico V -- New York, N.Y. -- Science. 2008 Jan 11;319(5860):202-6. doi: 10.1126/science.1147674.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto di Scienze dell'Alimentazione, Consiglio Nazionale delle Ricerche (C.N.R.), 83100 Avellino, Italy. perillo@unina.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18187655" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cells, Cultured ; Chromatin/metabolism ; DNA/*metabolism ; DNA Damage ; DNA Glycosylases/metabolism ; DNA Repair ; DNA Topoisomerases, Type II/metabolism ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; Estradiol/*metabolism ; Estrogen Receptor alpha/metabolism ; *Gene Expression Regulation ; Genes, bcl-2 ; Guanine/analogs & derivatives/metabolism ; Histone Demethylases ; Histones/*metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Lysine/metabolism ; Methylation ; Nucleic Acid Conformation ; Oxidation-Reduction ; Oxidoreductases, N-Demethylating/metabolism ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; *Transcription, Genetic
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    Maternal alloantigens promote the development of tolerogenic fetal regulatory T cells in utero (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-06
    Description: As the immune system develops, T cells are selected or regulated to become tolerant of self antigens and reactive against foreign antigens. In mice, the induction of such tolerance is thought to be attributable to the deletion of self-reactive cells. Here, we show that the human fetal immune system takes advantage of an additional mechanism: the generation of regulatory T cells (Tregs) that suppress fetal immune responses. We find that substantial numbers of maternal cells cross the placenta to reside in fetal lymph nodes, inducing the development of CD4+CD25highFoxP3+ Tregs that suppress fetal antimaternal immunity and persist at least until early adulthood. These findings reveal a form of antigen-specific tolerance in humans, induced in utero and probably active in regulating immune responses after birth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648820/" 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/PMC2648820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mold, Jeff E -- Michaelsson, Jakob -- Burt, Trevor D -- Muench, Marcus O -- Beckerman, Karen P -- Busch, Michael P -- Lee, Tzong-Hae -- Nixon, Douglas F -- McCune, Joseph M -- AI40312/AI/NIAID NIH HHS/ -- AI68498/AI/NIAID NIH HHS/ -- DP1 OD000329/OD/NIH HHS/ -- DP1 OD000329-01/OD/NIH HHS/ -- DP1 OD000329-02/OD/NIH HHS/ -- DP1 OD000329-03/OD/NIH HHS/ -- DP1 OD000329-04/OD/NIH HHS/ -- HD00850/HD/NICHD NIH HHS/ -- HL083388/HL/NHLBI NIH HHS/ -- OD000329/OD/NIH HHS/ -- R01 HL083388/HL/NHLBI NIH HHS/ -- R01 HL083388-02/HL/NHLBI NIH HHS/ -- R37 AI040312/AI/NIAID NIH HHS/ -- R37 AI040312-09/AI/NIAID NIH HHS/ -- R37 AI040312-10/AI/NIAID NIH HHS/ -- R37 AI040312-11/AI/NIAID NIH HHS/ -- R37 AI040312-12/AI/NIAID NIH HHS/ -- R37 AI040312-13/AI/NIAID NIH HHS/ -- RR024131/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1562-5. doi: 10.1126/science.1164511.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Medicine, Department of Medicine, University of California at San Francisco (UCSF), San Francisco, CA 94110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056990" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Antigen-Presenting Cells/immunology ; Cells, Cultured ; Child ; Chimerism ; Female ; Fetus/*immunology ; Forkhead Transcription Factors/metabolism ; Gene Expression Profiling ; Humans ; *Immune Tolerance ; Isoantigens/*immunology ; Lymph Nodes/cytology/*immunology ; Lymphocyte Activation ; *Maternal-Fetal Exchange ; Pregnancy ; Self Tolerance ; T-Lymphocytes, Regulatory/*immunology ; Thymus Gland/immunology ; Transforming Growth Factors/genetics/metabolism ; Tumor Necrosis Factors/genetics/metabolism
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    Segregation of axial motor and sensory pathways via heterotypic trans-axonal signaling (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: Execution of motor behaviors relies on circuitries effectively integrating immediate sensory feedback to efferent pathways controlling muscle activity. It remains unclear how, during neuromuscular circuit assembly, sensory and motor projections become incorporated into tightly coordinated, yet functionally separate pathways. We report that, within axial nerves, establishment of discrete afferent and efferent pathways depends on coordinate signaling between coextending sensory and motor projections. These heterotypic axon-axon interactions require motor axonal EphA3/EphA4 receptor tyrosine kinases activated by cognate sensory axonal ephrin-A ligands. Genetic elimination of trans-axonal ephrin-A --〉 EphA signaling in mice triggers drastic motor-sensory miswiring, culminating in functional efferents within proximal afferent pathways. Effective assembly of a key circuit underlying motor behaviors thus critically depends on trans-axonal signaling interactions resolving motor and sensory projections into discrete pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158657/" 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/PMC3158657/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gallarda, Benjamin W -- Bonanomi, Dario -- Muller, Daniel -- Brown, Arthur -- Alaynick, William A -- Andrews, Shane E -- Lemke, Greg -- Pfaff, Samuel L -- Marquardt, Till -- NS031249-14A1/NS/NINDS NIH HHS/ -- NS054172-01A2/NS/NINDS NIH HHS/ -- R01 NS054172/NS/NINDS NIH HHS/ -- R01 NS054172-01A2/NS/NINDS NIH HHS/ -- R01 NS054172-02/NS/NINDS NIH HHS/ -- R01 NS054172-03/NS/NINDS NIH HHS/ -- R01 NS054172-04/NS/NINDS NIH HHS/ -- R01 NS054172-05/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):233-6. doi: 10.1126/science.1153758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403711" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/physiology ; Animals ; Axons/*physiology ; Cells, Cultured ; Coculture Techniques ; Efferent Pathways/physiology ; Electrophysiology ; Ephrins/*metabolism ; Ganglia, Spinal/cytology/physiology ; Growth Cones/physiology ; Ligands ; Mice ; Mice, Transgenic ; Motor Activity ; Motor Neurons/*physiology ; Muscle, Skeletal/innervation ; Mutation ; Neurons, Afferent/*physiology ; Peripheral Nerves/cytology/physiology ; Receptor, EphA3/genetics/*metabolism ; Receptor, EphA4/genetics/*metabolism ; Signal Transduction
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    Electric fields due to synaptic currents sharpen excitatory transmission (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-29
    Description: The synaptic response waveform, which determines signal integration properties in the brain, depends on the spatiotemporal profile of neurotransmitter in the synaptic cleft. Here, we show that electrophoretic interactions between AMPA receptor-mediated excitatory currents and negatively charged glutamate molecules accelerate the clearance of glutamate from the synaptic cleft, speeding up synaptic responses. This phenomenon is reversed upon depolarization and diminished when intracleft electric fields are weakened through a decrease in the AMPA receptor density. In contrast, the kinetics of receptor-mediated currents evoked by direct application of glutamate are voltage-independent, as are synaptic currents mediated by the electrically neutral neurotransmitter GABA. Voltage-dependent temporal tuning of excitatory synaptic responses may thus contribute to signal integration in neural circuits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685065/" 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/PMC2685065/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sylantyev, Sergiy -- Savtchenko, Leonid P -- Niu, Yin-Ping -- Ivanov, Anton I -- Jensen, Thomas P -- Kullmann, Dimitri M -- Xiao, Min-Yi -- Rusakov, Dmitri A -- 071179/Wellcome Trust/United Kingdom -- G0400627/Medical Research Council/United Kingdom -- G0400627(71256)/Medical Research Council/United Kingdom -- G0400627(76527)/Medical Research Council/United Kingdom -- G0600368/Medical Research Council/United Kingdom -- G0600368(77987)/Medical Research Council/United Kingdom -- G116/147/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1845-9. doi: 10.1126/science.1154330.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/physiology ; Diffusion ; Dipeptides/pharmacology ; *Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; Magnesium/pharmacology ; Male ; Monte Carlo Method ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Quinoxalines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/antagonists & inhibitors/*metabolism ; Receptors, GABA/metabolism ; Synapses/*physiology ; gamma-Aminobutyric Acid/metabolism
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    Cell biology. Arrestin' movement in cilia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-06-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohatgi, Rajat -- Scott, Matthew P -- 1K99CA129174/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jun 27;320(5884):1726-7. doi: 10.1126/science.1160448.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305-5439, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18583599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/genetics/*metabolism ; Cells, Cultured ; Cilia/*metabolism ; Hedgehog Proteins/metabolism ; Kinesin/*metabolism ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Molecular Motor Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Protein Transport ; RNA Interference ; Receptors, G-Protein-Coupled/*metabolism ; Signal Transduction
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  • 45
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    Motile cilia of human airway epithelia are chemosensory (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-25
    Description: Cilia are microscopic projections that extend from eukaryotic cells. There are two general types of cilia; primary cilia serve as sensory organelles, whereas motile cilia exert mechanical force. The motile cilia emerging from human airway epithelial cells propel harmful inhaled material out of the lung. We found that these cells express sensory bitter taste receptors, which localized on motile cilia. Bitter compounds increased the intracellular calcium ion concentration and stimulated ciliary beat frequency. Thus, airway epithelia contain a cell-autonomous system in which motile cilia both sense noxious substances entering airways and initiate a defensive mechanical mechanism to eliminate the offending compound. Hence, like primary cilia, classical motile cilia also contain sensors to detect the external environment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894709/" 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/PMC2894709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Alok S -- Ben-Shahar, Yehuda -- Moninger, Thomas O -- Kline, Joel N -- Welsh, Michael J -- DK54759/DK/NIDDK NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- P01 HL051670/HL/NHLBI NIH HHS/ -- P01 HL051670-15/HL/NHLBI NIH HHS/ -- P30 DK054759/DK/NIDDK NIH HHS/ -- P30 DK054759-109004/DK/NIDDK NIH HHS/ -- P30 DK054759-13/DK/NIDDK NIH HHS/ -- R01 DK051315/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1131-4. doi: 10.1126/science.1173869. Epub 2009 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628819" target="_blank"〉PubMed〈/a〉
    Keywords: Bronchi/cytology ; Calcium/metabolism ; Cells, Cultured ; Cilia/metabolism/*physiology ; Epithelial Cells/*metabolism ; Humans ; Monoterpenes/metabolism/pharmacology ; Movement ; Noxae ; Phospholipase C beta/metabolism ; Quaternary Ammonium Compounds/metabolism/pharmacology ; Receptors, G-Protein-Coupled/*metabolism ; Respiratory Mucosa/cytology/*metabolism ; *Signal Transduction ; *Taste ; Trachea/cytology ; Transducin/metabolism
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    Function of mitochondrial Stat3 in cellular respiration (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-10
    Description: Cytokines such as interleukin-6 induce tyrosine and serine phosphorylation of Stat3 that results in activation of Stat3-responsive genes. We provide evidence that Stat3 is present in the mitochondria of cultured cells and primary tissues, including the liver and heart. In Stat3(-/-) cells, the activities of complexes I and II of the electron transport chain (ETC) were significantly decreased. We identified Stat3 mutants that selectively restored the protein's function as a transcription factor or its functions within the ETC. In mice that do not express Stat3 in the heart, there were also selective defects in the activities of complexes I and II of the ETC. These data indicate that Stat3 is required for optimal function of the ETC, which may allow it to orchestrate responses to cellular homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2758306/" 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/PMC2758306/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wegrzyn, Joanna -- Potla, Ramesh -- Chwae, Yong-Joon -- Sepuri, Naresh B V -- Zhang, Qifang -- Koeck, Thomas -- Derecka, Marta -- Szczepanek, Karol -- Szelag, Magdalena -- Gornicka, Agnieszka -- Moh, Akira -- Moghaddas, Shadi -- Chen, Qun -- Bobbili, Santha -- Cichy, Joanna -- Dulak, Jozef -- Baker, Darren P -- Wolfman, Alan -- Stuehr, Dennis -- Hassan, Medhat O -- Fu, Xin-Yuan -- Avadhani, Narayan -- Drake, Jennifer I -- Fawcett, Paul -- Lesnefsky, Edward J -- Larner, Andrew C -- CA098924/CA/NCI NIH HHS/ -- P01AG15885/AG/NIA NIH HHS/ -- R01 AI059710/AI/NIAID NIH HHS/ -- R01 AI059710-03/AI/NIAID NIH HHS/ -- R01 AI059710-04/AI/NIAID NIH HHS/ -- R01 CA098924/CA/NCI NIH HHS/ -- R01 CA098924-03/CA/NCI NIH HHS/ -- R01 CA098924-04/CA/NCI NIH HHS/ -- R01 CA098924-05/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):793-7. doi: 10.1126/science.1164551. Epub 2009 Jan 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology and Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19131594" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Respiration ; Cells, Cultured ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Homeostasis ; Mice ; Mitochondria/*metabolism ; Mitochondria, Heart/metabolism ; Mitochondria, Liver/metabolism ; Mitochondrial Membranes/metabolism ; NADH, NADPH Oxidoreductases/metabolism ; Oxidative Phosphorylation ; Phosphorylation ; Precursor Cells, B-Lymphoid/metabolism ; STAT3 Transcription Factor/chemistry/*metabolism ; Serine/metabolism ; Signal Transduction
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    Biochemistry. A glucose-to-gene link (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2788238/" 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/PMC2788238/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rathmell, Jeffrey C -- Newgard, Christopher B -- R01 CA123350/CA/NCI NIH HHS/ -- R01 CA123350-03/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 May 22;324(5930):1021-2. doi: 10.1126/science.1174665.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Cancer Biology, Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19460991" target="_blank"〉PubMed〈/a〉
    Keywords: ATP Citrate (pro-S)-Lyase/genetics/*metabolism ; Acetate-CoA Ligase/metabolism ; Acetyl Coenzyme A/*metabolism ; Acetylation ; Animals ; Cell Nucleus/enzymology ; Cells, Cultured ; Chromatin/*metabolism ; Citric Acid/metabolism ; Gene Expression Regulation ; Glucose/*metabolism ; Glycolysis ; Histones/*metabolism ; Humans ; *Transcription, Genetic
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    Small-molecule activators of a proenzyme (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-07
    Description: Virtually all of the 560 human proteases are stored as inactive proenyzmes and are strictly regulated. We report the identification and characterization of the first small molecules that directly activate proenzymes, the apoptotic procaspases-3 and -6. It is surprising that these compounds induce autoproteolytic activation by stabilizing a conformation that is both more active and more susceptible to intermolecular proteolysis. These procaspase activators bypass the normal upstream proapoptotic signaling cascades and induce rapid apoptosis in a variety of cell lines. Systematic biochemical and biophysical analyses identified a cluster of mutations in procaspase-3 that resist small-molecule activation both in vitro and in cells. Compounds that induce gain of function are rare, and the activators reported here will enable direct control of the executioner caspases in apoptosis and in cellular differentiation. More generally, these studies presage the discovery of other proenzyme activators to explore fundamental processes of proenzyme activation and their fate-determining roles in biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886848/" 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/PMC2886848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolan, Dennis W -- Zorn, Julie A -- Gray, Daniel C -- Wells, James A -- F32 CA119641/CA/NCI NIH HHS/ -- F32 CA119641-03/CA/NCI NIH HHS/ -- R01 CA136779/CA/NCI NIH HHS/ -- R21 N5057022/PHS HHS/ -- New York, N.Y. -- Science. 2009 Nov 6;326(5954):853-8. doi: 10.1126/science.1177585.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Chemistry, University of California, San Francisco, Byers Hall, 1700 4th Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19892984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Benzopyrans/chemistry/*metabolism/pharmacology ; Biocatalysis ; Caspase 3/chemistry/genetics/*metabolism ; Caspase 6/chemistry/genetics/*metabolism ; Caspase Inhibitors ; Catalytic Domain ; Cell Line, Transformed ; Cell Line, Tumor ; Cells, Cultured ; Enzyme Activation ; Enzyme Activators/chemistry/*metabolism/pharmacology ; Enzyme Inhibitors/metabolism/pharmacology ; Enzyme Precursors/antagonists & inhibitors/chemistry/genetics/*metabolism ; Granzymes/metabolism ; Humans ; Imidazoles/chemistry/*metabolism/pharmacology ; Kinetics ; Mice ; Molecular Structure ; Mutagenesis ; Pyridines/chemistry/*metabolism/pharmacology ; Signal Transduction ; Small Molecule Libraries/chemistry/metabolism
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    The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: The sigma-1 receptor is widely distributed in the central nervous system and periphery. Originally mischaracterized as an opioid receptor, the sigma-1 receptor binds a vast number of synthetic compounds but does not bind opioid peptides; it is currently considered an orphan receptor. The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" 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/PMC2947205/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontanilla, Dominique -- Johannessen, Molly -- Hajipour, Abdol R -- Cozzi, Nicholas V -- Jackson, Meyer B -- Ruoho, Arnold E -- F31 DA022932/DA/NIDA NIH HHS/ -- NS30016/NS/NINDS NIH HHS/ -- R01 MH065503/MH/NIMH NIH HHS/ -- R01 MH065503-01A1/MH/NIMH NIH HHS/ -- R01 NS030016/NS/NINDS NIH HHS/ -- R01 NS030016-08/NS/NINDS NIH HHS/ -- R01 NS030016-09/NS/NINDS NIH HHS/ -- T32 GM08688/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):934-7. doi: 10.1126/science.1166127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Guinea Pigs ; Hallucinogens/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; N,N-Dimethyltryptamine/*metabolism ; Rats ; Receptors, sigma/agonists/antagonists & inhibitors/*metabolism ; Tryptamines/metabolism
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    KLF family members regulate intrinsic axon regeneration ability (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Neurons in the central nervous system (CNS) lose their ability to regenerate early in development, but the underlying mechanisms are unknown. By screening genes developmentally regulated in retinal ganglion cells (RGCs), we identified Kruppel-like factor-4 (KLF4) as a transcriptional repressor of axon growth in RGCs and other CNS neurons. RGCs lacking KLF4 showed increased axon growth both in vitro and after optic nerve injury in vivo. Related KLF family members suppressed or enhanced axon growth to differing extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhancing KLFs were down-regulated. Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882032/" 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/PMC2882032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Darcie L -- Blackmore, Murray G -- Hu, Ying -- Kaestner, Klaus H -- Bixby, John L -- Lemmon, Vance P -- Goldberg, Jeffrey L -- P30 EY014801/EY/NEI NIH HHS/ -- R01 NS059866/NS/NINDS NIH HHS/ -- R01 NS059866-01A2/NS/NINDS NIH HHS/ -- R01 NS061348/NS/NINDS NIH HHS/ -- R01 NS061348-01A2/NS/NINDS NIH HHS/ -- R01 NS061348-02/NS/NINDS NIH HHS/ -- R01 NS061348-03/NS/NINDS NIH HHS/ -- R01 NS061348-04/NS/NINDS NIH HHS/ -- R03 EY016790/EY/NEI NIH HHS/ -- R03 EY016790-01/EY/NEI NIH HHS/ -- R03 EY016790-02/EY/NEI NIH HHS/ -- R03 EY016790-03/EY/NEI NIH HHS/ -- T32 NS007459/NS/NINDS NIH HHS/ -- T32 NS07492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):298-301. doi: 10.1126/science.1175737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Count ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Gene Knockout Techniques ; Growth Cones/physiology ; Hippocampus/cytology/physiology ; Kruppel-Like Transcription Factors/genetics/*physiology ; Mice ; Nerve Crush ; Nerve Regeneration ; Neurites/physiology ; Neurons/*physiology ; Optic Nerve Injuries/physiopathology ; Rats ; Retinal Ganglion Cells/cytology/*physiology ; Transcription, Genetic ; Transfection ; Up-Regulation
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    Input-specific spine entry of soma-derived Vesl-1S protein conforms to synaptic tagging (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-16
    Description: Late-phase synaptic plasticity depends on the synthesis of new proteins that must function only in the activated synapses. The synaptic tag hypothesis requires input-specific functioning of these proteins after undirected transport. Confirmation of this hypothesis requires specification of a biochemical tagging activity and an example protein that behaves as the hypothesis predicts. We found that in rat neurons, soma-derived Vesl-1S (Homer-1a) protein, a late-phase plasticity-related synaptic protein, prevailed in every dendrite and did not enter spines. N-methyl-d-aspartate receptor activation triggered input-specific spine entry of Vesl-1S proteins, which met many criteria for synaptic tagging. These results suggest that Vesl-1S supports the hypothesis and that the activity-dependent regulation of spine entry functions as a synaptic tag.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Daisuke -- Ozawa, Fumiko -- Inokuchi, Kaoru -- New York, N.Y. -- Science. 2009 May 15;324(5929):904-9. doi: 10.1126/science.1171498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan. dada@mitils.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; Dendrites/*metabolism ; Dendritic Spines/*metabolism/ultrastructure ; Hippocampus/cytology/metabolism ; Mice ; *Neuronal Plasticity ; Plasmids ; Protein Transport ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission ; Transfection
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    Cell biology. Hypoxic hookup (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guarente, Leonard -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1281-2. doi: 10.1126/science.1175679.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Paul F. Glenn Lab and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. leng@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498158" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Aging ; Animals ; Basic Helix-Loop-Helix Transcription Factors/*metabolism ; *Cell Hypoxia ; Cells, Cultured ; Erythropoietin/biosynthesis/genetics ; Gene Expression ; Gene Expression Regulation ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Liver/embryology/metabolism ; Mice ; NAD/metabolism ; Neoplasms/metabolism/pathology ; Oxidation-Reduction ; Sirtuin 1 ; Sirtuins/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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    Cell biology. Using taste to clear the air(ways) (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kinnamon, Sue C -- Reynolds, Susan D -- New York, N.Y. -- Science. 2009 Aug 28;325(5944):1081-2. doi: 10.1126/science.1179180.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Otolaryngology and Rocky Mountain Taste and Smell Center, University of Colorado Denver, 12700 East 19th Avenue, Aurora, CO 80045, USA. sue.kinnamon@ucdenver.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19713515" target="_blank"〉PubMed〈/a〉
    Keywords: Calcium/metabolism ; Cells, Cultured ; Cilia/*physiology ; Epithelial Cells/*metabolism ; Humans ; Movement ; Mucus/secretion ; Noxae ; Receptors, G-Protein-Coupled/*metabolism ; Respiratory Mucosa/cytology/*metabolism ; *Signal Transduction ; *Taste ; Transducin/metabolism ; Type C Phospholipases/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neurodegeneration. Huntington's research points to possible new therapies (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):43-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Clinical Trials as Topic ; Corpus Striatum/pathology ; Disease Models, Animal ; Gene Expression Regulation ; Humans ; Huntington Disease/*drug therapy/genetics/pathology/*physiopathology ; Mice ; Mitochondria/metabolism ; Mutation ; Nerve Tissue Proteins/chemistry/*genetics/metabolism/*physiology ; Neurons/*physiology ; Nuclear Proteins/chemistry/*genetics/metabolism/*physiology ; Peptides ; Transcription Factors/metabolism ; Trinucleotide Repeat Expansion
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    Achieving stability of lipopolysaccharide-induced NF-kappaB activation (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: The activation dynamics of the transcription factor NF-kappaB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor-alpha (TNFalpha) but stable behavior when stimulated by lipopolysaccharide (LPS). LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-kappaB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. Computational modeling of the two TLR4-dependent signaling pathways suggests that one pathway requires a time delay to establish early anti-phase activation of NF-kappaB by the two pathways. The MyD88-independent pathway required Inferon regulatory factor 3-dependent expression of TNFalpha to activate NF-kappaB, and the time required for TNFalpha synthesis established the delay.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Covert, Markus W -- Leung, Thomas H -- Gaston, Jahlionais E -- Baltimore, David -- GM039458-21/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1854-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166516" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/deficiency/physiology ; Animals ; Antigens, Differentiation/physiology ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cycloheximide/pharmacology ; DNA-Binding Proteins/genetics/physiology ; Gene Expression Profiling ; Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/biosynthesis/genetics/metabolism ; Interferon Regulatory Factor-3 ; Kinetics ; Lipopolysaccharides/*immunology/metabolism ; Mice ; Models, Biological ; Myeloid Differentiation Factor 88 ; NF-kappa B/*metabolism ; Oligonucleotide Array Sequence Analysis ; Protein Synthesis Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Immunologic/deficiency/metabolism/physiology ; Signal Transduction ; Time Factors ; Toll-Like Receptor 4 ; Transcription Factors/genetics/physiology ; Tumor Necrosis Factor-alpha/biosynthesis/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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    Self-propagating, molecular-level polymorphism in Alzheimer's beta-amyloid fibrils (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Amyloid fibrils commonly exhibit multiple distinct morphologies in electron microscope and atomic force microscope images, often within a single image field. By using electron microscopy and solid-state nuclear magnetic resonance measurements on fibrils formed by the 40-residue beta-amyloid peptide of Alzheimer's disease (Abeta(1-40)), we show that different fibril morphologies have different underlying molecular structures, that the predominant structure can be controlled by subtle variations in fibril growth conditions, and that both morphology and molecular structure are self-propagating when fibrils grow from preformed seeds. Different Abeta(1-40) fibril morphologies also have significantly different toxicities in neuronal cell cultures. These results have implications for the mechanism of amyloid formation, the phenomenon of strains in prion diseases, the role of amyloid fibrils in amyloid diseases, and the development of amyloid-based nano-materials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petkova, Aneta T -- Leapman, Richard D -- Guo, Zhihong -- Yau, Wai-Ming -- Mattson, Mark P -- Tycko, Robert -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, MD 20892-0520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653506" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amyloid beta-Peptides/*chemistry/toxicity/*ultrastructure ; Animals ; Cells, Cultured ; Chemistry, Physical ; Hippocampus/cytology ; Humans ; Hydrogen Bonding ; Microscopy, Atomic Force ; Microscopy, Electron, Transmission ; Molecular Structure ; Neurons/cytology/drug effects ; Nuclear Magnetic Resonance, Biomolecular ; Peptide Fragments/*chemistry/toxicity/*ultrastructure ; Physicochemical Phenomena ; Protein Conformation ; Protein Structure, Secondary ; Rats
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    Stimulus specificity of gene expression programs determined by temporal control of IKK activity (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-17
    Description: A small number of mammalian signaling pathways mediate a myriad of distinct physiological responses to diverse cellular stimuli. Temporal control of the signaling module that contains IkappaB kinase (IKK), its substrate inhibitor of NF-kappaB (IkappaB), and the key inflammatory transcription factor NF-kappaB can allow for selective gene activation. We have demonstrated that different inflammatory stimuli induce distinct IKK profiles, and we examined the underlying molecular mechanisms. Although tumor necrosis factor-alpha (TNFalpha)-induced IKK activity was rapidly attenuated by negative feedback, lipopolysaccharide (LPS) signaling and LPS-specific gene expression programs were dependent on a cytokine-mediated positive feedback mechanism. Thus, the distinct biological responses to LPS and TNFalpha depend on signaling pathway-specific mechanisms that regulate the temporal profile of IKK activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Werner, Shannon L -- Barken, Derren -- Hoffmann, Alexander -- GM071573/GM/NIGMS NIH HHS/ -- GM72024/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1857-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry, 9500 Gilman Drive, Mailcode 0375, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166517" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Autocrine Communication ; Cell Line ; Cells, Cultured ; Computer Simulation ; Cytokines/genetics ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation ; I-kappa B Kinase ; I-kappa B Proteins/metabolism ; Lipopolysaccharides/immunology/metabolism/pharmacology ; Mice ; Models, Biological ; NF-kappa B/deficiency/metabolism ; Oligonucleotide Array Sequence Analysis ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Immunologic/metabolism ; Signal Transduction ; Toll-Like Receptor 4 ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/deficiency/immunology/metabolism/pharmacology
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    Endosomal proteolysis of the Ebola virus glycoprotein is necessary for infection (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: Ebola virus (EboV) causes rapidly fatal hemorrhagic fever in humans and there is currently no effective treatment. We found that the infection of African green monkey kidney (Vero) cells by vesicular stomatitis viruses bearing the EboV glycoprotein (GP) requires the activity of endosomal cysteine proteases. Using selective protease inhibitors and protease-deficient cell lines, we identified an essential role for cathepsin B (CatB) and an accessory role for cathepsin L (CatL) in EboV GP-dependent entry. Biochemical studies demonstrate that CatB and CatL mediate entry by carrying out proteolysis of the EboV GP subunit GP1 and support a multistep mechanism that explains the relative contributions of these enzymes to infection. CatB and CatB/CatL inhibitors diminish the multiplication of infectious EboV-Zaire in cultured cells and may merit investigation as anti-EboV drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandran, Kartik -- Sullivan, Nancy J -- Felbor, Ute -- Whelan, Sean P -- Cunningham, James M -- R01 AI059371/AI/NIAID NIH HHS/ -- R01 AI059371-01A1/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Jun 10;308(5728):1643-5. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831716" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cathepsin B/antagonists & inhibitors/*metabolism ; Cathepsin L ; Cathepsins/antagonists & inhibitors/*metabolism ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Ebolavirus/metabolism/*physiology ; Endosomes/*metabolism ; Hydrogen-Ion Concentration ; Mice ; Vero Cells ; Vesicular stomatitis Indiana virus/genetics/physiology ; Viral Envelope Proteins/*metabolism ; Virion/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-22
    Description: Blood calcium concentration is maintained within a narrow range despite large variations in dietary input and body demand. The Transient Receptor Potential ion channel TRPV5 has been implicated in this process. We report here that TRPV5 is stimulated by the mammalian hormone klotho. Klotho, a beta-glucuronidase, hydrolyzes extracellular sugar residues on TRPV5, entrapping the channel in the plasma membrane. This maintains durable calcium channel activity and membrane calcium permeability in kidney. Thus, klotho activates a cell surface channel by hydrolysis of its extracellular N-linked oligosaccharides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Q -- Hoefs, S -- van der Kemp, A W -- Topala, C N -- Bindels, R J -- Hoenderop, J G -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):490-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16239475" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Calcium Channels/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Glucuronidase/antagonists & inhibitors/metabolism ; Glycosylation ; Humans ; Hydrolysis ; Kidney/cytology/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Patch-Clamp Techniques ; Protein Transport ; Rabbits ; Sodium/metabolism ; TRPV Cation Channels/genetics/*metabolism ; Transfection
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    Glial membranes at the node of Ranvier prevent neurite outgrowth (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
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    Neuroscience. Brain under surveillance: the microglia patrol (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fetler, Luc -- Amigorena, Sebastian -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):392-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire Physico-Chimie Curie, CNRS UMR 168, Institut Curie, Paris, France. luc.fetler@curie.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020721" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Astrocytes/metabolism ; Brain/blood supply/*cytology/pathology/*physiology ; Brain Injuries/immunology/pathology/*physiopathology ; Capillaries/injuries ; Cell Surface Extensions/physiology/ultrastructure ; Cells, Cultured ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy/methods ; Movement ; Phagocytosis ; Photons ; Receptors, Purinergic P2/metabolism
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    Neuroscience. Making synapses: a balancing act (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussain, Natasha K -- Sheng, Morgan -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Center for Learning and Memory, RIKEN-MIT Neuroscience Research Center, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. natashah@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules, Neuronal ; Cells, Cultured ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Binding ; Rats ; Synapses/*physiology ; Synaptic Membranes/*physiology ; gamma-Aminobutyric Acid/metabolism
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    Cell signaling. Stat acetylation--a key facet of cytokine signaling? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Shea, John J -- Kanno, Yuka -- Chen, Xiaomin -- Levy, David E -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):217-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653493" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Active Transport, Cell Nucleus ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*physiology ; Cytoplasm/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dimerization ; Histone Acetyltransferases ; Histone Deacetylases/metabolism ; Lysine/*metabolism ; Mutation ; NF-kappa B/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Processing, Post-Translational ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transcriptional Activation ; src Homology Domains
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    Cell biology. Ras on the roundabout (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meder, Doris -- Simons, Kai -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1731-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany. meder@mpi-cbg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774748" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Animals ; Cell Differentiation ; Cell Membrane/*metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytosol/metabolism ; Dogs ; Fluorescence Resonance Energy Transfer ; Genes, ras ; Golgi Apparatus/*metabolism ; Guanosine Triphosphate/metabolism ; Humans ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/metabolism ; Models, Biological ; Palmitic Acid/metabolism ; Protein Isoforms/chemistry/metabolism ; Proto-Oncogene Proteins p21(ras)/chemistry/*metabolism ; ras Proteins
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    Stem cells. Scientists chase after immortality in a petri dish (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):1982-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16179446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Embryo, Mammalian/*cytology ; Female ; Genomic Imprinting ; Humans ; Male ; Meiosis ; *Oocytes/cytology/physiology ; Ovary/cytology/physiology ; *Spermatozoa/cytology/physiology ; *Stem Cells/cytology/physiology ; Testis/cytology/physiology
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    Bone marrow stromal cells generate muscle cells and repair muscle degeneration (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: Bone marrow stromal cells (MSCs) have great potential as therapeutic agents. We report a method for inducing skeletal muscle lineage cells from human and rat general adherent MSCs with an efficiency of 89%. Induced cells differentiated into muscle fibers upon transplantation into degenerated muscles of rats and mdx-nude mice. The induced population contained Pax7-positive cells that contributed to subsequent regeneration of muscle upon repetitive damage without additional transplantation of cells. These MSCs represent a more ready supply of myogenic cells than do the rare myogenic stem cells normally found in muscle and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dezawa, Mari -- Ishikawa, Hiroto -- Itokazu, Yutaka -- Yoshihara, Tomoyuki -- Hoshino, Mikio -- Takeda, Shin-ichi -- Ide, Chizuka -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Kyoto University Graduate School of Medicine, Yoshidakonoecho, Sakyo-ku, Kyoto, 606-8501 Japan. dezawa@anat2.med.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology/physiology ; Bone Marrow Transplantation ; *Cell Differentiation ; Cell Fusion ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Colforsin/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression Profiling ; Homeodomain Proteins/analysis ; Humans ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Cells/*cytology ; Muscle Development/genetics ; Muscle Fibers, Skeletal/*cytology ; Muscle Proteins/analysis ; Muscle, Skeletal/cytology ; Muscular Diseases/*therapy ; Muscular Dystrophy, Duchenne/therapy ; Neuregulins/pharmacology ; PAX7 Transcription Factor ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology/physiology ; Stem Cells/cytology/physiology ; Stromal Cells/*cytology/physiology/transplantation ; Transfection
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    Altered TCR signaling from geometrically repatterned immunological synapses (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: The immunological synapse is a specialized cell-cell junction that is defined by large-scale spatial patterns of receptors and signaling molecules yet remains largely enigmatic in terms of formation and function. We used supported bilayer membranes and nanometer-scale structures fabricated onto the underlying substrate to impose geometric constraints on immunological synapse formation. Analysis of the resulting alternatively patterned synapses revealed a causal relation between the radial position of T cell receptors (TCRs) and signaling activity, with prolonged signaling from TCR microclusters that had been mechanically trapped in the peripheral regions of the synapse. These results are consistent with a model of the synapse in which spatial translocation of TCRs represents a direct mechanism of signal regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mossman, Kaspar D -- Campi, Gabriele -- Groves, Jay T -- Dustin, Michael L -- GM64900/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1191-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biophysics Graduate Group, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293763" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Antigen-Presenting Cells/metabolism ; Cells, Cultured ; Lipid Bilayers ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell/chemistry/*metabolism ; *Signal Transduction ; Structure-Activity Relationship ; T-Lymphocytes/immunology/*metabolism
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    Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans. Axonal defects consisted of swellings that accumulated abnormal amounts of microtubule-associated and molecular motor proteins, organelles, and vesicles. Impairing axonal transport by reducing the dosage of a kinesin molecular motor protein enhanced the frequency of axonal defects and increased amyloid-beta peptide levels and amyloid deposition. Reductions in microtubule-dependent transport may stimulate proteolytic processing of beta-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokin, Gorazd B -- Lillo, Concepcion -- Falzone, Tomas L -- Brusch, Richard G -- Rockenstein, Edward -- Mount, Stephanie L -- Raman, Rema -- Davies, Peter -- Masliah, Eliezer -- Williams, David S -- Goldstein, Lawrence S B -- EY12598/EY/NEI NIH HHS/ -- EY13408/EY/NEI NIH HHS/ -- P50 AG05131/AG/NIA NIH HHS/ -- R01 EY007042/EY/NEI NIH HHS/ -- R01 EY007042-19/EY/NEI NIH HHS/ -- R01 EY013408/EY/NEI NIH HHS/ -- R01 EY013408-02/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1282-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cellular and Molecular Medicine, School of Medicine, University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731448" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Alzheimer Disease/genetics/*metabolism/*pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; *Axonal Transport ; Axons/*pathology/physiology ; Basal Nucleus of Meynert/pathology ; Brain/*metabolism/*pathology ; Cells, Cultured ; Cytoplasmic Vesicles/ultrastructure ; Female ; Hippocampus ; Humans ; Kinesin/metabolism ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics/metabolism ; Neurons/metabolism ; Organelles/ultrastructure ; Plaque, Amyloid/pathology ; Time Factors
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    Recognition of host immune activation by Pseudomonas aeruginosa (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-07-30
    Description: It is generally reasoned that lethal infections caused by opportunistic pathogens develop permissively by invading a host that is both physiologically stressed and immunologically compromised. However, an alternative hypothesis might be that opportunistic pathogens actively sense alterations in host immune function and respond by enhancing their virulence phenotype. We demonstrate that interferon-gamma binds to an outer membrane protein in Pseudomonas aeruginosa, OprF, resulting in the expression of a quorum-sensing dependent virulence determinant, the PA-I lectin. These observations provide details of the mechanisms by which prokaryotic organisms are directly signaled by immune activation in their eukaryotic host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Licheng -- Estrada, Oscar -- Zaborina, Olga -- Bains, Manjeet -- Shen, Le -- Kohler, Jonathan E -- Patel, Nachiket -- Musch, Mark W -- Chang, Eugene B -- Fu, Yang-Xin -- Jacobs, Michael A -- Nishimura, Michael I -- Hancock, Robert E W -- Turner, Jerrold R -- Alverdy, John C -- 2-RO1 GM062344-05/GM/NIGMS NIH HHS/ -- DK-38510/DK/NIDDK NIH HHS/ -- DK-47722/DK/NIDDK NIH HHS/ -- R01DK61931/DK/NIDDK NIH HHS/ -- R01DK68271/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Jul 29;309(5735):774-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16051797" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Cytokines/immunology/metabolism/pharmacology ; Humans ; Interferon-gamma/immunology/*metabolism/pharmacology ; Lectins/*biosynthesis ; Lymphocyte Activation ; Porins/isolation & purification/*metabolism ; Protein Binding ; Pseudomonas aeruginosa/growth & development/*immunology/metabolism/*pathogenicity ; Pyocyanine/biosynthesis ; Recombinant Proteins/pharmacology ; Signal Transduction ; T-Lymphocytes/*immunology ; Up-Regulation ; Virulence
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    Control of excitatory and inhibitory synapse formation by neuroligins (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: The normal function of neural networks depends on a delicate balance between excitatory and inhibitory synaptic inputs. Synapse formation is thought to be regulated by bidirectional signaling between pre- and postsynaptic cells. We demonstrate that members of the Neuroligin family promote postsynaptic differentiation in cultured rat hippocampal neurons. Down-regulation of neuroligin isoform expression by RNA interference results in a loss of excitatory and inhibitory synapses. Electrophysiological analysis revealed a predominant reduction of inhibitory synaptic function. Thus, neuroligins control the formation and functional balance of excitatory and inhibitory synapses in hippocampal neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chih, Ben -- Engelman, Holly -- Scheiffele, Peter -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1324-8. Epub 2005 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cellular Biophysics, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681343" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Adhesion Molecules, Neuronal ; Cell Line ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Down-Regulation ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; Membrane Proteins/genetics/*metabolism ; Membrane Transport Proteins/metabolism ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Isoforms ; RNA Interference ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Membranes/*physiology ; Synaptic Transmission ; Transfection ; Vesicular Glutamate Transport Protein 1 ; Vesicular Inhibitory Amino Acid Transport Proteins
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    Equivalent effects of snake PLA2 neurotoxins and lysophospholipid-fatty acid mixtures (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-13
    Description: Snake presynaptic phospholipase A2 neurotoxins (SPANs) paralyze the neuromuscular junction (NMJ). Upon intoxication, the NMJ enlarges and has a reduced content of synaptic vesicles, and primary neuronal cultures show synaptic swelling with surface exposure of the lumenal domain of the synaptic vesicle protein synaptotagmin I. Concomitantly, these neurotoxins induce exocytosis of neurotransmitters. We found that an equimolar mixture of lysophospholipids and fatty acids closely mimics all of the biological effects of SPANs. These results draw attention to the possible role of local lipid changes in synaptic vesicle release and provide new tools for the study of exocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rigoni, Michela -- Caccin, Paola -- Gschmeissner, Steve -- Koster, Grielof -- Postle, Anthony D -- Rossetto, Ornella -- Schiavo, Giampietro -- Montecucco, Cesare -- GP0272Y01/Telethon/Italy -- New York, N.Y. -- Science. 2005 Dec 9;310(5754):1678-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Sciences and Consiglio Nazionale Ricerche Institute of Neuroscience, University of Padova, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16339444" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Elapid Venoms/toxicity ; Esterification ; Exocytosis ; Fatty Acids/*metabolism/toxicity ; Glutamic Acid/metabolism ; Hydrolysis ; Kinetics ; Lipid Bilayers ; Lysophospholipids/*metabolism/toxicity ; Male ; Mass Spectrometry ; Membrane Fusion ; Membrane Lipids/metabolism ; Mice ; Neuromuscular Junction/drug effects/metabolism/physiology ; Neurons/drug effects/metabolism/ultrastructure ; Neurotoxins/*metabolism/toxicity ; Neurotransmitter Agents/metabolism ; Phospholipases A/*metabolism/toxicity ; Phospholipases A2 ; Synapses/drug effects/ultrastructure ; Synaptic Membranes/metabolism/*physiology ; Synaptic Vesicles/drug effects/physiology/ultrastructure
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    Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-02-05
    Description: Variants of NOD2, an intracellular sensor of bacteria-derived muramyl dipeptide (MDP), increase susceptibility to Crohn's disease (CD). These variants are thought to be defective in activation of nuclear factor kappaB (NF-kappaB) and antibacterial defenses, but CD clinical specimens display elevated NF-kappaB activity. To illuminate the pathophysiological function of NOD2, we introduced such a variant to the mouse Nod2 locus. Mutant mice exhibited elevated NF-kappaB activation in response to MDP and more efficient processing and secretion of the cytokine interleukin-1beta (IL-1beta). These effects are linked to increased susceptibility to bacterial-induced intestinal inflammation and identify NOD2 as a positive regulator of NF-kappaB activation and IL-1beta secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maeda, Shin -- Hsu, Li-Chung -- Liu, Hongjun -- Bankston, Laurie A -- Iimura, Mitsutoshi -- Kagnoff, Martin F -- Eckmann, Lars -- Karin, Michael -- AI43477/AI/NIAID NIH HHS/ -- AI56075/AI/NIAID NIH HHS/ -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):734-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0723, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15692052" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylmuramyl-Alanyl-Isoglutamine/immunology ; Animals ; Anti-Bacterial Agents/pharmacology ; Apoptosis ; Bacteria/immunology ; Cells, Cultured ; Colitis/immunology/pathology ; Colon/*immunology/microbiology ; Crohn Disease/genetics/*immunology ; Cytokines/biosynthesis/genetics ; Dextran Sulfate/pharmacology ; Interleukin-1/*metabolism ; Intestinal Mucosa/immunology ; Intracellular Signaling Peptides and Proteins/*genetics/*physiology ; Lipopolysaccharides/immunology ; Macrophage Activation ; Macrophages/*immunology/metabolism ; Mice ; Mutation ; NF-kappa B/*metabolism ; Nod2 Signaling Adaptor Protein ; Peptidoglycan/immunology ; Signal Transduction
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    Obligate role of anti-apoptotic MCL-1 in the survival of hematopoietic stem cells (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-02-19
    Description: Apoptosis is important in controlling hematopoietic stem cell (HSC) numbers. However, the specific BCL-2 family member(s) that regulate HSC homeostasis are not precisely defined. We tested myeloid leukemia-1 (MCL-1) as an attractive candidate that is highly expressed in HSCs and regulated by growth factor signals. Inducible deletion of Mcl-1 in mice resulted in ablation of bone marrow. This resulted in the loss of early bone marrow progenitor populations, including HSCs. Moreover, growth factors including stem cell factor increased transcription of the Mcl-1 gene and required MCL-1 to augment survival of purified bone marrow progenitors. Deletion of Mcl-1 in other tissues, including liver, did not impair survival. Thus, MCL-1 is a critical and specific regulator essential for ensuring the homeostasis of early hematopoietic progenitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Opferman, Joseph T -- Iwasaki, Hiromi -- Ong, Christy C -- Suh, Heikyung -- Mizuno, Shin-ichi -- Akashi, Koichi -- Korsmeyer, Stanley J -- CA072009/CA/NCI NIH HHS/ -- DK061320/DK/NIDDK NIH HHS/ -- R37CA50239/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1101-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Cancer Immunology and AIDS, Pathology and Medicine, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Bone Marrow Cells/cytology/physiology ; Cell Count ; Cell Lineage ; Cell Shape ; Cell Survival ; Cells, Cultured ; Colony-Forming Units Assay ; Gene Deletion ; Gene Expression ; Hematopoietic Stem Cells/cytology/*physiology ; Homeostasis ; Interleukin-6/pharmacology ; Liver/cytology/physiology ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/genetics/*physiology ; Poly I-C/pharmacology ; Polymerase Chain Reaction ; Proto-Oncogene Proteins c-bcl-2/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Signal Transduction ; Stem Cell Factor/pharmacology ; Transduction, Genetic
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    Astrocytic purinergic signaling coordinates synaptic networks (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-10-08
    Description: To investigate the role of astrocytes in regulating synaptic transmission, we generated inducible transgenic mice that express a dominant-negative SNARE domain selectively in astrocytes to block the release of transmitters from these glial cells. By releasing adenosine triphosphate, which accumulates as adenosine, astrocytes tonically suppressed synaptic transmission, thereby enhancing the dynamic range for long-term potentiation and mediated activity-dependent, heterosynaptic depression. These results indicate that astrocytes are intricately linked in the regulation of synaptic strength and plasticity and provide a pathway for synaptic cross-talk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pascual, Olivier -- Casper, Kristen B -- Kubera, Cathryn -- Zhang, Jing -- Revilla-Sanchez, Raquel -- Sul, Jai-Yoon -- Takano, Hajime -- Moss, Stephen J -- McCarthy, Ken -- Haydon, Philip G -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):113-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Conte Center for Integration at the Tripartite Synapse, 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/16210541" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*metabolism ; Adenosine A1 Receptor Antagonists ; Adenosine Triphosphatases/antagonists & inhibitors ; Adenosine Triphosphate/analogs & derivatives/metabolism/pharmacology ; Animals ; Astrocytes/drug effects/*physiology ; Cells, Cultured ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/physiology ; In Vitro Techniques ; Long-Term Potentiation/drug effects ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Purinergic P1 Receptor Antagonists ; Purinergic P2 Receptor Antagonists ; Receptor, Adenosine A1/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Receptors, Purinergic P1/metabolism ; Receptors, Purinergic P2/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Xanthines/pharmacology
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    Neuroscience. Cancer drugs may help injured nerve cells regrow their axons (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-10-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210503" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*pharmacology ; Axons/drug effects/*physiology ; Cells, Cultured ; Erlotinib Hydrochloride ; Mice ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurons/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Quinazolines/*pharmacology ; Rats ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/metabolism ; Signal Transduction/*drug effects ; Spinal Cord Injuries/drug therapy
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    American Chemical Society meeting. Nanofibers seed blood vessels (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):44-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/*growth & development ; Cells, Cultured ; Fibroblast Growth Factors/chemistry/metabolism ; Heparin/chemistry/metabolism ; *Nanostructures ; *Neovascularization, Physiologic ; Peptides/*chemistry/metabolism ; Vascular Endothelial Growth Factor A/chemistry/metabolism
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    Differential lysosomal proteolysis in antigen-presenting cells determines antigen fate (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-03-12
    Description: Antigen-presenting cells (APCs) internalize antigens and present antigen-derived peptides to T cells. Although APCs have been thought to exhibit a well-developed capacity for lysosomal proteolysis, here we found that they can exhibit two distinct strategies upon antigen encounter. Whereas macrophages contained high levels of lysosomal proteases and rapidly degraded internalized proteins, dendritic cells (DCs) and B lymphocytes were protease-poor, resulting in a limited capacity for lysosomal degradation. Consistent with these findings, DCs in vivo degraded internalized antigens slowly and thus retained antigen in lymphoid organs for extended periods. Limited lysosomal proteolysis also favored antigen presentation. These results help explain why DCs are able to efficiently accumulate, process, and disseminate antigens and microbes systemically for purposes of tolerance and immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delamarre, Lelia -- Pack, Margit -- Chang, Henry -- Mellman, Ira -- Trombetta, E Sergio -- R37-AI34098/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 11;307(5715):1630-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology and Department of Immunobiology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, Post Office Box 208002, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15761154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigen-Presenting Cells/*enzymology/*immunology/metabolism ; Antigens/*metabolism ; B-Lymphocytes/enzymology/immunology/metabolism ; Cells, Cultured ; Dendritic Cells/*enzymology/immunology/metabolism ; Endocytosis ; Green Fluorescent Proteins/immunology/metabolism ; Histocompatibility Antigens Class II/immunology ; Horseradish Peroxidase/immunology/metabolism ; Lymphoid Tissue/cytology/enzymology/immunology ; Lysosome-Associated Membrane Glycoproteins ; Lysosomes/*enzymology/ultrastructure ; Macrophages/enzymology/immunology/metabolism ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C3H ; Peptide Hydrolases/*metabolism ; Ribonuclease, Pancreatic/immunology/metabolism ; Ribonucleases/immunology/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Direct isolation of satellite cells for skeletal muscle regeneration (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-09-06
    Description: Muscle satellite cells contribute to muscle regeneration. We have used a Pax3(GFP/+) mouse line to directly isolate (Pax3)(green fluorescent protein)-expressing muscle satellite cells, by flow cytometry from adult skeletal muscles, as a homogeneous population of small, nongranular, Pax7+, CD34+, CD45-, Sca1- cells. The flow cytometry parameters thus established enabled us to isolate satellite cells from wild-type muscles. Such cells, grafted into muscles of mdx nu/nu mice, contributed both to fiber repair and to the muscle satellite cell compartment. Expansion of these cells in culture before engraftment reduced their regenerative capacity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Montarras, Didier -- Morgan, Jennifer -- Collins, Charlotte -- Relaix, Frederic -- Zaffran, Stephane -- Cumano, Ana -- Partridge, Terence -- Buckingham, Margaret -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2064-7. Epub 2005 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS Unite de Recherche Associee 2578, Department of Developmental Biology, INSERM, Pasteur Institute, 75724 Paris Cedex 15, France. dmontarr@pasteur.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141372" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; *Cell Separation ; Cells, Cultured ; DNA-Binding Proteins/analysis/biosynthesis ; Diaphragm ; Dystrophin/biosynthesis ; Flow Cytometry ; Green Fluorescent Proteins/analysis ; Homeodomain Proteins/analysis/biosynthesis ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Development ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/cytology/*physiology ; PAX7 Transcription Factor ; Paired Box Transcription Factors ; *Regeneration ; Satellite Cells, Skeletal Muscle/*cytology/physiology/transplantation ; Stem Cell Transplantation ; Transcription Factors/analysis/biosynthesis
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  • 79
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    Impaired thermosensation in mice lacking TRPV3, a heat and camphor sensor in the skin (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-05
    Description: Environmental temperature is thought to be directly sensed by neurons through their projections in the skin. A subset of the mammalian transient receptor potential (TRP) family of ion channels has been implicated in this process. These "thermoTRPs" are activated at distinct temperature thresholds and are typically expressed in sensory neurons. TRPV3 is activated by heat (〉33 degrees C) and, unlike most thermoTRPs, is expressed in mouse keratinocytes. We found that TRPV3 null mice have strong deficits in responses to innocuous and noxious heat but not in other sensory modalities; hence, TRPV3 has a specific role in thermosensation. The natural compound camphor, which modulates sensations of warmth in humans, proved to be a specific activator of TRPV3. Camphor activated cultured primary keratinocytes but not sensory neurons, and this activity was abolished in TRPV3 null mice. Therefore, heat-activated receptors in keratinocytes are important for mammalian thermosensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moqrich, Aziz -- Hwang, Sun Wook -- Earley, Taryn J -- Petrus, Matt J -- Murray, Amber N -- Spencer, Kathryn S R -- Andahazy, Mary -- Story, Gina M -- Patapoutian, Ardem -- New York, N.Y. -- Science. 2005 Mar 4;307(5714):1468-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15746429" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bradykinin/pharmacology ; CHO Cells ; Camphor/pharmacology ; Cation Transport Proteins/genetics/*physiology ; Cells, Cultured ; Cricetinae ; Dermis/anatomy & histology/innervation/ultrastructure ; Epidermis/anatomy & histology/innervation/ultrastructure ; Ganglia, Spinal/cytology/metabolism ; *Hot Temperature ; Humans ; Ion Channels/genetics/*physiology ; Keratinocytes/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons, Afferent/physiology ; Patch-Clamp Techniques ; TRPV Cation Channels ; Temperature ; Thermoreceptors/*physiology ; *Thermosensing ; Time Factors
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    PUMA couples the nuclear and cytoplasmic proapoptotic function of p53 (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-10
    Description: The Trp53 tumor suppressor gene product (p53) functions in the nucleus to regulate proapoptotic genes, whereas cytoplasmic p53 directly activates proapoptotic Bcl-2 proteins to permeabilize mitochondria and initiate apoptosis. Here, we demonstrate that a tripartite nexus between Bcl-xL, cytoplasmic p53, and PUMA coordinates these distinct p53 functions. After genotoxic stress, Bcl-xL sequestered cytoplasmic p53. Nuclear p53 caused expression of PUMA, which then displaced p53 from Bcl-xL, allowing p53 to induce mitochondrial permeabilization. Mutant Bcl-xL that bound p53, but not PUMA, rendered cells resistant to p53-induced apoptosis irrespective of PUMA expression. Thus, PUMA couples the nuclear and cytoplasmic proapoptotic functions of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chipuk, Jerry E -- Bouchier-Hayes, Lisa -- Kuwana, Tomomi -- Newmeyer, Donald D -- Green, Douglas R -- New York, N.Y. -- Science. 2005 Sep 9;309(5741):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16151013" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Cell Line, Tumor ; Cell Nucleus/*metabolism ; Cells, Cultured ; Cytoplasm/*metabolism ; DNA Damage ; Gene Expression Regulation ; Humans ; Immunoprecipitation ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Models, Biological ; Permeability ; Protein Binding ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Recombinant Proteins/metabolism ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins/chemistry/*metabolism ; Ultraviolet Rays ; bcl-2-Associated X Protein ; bcl-X Protein
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    Synapses form in skeletal muscles lacking neuregulin receptors (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-25
    Description: The formation of the neuromuscular junction (NMJ) is directed by reciprocal interactions between motor neurons and muscle fibers. Neuregulin (NRG) and Agrin from motor nerve terminals are both implicated. Here, we demonstrate that NMJs can form in the absence of the NRG receptors ErbB2 and ErbB4 in mouse muscle. Postsynaptic differentiation is, however, induced by Agrin. We therefore conclude that NRG signaling to muscle is not required for NMJ formation. The effects of NRG signaling to muscle may be mediated indirectly through Schwann cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escher, P -- Lacazette, E -- Courtet, M -- Blindenbacher, A -- Landmann, L -- Bezakova, G -- Lloyd, K C -- Mueller, U -- Brenner, H R -- New York, N.Y. -- Science. 2005 Jun 24;308(5730):1920-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, Biozentrum, University of Basel, 4056 Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15976301" target="_blank"〉PubMed〈/a〉
    Keywords: Agrin/physiology ; Animals ; Animals, Newborn ; Cells, Cultured ; Genes, erbB ; Genes, erbB-2 ; Membrane Potentials ; Mice ; Motor Endplate/metabolism/physiology/ultrastructure ; Muscle, Skeletal/*innervation/ultrastructure ; Mutation ; Neuregulins/*metabolism ; Neuromuscular Junction/embryology/metabolism/*physiology/ultrastructure ; Presynaptic Terminals/physiology ; RNA, Messenger/genetics/metabolism ; Receptor, Epidermal Growth Factor/genetics/*physiology ; Receptor, ErbB-2/genetics/*physiology ; Receptor, ErbB-4 ; Receptors, Cholinergic/chemistry/genetics/metabolism ; Recombination, Genetic ; Schwann Cells/physiology ; *Signal Transduction ; Synaptic Transmission
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    Stem cell depletion through epidermal deletion of Rac1 (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-08-06
    Description: Mammalian epidermis is maintained by self-renewal of stem cells, but the underlying mechanisms are unknown. Deletion of Rac1, a Rho guanosine triphosphatase, in adult mouse epidermis stimulated stem cells to divide and undergo terminal differentiation, leading to failure to maintain the interfollicular epidermis, hair follicles, and sebaceous glands. Rac1 exerts its effects in the epidermis by negatively regulating c-Myc through p21-activated kinase 2 (PAK2) phosphorylation. We conclude that a pleiotropic regulator of cell adhesion and the cytoskeleton plays a critical role in controlling exit from the stem cell niche and propose that Rac and Myc represent a global stem cell regulatory axis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benitah, Salvador Aznar -- Frye, Michaela -- Glogauer, Michael -- Watt, Fiona M -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):933-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Keratinocyte Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation/metabolism ; Apoptosis ; Carcinoma, Squamous Cell/metabolism ; Cell Differentiation/*physiology ; Cells, Cultured ; Epidermis/*cytology ; Gene Deletion ; Humans ; Keratinocytes ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuropeptides/genetics/*physiology ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Skin Neoplasms/metabolism ; Stem Cells/*cytology ; Tamoxifen/*analogs & derivatives ; p21-Activated Kinases ; rac GTP-Binding Proteins/genetics/*physiology ; rac1 GTP-Binding Protein
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    Mammalian SAD kinases are required for neuronal polarization (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-12
    Description: Electrical activity in neurons is generally initiated in dendritic processes then propagated along axons to synapses, where it is passed to other neurons. Major structural features of neurons-their dendrites and axons-are thus related to their fundamental functions: the receipt and transmission of information. The acquisition of these distinct properties by dendrites and axons, called polarization, is a critical step in neuronal differentiation. We show here that SAD-A and SAD-B, mammalian orthologs of a kinase needed for presynaptic differentiation in Caenorhabditis elegans, are required for neuronal polarization. These kinases will provide entry points for unraveling signaling mechanisms that polarize neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kishi, Masashi -- Pan, Y Albert -- Crump, Justin Gage -- Sanes, Joshua R -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):929-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Washington University Medical School, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705853" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Axons/physiology/ultrastructure ; Brain/*cytology/embryology/metabolism ; Brain Chemistry ; Cell Differentiation ; Cell Line ; *Cell Polarity ; Cell Shape ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/metabolism ; Dendrites/physiology/ultrastructure ; Hippocampus/cytology ; Mice ; Microtubule-Associated Proteins/metabolism ; Mutation ; Neurons/*cytology/*physiology/ultrastructure ; Phosphorylation ; Prosencephalon/cytology/embryology/metabolism ; Protein-Serine-Threonine Kinases/genetics/*physiology ; Spinal Cord/chemistry/embryology ; tau Proteins/metabolism
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    EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-10-08
    Description: Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in the adult central nervous system (CNS), but the underlying signaling mechanisms of regeneration inhibition are not fully understood. Here, we show that suppressing the kinase function of the epidermal growth factor receptor (EGFR) blocks the activities of both myelin inhibitors and chondroitin sulfate proteoglycans in inhibiting neurite outgrowth. In addition, regeneration inhibitors trigger the phosphorylation of EGFR in a calcium-dependent manner. Local administration of EGFR inhibitors promotes significant regeneration of injured optic nerve fibers, pointing to a promising therapeutic avenue for enhancing axon regeneration after CNS injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koprivica, Vuk -- Cho, Kin-Sang -- Park, Jong Bae -- Yiu, Glenn -- Atwal, Jasvinder -- Gore, Bryan -- Kim, Jieun A -- Lin, Estelle -- Tessier-Lavigne, Marc -- Chen, Dong Feng -- He, Zhigang -- New York, N.Y. -- Science. 2005 Oct 7;310(5745):106-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16210539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/*physiology ; Calcium/metabolism ; Cells, Cultured ; Chondroitin Sulfate Proteoglycans/*metabolism ; Enzyme Inhibitors/pharmacology ; Erlotinib Hydrochloride ; GPI-Linked Proteins ; Humans ; Mice ; Myelin Proteins/*metabolism/pharmacology ; Nerve Crush ; *Nerve Regeneration/drug effects ; Neurites/drug effects/physiology ; Optic Nerve/drug effects/physiology ; Optic Nerve Injuries/drug therapy ; Phosphorylation ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/*antagonists & inhibitors/*metabolism ; Receptors, Cell Surface/metabolism ; Retinal Ganglion Cells/drug effects/physiology ; Signal Transduction/drug effects ; Tyrphostins/pharmacology
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    Nucleus accumbens long-term depression and the expression of behavioral sensitization (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-11-29
    Description: Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brebner, Karen -- Wong, Tak Pan -- Liu, Lidong -- Liu, Yitao -- Campsall, Paul -- Gray, Sarah -- Phelps, Lindsay -- Phillips, Anthony G -- Wang, Yu Tian -- New York, N.Y. -- Science. 2005 Nov 25;310(5752):1340-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Centre, University of British Columbia, Vancouver, British Columbia V6T 2B5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16311338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Behavior, Animal/*drug effects ; Cells, Cultured ; Clathrin/physiology ; Dextroamphetamine/*administration & dosage/pharmacology ; Dynamins/pharmacology ; Endocytosis ; Excitatory Postsynaptic Potentials ; *Long-Term Synaptic Depression/drug effects ; Male ; Membrane Potentials ; Models, Animal ; Motor Activity/*drug effects ; Nucleus Accumbens/drug effects/*physiology ; Patch-Clamp Techniques ; Peptides/pharmacology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/metabolism ; Recombinant Fusion Proteins/pharmacology ; Stereotyped Behavior/*drug effects ; Synaptic Transmission/drug effects ; Ventral Tegmental Area/drug effects/physiology
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    Genetics. Jumping DNA mixes it up in the developing brain (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Jun 17;308(5729):1729.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15961641" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*growth & development ; Cell Differentiation ; Cells, Cultured ; *Gene Expression Regulation ; Humans ; *Long Interspersed Nucleotide Elements ; Mice ; Mice, Transgenic ; Neurons/*cytology/physiology ; Rats ; Stem Cells/*cytology/physiology
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    A plant peptide encoded by CLV3 identified by in situ MALDI-TOF MS analysis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: The Arabidopsis CLAVATA3 (CLV3) gene encodes a stem cell-specific protein presumed to be a precursor of a secreted peptide hormone. Matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) applied to in situ Arabidopsis tissues determined the structure of a modified 12-amino acid peptide (MCLV3), which was derived from a conserved motif in the CLV3 sequence. Synthetic MCLV3 induced shoot and root meristem consumption as cells differentiated into other organs, displaying the typical phenotype of transgenic plants overexpressing CLV3. These results suggest that the functional peptide of CLV3 is MCLV3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, Tatsuhiko -- Sawa, Shinichiro -- Kinoshita, Atsuko -- Mizuno, Satoko -- Kakimoto, Tatsuo -- Fukuda, Hiroo -- Sakagami, Youji -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):845-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Bio-Agricultural Sciences, Nagoya University, Chikusa, Nagoya, 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902141" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amino Acid Sequence ; Arabidopsis/*cytology/genetics/metabolism ; Arabidopsis Proteins/*chemistry/genetics/*metabolism/pharmacology ; Cell Differentiation ; Cells, Cultured ; Hydroxyproline/chemistry ; Meristem/*cytology/drug effects/metabolism ; Molecular Sequence Data ; Oligopeptides/chemistry/*metabolism/pharmacology ; Plant Roots/growth & development ; Plants, Genetically Modified ; Signal Transduction ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Stem Cells/cytology
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    PIN proteins perform a rate-limiting function in cellular auxin efflux (2006)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2006-04-08
    Description: Intercellular flow of the phytohormone auxin underpins multiple developmental processes in plants. Plant-specific pin-formed (PIN) proteins and several phosphoglycoprotein (PGP) transporters are crucial factors in auxin transport-related development, yet the molecular function of PINs remains unknown. Here, we show that PINs mediate auxin efflux from mammalian and yeast cells without needing additional plant-specific factors. Conditional gain-of-function alleles and quantitative measurements of auxin accumulation in Arabidopsis and tobacco cultured cells revealed that the action of PINs in auxin efflux is distinct from PGP, rate-limiting, specific to auxins, and sensitive to auxin transport inhibitors. This suggests a direct involvement of PINs in catalyzing cellular auxin efflux.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrasek, Jan -- Mravec, Jozef -- Bouchard, Rodolphe -- Blakeslee, Joshua J -- Abas, Melinda -- Seifertova, Daniela -- Wisniewska, Justyna -- Tadele, Zerihun -- Kubes, Martin -- Covanova, Milada -- Dhonukshe, Pankaj -- Skupa, Petr -- Benkova, Eva -- Perry, Lucie -- Krecek, Pavel -- Lee, Ok Ran -- Fink, Gerald R -- Geisler, Markus -- Murphy, Angus S -- Luschnig, Christian -- Zazimalova, Eva -- Friml, Jiri -- New York, N.Y. -- Science. 2006 May 12;312(5775):914-8. Epub 2006 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Botany, the Academy of Sciences of the Czech Republic, 165 02 Prague 6, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601150" target="_blank"〉PubMed〈/a〉
    Keywords: ATP-Binding Cassette Transporters/genetics/metabolism ; Arabidopsis/cytology/growth & development/*metabolism/physiology ; Arabidopsis Proteins/genetics/*metabolism ; Biological Transport ; Cell Membrane/metabolism ; Cells, Cultured ; Gravitropism ; HeLa Cells ; Humans ; Indoleacetic Acids/*metabolism ; Kinetics ; Membrane Transport Proteins/genetics/*metabolism ; Mutation ; Naphthaleneacetic Acids/metabolism ; Phthalimides/pharmacology ; Plant Roots/physiology ; Saccharomyces cerevisiae/genetics ; Tobacco ; Transfection ; Transformation, Genetic
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    Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: Normal intestinal mucosa contains abundant immunoglobulin A (IgA)-secreting cells, which are generated from B cells in gut-associated lymphoid tissues (GALT). We show that dendritic cells (DC) from GALT induce T cell-independent expression of IgA and gut-homing receptors on B cells. GALT-DC-derived retinoic acid (RA) alone conferred gut tropism but could not promote IgA secretion. However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Thus, GALT-DC shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mora, J Rodrigo -- Iwata, Makoto -- Eksteen, Bertus -- Song, Si-Young -- Junt, Tobias -- Senman, Balimkiz -- Otipoby, Kevin L -- Yokota, Aya -- Takeuchi, Hajime -- Ricciardi-Castagnoli, Paola -- Rajewsky, Klaus -- Adams, David H -- von Andrian, Ulrich H -- AI-061663/AI/NIAID NIH HHS/ -- G0601816/Medical Research Council/United Kingdom -- HL54936/HL/NHLBI NIH HHS/ -- HL56949/HL/NHLBI NIH HHS/ -- HL62524/HL/NHLBI NIH HHS/ -- R37 AI054636/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1157-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CBR Institute for Biomedical Research and Department of Pathology, Harvard Medical School, Boston, MA 02115, USA. mora@cbr.med.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110582" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology/secretion ; Cell Movement ; Cells, Cultured ; Chemotaxis, Leukocyte ; Dendritic Cells/*immunology ; Immunity, Mucosal ; Immunoglobulin A/*biosynthesis/immunology ; Interleukin-5/immunology ; Interleukin-6/immunology ; Intestinal Mucosa/immunology ; Intestines/cytology/*immunology ; Lymphoid Tissue/cytology/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/biosynthesis ; Tretinoin/immunology ; Vitamin A/physiology ; Vitamin A Deficiency/immunology ; Vitamins/immunology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Caspases 3 and 7: key mediators of mitochondrial events of apoptosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738210/" 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/PMC3738210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lakhani, Saquib A -- Masud, Ali -- Kuida, Keisuke -- Porter, George A Jr -- Booth, Carmen J -- Mehal, Wajahat Z -- Inayat, Irteza -- Flavell, Richard A -- 1 K08 HD044580/HD/NICHD NIH HHS/ -- 5 K12 HD01401/HD/NICHD NIH HHS/ -- K08 DK002965/DK/NIDDK NIH HHS/ -- K08 DK002965-04/DK/NIDDK NIH HHS/ -- K12 HD00850/HD/NICHD NIH HHS/ -- NIDDK P30-34989/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):847-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Inducing Factor/metabolism ; Caspase 3 ; Caspase 7 ; Caspases/deficiency/*metabolism ; Cell Nucleus/metabolism ; Cell Shape ; Cell Survival ; Cells, Cultured ; Cytochromes c/metabolism ; DNA Fragmentation ; Female ; Fibroblasts/cytology ; Heart/embryology ; Heart Defects, Congenital/etiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/*physiology ; Mitochondrial Membranes/physiology ; Permeability ; T-Lymphocytes/cytology ; bcl-2-Associated X Protein/metabolism
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    Botany. Plant cells CLEave their way to differentiation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Simon, Rudiger -- Stahl, Yvonne -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):773-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut fur Genetik, Heinrich Heine Universitat, 40225 Dusseldorf, Germany. ruediger.simon@uni-duesseldorf.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902118" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Arabidopsis/cytology ; Arabidopsis Proteins/*chemistry/metabolism ; Asteraceae/cytology ; *Cell Communication ; *Cell Differentiation ; Cells, Cultured ; Meristem/*cytology ; Oligopeptides/chemistry/isolation & purification/*metabolism ; Plant Leaves/cytology ; Plant Roots/cytology ; Plant Shoots/cytology ; Plant Structures/cytology ; *Signal Transduction ; Stem Cells/*cytology
    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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  • 92
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    Dodeca-CLE peptides as suppressors of plant stem cell differentiation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-08-12
    Description: In plants and animals, small peptide ligands that signal in cell-cell communication have been suggested to be a crucial component of development. A bioassay of single-cell transdifferentation demonstrates that a dodecapeptide with two hydroxyproline residues is the functional product of genes from the CLE family, which includes CLAVATA3 in Arabidopsis. The dodecapeptide suppresses xylem cell development at a concentration of 10(-11) M and promotes cell division. An application, corresponding to all 26 Arabidopsis CLE protein family members, of synthetic dodecapeptides reveals two counteracting signaling pathways involved in stem cell fate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Yasuko -- Nakanomyo, Ikuko -- Motose, Hiroyasu -- Iwamoto, Kuninori -- Sawa, Shinichiro -- Dohmae, Naoshi -- Fukuda, Hiroo -- New York, N.Y. -- Science. 2006 Aug 11;313(5788):842-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16902140" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/cytology ; Arabidopsis Proteins/chemistry/metabolism ; Asteraceae/*cytology ; Base Sequence ; Biological Assay ; Cell Communication ; *Cell Differentiation ; Cells, Cultured ; Ligands ; Meristem/cytology ; Molecular Sequence Data ; Oligopeptides/chemistry/isolation & purification/*metabolism/pharmacology ; Plant Proteins/chemistry/*metabolism ; Plant Roots/cytology/growth & development ; Plant Structures/*cytology ; *Signal Transduction ; Stem Cells/*cytology
    Print ISSN: 0036-8075
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  • 93
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    Regulation of adult bone mass by the zinc finger adapter protein Schnurri-3 (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-05-27
    Description: Genetic mutations that disrupt osteoblast function can result in skeletal dysmorphogenesis or, more rarely, in increased postnatal bone formation. Here we show that Schnurri-3 (Shn3), a mammalian homolog of the Drosophila zinc finger adapter protein Shn, is an essential regulator of adult bone formation. Mice lacking Shn3 display adult-onset osteosclerosis with increased bone mass due to augmented osteoblast activity. Shn3 was found to control protein levels of Runx2, the principal transcriptional regulator of osteoblast differentiation, by promoting its degradation through recruitment of the E3 ubiquitin ligase WWP1 to Runx2. By this means, Runx2-mediated extracellular matrix mineralization was antagonized, revealing an essential role for Shn3 as a central regulator of postnatal bone mass.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, Dallas C -- Wein, Marc N -- Oukka, Mohamed -- Hofstaetter, Jochen G -- Glimcher, Melvin J -- Glimcher, Laurie H -- AI29673/AI/NIAID NIH HHS/ -- AR46983/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1223-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16728642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; *Bone Density ; Bone and Bones/*anatomy & histology/chemistry/physiology ; Cell Line ; Cells, Cultured ; Core Binding Factor Alpha 1 Subunit/genetics/metabolism ; DNA-Binding Proteins/analysis/genetics/*metabolism ; Gene Expression Regulation ; Immunoprecipitation ; Mice ; Osteoblasts/chemistry/physiology ; Osteoclasts/physiology ; Osteogenesis ; Protein Binding ; Protein Structure, Tertiary ; RNA Interference ; RNA, Messenger/genetics/metabolism ; Transcriptional Activation ; Transfection ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism ; Zinc Fingers
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    Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-24
    Description: Alpha-synuclein (alphaSyn) misfolding is associated with several devastating neurodegenerative disorders, including Parkinson's disease (PD). In yeast cells and in neurons alphaSyn accumulation is cytotoxic, but little is known about its normal function or pathobiology. The earliest defect following alphaSyn expression in yeast was a block in endoplasmic reticulum (ER)-to-Golgi vesicular trafficking. In a genomewide screen, the largest class of toxicity modifiers were proteins functioning at this same step, including the Rab guanosine triphosphatase Ypt1p, which associated with cytoplasmic alphaSyn inclusions. Elevated expression of Rab1, the mammalian YPT1 homolog, protected against alphaSyn-induced dopaminergic neuron loss in animal models of PD. Thus, synucleinopathies may result from disruptions in basic cellular functions that interface with the unique biology of particular neurons to make them especially vulnerable.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1983366/" 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/PMC1983366/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cooper, Antony A -- Gitler, Aaron D -- Cashikar, Anil -- Haynes, Cole M -- Hill, Kathryn J -- Bhullar, Bhupinder -- Liu, Kangning -- Xu, Kexiang -- Strathearn, Katherine E -- Liu, Fang -- Cao, Songsong -- Caldwell, Kim A -- Caldwell, Guy A -- Marsischky, Gerald -- Kolodner, Richard D -- Labaer, Joshua -- Rochet, Jean-Christophe -- Bonini, Nancy M -- Lindquist, Susan -- P50 NS038372/NS/NINDS NIH HHS/ -- R01-HG002923/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 21;313(5785):324-8. Epub 2006 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biological Sciences, University of Missouri-Kansas City, Kansas City, MO 64110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16794039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Caenorhabditis elegans ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Dopamine/physiology ; Drosophila ; Endoplasmic Reticulum/*metabolism ; Gene Expression ; Gene Library ; Golgi Apparatus/*metabolism ; Humans ; Mice ; Nerve Degeneration ; Neurons/cytology/*physiology ; Parkinsonian Disorders/metabolism/pathology/*physiopathology ; Proteasome Endopeptidase Complex/metabolism ; Protein Folding ; *Protein Transport ; Proteins/chemistry/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Saccharomyces cerevisiae/genetics/metabolism ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; alpha-Synuclein/chemistry/genetics/*metabolism ; rab GTP-Binding Proteins/genetics/metabolism ; rab1 GTP-Binding Proteins/genetics/*metabolism
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    RIG-I-mediated antiviral responses to single-stranded RNA bearing 5'-phosphates (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-14
    Description: Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pichlmair, Andreas -- Schulz, Oliver -- Tan, Choon Ping -- Naslund, Tanja I -- Liljestrom, Peter -- Weber, Friedemann -- Reis e Sousa, Caetano -- New York, N.Y. -- Science. 2006 Nov 10;314(5801):997-1001. Epub 2006 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology Laboratory, Cancer Research UK, London Research Institute, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17038589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cells, Cultured ; Cytoplasm/metabolism/virology ; DEAD-box RNA Helicases/genetics/*metabolism ; Dendritic Cells/virology ; Encephalomyocarditis virus/genetics/immunology/metabolism ; Genome, Viral ; Humans ; *Immunity, Innate ; Influenza A virus/*genetics/*immunology/metabolism/physiology ; Interferon-alpha/biosynthesis ; Interferon-beta/biosynthesis ; Mice ; Mice, Inbred C57BL ; Phosphates/metabolism ; Phosphorylation ; RNA Caps/metabolism ; RNA, Double-Stranded/metabolism ; RNA, Viral/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Transfection ; Vesicular stomatitis Indiana virus/genetics/immunology/metabolism ; Viral Nonstructural Proteins/genetics/metabolism ; Virus Replication
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    Regulation of B cell tolerance by the lupus susceptibility gene Ly108 (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: The susceptibility locus for the autoimmune disease lupus on murine chromosome 1, Sle1z/Sle1bz, and the orthologous human locus are associated with production of autoantibody to chromatin. We report that the presence of Sle1z/Sle1bz impairs B cell anergy, receptor revision, and deletion. Members of the SLAM costimulatory molecule family constitute prime candidates for Sle1bz, among which the Ly108.1 isoform of the Ly108 gene was most highly expressed in immature B cells from lupus-prone B6.Sle1z mice. The normal Ly108.2 allele, but not the lupus-associated Ly108.1 allele, was found to sensitize immature B cells to deletion and RAG reexpression. As a potential regulator of tolerance checkpoints, Ly108 may censor self-reactive B cells, hence safeguarding against autoimmunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kumar, Kirthi Raman -- Li, Liunan -- Yan, Mei -- Bhaskarabhatla, Madhavi -- Mobley, Angela B -- Nguyen, Charles -- Mooney, Jill M -- Schatzle, John D -- Wakeland, Edward K -- Mohan, Chandra -- AI54902/AI/NIAID NIH HHS/ -- NIH RO1 AR44894/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1665-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine (Rheumatology), University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Ly/*genetics ; Autoantigens/immunology ; B-Lymphocytes/*immunology ; Bone Marrow Cells/immunology ; Cell Death ; Cell Line, Tumor ; Cells, Cultured ; Clonal Anergy ; Clonal Deletion ; *Genetic Predisposition to Disease ; *Immune Tolerance ; Lupus Erythematosus, Systemic/*genetics/immunology ; Mice ; Mice, Transgenic ; Multifactorial Inheritance ; Muramidase/immunology ; Receptors, Antigen, B-Cell/immunology ; Spleen/immunology ; Transfection
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    Microbiology. Malaria's stealth shuttle (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cowman, Alan F -- Kappe, Stefan H I -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1245-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia. cowman@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946056" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Adhesion ; Cell Death ; Cell Membrane/metabolism ; Cells, Cultured ; Cellular Structures/*parasitology/ultrastructure ; Endothelial Cells/parasitology ; Erythrocytes/parasitology ; Hepatocytes/*parasitology/physiology/ultrastructure ; Liver/blood supply/parasitology ; Malaria/*parasitology ; Mice ; Phagocytosis ; Phosphatidylserines/metabolism ; Plasmodium berghei/growth & development/*pathogenicity ; Sporozoites/growth & development ; Vacuoles/parasitology/ultrastructure
    Print ISSN: 0036-8075
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    Activity- and mTOR-dependent suppression of Kv1.1 channel mRNA translation in dendrites (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-d-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raab-Graham, Kimberly F -- Haddick, Patrick C G -- Jan, Yuh Nung -- Jan, Lily Yeh -- MH13010/MH/NIMH NIH HHS/ -- MH65334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):144-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023663" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Cells, Cultured ; Dendrites/drug effects/*metabolism ; Excitatory Postsynaptic Potentials ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; Kv1.1 Potassium Channel/*biosynthesis/*genetics ; Neuronal Plasticity ; Neurons/metabolism/virology ; Oligonucleotide Array Sequence Analysis ; Phosphorylation ; Protein Biosynthesis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinases/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Recombinant Fusion Proteins/metabolism ; Sindbis Virus/physiology ; Sirolimus/pharmacology ; Synapses/physiology ; TOR Serine-Threonine Kinases
    Print ISSN: 0036-8075
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  • 99
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    Cancer regression in patients after transfer of genetically engineered lymphocytes (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: Through the adoptive transfer of lymphocytes after host immunodepletion, it is possible to mediate objective cancer regression in human patients with metastatic melanoma. However, the generation of tumor-specific T cells in this mode of immunotherapy is often limiting. Here we report the ability to specifically confer tumor recognition by autologous lymphocytes from peripheral blood by using a retrovirus that encodes a T cell receptor. Adoptive transfer of these transduced cells in 15 patients resulted in durable engraftment at levels exceeding 10% of peripheral blood lymphocytes for at least 2 months after the infusion. We observed high sustained levels of circulating, engineered cells at 1 year after infusion in two patients who both demonstrated objective regression of metastatic melanoma lesions. This study suggests the therapeutic potential of genetically engineered cells for the biologic therapy of cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267026/" 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/PMC2267026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morgan, Richard A -- Dudley, Mark E -- Wunderlich, John R -- Hughes, Marybeth S -- Yang, James C -- Sherry, Richard M -- Royal, Richard E -- Topalian, Suzanne L -- Kammula, Udai S -- Restifo, Nicholas P -- Zheng, Zhili -- Nahvi, Azam -- de Vries, Christiaan R -- Rogers-Freezer, Linda J -- Mavroukakis, Sharon A -- Rosenberg, Steven A -- Z01 BC010763-01/Intramural NIH HHS/ -- Z01 SC003811-32/Intramural NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):126-9. Epub 2006 Aug 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946036" target="_blank"〉PubMed〈/a〉
    Keywords: *Adoptive Transfer ; Adult ; Antigens, Neoplasm/*immunology ; CD8-Positive T-Lymphocytes/*immunology ; Cancer Vaccines/therapeutic use ; Cells, Cultured ; Electroporation ; Female ; Genetic Engineering ; *Genetic Therapy ; HLA-A Antigens/immunology ; HLA-A2 Antigen ; Humans ; Interleukin-2/immunology/therapeutic use ; MART-1 Antigen ; Male ; Melanoma/immunology/secondary/*therapy ; Middle Aged ; Neoplasm Proteins/*immunology ; Receptors, Antigen, T-Cell, alpha-beta/*genetics/*immunology ; Transduction, Genetic ; Transgenes
    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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  • 100
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    Comment on "PDK1 nucleates T cell receptor-induced signaling complex for NF-kappaB activation" (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: We observe that protein kinase C (PKC) is phosphorylated on the activation loop at threonine 538 (Thr-538) before T cell activation. Our results are inconsistent with the conclusions of Lee et al. (Reports, 1 April 2005, p. 114) that the Thr-538 phosphorylation of PKC is regulated by T cell receptor activation. Other mechanisms, such as autophosphorylation of Thr-219, might orchestrate the cellular function of PKC in T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gruber, Thomas -- Freeley, Michael -- Thuille, Nikolaus -- Heit, Isabelle -- Shaw, Stephen -- Long, Aideen -- Baier, Gottfried -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):55; author reply 55.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department for Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601177" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Animals ; Antibodies/immunology ; Antigens, CD28/immunology ; Antigens, CD3/immunology ; Cells, Cultured ; Humans ; Isoenzymes/*metabolism ; Jurkat Cells ; Lymphocyte Activation ; Mice ; NF-kappa B/*metabolism ; Phosphorylation ; Protein Kinase C/*metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/enzymology/immunology/*metabolism ; Threonine/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)
    Location Call Number Expected Availability
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