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  • Mice  (35)
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  • 1
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    BAFF-R, a newly identified TNF receptor that specifically interacts with BAFF (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-18
    Description: B cell homeostasis has been shown to critically depend on BAFF, the B cell activation factor from the tumor necrosis factor (TNF) family. Although BAFF is already known to bind two receptors, BCMA and TACI, we have identified a third receptor for BAFF that we have termed BAFF-R. BAFF-R binding appears to be highly specific for BAFF, suggesting a unique role for this ligand-receptor interaction. Consistent with this, the BAFF-R locus is disrupted in A/WySnJ mice, which display a B cell phenotype qualitatively similar to that of the BAFF-deficient mice. Thus, BAFF-R appears to be the principal receptor for BAFF-mediated mature B cell survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, J S -- Bixler, S A -- Qian, F -- Vora, K -- Scott, M L -- Cachero, T G -- Hession, C -- Schneider, P -- Sizing, I D -- Mullen, C -- Strauch, K -- Zafari, M -- Benjamin, C D -- Tschopp, J -- Browning, J L -- Ambrose, C -- New York, N.Y. -- Science. 2001 Sep 14;293(5537):2108-11. Epub 2001 Aug 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biogen, 12 Cambridge Center, Cambridge, MA 02142, USA., The Institute of Biochemistry, University of Lausanne, CH-1066, Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11509692" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Cell Activating Factor ; B-Cell Activation Factor Receptor ; B-Cell Maturation Antigen ; B-Lymphocytes/immunology/metabolism/*physiology ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 22 ; Cloning, Molecular ; Homeostasis ; Humans ; Ligands ; Lymphoid Tissue/metabolism ; Male ; Membrane Proteins/*metabolism ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Molecular Sequence Data ; RNA, Messenger/chemistry/genetics/metabolism ; Receptors, Tumor Necrosis Factor/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transfection ; Transmembrane Activator and CAML Interactor Protein ; Tumor Necrosis Factor-alpha/*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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  • 2
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    Axonal swellings and degeneration in mice lacking the major proteolipid of myelin (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-11
    Description: Glial cells produce myelin and contribute to axonal morphology in the nervous system. Two myelin membrane proteolipids, PLP and DM20, were shown to be essential for the integrity of myelinated axons. In the absence of PLP-DM20, mice assembled compact myelin sheaths but subsequently developed widespread axonal swellings and degeneration, associated predominantly with small-caliber nerve fibers. Similar swellings were absent in dysmyelinated shiverer mice, which lack myelin basic protein (MBP), but recurred in MBP*PLP double mutants. Thus, fiber degeneration, which was probably secondary to impaired axonal transport, could indicate that myelinated axons require local oligodendroglial support.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Griffiths, I -- Klugmann, M -- Anderson, T -- Yool, D -- Thomson, C -- Schwab, M H -- Schneider, A -- Zimmermann, F -- McCulloch, M -- Nadon, N -- Nave, K A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jun 5;280(5369):1610-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Applied Neurobiology Group, Department of Veterinary Clinical Studies, University of Glasgow, Glasgow G61 1QH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9616125" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Axons/*physiology/*ultrastructure ; Cell Communication ; Central Nervous System/*ultrastructure ; Female ; Mice ; Mice, Neurologic Mutants ; Models, Neurological ; Motor Activity ; Myelin Proteolipid Protein/analysis/genetics/*physiology ; Myelin Sheath/chemistry/physiology/ultrastructure ; Nerve Degeneration/*pathology ; *Nerve Tissue Proteins ; Oligodendroglia/physiology ; Optic Nerve/ultrastructure ; Organelles/ultrastructure ; Spinal Cord/ultrastructure ; Transgenes
    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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    Chromatin dynamics during epigenetic reprogramming in the mouse germ line (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-03-21
    Description: A unique feature of the germ cell lineage is the generation of totipotency. A critical event in this context is DNA demethylation and the erasure of parental imprints in mouse primordial germ cells (PGCs) on embryonic day 11.5 (E11.5) after they enter into the developing gonads. Little is yet known about the mechanism involved, except that it is apparently an active process. We have examined the associated changes in the chromatin to gain further insights into this reprogramming event. Here we show that the chromatin changes occur in two steps. The first changes in nascent PGCs at E8.5 establish a distinctive chromatin signature that is reminiscent of pluripotency. Next, when PGCs are residing in the gonads, major changes occur in nuclear architecture accompanied by an extensive erasure of several histone modifications and exchange of histone variants. Furthermore, the histone chaperones HIRA and NAP-1 (NAP111), which are implicated in histone exchange, accumulate in PGC nuclei undergoing reprogramming. We therefore suggest that the mechanism of histone replacement is critical for these chromatin rearrangements to occur. The marked chromatin changes are intimately linked with genome-wide DNA demethylation. On the basis of the timing of the observed events, we propose that if DNA demethylation entails a DNA repair-based mechanism, the evident histone replacement would represent a repair-induced response event rather than being a prerequisite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3847605/" 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/PMC3847605/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hajkova, Petra -- Ancelin, Katia -- Waldmann, Tanja -- Lacoste, Nicolas -- Lange, Ulrike C -- Cesari, Francesca -- Lee, Caroline -- Almouzni, Genevieve -- Schneider, Robert -- Surani, M Azim -- 083089/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Apr 17;452(7189):877-81. doi: 10.1038/nature06714. Epub 2008 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust/Cancer Research UK Gurdon Institute of Cancer and Developmental Biology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18354397" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/*metabolism ; *Chromatin Assembly and Disassembly ; DNA Methylation ; *Epigenesis, Genetic ; Germ Cells/*metabolism ; Gonads/cytology/metabolism ; Histones/metabolism ; Mice ; Stem Cells/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-06-06
    Description: Inflammation is a protective attempt by the host to remove injurious stimuli and initiate the tissue healing process. The inflammatory response must be actively terminated, however, because failure to do so can result in 'bystander' damage to tissues and diseases such as arthritis or type-2 diabetes. Yet the mechanisms controlling excessive inflammatory responses are still poorly understood. Here we show that mouse effector and memory CD4(+) T cells abolish macrophage inflammasome-mediated caspase-1 activation and subsequent interleukin 1beta release in a cognate manner. Inflammasome inhibition is observed for all tested NLRP1 (commonly called NALP1) and NLRP3 (NALP3 or cryopyrin) activators, whereas NLRC4 (IPAF) inflammasome function and release of other inflammatory mediators such as CXCL2, interleukin 6 and tumour necrosis factor are not affected. Suppression of the NLRP3 inflammasome requires cell-to-cell contact and can be mimicked by macrophage stimulation with selected ligands of the tumour necrosis factor family, such as CD40L (also known as CD40LG). In a NLRP3-dependent peritonitis model, effector CD4(+) T cells are responsible for decreasing neutrophil recruitment in an antigen-dependent manner. Our findings reveal an unexpected mechanism of inflammasome inhibition, whereby effector and memory T cells suppress potentially damaging inflammation, yet leave the primary inflammatory response, crucial for the onset of immunity, intact.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guarda, Greta -- Dostert, Catherine -- Staehli, Francesco -- Cabalzar, Katrin -- Castillo, Rosa -- Tardivel, Aubry -- Schneider, Pascal -- Tschopp, Jurg -- England -- Nature. 2009 Jul 9;460(7252):269-73. doi: 10.1038/nature08100. Epub 2009 Jun 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Lausanne, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19494813" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*antagonists & inhibitors/metabolism ; Animals ; Antigens/immunology ; Apoptosis Regulatory Proteins/*antagonists & inhibitors/metabolism ; Bone Marrow Cells/cytology ; CD4-Positive T-Lymphocytes/*immunology ; Carrier Proteins/*antagonists & inhibitors/metabolism ; Caspase 1/metabolism ; Cells, Cultured ; Immunity, Innate/*immunology ; Immunologic Memory ; Inflammation/immunology/*metabolism/pathology ; Interleukin-1beta/immunology ; Ligands ; Macrophages/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neutrophils/immunology ; Peritoneal Cavity/cytology ; Tumor Necrosis Factors/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Innate immune and chemically triggered oxidative stress modifies translational fidelity (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-11-27
    Description: Translational fidelity, essential for protein and cell function, requires accurate transfer RNA (tRNA) aminoacylation. Purified aminoacyl-tRNA synthetases exhibit a fidelity of one error per 10,000 to 100,000 couplings. The accuracy of tRNA aminoacylation in vivo is uncertain, however, and might be considerably lower. Here we show that in mammalian cells, approximately 1% of methionine (Met) residues used in protein synthesis are aminoacylated to non-methionyl-tRNAs. Remarkably, Met-misacylation increases up to tenfold upon exposing cells to live or non-infectious viruses, toll-like receptor ligands or chemically induced oxidative stress. Met is misacylated to specific non-methionyl-tRNA families, and these Met-misacylated tRNAs are used in translation. Met-misacylation is blocked by an inhibitor of cellular oxidases, implicating reactive oxygen species (ROS) as the misacylation trigger. Among six amino acids tested, tRNA misacylation occurs exclusively with Met. As Met residues are known to protect proteins against ROS-mediated damage, we propose that Met-misacylation functions adaptively to increase Met incorporation into proteins to protect cells against oxidative stress. In demonstrating an unexpected conditional aspect of decoding mRNA, our findings illustrate the importance of considering alternative iterations of the genetic code.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785853/" 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/PMC2785853/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Netzer, Nir -- Goodenbour, Jeffrey M -- David, Alexandre -- Dittmar, Kimberly A -- Jones, Richard B -- Schneider, Jeffrey R -- Boone, David -- Eves, Eva M -- Rosner, Marsha R -- Gibbs, James S -- Embry, Alan -- Dolan, Brian -- Das, Suman -- Hickman, Heather D -- Berglund, Peter -- Bennink, Jack R -- Yewdell, Jonathan W -- Pan, Tao -- Z01 AI000542-20/Intramural NIH HHS/ -- Z01 AI000653-16/Intramural NIH HHS/ -- Z01 AI000658-16/Intramural NIH HHS/ -- Z01 AI001014-01/Intramural NIH HHS/ -- England -- Nature. 2009 Nov 26;462(7272):522-6. doi: 10.1038/nature08576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19940929" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/physiology ; Animals ; Genetic Code ; HeLa Cells ; Humans ; *Immunity, Innate ; Ligands ; Methionine/genetics/*metabolism ; Mice ; Models, Genetic ; NADPH Oxidase/metabolism ; Orthomyxoviridae/physiology ; Oxidative Stress/drug effects/genetics/*physiology ; RNA, Transfer, Met/genetics/metabolism ; Reactive Oxygen Species/metabolism ; Substrate Specificity ; Toll-Like Receptors/immunology/metabolism ; Transfer RNA Aminoacylation/drug effects/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-08-13
    Description: Influenza A viruses cause recurrent outbreaks at local or global scale with potentially severe consequences for human health and the global economy. Recently, a new strain of influenza A virus was detected that causes disease in and transmits among humans, probably owing to little or no pre-existing immunity to the new strain. On 11 June 2009 the World Health Organization declared that the infections caused by the new strain had reached pandemic proportion. Characterized as an influenza A virus of the H1N1 subtype, the genomic segments of the new strain were most closely related to swine viruses. Most human infections with swine-origin H1N1 influenza viruses (S-OIVs) seem to be mild; however, a substantial number of hospitalized individuals do not have underlying health issues, attesting to the pathogenic potential of S-OIVs. To achieve a better assessment of the risk posed by the new virus, we characterized one of the first US S-OIV isolates, A/California/04/09 (H1N1; hereafter referred to as CA04), as well as several other S-OIV isolates, in vitro and in vivo. In mice and ferrets, CA04 and other S-OIV isolates tested replicate more efficiently than a currently circulating human H1N1 virus. In addition, CA04 replicates efficiently in non-human primates, causes more severe pathological lesions in the lungs of infected mice, ferrets and non-human primates than a currently circulating human H1N1 virus, and transmits among ferrets. In specific-pathogen-free miniature pigs, CA04 replicates without clinical symptoms. The assessment of human sera from different age groups suggests that infection with human H1N1 viruses antigenically closely related to viruses circulating in 1918 confers neutralizing antibody activity to CA04. Finally, we show that CA04 is sensitive to approved and experimental antiviral drugs, suggesting that these compounds could function as a first line of defence against the recently declared S-OIV pandemic.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748827/" 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/PMC2748827/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Itoh, Yasushi -- Shinya, Kyoko -- Kiso, Maki -- Watanabe, Tokiko -- Sakoda, Yoshihiro -- Hatta, Masato -- Muramoto, Yukiko -- Tamura, Daisuke -- Sakai-Tagawa, Yuko -- Noda, Takeshi -- Sakabe, Saori -- Imai, Masaki -- Hatta, Yasuko -- Watanabe, Shinji -- Li, Chengjun -- Yamada, Shinya -- Fujii, Ken -- Murakami, Shin -- Imai, Hirotaka -- Kakugawa, Satoshi -- Ito, Mutsumi -- Takano, Ryo -- Iwatsuki-Horimoto, Kiyoko -- Shimojima, Masayuki -- Horimoto, Taisuke -- Goto, Hideo -- Takahashi, Kei -- Makino, Akiko -- Ishigaki, Hirohito -- Nakayama, Misako -- Okamatsu, Masatoshi -- Takahashi, Kazuo -- Warshauer, David -- Shult, Peter A -- Saito, Reiko -- Suzuki, Hiroshi -- Furuta, Yousuke -- Yamashita, Makoto -- Mitamura, Keiko -- Nakano, Kunio -- Nakamura, Morio -- Brockman-Schneider, Rebecca -- Mitamura, Hiroshi -- Yamazaki, Masahiko -- Sugaya, Norio -- Suresh, M -- Ozawa, Makoto -- Neumann, Gabriele -- Gern, James -- Kida, Hiroshi -- Ogasawara, Kazumasa -- Kawaoka, Yoshihiro -- HHNSN266200700010C/NS/NINDS NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200800060C/AI/NIAID NIH HHS/ -- R01 AI069274/AI/NIAID NIH HHS/ -- R01 AI069274-04/AI/NIAID NIH HHS/ -- U19 AI070503/AI/NIAID NIH HHS/ -- England -- Nature. 2009 Aug 20;460(7258):1021-5. doi: 10.1038/nature08260.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Shiga University of Medical Science, Ohtsu, Shiga 520-2192, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19672242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/immunology ; Antiviral Agents/pharmacology ; Cell Line ; Dogs ; Female ; Ferrets/virology ; HN Protein/metabolism ; Humans ; Influenza A Virus, H1N1 Subtype/drug effects/enzymology/pathogenicity/*physiology ; Lung/immunology/pathology/virology ; Macaca fascicularis/immunology/virology ; Male ; Mice ; Mice, Inbred BALB C ; Neutralization Tests ; Orthomyxoviridae Infections/immunology/transmission/virology ; Primate Diseases/pathology/virology ; Swine/*virology ; Swine Diseases/pathology/virology ; Swine, Miniature/virology ; Virus Replication
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Phenotypic profiling of the human genome by time-lapse microscopy reveals cell division genes (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-03
    Description: Despite our rapidly growing knowledge about the human genome, we do not know all of the genes required for some of the most basic functions of life. To start to fill this gap we developed a high-throughput phenotypic screening platform combining potent gene silencing by RNA interference, time-lapse microscopy and computational image processing. We carried out a genome-wide phenotypic profiling of each of the approximately 21,000 human protein-coding genes by two-day live imaging of fluorescently labelled chromosomes. Phenotypes were scored quantitatively by computational image processing, which allowed us to identify hundreds of human genes involved in diverse biological functions including cell division, migration and survival. As part of the Mitocheck consortium, this study provides an in-depth analysis of cell division phenotypes and makes the entire high-content data set available as a resource to the community.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108885/" 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/PMC3108885/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Neumann, Beate -- Walter, Thomas -- Heriche, Jean-Karim -- Bulkescher, Jutta -- Erfle, Holger -- Conrad, Christian -- Rogers, Phill -- Poser, Ina -- Held, Michael -- Liebel, Urban -- Cetin, Cihan -- Sieckmann, Frank -- Pau, Gregoire -- Kabbe, Rolf -- Wunsche, Annelie -- Satagopam, Venkata -- Schmitz, Michael H A -- Chapuis, Catherine -- Gerlich, Daniel W -- Schneider, Reinhard -- Eils, Roland -- Huber, Wolfgang -- Peters, Jan-Michael -- Hyman, Anthony A -- Durbin, Richard -- Pepperkok, Rainer -- Ellenberg, Jan -- 077192/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Apr 1;464(7289):721-7. doi: 10.1038/nature08869.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MitoCheck Project Group, European Molecular Biology Laboratory (EMBL), Meyerhofstrasse 1, D-69117 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360735" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/*genetics ; Cell Movement/genetics ; Cell Survival/genetics ; Color ; Gene Knockdown Techniques ; Genes/genetics ; Genome, Human/*genetics ; HeLa Cells ; Humans ; Kinetics ; Mice ; Microscopy, Fluorescence/*methods ; Mitosis/genetics ; *Phenotype ; RNA Interference ; Reproducibility of Results ; Spindle Apparatus/genetics/metabolism ; Time Factors
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    A synaptic and circuit basis for corollary discharge in the auditory cortex (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-08-28
    Description: Sensory regions of the brain integrate environmental cues with copies of motor-related signals important for imminent and ongoing movements. In mammals, signals propagating from the motor cortex to the auditory cortex are thought to have a critical role in normal hearing and behaviour, yet the synaptic and circuit mechanisms by which these motor-related signals influence auditory cortical activity remain poorly understood. Using in vivo intracellular recordings in behaving mice, we find that excitatory neurons in the auditory cortex are suppressed before and during movement, owing in part to increased activity of local parvalbumin-positive interneurons. Electrophysiology and optogenetic gain- and loss-of-function experiments reveal that motor-related changes in auditory cortical dynamics are driven by a subset of neurons in the secondary motor cortex that innervate the auditory cortex and are active during movement. These findings provide a synaptic and circuit basis for the motor-related corollary discharge hypothesized to facilitate hearing and auditory-guided behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4248668/" 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/PMC4248668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, David M -- Nelson, Anders -- Mooney, Richard -- NS079929/NS/NINDS NIH HHS/ -- R01 DC013826/DC/NIDCD NIH HHS/ -- R21 NS079929/NS/NINDS NIH HHS/ -- T32 GM008441/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Sep 11;513(7517):189-94. doi: 10.1038/nature13724. Epub 2014 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA [2]. ; Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25162524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Auditory Cortex/*physiology ; Electrical Synapses/*physiology ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity/*physiology ; Optogenetics ; Sensory Receptor Cells/metabolism
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  • 9
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    GABAergic pathway from zona incerta to neocortex: clarification (1991)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1991-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, C S -- Nicolelis, M A -- Schneider, J S -- Chapin, J K Jr -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1162.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1706534" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; Cerebral Cortex/*anatomy & histology ; Diencephalon/*anatomy & histology ; Horseradish Peroxidase ; Mice ; Neurons/cytology ; Rats ; Thalamus/*anatomy & histology ; gamma-Aminobutyric Acid/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Efficient inhibition of the Alzheimer's disease beta-secretase by membrane targeting (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-26
    Description: beta-Secretase plays a critical role in beta-amyloid formation and thus provides a therapeutic target for Alzheimer's disease. Inhibitor design has usually focused on active-site binding, neglecting the subcellular localization of active enzyme. We have addressed this issue by synthesizing a membrane-anchored version of a beta-secretase transition-state inhibitor by linking it to a sterol moiety. Thus, we targeted the inhibitor to active beta-secretase found in endosomes and also reduced the dimensionality of the inhibitor, increasing its local membrane concentration. This inhibitor reduced enzyme activity much more efficiently than did the free inhibitor in cultured cells and in vivo. In addition to effectively targeting beta-secretase, this strategy could also be used in designing potent drugs against other membrane protein targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajendran, Lawrence -- Schneider, Anja -- Schlechtingen, Georg -- Weidlich, Sebastian -- Ries, Jonas -- Braxmeier, Tobias -- Schwille, Petra -- Schulz, Jorg B -- Schroeder, Cornelia -- Simons, Mikael -- Jennings, Gary -- Knolker, Hans-Joachim -- Simons, Kai -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):520-3. doi: 10.1126/science.1156609.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstr. 108, 01307 Dresden, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436784" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/enzymology ; Amyloid Precursor Protein Secretases/*antagonists & inhibitors/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Animals, Genetically Modified ; Drosophila/genetics ; Drug Delivery Systems ; *Drug Design ; Endocytosis ; Endosomes/*enzymology ; HeLa Cells ; Humans ; Intracellular Membranes/metabolism ; Membrane Microdomains/enzymology ; Mice ; Peptides/chemistry/metabolism/*pharmacology ; Protease Inhibitors/chemical synthesis/chemistry/metabolism/*pharmacology ; *Sterols
    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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