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  • 1
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    Ars2 maintains neural stem-cell identity through direct transcriptional activation of Sox2 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-27
    Description: Fundamental questions remain unanswered about the transcriptional networks that control the identity and self-renewal of neural stem cells (NSCs), a specialized subset of astroglial cells that are endowed with stem properties and neurogenic capacity. Here we report that the zinc finger protein Ars2 (arsenite-resistance protein 2; also known as Srrt) is expressed by adult NSCs from the subventricular zone (SVZ) of mice, and that selective knockdown of Ars2 in cells expressing glial fibrillary acidic protein within the adult SVZ depletes the number of NSCs and their neurogenic capacity. These phenotypes are recapitulated in the postnatal SVZ of hGFAP-cre::Ars2(fl/fl) conditional knockout mice, but are more severe. Ex vivo assays show that Ars2 is necessary and sufficient to promote NSC self-renewal, and that it does so by positively regulating the expression of Sox2. Although plant and animal orthologues of Ars2 are known for their conserved roles in microRNA biogenesis, we unexpectedly observed that Ars2 retains its capacity to promote self-renewal in Drosha and Dicer1 knockout NSCs. Instead, chromatin immunoprecipitation revealed that Ars2 binds a specific region within the 6-kilobase NSC enhancer of Sox2. This association is RNA-independent, and the region that is bound is required for Ars2-mediated activation of Sox2. We used gel-shift analysis to refine the Sox2 region bound by Ars2 to a specific conserved DNA sequence. The importance of Sox2 as a critical downstream effector is shown by its ability to restore the self-renewal and multipotency defects of Ars2 knockout NSCs. Our findings reveal Ars2 as a new transcription factor that controls the multipotent progenitor state of NSCs through direct activation of the pluripotency factor Sox2.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261657/" 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/PMC3261657/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andreu-Agullo, Celia -- Maurin, Thomas -- Thompson, Craig B -- Lai, Eric C -- R01 GM083300/GM/NIGMS NIH HHS/ -- R01 GM083300-05/GM/NIGMS NIH HHS/ -- R01-GM083300/GM/NIGMS NIH HHS/ -- England -- Nature. 2011 Dec 25;481(7380):195-8. doi: 10.1038/nature10712.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Sloan-Kettering Institute, 1275 York Avenue, Box 252, New York, New York 10065, USA. andreuac@mskcc.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22198669" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology ; Cell Proliferation ; Cells, Cultured ; Chromatin Immunoprecipitation ; Conserved Sequence/genetics ; DEAD-box RNA Helicases/deficiency ; Electrophoretic Mobility Shift Assay ; Enhancer Elements, Genetic/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Mice ; Mice, Knockout ; Neural Stem Cells/*cytology/*metabolism ; Neurogenesis/genetics ; Nuclear Proteins/chemistry/deficiency/genetics/*metabolism ; Olfactory Bulb/cytology ; Ribonuclease III/deficiency ; SOXB1 Transcription Factors/*genetics ; Transcription Factors/chemistry/deficiency/genetics/*metabolism ; *Transcriptional Activation ; Zinc Fingers
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Purkinje neuron synchrony elicits time-locked spiking in the cerebellar nuclei (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-27
    Description: An unusual feature of the cerebellar cortex is that its output neurons, Purkinje cells, release GABA (gamma-aminobutyric acid). Their high intrinsic firing rates (50 Hz) and extensive convergence predict that their target neurons in the cerebellar nuclei would be largely inhibited unless Purkinje cells pause their spiking, yet Purkinje and nuclear neuron firing rates do not always vary inversely. One indication of how these synapses transmit information is that populations of Purkinje neurons synchronize their spikes during cerebellar behaviours. If nuclear neurons respond to Purkinje synchrony, they may encode signals from subsets of inhibitory inputs. Here we show in weanling and adult mice that nuclear neurons transmit the timing of synchronous Purkinje afferent spikes, owing to modest Purkinje-to-nuclear convergence ratios ( approximately 40:1), fast inhibitory postsynaptic current kinetics (tau(decay) = 2.5 ms) and high intrinsic firing rates ( approximately 90 Hz). In vitro, dynamically clamped asynchronous inhibitory postsynaptic potentials mimicking Purkinje afferents suppress nuclear cell spiking, whereas synchronous inhibitory postsynaptic potentials entrain nuclear cell spiking. With partial synchrony, nuclear neurons time-lock their spikes to the synchronous subpopulation of inputs, even when only 2 out of 40 afferents synchronize. In vivo, nuclear neurons reliably phase-lock to regular trains of molecular layer stimulation. Thus, cerebellar nuclear neurons can preferentially relay the spike timing of synchronized Purkinje cells to downstream premotor areas.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268051/" 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/PMC3268051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Person, Abigail L -- Raman, Indira M -- F32 NS067831/NS/NINDS NIH HHS/ -- F32 NS067831-02/NS/NINDS NIH HHS/ -- F32-NS067831/NS/NINDS NIH HHS/ -- R01 NS039395/NS/NINDS NIH HHS/ -- R01 NS039395-13/NS/NINDS NIH HHS/ -- R01-NS39395/NS/NINDS NIH HHS/ -- England -- Nature. 2011 Dec 25;481(7382):502-5. doi: 10.1038/nature10732.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Northwestern University, Evanston, Illinois 60208, USA. a-person@northwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22198670" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Cerebellar Cortex/cytology ; Cerebellar Nuclei/*physiology ; Inhibitory Postsynaptic Potentials/*physiology ; Kinetics ; Mice ; Mice, Inbred C57BL ; Purkinje Cells/*physiology ; Time Factors ; Weaning
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Npas4 regulates a transcriptional program in CA3 required for contextual memory formation (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-24
    Description: The rapid encoding of contextual memory requires the CA3 region of the hippocampus, but the necessary genetic pathways remain unclear. We found that the activity-dependent transcription factor Npas4 regulates a transcriptional program in CA3 that is required for contextual memory formation. Npas4 was specifically expressed in CA3 after contextual learning. Global knockout or selective deletion of Npas4 in CA3 both resulted in impaired contextual memory, and restoration of Npas4 in CA3 was sufficient to reverse the deficit in global knockout mice. By recruiting RNA polymerase II to promoters and enhancers of target genes, Npas4 regulates a learning-specific transcriptional program in CA3 that includes many well-known activity-regulated genes, which suggests that Npas4 is a master regulator of activity-regulated gene programs and is central to memory formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038289/" 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/PMC4038289/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ramamoorthi, Kartik -- Fropf, Robin -- Belfort, Gabriel M -- Fitzmaurice, Helen L -- McKinney, Ross M -- Neve, Rachael L -- Otto, Tim -- Lin, Yingxi -- MH091220-01/MH/NIMH NIH HHS/ -- R01 MH091220/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1669-75. doi: 10.1126/science.1208049.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGovern Institute for Brain Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism ; CA3 Region, Hippocampal/cytology/*physiology ; Conditioning (Psychology) ; Enhancer Elements, Genetic ; Fear ; Gene Deletion ; *Gene Expression Regulation ; Genes, Immediate-Early ; Learning ; *Memory ; Mice ; Mice, Knockout ; Neurons/physiology ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; *Transcription, Genetic ; Transcriptional Activation
    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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    Neurodevelopmental disorders. New hope for a devastating neurological disorder (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1615. doi: 10.1126/science.334.6063.1615.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194537" target="_blank"〉PubMed〈/a〉
    Keywords: Angelman Syndrome/*drug therapy/*genetics/therapy ; Animals ; Brain/cytology/drug effects ; Camptothecin/*analogs & derivatives/pharmacology ; Drug Evaluation, Preclinical ; Gene Expression Regulation ; Genetic Therapy ; Humans ; Mice ; Neurons/drug effects/physiology ; Topotecan/administration & dosage/*pharmacology/therapeutic use ; *Transcriptional Activation ; Ubiquitin-Protein Ligases/*genetics/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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  • 5
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    Fear erasure in mice requires synergy between antidepressant drugs and extinction training (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-24
    Description: Antidepressant drugs and psychotherapy combined are more effective in treating mood disorders than either treatment alone, but the neurobiological basis of this interaction is unknown. To investigate how antidepressants influence the response of mood-related systems to behavioral experience, we used a fear-conditioning and extinction paradigm in mice. Combining extinction training with chronic fluoxetine, but neither treatment alone, induced an enduring loss of conditioned fear memory in adult animals. Fluoxetine treatment increased synaptic plasticity, converted the fear memory circuitry to a more immature state, and acted through local brain-derived neurotrophic factor. Fluoxetine-induced plasticity may allow fear erasure by extinction-guided remodeling of the memory circuitry. Thus, the pharmacological effects of antidepressants need to be combined with psychological rehabilitation to reorganize networks rendered more plastic by the drug treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929964/" 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/PMC3929964/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karpova, Nina N -- Pickenhagen, Anouchka -- Lindholm, Jesse -- Tiraboschi, Ettore -- Kulesskaya, Natalia -- Agustsdottir, Arna -- Antila, Hanna -- Popova, Dina -- Akamine, Yumiko -- Bahi, Amine -- Sullivan, Regina -- Hen, Rene -- Drew, Liam J -- Castren, Eero -- DC 003906/DC/NIDCD NIH HHS/ -- DC 009910/DC/NIDCD NIH HHS/ -- R01 DC009910/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 23;334(6063):1731-4. doi: 10.1126/science.1214592.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sigrid Juselius Laboratory, Neuroscience Center, University of Helsinki, Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22194582" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/drug effects/physiology ; Animals ; Antidepressive Agents, Second-Generation/pharmacology/*therapeutic use ; Anxiety Disorders/*therapy ; *Behavior Therapy ; Brain-Derived Neurotrophic Factor/genetics/metabolism ; Combined Modality Therapy ; Conditioning, Classical ; Excitatory Postsynaptic Potentials/drug effects ; *Extinction, Psychological ; *Fear ; Fluoxetine/pharmacology/*therapeutic use ; Interneurons/drug effects/physiology ; Male ; Memory ; Mice ; Mice, Inbred C57BL ; Nerve Net/drug effects/physiology ; Neuronal Plasticity/*drug effects ; Neurons/cytology/drug effects ; Synaptic Transmission/drug effects
    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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    Topoisomerase inhibitors unsilence the dormant allele of Ube3a in neurons (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-23
    Description: Angelman syndrome is a severe neurodevelopmental disorder caused by deletion or mutation of the maternal allele of the ubiquitin protein ligase E3A (UBE3A). In neurons, the paternal allele of UBE3A is intact but epigenetically silenced, raising the possibility that Angelman syndrome could be treated by activating this silenced allele to restore functional UBE3A protein. Using an unbiased, high-content screen in primary cortical neurons from mice, we identify twelve topoisomerase I inhibitors and four topoisomerase II inhibitors that unsilence the paternal Ube3a allele. These drugs included topotecan, irinotecan, etoposide and dexrazoxane (ICRF-187). At nanomolar concentrations, topotecan upregulated catalytically active UBE3A in neurons from maternal Ube3a-null mice. Topotecan concomitantly downregulated expression of the Ube3a antisense transcript that overlaps the paternal copy of Ube3a. These results indicate that topotecan unsilences Ube3a in cis by reducing transcription of an imprinted antisense RNA. When administered in vivo, topotecan unsilenced the paternal Ube3a allele in several regions of the nervous system, including neurons in the hippocampus, neocortex, striatum, cerebellum and spinal cord. Paternal expression of Ube3a remained elevated in a subset of spinal cord neurons for at least 12 weeks after cessation of topotecan treatment, indicating that transient topoisomerase inhibition can have enduring effects on gene expression. Although potential off-target effects remain to be investigated, our findings suggest a therapeutic strategy for reactivating the functional but dormant allele of Ube3a in patients with Angelman syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257422/" 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/PMC3257422/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Hsien-Sung -- Allen, John A -- Mabb, Angela M -- King, Ian F -- Miriyala, Jayalakshmi -- Taylor-Blake, Bonnie -- Sciaky, Noah -- Dutton, J Walter Jr -- Lee, Hyeong-Min -- Chen, Xin -- Jin, Jian -- Bridges, Arlene S -- Zylka, Mark J -- Roth, Bryan L -- Philpot, Benjamin D -- 5F32NS067712/NS/NINDS NIH HHS/ -- 5P30NS045892/NS/NINDS NIH HHS/ -- HHSN-271-2008-00025-C/PHS HHS/ -- P30 HD003110/HD/NICHD NIH HHS/ -- P30 HD003110-45/HD/NICHD NIH HHS/ -- P30HD03110/HD/NICHD NIH HHS/ -- R01EY018323/EY/NEI NIH HHS/ -- R01MH093372/MH/NIMH NIH HHS/ -- R01NS060725/NS/NINDS NIH HHS/ -- R01NS067688/NS/NINDS NIH HHS/ -- T32 HD040127/HD/NICHD NIH HHS/ -- T32 HD040127-10/HD/NICHD NIH HHS/ -- T32HD040127-07/HD/NICHD NIH HHS/ -- England -- Nature. 2011 Dec 21;481(7380):185-9. doi: 10.1038/nature10726.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22190039" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Angelman Syndrome/drug therapy/genetics ; Animals ; Cells, Cultured ; Cerebral Cortex/cytology/drug effects/metabolism ; Drug Evaluation, Preclinical ; Fathers ; Female ; Gene Silencing/*drug effects ; Genomic Imprinting/drug effects/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mothers ; Neurons/*drug effects/*metabolism ; Small Molecule Libraries/administration & dosage/chemistry/pharmacology ; Topoisomerase Inhibitors/administration & ; dosage/analysis/pharmacokinetics/*pharmacology ; Topotecan/administration & dosage/pharmacokinetics/pharmacology ; Ubiquitin-Protein Ligases/deficiency/*genetics
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Molecular biology. Translation goes global (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiss, Robert B -- Atkins, John F -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1509-10. doi: 10.1126/science.1216974.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA. bob.weiss@genetics.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174241" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Profiling ; Gene Expression Regulation ; Humans ; Mice ; Open Reading Frames ; *Protein Biosynthesis ; *Proteome ; *RNA, Messenger/metabolism ; Ribosomes/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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  • 8
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    The molecular basis of acid insensitivity in the African naked mole-rat (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-17
    Description: Acid evokes pain by exciting nociceptors; the acid sensors are proton-gated ion channels that depolarize neurons. The naked mole-rat (Heterocephalus glaber) is exceptional in its acid insensitivity, but acid sensors (acid-sensing ion channels and the transient receptor potential vanilloid-1 ion channel) in naked mole-rat nociceptors are similar to those in other vertebrates. Acid inhibition of voltage-gated sodium currents is more profound in naked mole-rat nociceptors than in mouse nociceptors, however, which effectively prevents acid-induced action potential initiation. We describe a species-specific variant of the nociceptor sodium channel Na(V)1.7, which is potently blocked by protons and can account for acid insensitivity in this species. Thus, evolutionary pressure has selected for an Na(V)1.7 gene variant that tips the balance from proton-induced excitation to inhibition of action potential initiation to abolish acid nociception.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Ewan St John -- Omerbasic, Damir -- Lechner, Stefan G -- Anirudhan, Gireesh -- Lapatsina, Liudmila -- Lewin, Gary R -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1557-60. doi: 10.1126/science.1213760.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Max-Delbruck Center for Molecular Medicine, Berlin-Buch, Germany. ewan.smith@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174253" target="_blank"〉PubMed〈/a〉
    Keywords: Acid Sensing Ion Channels ; Acids/metabolism/*pharmacology ; Action Potentials ; Amino Acid Motifs ; Animals ; Ganglia, Spinal/cytology/physiology ; Mice ; Mole Rats/genetics/*physiology ; NAV1.7 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins/metabolism ; Nociception/*physiology ; Rats ; Sodium Channels/genetics/*metabolism ; TRPV Cation Channels/metabolism
    Print ISSN: 0036-8075
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  • 9
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    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/physiology
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  • 10
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    Detecting novel associations in large data sets (2011)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2011-12-17
    Description: Identifying interesting relationships between pairs of variables in large data sets is increasingly important. Here, we present a measure of dependence for two-variable relationships: the maximal information coefficient (MIC). MIC captures a wide range of associations both functional and not, and for functional relationships provides a score that roughly equals the coefficient of determination (R(2)) of the data relative to the regression function. MIC belongs to a larger class of maximal information-based nonparametric exploration (MINE) statistics for identifying and classifying relationships. We apply MIC and MINE to data sets in global health, gene expression, major-league baseball, and the human gut microbiota and identify known and novel relationships.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325791/" 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/PMC3325791/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reshef, David N -- Reshef, Yakir A -- Finucane, Hilary K -- Grossman, Sharon R -- McVean, Gilean -- Turnbaugh, Peter J -- Lander, Eric S -- Mitzenmacher, Michael -- Sabeti, Pardis C -- 090532/Wellcome Trust/United Kingdom -- P50 GM068763/GM/NIGMS NIH HHS/ -- P50 GM068763-09/GM/NIGMS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U54 GM088558/GM/NIGMS NIH HHS/ -- U54 GM088558-03/GM/NIGMS NIH HHS/ -- U54GM088558/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Dec 16;334(6062):1518-24. doi: 10.1126/science.1205438.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Computer Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dnreshef@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174245" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Baseball/statistics & numerical data ; *Data Interpretation, Statistical ; Female ; Gene Expression ; Genes, Fungal ; Genomics/methods ; Humans ; Intestines/microbiology ; Male ; Metagenome ; Mice ; Obesity ; Saccharomyces cerevisiae/genetics
    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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