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  • 1
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    Impaired cued and contextual memory in NPAS2-deficient mice (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-24
    Description: Neuronal PAS domain protein 2 (NPAS2) is a basic helix-loop-helix (bHLH) PAS domain transcription factor expressed in multiple regions of the vertebrate brain. Targeted insertion of a beta-galactosidase reporter gene (lacZ) resulted in the production of an NPAS2-lacZ fusion protein and an altered form of NPAS2 lacking the bHLH domain. The neuroanatomical expression pattern of NPAS2-lacZ was temporally and spatially coincident with formation of the mature frontal association/limbic forebrain pathway. NPAS2-deficient mice were subjected to a series of behavioral tests and were found to exhibit deficits in the long-term memory arm of the cued and contextual fear task. Thus, NPAS2 may serve a dedicated regulatory role in the acquisition of specific types of memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia, J A -- Zhang, D -- Estill, S J -- Michnoff, C -- Rutter, J -- Reick, M -- Scott, K -- Diaz-Arrastia, R -- McKnight, S L -- AG12297/AG/NIA NIH HHS/ -- AG16450/AG/NIA NIH HHS/ -- NS01763/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Jun 23;288(5474):2226-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10864874" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning ; Basic Helix-Loop-Helix Transcription Factors ; Behavior, Animal ; Brain/metabolism/*physiology ; Conditioning (Psychology) ; Cues ; Fear ; Gene Targeting ; Helix-Loop-Helix Motifs ; Learning/*physiology ; Limbic System/metabolism/physiology ; Male ; Memory/*physiology ; Mice ; Nerve Tissue Proteins/chemistry/genetics/*physiology ; Prosencephalon/metabolism/physiology ; Recombinant Fusion Proteins/chemistry/metabolism ; Touch ; Transcription Factors/chemistry/genetics/*physiology ; Transcriptional Activation ; Transfection ; beta-Galactosidase/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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    Spermiogenesis deficiency in mice lacking the Trf2 gene (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-05-16
    Description: The discovery of TATA-binding protein-related factors (TRFs) has suggested alternative mechanisms for gene-specific transcriptional regulation and raised interest in their biological functions. In contrast to recent observations of an embryonic lethal phenotype for TRF2 inactivation in Caenorhabditis elegans and Xenopus laevis, we found that Trf2-deficient mice are viable. However, Trf2-/- mice are sterile because of a severe defect in spermiogenesis. Postmeiotic round spermatids advance at most to step 7 of differentiation but fail to progress to the elongated form, and gene-specific transcription deficiencies were identified. We speculate that mammals may have evolved more specialized TRF2 functions in the testis that involve transcriptional regulation of genes essential for spermiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, D -- Penttila, T L -- Morris, P L -- Teichmann, M -- Roeder, R G -- New York, N.Y. -- Science. 2001 May 11;292(5519):1153-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11352070" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Differentiation ; Cell Size ; DNA-Binding Proteins/*deficiency/genetics/*physiology ; Female ; *Gene Deletion ; Gene Expression Regulation, Developmental ; Gene Targeting ; Genotype ; Infertility, Male/genetics/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Organ Size ; RNA, Messenger/genetics/metabolism ; Spermatogenesis/*genetics ; Spermatozoa/metabolism/pathology ; Telomeric Repeat Binding Protein 2 ; Testis/abnormalities/metabolism/pathology
    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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    An antimicrobial peptide gene found in the male reproductive system of rats (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-07
    Description: Little is known about the innate defense mechanisms of the male reproductive tract. We cloned a 385-base pair complementary DNA and its genomic DNA named Bin1b that is exclusively expressed in the caput region of the rat epididymis and that is responsible for sperm maturation, storage, and protection. Bin1b exhibits structural characteristics and antimicrobial activity similar to that of cationic antimicrobial peptides, beta-defensins. Bin1b is maximally expressed when the rats are sexually mature and can be up-regulated by inflammation. Bin1b appears to be a natural epididymis-specific antimicrobial peptide that plays a role in reproductive tract host defense and male fertility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, P -- Chan, H C -- He, B -- So, S C -- Chung, Y W -- Shang, Q -- Zhang, Y D -- Zhang, Y L -- New York, N.Y. -- Science. 2001 Mar 2;291(5509):1783-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, 320, Yue-Yang Road, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11230693" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cloning, Molecular ; DNA, Complementary ; Epididymis/*immunology/physiology ; Epididymitis/immunology ; Escherichia coli/growth & development ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genes ; Humans ; Male ; Molecular Sequence Data ; Oligonucleotides, Antisense/pharmacology ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Sequence Alignment ; Sexual Maturation ; Spermatozoa/physiology ; Up-Regulation ; beta-Defensins/chemistry/*genetics/pharmacology/*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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  • 4
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    Neutrophil ageing is regulated by the microbiome (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-09-17
    Description: Blood polymorphonuclear neutrophils provide immune protection against pathogens, but may also promote tissue injury in inflammatory diseases. Although neutrophils are generally considered to be a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and replenishment by newly released neutrophils from the bone marrow. Aged neutrophils upregulate CXCR4, a receptor allowing their clearance in the bone marrow, with feedback inhibition of neutrophil production via the IL-17/G-CSF axis, and rhythmic modulation of the haematopoietic stem-cell niche. The aged subset also expresses low levels of L-selectin. Previous studies have suggested that in vitro-aged neutrophils exhibit impaired migration and reduced pro-inflammatory properties. Here, using in vivo ageing analyses in mice, we show that neutrophil pro-inflammatory activity correlates positively with their ageing whilst in circulation. Aged neutrophils represent an overly active subset exhibiting enhanced alphaMbeta2 integrin activation and neutrophil extracellular trap formation under inflammatory conditions. Neutrophil ageing is driven by the microbiota via Toll-like receptor and myeloid differentiation factor 88-mediated signalling pathways. Depletion of the microbiota significantly reduces the number of circulating aged neutrophils and dramatically improves the pathogenesis and inflammation-related organ damage in models of sickle-cell disease or endotoxin-induced septic shock. These results identify a role for the microbiota in regulating a disease-promoting neutrophil subset.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712631/" 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/PMC4712631/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Dachuan -- Chen, Grace -- Manwani, Deepa -- Mortha, Arthur -- Xu, Chunliang -- Faith, Jeremiah J -- Burk, Robert D -- Kunisaki, Yuya -- Jang, Jung-Eun -- Scheiermann, Christoph -- Merad, Miriam -- Frenette, Paul S -- R01 CA154947/CA/NCI NIH HHS/ -- R01 CA173861/CA/NCI NIH HHS/ -- R01 CA190400/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Sep 24;525(7570):528-32. doi: 10.1038/nature15367. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Immunology Institute, Mount Sinai School of Medicine, New York, New York 10029, USA. ; The Institute for Genomics and Multiscale Biology, Mount Sinai School of Medicine, New York, New York 10029, USA. ; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374999" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/blood/microbiology/pathology ; Animals ; Cell Aging/*immunology ; Disease Models, Animal ; Erythrocytes, Abnormal/pathology ; Inflammation/immunology/pathology ; Macrophage-1 Antigen/metabolism ; Male ; Mice ; Microbiota/*immunology ; Myeloid Differentiation Factor 88/metabolism ; Neutrophils/*cytology/*immunology ; Shock, Septic/immunology/microbiology/pathology ; Signal Transduction ; Toll-Like Receptors/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Arteriolar niches maintain haematopoietic stem cell quiescence (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-10-11
    Description: Cell cycle quiescence is a critical feature contributing to haematopoietic stem cell (HSC) maintenance. Although various candidate stromal cells have been identified as potential HSC niches, the spatial localization of quiescent HSCs in the bone marrow remains unclear. Here, using a novel approach that combines whole-mount confocal immunofluorescence imaging techniques and computational modelling to analyse significant three-dimensional associations in the mouse bone marrow among vascular structures, stromal cells and HSCs, we show that quiescent HSCs associate specifically with small arterioles that are preferentially found in endosteal bone marrow. These arterioles are ensheathed exclusively by rare NG2 (also known as CSPG4)(+) pericytes, distinct from sinusoid-associated leptin receptor (LEPR)(+) cells. Pharmacological or genetic activation of the HSC cell cycle alters the distribution of HSCs from NG2(+) periarteriolar niches to LEPR(+) perisinusoidal niches. Conditional depletion of NG2(+) cells induces HSC cycling and reduces functional long-term repopulating HSCs in the bone marrow. These results thus indicate that arteriolar niches are indispensable for maintaining HSC quiescence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821873/" 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/PMC3821873/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kunisaki, Yuya -- Bruns, Ingmar -- Scheiermann, Christoph -- Ahmed, Jalal -- Pinho, Sandra -- Zhang, Dachuan -- Mizoguchi, Toshihide -- Wei, Qiaozhi -- Lucas, Daniel -- Ito, Keisuke -- Mar, Jessica C -- Bergman, Aviv -- Frenette, Paul S -- HL069438/HL/NHLBI NIH HHS/ -- HL097700/HL/NHLBI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL097700/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- T32 063754/PHS HHS/ -- England -- Nature. 2013 Oct 31;502(7473):637-43. doi: 10.1038/nature12612. Epub 2013 Oct 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24107994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arterioles/*cytology ; Bone Marrow/blood supply ; Cell Division ; Cell Separation ; Female ; Flow Cytometry ; Hematopoietic Stem Cells/*cytology/metabolism ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Nestin/metabolism ; *Stem Cell Niche
    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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    Diversity and dynamics of the Drosophila transcriptome (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-03-29
    Description: Animal transcriptomes are dynamic, with each cell type, tissue and organ system expressing an ensemble of transcript isoforms that give rise to substantial diversity. Here we have identified new genes, transcripts and proteins using poly(A)+ RNA sequencing from Drosophila melanogaster in cultured cell lines, dissected organ systems and under environmental perturbations. We found that a small set of mostly neural-specific genes has the potential to encode thousands of transcripts each through extensive alternative promoter usage and RNA splicing. The magnitudes of splicing changes are larger between tissues than between developmental stages, and most sex-specific splicing is gonad-specific. Gonads express hundreds of previously unknown coding and long non-coding RNAs (lncRNAs), some of which are antisense to protein-coding genes and produce short regulatory RNAs. Furthermore, previously identified pervasive intergenic transcription occurs primarily within newly identified introns. The fly transcriptome is substantially more complex than previously recognized, with this complexity arising from combinatorial usage of promoters, splice sites and polyadenylation sites.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4152413/" 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/PMC4152413/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, James B -- Boley, Nathan -- Eisman, Robert -- May, Gemma E -- Stoiber, Marcus H -- Duff, Michael O -- Booth, Ben W -- Wen, Jiayu -- Park, Soo -- Suzuki, Ana Maria -- Wan, Kenneth H -- Yu, Charles -- Zhang, Dayu -- Carlson, Joseph W -- Cherbas, Lucy -- Eads, Brian D -- Miller, David -- Mockaitis, Keithanne -- Roberts, Johnny -- Davis, Carrie A -- Frise, Erwin -- Hammonds, Ann S -- Olson, Sara -- Shenker, Sol -- Sturgill, David -- Samsonova, Anastasia A -- Weiszmann, Richard -- Robinson, Garret -- Hernandez, Juan -- Andrews, Justen -- Bickel, Peter J -- Carninci, Piero -- Cherbas, Peter -- Gingeras, Thomas R -- Hoskins, Roger A -- Kaufman, Thomas C -- Lai, Eric C -- Oliver, Brian -- Perrimon, Norbert -- Graveley, Brenton R -- Celniker, Susan E -- 1U01HG007031-01/HG/NHGRI NIH HHS/ -- 5U01HG004695-04/HG/NHGRI NIH HHS/ -- K99 HG006698/HG/NHGRI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 GM076655/GM/NIGMS NIH HHS/ -- R01 GM083300/GM/NIGMS NIH HHS/ -- R01 GM097231/GM/NIGMS NIH HHS/ -- RC2-HG005639/HG/NHGRI NIH HHS/ -- U01 HG004271/HG/NHGRI NIH HHS/ -- U01 HG007031/HG/NHGRI NIH HHS/ -- U01-HG004261/HG/NHGRI NIH HHS/ -- U54 HG006944/HG/NHGRI NIH HHS/ -- ZIA DK015600-18/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 28;512(7515):393-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670639" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/genetics ; Animals ; Drosophila melanogaster/anatomy & histology/cytology/*genetics ; Female ; *Gene Expression Profiling ; Male ; Molecular Sequence Annotation ; Nerve Tissue/metabolism ; Organ Specificity ; Poly A/genetics ; Polyadenylation ; Promoter Regions, Genetic/genetics ; RNA, Long Noncoding/genetics ; RNA, Messenger/genetics/metabolism ; Sex Characteristics ; Stress, Physiological/genetics ; Transcriptome/*genetics
    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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    The developmental transcriptome of Drosophila melanogaster (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Drosophila melanogaster is one of the most well studied genetic model organisms; nonetheless, its genome still contains unannotated coding and non-coding genes, transcripts, exons and RNA editing sites. Full discovery and annotation are pre-requisites for understanding how the regulation of transcription, splicing and RNA editing directs the development of this complex organism. Here we used RNA-Seq, tiling microarrays and cDNA sequencing to explore the transcriptome in 30 distinct developmental stages. We identified 111,195 new elements, including thousands of genes, coding and non-coding transcripts, exons, splicing and editing events, and inferred protein isoforms that previously eluded discovery using established experimental, prediction and conservation-based approaches. These data substantially expand the number of known transcribed elements in the Drosophila genome and provide a high-resolution view of transcriptome dynamics throughout development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075879/" 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/PMC3075879/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graveley, Brenton R -- Brooks, Angela N -- Carlson, Joseph W -- Duff, Michael O -- Landolin, Jane M -- Yang, Li -- Artieri, Carlo G -- van Baren, Marijke J -- Boley, Nathan -- Booth, Benjamin W -- Brown, James B -- Cherbas, Lucy -- Davis, Carrie A -- Dobin, Alex -- Li, Renhua -- Lin, Wei -- Malone, John H -- Mattiuzzo, Nicolas R -- Miller, David -- Sturgill, David -- Tuch, Brian B -- Zaleski, Chris -- Zhang, Dayu -- Blanchette, Marco -- Dudoit, Sandrine -- Eads, Brian -- Green, Richard E -- Hammonds, Ann -- Jiang, Lichun -- Kapranov, Phil -- Langton, Laura -- Perrimon, Norbert -- Sandler, Jeremy E -- Wan, Kenneth H -- Willingham, Aarron -- Zhang, Yu -- Zou, Yi -- Andrews, Justen -- Bickel, Peter J -- Brenner, Steven E -- Brent, Michael R -- Cherbas, Peter -- Gingeras, Thomas R -- Hoskins, Roger A -- Kaufman, Thomas C -- Oliver, Brian -- Celniker, Susan E -- U01 HB004271/HB/NHLBI NIH HHS/ -- U01 HG004271/HG/NHGRI NIH HHS/ -- U01 HG004271-01/HG/NHGRI NIH HHS/ -- ZIA DK015600-14/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):473-9. doi: 10.1038/nature09715. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Developmental Biology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-6403, USA. graveley@neuron.uchc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179090" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/genetics ; Animals ; Base Sequence ; Drosophila Proteins/genetics ; Drosophila melanogaster/embryology/*genetics/*growth & development ; Exons/genetics ; Female ; *Gene Expression Profiling ; Gene Expression Regulation, Developmental/*genetics ; Genes, Insect/genetics ; Genome, Insect/genetics ; Male ; MicroRNAs/genetics ; Oligonucleotide Array Sequence Analysis ; Protein Isoforms/genetics ; RNA Editing/genetics ; RNA, Messenger/analysis/genetics ; RNA, Small Untranslated/analysis/genetics ; Sequence Analysis ; Sex Characteristics ; Transcription, Genetic/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-02-28
    Description: Nonalcoholic fatty liver disease (NAFLD) is a major factor in the pathogenesis of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH). The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effects on NAFLD, insulin resistance, and obesity in preclinical models but is too toxic for clinical use. We developed a controlled-release oral formulation of DNP, called CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial uncoupling. In rat models, CRMP reduced hypertriglyceridemia, insulin resistance, hepatic steatosis, and diabetes. It also normalized plasma transaminase concentrations, ameliorated liver fibrosis, and improved hepatic protein synthetic function in a methionine/choline-deficient rat model of NASH. Chronic treatment with CRMP was not associated with any systemic toxicity. These data offer proof of concept that mild hepatic mitochondrial uncoupling may be a safe and effective therapy for the related epidemics of metabolic syndrome, T2D, and NASH.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495920/" 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/PMC4495920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perry, Rachel J -- Zhang, Dongyan -- Zhang, Xian-Man -- Boyer, James L -- Shulman, Gerald I -- P30 DK-34989/DK/NIDDK NIH HHS/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- R01 DK-40936/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R24 DK-085638/DK/NIDDK NIH HHS/ -- T32 DK-101019/DK/NIDDK NIH HHS/ -- U24 DK-059635/DK/NIDDK NIH HHS/ -- UL1 TR-000142/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1253-6. doi: 10.1126/science.aaa0672. Epub 2015 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Yale Liver Center, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. gerald.shulman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25721504" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4-Dinitrophenol/*administration & dosage/toxicity ; Animals ; Blood Glucose/metabolism ; Delayed-Action Preparations/*administration & dosage ; Diabetes Mellitus, Type 2/*drug therapy/metabolism ; Glucose Tolerance Test ; Insulin Resistance ; Lipid Metabolism ; Liver Cirrhosis/drug therapy ; Male ; Mice ; Mitochondria, Liver/drug effects/metabolism ; Muscle, Skeletal/metabolism ; Non-alcoholic Fatty Liver Disease/*drug therapy/metabolism ; Oxidation-Reduction ; Proton Ionophores/*administration & dosage/toxicity ; Random Allocation ; Rats ; Rats, Zucker
    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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    Autism-like behaviours and germline transmission in transgenic monkeys overexpressing MeCP2 (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-26
    Description: Methyl-CpG binding protein 2 (MeCP2) has crucial roles in transcriptional regulation and microRNA processing. Mutations in the MECP2 gene are found in 90% of patients with Rett syndrome, a severe developmental disorder with autistic phenotypes. Duplications of MECP2-containing genomic segments cause the MECP2 duplication syndrome, which shares core symptoms with autism spectrum disorders. Although Mecp2-null mice recapitulate most developmental and behavioural defects seen in patients with Rett syndrome, it has been difficult to identify autism-like behaviours in the mouse model of MeCP2 overexpression. Here we report that lentivirus-based transgenic cynomolgus monkeys (Macaca fascicularis) expressing human MeCP2 in the brain exhibit autism-like behaviours and show germline transmission of the transgene. Expression of the MECP2 transgene was confirmed by western blotting and immunostaining of brain tissues of transgenic monkeys. Genomic integration sites of the transgenes were characterized by a deep-sequencing-based method. As compared to wild-type monkeys, MECP2 transgenic monkeys exhibited a higher frequency of repetitive circular locomotion and increased stress responses, as measured by the threat-related anxiety and defensive test. The transgenic monkeys showed less interaction with wild-type monkeys within the same group, and also a reduced interaction time when paired with other transgenic monkeys in social interaction tests. The cognitive functions of the transgenic monkeys were largely normal in the Wisconsin general test apparatus, although some showed signs of stereotypic cognitive behaviours. Notably, we succeeded in generating five F1 offspring of MECP2 transgenic monkeys by intracytoplasmic sperm injection with sperm from one F0 transgenic monkey, showing germline transmission and Mendelian segregation of several MECP2 transgenes in the F1 progeny. Moreover, F1 transgenic monkeys also showed reduced social interactions when tested in pairs, as compared to wild-type monkeys of similar age. Together, these results indicate the feasibility and reliability of using genetically engineered non-human primates to study brain disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Zhen -- Li, Xiao -- Zhang, Jun-Tao -- Cai, Yi-Jun -- Cheng, Tian-Lin -- Cheng, Cheng -- Wang, Yan -- Zhang, Chen-Chen -- Nie, Yan-Hong -- Chen, Zhi-Fang -- Bian, Wen-Jie -- Zhang, Ling -- Xiao, Jianqiu -- Lu, Bin -- Zhang, Yue-Fang -- Zhang, Xiao-Di -- Sang, Xiao -- Wu, Jia-Jia -- Xu, Xiu -- Xiong, Zhi-Qi -- Zhang, Feng -- Yu, Xiang -- Gong, Neng -- Zhou, Wen-Hao -- Sun, Qiang -- Qiu, Zilong -- England -- Nature. 2016 Feb 4;530(7588):98-102. doi: 10.1038/nature16533. Epub 2016 Jan 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience, CAS Key Laboratory of Primate Neurobiology, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-Yang Road, Shanghai 200031, China. ; State Key Laboratory of Genetic Engineering and Ministry of Education Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200438, China. ; Department of Child Healthcare, Children's Hospital of Fudan University, Shanghai 201102, China. ; Department of Neonatology, Children's Hospital of Fudan University, Shanghai 201102, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26808898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Anxiety/genetics/psychology ; Autistic Disorder/*genetics/metabolism/physiopathology/*psychology ; Brain/metabolism ; Cognition/physiology ; *Disease Models, Animal ; Female ; Germ-Line Mutation/*genetics ; Heredity/*genetics ; Humans ; Locomotion/genetics/physiology ; Macaca fascicularis ; Male ; Methyl-CpG-Binding Protein 2/*genetics/*metabolism ; Phenotype ; Social Behavior ; Sperm Injections, Intracytoplasmic ; Transgenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    IkappaBbeta acts to inhibit and activate gene expression during the inflammatory response (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-27
    Description: The activation of pro-inflammatory gene programs by nuclear factor-kappaB (NF-kappaB) is primarily regulated through cytoplasmic sequestration of NF-kappaB by the inhibitor of kappaB (IkappaB) family of proteins. IkappaBbeta, a major isoform of IkappaB, can sequester NF-kappaB in the cytoplasm, although its biological role remains unclear. Although cells lacking IkappaBbeta have been reported, in vivo studies have been limited and suggested redundancy between IkappaBalpha and IkappaBbeta. Like IkappaBalpha, IkappaBbeta is also inducibly degraded; however, upon stimulation by lipopolysaccharide (LPS), it is degraded slowly and re-synthesized as a hypophosphorylated form that can be detected in the nucleus. The crystal structure of IkappaBbeta bound to p65 suggested this complex might bind DNA. In vitro, hypophosphorylated IkappaBbeta can bind DNA with p65 and c-Rel, and the DNA-bound NF-kappaB:IkappaBbeta complexes are resistant to IkappaBalpha, suggesting hypophosphorylated, nuclear IkappaBbeta may prolong the expression of certain genes. Here we report that in vivo IkappaBbeta serves both to inhibit and facilitate the inflammatory response. IkappaBbeta degradation releases NF-kappaB dimers which upregulate pro-inflammatory target genes such as tumour necrosis factor-alpha (TNF-alpha). Surprisingly, absence of IkappaBbeta results in a dramatic reduction of TNF-alpha in response to LPS even though activation of NF-kappaB is normal. The inhibition of TNF-alpha messenger RNA (mRNA) expression correlates with the absence of nuclear, hypophosphorylated-IkappaBbeta bound to p65:c-Rel heterodimers at a specific kappaB site on the TNF-alpha promoter. Therefore IkappaBbeta acts through p65:c-Rel dimers to maintain prolonged expression of TNF-alpha. As a result, IkappaBbeta(-/-) mice are resistant to LPS-induced septic shock and collagen-induced arthritis. Blocking IkappaBbeta might be a promising new strategy for selectively inhibiting the chronic phase of TNF-alpha production during the inflammatory response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2946371/" 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/PMC2946371/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rao, Ping -- Hayden, Mathew S -- Long, Meixiao -- Scott, Martin L -- West, A Philip -- Zhang, Dekai -- Oeckinghaus, Andrea -- Lynch, Candace -- Hoffmann, Alexander -- Baltimore, David -- Ghosh, Sankar -- R01 AI083453/AI/NIAID NIH HHS/ -- R01 GM071573/GM/NIGMS NIH HHS/ -- R01 GM071573-06/GM/NIGMS NIH HHS/ -- R37 AI033443/AI/NIAID NIH HHS/ -- R37 AI033443-19/AI/NIAID NIH HHS/ -- R37-AI03343/AI/NIAID NIH HHS/ -- England -- Nature. 2010 Aug 26;466(7310):1115-9. doi: 10.1038/nature09283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology and Department of Molecular Biophysics & Biochemistry, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20740013" target="_blank"〉PubMed〈/a〉
    Keywords: Adjuvants, Immunologic/pharmacology ; Animals ; Arthritis, Experimental/*metabolism ; Cell Line ; Cytokines/blood ; Female ; *Gene Expression Regulation/drug effects ; I-kappa B Proteins/*genetics/*metabolism ; Lipopolysaccharides/pharmacology ; Male ; Mice ; Mice, Inbred DBA ; Mice, Knockout ; Tumor Necrosis Factor-alpha/blood/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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