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  • Articles  (9)
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  • 2020-2022
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  • 1
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    Endocannabinoid hydrolysis generates brain prostaglandins that promote neuroinflammation (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-25
    Description: Phospholipase A(2)(PLA(2)) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here, we show that a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannabinoid 2-arachidonoylglycerol to generate a major arachidonate precursor pool for neuroinflammatory prostaglandins. MAGL-disrupted animals show neuroprotection in a parkinsonian mouse model. These animals are spared the hemorrhaging caused by COX inhibitors in the gut, where prostaglandins are instead regulated by cytosolic PLA(2). These findings identify MAGL as a distinct metabolic node that couples endocannabinoid to prostaglandin signaling networks in the nervous system and suggest that inhibition of this enzyme may be a new and potentially safer way to suppress the proinflammatory cascades that underlie neurodegenerative disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nomura, Daniel K -- Morrison, Bradley E -- Blankman, Jacqueline L -- Long, Jonathan Z -- Kinsey, Steven G -- Marcondes, Maria Cecilia G -- Ward, Anna M -- Hahn, Yun Kyung -- Lichtman, Aron H -- Conti, Bruno -- Cravatt, Benjamin F -- 5P01DA009789/DA/NIDA NIH HHS/ -- AG028040/AG/NIA NIH HHS/ -- DA017259/DA/NIDA NIH HHS/ -- DA026261/DA/NIDA NIH HHS/ -- F31 DA026261-03/DA/NIDA NIH HHS/ -- K99 DA030908/DA/NIDA NIH HHS/ -- K99 DA030908-01/DA/NIDA NIH HHS/ -- K99DA030908/DA/NIDA NIH HHS/ -- P01 DA009789/DA/NIDA NIH HHS/ -- P01 DA009789-14/DA/NIDA NIH HHS/ -- P01 DA017259/DA/NIDA NIH HHS/ -- P01 DA017259-08/DA/NIDA NIH HHS/ -- P01DA01725/DA/NIDA NIH HHS/ -- R00 DA030908/DA/NIDA NIH HHS/ -- R00 DA030908-02/DA/NIDA NIH HHS/ -- R00DA030908/DA/NIDA NIH HHS/ -- R01 AG028040/AG/NIA NIH HHS/ -- R01 AG028040-04/AG/NIA NIH HHS/ -- R03 DA027936/DA/NIDA NIH HHS/ -- R03 DA027936-02/DA/NIDA NIH HHS/ -- R03DA027936/DA/NIDA NIH HHS/ -- T32 DA007027/DA/NIDA NIH HHS/ -- T32 DA007027-33/DA/NIDA NIH HHS/ -- T32DA007027/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):809-13. doi: 10.1126/science.1209200. Epub 2011 Oct 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Skaggs Institute for Chemical Biology and Department of Chemical Physiology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. dnomura@berkeley.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22021672" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acid/metabolism ; Arachidonic Acids/*metabolism ; Benzodioxoles/pharmacology ; Brain/drug effects/*metabolism/pathology ; Cannabinoid Receptor Modulators/*metabolism ; Cyclooxygenase 1/metabolism ; Cytokines/metabolism ; Eicosanoids/metabolism ; *Endocannabinoids ; Enzyme Inhibitors/pharmacology ; Glycerides/*metabolism ; Hydrolysis ; Inflammation/*metabolism/pathology ; Inflammation Mediators/pharmacology ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Lung/metabolism ; Metabolomics ; Mice ; Mice, Inbred C57BL ; Monoacylglycerol Lipases/antagonists & inhibitors/genetics/*metabolism ; Neuroprotective Agents/pharmacology ; Parkinsonian Disorders/metabolism/pathology ; Phospholipases A2/genetics/metabolism ; Piperidines/pharmacology ; Prostaglandins/biosynthesis/*metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    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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    Partitioning regulatory mechanisms of within-host malaria dynamics using the effective propagation number (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: Immune clearance and resource limitation (via red blood cell depletion) shape the peaks and troughs of malaria parasitemia, which in turn affect disease severity and transmission. Quantitatively partitioning the relative roles of these effects through time is challenging. Using data from rodent malaria, we estimated the effective propagation number, which reflects the relative importance of contrasting within-host control mechanisms through time and is sensitive to the inoculating parasite dose. Our analysis showed that the capacity of innate responses to restrict initial parasite growth saturates with parasite dose and that experimentally enhanced innate immunity can affect parasite density indirectly via resource depletion. Such a statistical approach offers a tool to improve targeting of drugs or vaccines for human therapy by revealing the dynamics and interactions of within-host regulatory mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891600/" 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/PMC3891600/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, C J E -- Graham, A L -- Huijben, S -- Barclay, V C -- Long, G H -- Grenfell, B T -- Read, A F -- Bjornstad, O N -- R01 GM089932/GM/NIGMS NIH HHS/ -- R01GM089932/GM/NIGMS NIH HHS/ -- R24 HD047879/HD/NICHD NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):984-8. doi: 10.1126/science.1204588.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, Oxford University, Oxford OX1 3PS, UK. charlotte.metcalf@zoo.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852493" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Antibodies/immunology ; CD4-Positive T-Lymphocytes/immunology ; Erythrocyte Aging ; Erythrocyte Count ; Erythrocytes/*parasitology/physiology ; Host-Parasite Interactions ; Humans ; Immunity, Innate ; Interleukin-10/immunology/metabolism ; Malaria/blood/*immunology/*parasitology ; Mice ; Models, Biological ; Models, Statistical ; *Parasitemia/blood/immunology/parasitology ; Plasmodium chabaudi/immunology/*physiology ; Receptors, Interleukin-10/immunology ; Regression Analysis
    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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    DHODH modulates transcriptional elongation in the neural crest and melanoma (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-03-25
    Description: Melanoma is a tumour of transformed melanocytes, which are originally derived from the embryonic neural crest. It is unknown to what extent the programs that regulate neural crest development interact with mutations in the BRAF oncogene, which is the most commonly mutated gene in human melanoma. We have used zebrafish embryos to identify the initiating transcriptional events that occur on activation of human BRAF(V600E) (which encodes an amino acid substitution mutant of BRAF) in the neural crest lineage. Zebrafish embryos that are transgenic for mitfa:BRAF(V600E) and lack p53 (also known as tp53) have a gene signature that is enriched for markers of multipotent neural crest cells, and neural crest progenitors from these embryos fail to terminally differentiate. To determine whether these early transcriptional events are important for melanoma pathogenesis, we performed a chemical genetic screen to identify small-molecule suppressors of the neural crest lineage, which were then tested for their effects on melanoma. One class of compound, inhibitors of dihydroorotate dehydrogenase (DHODH), for example leflunomide, led to an almost complete abrogation of neural crest development in zebrafish and to a reduction in the self-renewal of mammalian neural crest stem cells. Leflunomide exerts these effects by inhibiting the transcriptional elongation of genes that are required for neural crest development and melanoma growth. When used alone or in combination with a specific inhibitor of the BRAF(V600E) oncogene, DHODH inhibition led to a marked decrease in melanoma growth both in vitro and in mouse xenograft studies. Taken together, these studies highlight developmental pathways in neural crest cells that have a direct bearing on melanoma formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759979/" 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/PMC3759979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, Richard Mark -- Cech, Jennifer -- Ratanasirintrawoot, Sutheera -- Lin, Charles Y -- Rahl, Peter B -- Burke, Christopher J -- Langdon, Erin -- Tomlinson, Matthew L -- Mosher, Jack -- Kaufman, Charles -- Chen, Frank -- Long, Hannah K -- Kramer, Martin -- Datta, Sumon -- Neuberg, Donna -- Granter, Scott -- Young, Richard A -- Morrison, Sean -- Wheeler, Grant N -- Zon, Leonard I -- K08 AR055368/AR/NIAMS NIH HHS/ -- R01 CA103846/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-08/HG/NHGRI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):518-22. doi: 10.1038/nature09882.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430780" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Cell Lineage/drug effects ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Genes, p53/genetics ; Humans ; Isoxazoles/pharmacology/therapeutic use ; Melanoma/drug therapy/enzymology/*genetics/*pathology ; Mice ; Neural Crest/drug effects/*enzymology/metabolism/pathology ; Oxidoreductases Acting on CH-CH Group Donors/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins B-raf/antagonists & ; inhibitors/chemistry/genetics/metabolism ; Rats ; Stem Cells/cytology/drug effects/pathology ; *Transcription, Genetic/drug effects/physiology ; Xenograft Model Antitumor Assays ; Zebrafish/embryology/genetics
    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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    RIP3 mediates the embryonic lethality of caspase-8-deficient mice (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Apoptosis and necroptosis are complementary pathways controlled by common signalling adaptors, kinases and proteases; among these, caspase-8 (Casp8) is critical for death receptor-induced apoptosis. This caspase has also been implicated in non-apoptotic pathways that regulate Fas-associated via death domain (FADD)-dependent signalling and other less defined biological processes as diverse as innate immune signalling and myeloid or lymphoid differentiation patterns. Casp8 suppresses RIP3-RIP1 (also known as RIPK3-RIPK1) kinase complex-dependent necroptosis that follows death receptor activation as well as a RIP3-dependent, RIP1-independent necrotic pathway that has emerged as a host defence mechanism against murine cytomegalovirus. Disruption of Casp8 expression leads to embryonic lethality in mice between embryonic days 10.5 and 11.5 (ref. 7). Thus, Casp8 may naturally hold alternative RIP3-dependent death pathways in check in addition to promoting apoptosis. We find that RIP3 is responsible for the mid-gestational death of Casp8-deficient embryos. Remarkably, Casp8(-/-)Rip3(-/-) double mutant mice are viable and mature into fertile adults with a full immune complement of myeloid and lymphoid cell types. These mice seem immunocompetent but develop lymphadenopathy by four months of age marked by accumulation of abnormal T cells in the periphery, a phenotype reminiscent of mice with Fas-deficiency (lpr/lpr; also known as Fas). Thus, Casp8 contributes to homeostatic control in the adult immune system; however, RIP3 and Casp8 are together completely dispensable for mammalian development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060292/" 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/PMC3060292/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, William J -- Upton, Jason W -- Long, Alyssa B -- Livingston-Rosanoff, Devon -- Daley-Bauer, Lisa P -- Hakem, Razqallah -- Caspary, Tamara -- Mocarski, Edward S -- AI30363/AI/NIAID NIH HHS/ -- DP5 OD012198/OD/NIH HHS/ -- R01 AI020211/AI/NIAID NIH HHS/ -- R01 AI020211-24/AI/NIAID NIH HHS/ -- R01 AI030363/AI/NIAID NIH HHS/ -- R01 AI030363-13A2/AI/NIAID NIH HHS/ -- R01 AI20211/AI/NIAID NIH HHS/ -- England -- Nature. 2011 Mar 17;471(7338):368-72. doi: 10.1038/nature09857. Epub 2011 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA. wkaiser@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 8/*genetics/*metabolism ; Caspase Inhibitors ; Cell Line ; Embryo Loss/enzymology/*genetics/*metabolism ; Embryo, Mammalian/cytology/embryology ; Female ; GTPase-Activating Proteins/metabolism ; *Gene Deletion ; Immunocompetence/genetics/immunology ; Lymphatic Diseases/genetics/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; *Necrosis ; Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & ; inhibitors/deficiency/genetics/*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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    A PGC1-alpha-dependent myokine that drives brown-fat-like development of white fat and thermogenesis (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-01-13
    Description: Exercise benefits a variety of organ systems in mammals, and some of the best-recognized effects of exercise on muscle are mediated by the transcriptional co-activator PPAR-gamma co-activator-1 alpha (PGC1-alpha). Here we show in mouse that PGC1-alpha expression in muscle stimulates an increase in expression of FNDC5, a membrane protein that is cleaved and secreted as a newly identified hormone, irisin. Irisin acts on white adipose cells in culture and in vivo to stimulate UCP1 expression and a broad program of brown-fat-like development. Irisin is induced with exercise in mice and humans, and mildly increased irisin levels in the blood cause an increase in energy expenditure in mice with no changes in movement or food intake. This results in improvements in obesity and glucose homeostasis. Irisin could be therapeutic for human metabolic disease and other disorders that are improved with exercise.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522098/" 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/PMC3522098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bostrom, Pontus -- Wu, Jun -- Jedrychowski, Mark P -- Korde, Anisha -- Ye, Li -- Lo, James C -- Rasbach, Kyle A -- Bostrom, Elisabeth Almer -- Choi, Jang Hyun -- Long, Jonathan Z -- Kajimura, Shingo -- Zingaretti, Maria Cristina -- Vind, Birgitte F -- Tu, Hua -- Cinti, Saverio -- Hojlund, Kurt -- Gygi, Steven P -- Spiegelman, Bruce M -- DK31405/DK/NIDDK NIH HHS/ -- DK54477/DK/NIDDK NIH HHS/ -- K99 DK087853/DK/NIDDK NIH HHS/ -- R01 DK054477/DK/NIDDK NIH HHS/ -- R01 DK061562/DK/NIDDK NIH HHS/ -- R37 DK031405/DK/NIDDK NIH HHS/ -- England -- Nature. 2012 Jan 11;481(7382):463-8. doi: 10.1038/nature10777.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22237023" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology/drug effects/metabolism ; Adipose Tissue, Brown/*cytology/drug effects/metabolism ; Adipose Tissue, White/*cytology/drug effects/metabolism ; Animals ; Cell Respiration/drug effects ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Energy Metabolism/drug effects/genetics/physiology ; Exercise/physiology ; Gene Expression Regulation/drug effects/genetics ; Hormones/metabolism/secretion ; Humans ; Insulin Resistance/physiology ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Ion Channels/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Mitochondrial Proteins/metabolism ; Models, Animal ; Muscle Cells/metabolism ; Obesity/blood/chemically induced/prevention & control ; Physical Conditioning, Animal/physiology ; Plasma/chemistry ; Subcutaneous Fat/cytology/drug effects/metabolism ; *Thermogenesis/drug effects/genetics ; Trans-Activators/deficiency/genetics/*metabolism/secretion ; Transcription Factors
    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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    Broadly permissive intestinal chromatin underlies lateral inhibition and cell plasticity (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-01-15
    Description: Cells differentiate when transcription factors bind accessible cis-regulatory elements to establish specific gene expression programs. In differentiating embryonic stem cells, chromatin at lineage-restricted genes becomes sequentially accessible, probably by means of 'pioneer' transcription factor activity, but tissues may use other strategies in vivo. Lateral inhibition is a pervasive process in which one cell forces a different identity on its neighbours, and it is unclear how chromatin in equipotent progenitors undergoing lateral inhibition quickly enables distinct, transiently reversible cell fates. Here we report the chromatin and transcriptional underpinnings of differentiation in mouse small intestine crypts, where notch signalling mediates lateral inhibition to assign progenitor cells into absorptive or secretory lineages. Transcript profiles in isolated LGR5(+) intestinal stem cells and secretory and absorptive progenitors indicated that each cell population was distinct and the progenitors specified. Nevertheless, secretory and absorptive progenitors showed comparable levels of H3K4me2 and H3K27ac histone marks and DNase I hypersensitivity--signifying accessible, permissive chromatin-at most of the same cis-elements. Enhancers acting uniquely in progenitors were well demarcated in LGR5(+) intestinal stem cells, revealing early priming of chromatin for divergent transcriptional programs, and retained active marks well after lineages were specified. On this chromatin background, ATOH1, a secretory-specific transcription factor, controls lateral inhibition through delta-like notch ligand genes and also drives the expression of numerous secretory lineage genes. Depletion of ATOH1 from specified secretory cells converted them into functional enterocytes, indicating prolonged responsiveness of marked enhancers to the presence or absence of a key transcription factor. Thus, lateral inhibition and intestinal crypt lineage plasticity involve interaction of a lineage-restricted transcription factor with broadly permissive chromatin established in multipotent stem cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151315/" 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/PMC4151315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Tae-Hee -- Li, Fugen -- Ferreiro-Neira, Isabel -- Ho, Li-Lun -- Luyten, Annouck -- Nalapareddy, Kodandaramireddy -- Long, Henry -- Verzi, Michael -- Shivdasani, Ramesh A -- K01 DK088868/DK/NIDDK NIH HHS/ -- K01DK088868/DK/NIDDK NIH HHS/ -- K99 DK095983/DK/NIDDK NIH HHS/ -- K99DK095983/DK/NIDDK NIH HHS/ -- P50 CA127003/CA/NCI NIH HHS/ -- P50CA127003/CA/NCI NIH HHS/ -- R01 DK081113/DK/NIDDK NIH HHS/ -- R01 DK082889/DK/NIDDK NIH HHS/ -- R01DK081113/DK/NIDDK NIH HHS/ -- R01DK082889/DK/NIDDK NIH HHS/ -- England -- Nature. 2014 Feb 27;506(7489):511-5. doi: 10.1038/nature12903. Epub 2014 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02215, USA. ; Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24413398" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/deficiency/metabolism ; Cell Differentiation/*genetics ; Cell Lineage/genetics ; Chromatin/*genetics/*metabolism ; Deoxyribonuclease I/metabolism ; Enhancer Elements, Genetic/genetics ; Enterocytes/cytology/metabolism ; Female ; *Gene Expression Regulation ; Histones/metabolism ; Intestine, Small/cytology/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Notch/metabolism ; Stem Cells/cytology/metabolism ; Transcription, Genetic
    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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    Corticostriatal plasticity is necessary for learning intentional neuroprosthetic skills (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-06
    Description: The ability to learn new skills and perfect them with practice applies not only to physical skills but also to abstract skills, like motor planning or neuroprosthetic actions. Although plasticity in corticostriatal circuits has been implicated in learning physical skills, it remains unclear if similar circuits or processes are required for abstract skill learning. Here we use a novel behavioural task in rodents to investigate the role of corticostriatal plasticity in abstract skill learning. Rodents learned to control the pitch of an auditory cursor to reach one of two targets by modulating activity in primary motor cortex irrespective of physical movement. Degradation of the relation between action and outcome, as well as sensory-specific devaluation and omission tests, demonstrate that these learned neuroprosthetic actions are intentional and goal-directed, rather than habitual. Striatal neurons change their activity with learning, with more neurons modulating their activity in relation to target-reaching as learning progresses. Concomitantly, strong relations between the activity of neurons in motor cortex and the striatum emerge. Specific deletion of striatal NMDA receptors impairs the development of this corticostriatal plasticity, and disrupts the ability to learn neuroprosthetic skills. These results suggest that corticostriatal plasticity is necessary for abstract skill learning, and that neuroprosthetic movements capitalize on the neural circuitry involved in natural motor learning.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477868/" 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/PMC3477868/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koralek, Aaron C -- Jin, Xin -- Long, John D 2nd -- Costa, Rui M -- Carmena, Jose M -- 243393/European Research Council/International -- Z01 AA000416-03/Intramural NIH HHS/ -- England -- Nature. 2012 Mar 4;483(7389):331-5. doi: 10.1038/nature10845.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22388818" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Algorithms ; Animals ; Cues ; Learning/*physiology ; Male ; *Man-Machine Systems ; Mice ; Motor Cortex/cytology/*physiology ; Motor Skills/physiology ; Movement/physiology ; Neostriatum/cytology/*physiology ; Neuronal Plasticity/*physiology ; *Prostheses and Implants ; Psychomotor Performance/*physiology ; Rats ; Rats, Long-Evans ; Receptors, N-Methyl-D-Aspartate/deficiency/genetics/metabolism ; Reward
    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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  • 8
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    Prevention of muscular dystrophy in mice by CRISPR/Cas9-mediated editing of germline DNA (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-16
    Description: Duchenne muscular dystrophy (DMD) is an inherited X-linked disease caused by mutations in the gene encoding dystrophin, a protein required for muscle fiber integrity. DMD is characterized by progressive muscle weakness and a shortened life span, and there is no effective treatment. We used clustered regularly interspaced short palindromic repeat/Cas9 (CRISPR/Cas9)-mediated genome editing to correct the dystrophin gene (Dmd) mutation in the germ line of mdx mice, a model for DMD, and then monitored muscle structure and function. Genome editing produced genetically mosaic animals containing 2 to 100% correction of the Dmd gene. The degree of muscle phenotypic rescue in mosaic mice exceeded the efficiency of gene correction, likely reflecting an advantage of the corrected cells and their contribution to regenerating muscle. With the anticipated technological advances that will facilitate genome editing of postnatal somatic cells, this strategy may one day allow correction of disease-causing mutations in the muscle tissue of patients with DMD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398027/" 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/PMC4398027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Chengzu -- McAnally, John R -- Shelton, John M -- Mireault, Alex A -- Bassel-Duby, Rhonda -- Olson, Eric N -- DK-099653/DK/NIDDK NIH HHS/ -- HL-077439/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 DK099653/DK/NIDDK NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL111665/HL/NHLBI NIH HHS/ -- U01 HL100401/HL/NHLBI NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1184-8. doi: 10.1126/science.1254445. Epub 2014 Aug 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology and Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25123483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems/*genetics ; Caspase 9/*genetics ; DNA/genetics ; Dystrophin/*genetics ; Exons/genetics ; Gene Targeting/*methods ; Genetic Therapy/methods ; Germ Cells ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Duchenne/genetics/pathology/*prevention & control
    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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  • 9
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    Unknown
    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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