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  • Male  (9)
  • Nature Publishing Group (NPG)  (9)
  • American Geophysical Union (AGU)
  • Springer
  • 2005-2009  (9)
  • 1935-1939
  • 1
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    New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-23
    Description: Adipose tissue is central to the regulation of energy balance. Two functionally different types of fat are present in mammals: white adipose tissue, the primary site of triglyceride storage, and brown adipose tissue, which is specialized in energy expenditure and can counteract obesity. Factors that specify the developmental fate and function of white and brown adipose tissue remain poorly understood. Here we demonstrate that whereas some members of the family of bone morphogenetic proteins (BMPs) support white adipocyte differentiation, BMP7 singularly promotes differentiation of brown preadipocytes even in the absence of the normally required hormonal induction cocktail. BMP7 activates a full program of brown adipogenesis including induction of early regulators of brown fat fate PRDM16 (PR-domain-containing 16; ref. 4) and PGC-1alpha (peroxisome proliferator-activated receptor-gamma (PPARgamma) coactivator-1alpha; ref. 5), increased expression of the brown-fat-defining marker uncoupling protein 1 (UCP1) and adipogenic transcription factors PPARgamma and CCAAT/enhancer-binding proteins (C/EBPs), and induction of mitochondrial biogenesis via p38 mitogen-activated protein (MAP) kinase-(also known as Mapk14) and PGC-1-dependent pathways. Moreover, BMP7 triggers commitment of mesenchymal progenitor cells to a brown adipocyte lineage, and implantation of these cells into nude mice results in development of adipose tissue containing mostly brown adipocytes. Bmp7 knockout embryos show a marked paucity of brown fat and an almost complete absence of UCP1. Adenoviral-mediated expression of BMP7 in mice results in a significant increase in brown, but not white, fat mass and leads to an increase in energy expenditure and a reduction in weight gain. These data reveal an important role of BMP7 in promoting brown adipocyte differentiation and thermogenesis in vivo and in vitro, and provide a potential new therapeutic approach for the treatment of obesity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745972/" 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/PMC2745972/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tseng, Yu-Hua -- Kokkotou, Efi -- Schulz, Tim J -- Huang, Tian Lian -- Winnay, Jonathon N -- Taniguchi, Cullen M -- Tran, T Thien -- Suzuki, Ryo -- Espinoza, Daniel O -- Yamamoto, Yuji -- Ahrens, Molly J -- Dudley, Andrew T -- Norris, Andrew W -- Kulkarni, Rohit N -- Kahn, C Ronald -- K08 DK064906/DK/NIDDK NIH HHS/ -- K08 DK64906/DK/NIDDK NIH HHS/ -- P30 DK040561/DK/NIDDK NIH HHS/ -- P30 DK040561-13/DK/NIDDK NIH HHS/ -- P30 DK46200/DK/NIDDK NIH HHS/ -- R01 DK 060837/DK/NIDDK NIH HHS/ -- R01 DK077097/DK/NIDDK NIH HHS/ -- R01 DK077097-01A1/DK/NIDDK NIH HHS/ -- R01 DK077097-02/DK/NIDDK NIH HHS/ -- R01 DK67536/DK/NIDDK NIH HHS/ -- R21 DK070722/DK/NIDDK NIH HHS/ -- R21 DK070722-01/DK/NIDDK NIH HHS/ -- R21 DK070722-02/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Aug 21;454(7207):1000-4. doi: 10.1038/nature07221.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Obesity and Hormone Action, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA. yu-hua.tseng@joslin.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18719589" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3-L1 Cells ; *Adipogenesis ; Adipose Tissue, Brown/*growth & development/*metabolism ; Adipose Tissue, White/growth & development ; Animals ; Bone Morphogenetic Protein 7 ; Bone Morphogenetic Proteins/*metabolism ; Cell Line ; *Energy Metabolism/genetics ; Male ; Mesenchymal Stromal Cells/cytology/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Mitochondria/physiology ; Thermogenesis ; Transforming Growth Factor beta/*metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
    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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    HDAC2 negatively regulates memory formation and synaptic plasticity (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-05-09
    Description: Chromatin modifications, especially histone-tail acetylation, have been implicated in memory formation. Increased histone-tail acetylation induced by inhibitors of histone deacetylases (HDACis) facilitates learning and memory in wild-type mice as well as in mouse models of neurodegeneration. Harnessing the therapeutic potential of HDACis requires knowledge of the specific HDAC family member(s) linked to cognitive enhancement. Here we show that neuron-specific overexpression of HDAC2, but not that of HDAC1, decreased dendritic spine density, synapse number, synaptic plasticity and memory formation. Conversely, Hdac2 deficiency resulted in increased synapse number and memory facilitation, similar to chronic treatment with HDACis in mice. Notably, reduced synapse number and learning impairment of HDAC2-overexpressing mice were ameliorated by chronic treatment with HDACis. Correspondingly, treatment with HDACis failed to further facilitate memory formation in Hdac2-deficient mice. Furthermore, analysis of promoter occupancy revealed an association of HDAC2 with the promoters of genes implicated in synaptic plasticity and memory formation. Taken together, our results suggest that HDAC2 functions in modulating synaptic plasticity and long-lasting changes of neural circuits, which in turn negatively regulates learning and memory. These observations encourage the development and testing of HDAC2-selective inhibitors for human diseases associated with memory impairment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3498958/" 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/PMC3498958/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guan, Ji-Song -- Haggarty, Stephen J -- Giacometti, Emanuela -- Dannenberg, Jan-Hermen -- Joseph, Nadine -- Gao, Jun -- Nieland, Thomas J F -- Zhou, Ying -- Wang, Xinyu -- Mazitschek, Ralph -- Bradner, James E -- DePinho, Ronald A -- Jaenisch, Rudolf -- Tsai, Li-Huei -- R01 DA028301/DA/NIDA NIH HHS/ -- R01 DA028301-02/DA/NIDA NIH HHS/ -- R01 NS051874/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 May 7;459(7243):55-60. doi: 10.1038/nature07925.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19424149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Butyrates/pharmacology ; Dendritic Spines/physiology ; Electrical Synapses/*physiology ; Female ; Gene Expression Regulation ; Hippocampus/metabolism ; Histone Deacetylase 1 ; Histone Deacetylase 2 ; Histone Deacetylase Inhibitors ; Histone Deacetylases/deficiency/genetics/*metabolism ; Hydroxamic Acids/pharmacology ; Learning/drug effects ; Male ; Memory/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Promoter Regions, Genetic/genetics ; Repressor Proteins/antagonists & inhibitors/genetics/*metabolism ; Sodium/pharmacology
    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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    The avian Z-linked gene DMRT1 is required for male sex determination in the chicken (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-08-28
    Description: Sex in birds is chromosomally based, as in mammals, but the sex chromosomes are different and the mechanism of avian sex determination has been a long-standing mystery. In the chicken and all other birds, the homogametic sex is male (ZZ) and the heterogametic sex is female (ZW). Two hypotheses have been proposed for the mechanism of avian sex determination. The W (female) chromosome may carry a dominant-acting ovary determinant. Alternatively, the dosage of a Z-linked gene may mediate sex determination, two doses being required for male development (ZZ). A strong candidate avian sex-determinant under the dosage hypothesis is the conserved Z-linked gene, DMRT1 (doublesex and mab-3-related transcription factor 1). Here we used RNA interference (RNAi) to knock down DMRT1 in early chicken embryos. Reduction of DMRT1 protein expression in ovo leads to feminization of the embryonic gonads in genetically male (ZZ) embryos. Affected males show partial sex reversal, characterized by feminization of the gonads. The feminized left gonad shows female-like histology, disorganized testis cords and a decline in the testicular marker, SOX9. The ovarian marker, aromatase, is ectopically activated. The feminized right gonad shows a more variable loss of DMRT1 and ectopic aromatase activation, suggesting differential sensitivity to DMRT1 between left and right gonads. Germ cells also show a female pattern of distribution in the feminized male gonads. These results indicate that DMRT1 is required for testis determination in the chicken. Our data support the Z dosage hypothesis for avian sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Craig A -- Roeszler, Kelly N -- Ohnesorg, Thomas -- Cummins, David M -- Farlie, Peter G -- Doran, Timothy J -- Sinclair, Andrew H -- England -- Nature. 2009 Sep 10;461(7261):267-71. doi: 10.1038/nature08298. Epub 2009 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Murdoch Children's Research Institute and Department of Paediatrics, The University of Melbourne, Royal Children's Hospital, Melbourne, Victoria 3052, Australia. craig.smith@mcri.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19710650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Line ; Chick Embryo ; Chickens/*genetics/*physiology ; Disorders of Sex Development ; Down-Regulation ; Female ; Gene Dosage/genetics ; Male ; MicroRNAs/genetics/metabolism ; Models, Genetic ; Ovary/embryology/metabolism ; RNA Interference ; SOX9 Transcription Factor/genetics/metabolism ; *Sex Characteristics ; Sex Chromosomes/*genetics ; *Sex Determination Processes ; Testis/embryology/metabolism ; Transcription Factors/deficiency/*genetics/*metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Accurate whole human genome sequencing using reversible terminator chemistry (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-11-07
    Description: DNA sequence information underpins genetic research, enabling discoveries of important biological or medical benefit. Sequencing projects have traditionally used long (400-800 base pair) reads, but the existence of reference sequences for the human and many other genomes makes it possible to develop new, fast approaches to re-sequencing, whereby shorter reads are compared to a reference to identify intraspecies genetic variation. Here we report an approach that generates several billion bases of accurate nucleotide sequence per experiment at low cost. Single molecules of DNA are attached to a flat surface, amplified in situ and used as templates for synthetic sequencing with fluorescent reversible terminator deoxyribonucleotides. Images of the surface are analysed to generate high-quality sequence. We demonstrate application of this approach to human genome sequencing on flow-sorted X chromosomes and then scale the approach to determine the genome sequence of a male Yoruba from Ibadan, Nigeria. We build an accurate consensus sequence from 〉30x average depth of paired 35-base reads. We characterize four million single-nucleotide polymorphisms and four hundred thousand structural variants, many of which were previously unknown. Our approach is effective for accurate, rapid and economical whole-genome re-sequencing and many other biomedical applications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581791/" 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/PMC2581791/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bentley, David R -- Balasubramanian, Shankar -- Swerdlow, Harold P -- Smith, Geoffrey P -- Milton, John -- Brown, Clive G -- Hall, Kevin P -- Evers, Dirk J -- Barnes, Colin L -- Bignell, Helen R -- Boutell, Jonathan M -- Bryant, Jason -- Carter, Richard J -- Keira Cheetham, R -- Cox, Anthony J -- Ellis, Darren J -- Flatbush, Michael R -- Gormley, Niall A -- Humphray, Sean J -- Irving, Leslie J -- Karbelashvili, Mirian S -- Kirk, Scott M -- Li, Heng -- Liu, Xiaohai -- Maisinger, Klaus S -- Murray, Lisa J -- Obradovic, Bojan -- Ost, Tobias -- Parkinson, Michael L -- Pratt, Mark R -- Rasolonjatovo, Isabelle M J -- Reed, Mark T -- Rigatti, Roberto -- Rodighiero, Chiara -- Ross, Mark T -- Sabot, Andrea -- Sankar, Subramanian V -- Scally, Aylwyn -- Schroth, Gary P -- Smith, Mark E -- Smith, Vincent P -- Spiridou, Anastassia -- Torrance, Peta E -- Tzonev, Svilen S -- Vermaas, Eric H -- Walter, Klaudia -- Wu, Xiaolin -- Zhang, Lu -- Alam, Mohammed D -- Anastasi, Carole -- Aniebo, Ify C -- Bailey, David M D -- Bancarz, Iain R -- Banerjee, Saibal -- Barbour, Selena G -- Baybayan, Primo A -- Benoit, Vincent A -- Benson, Kevin F -- Bevis, Claire -- Black, Phillip J -- Boodhun, Asha -- Brennan, Joe S -- Bridgham, John A -- Brown, Rob C -- Brown, Andrew A -- Buermann, Dale H -- Bundu, Abass A -- Burrows, James C -- Carter, Nigel P -- Castillo, Nestor -- Chiara E Catenazzi, Maria -- Chang, Simon -- Neil Cooley, R -- Crake, Natasha R -- Dada, Olubunmi O -- Diakoumakos, Konstantinos D -- Dominguez-Fernandez, Belen -- Earnshaw, David J -- Egbujor, Ugonna C -- Elmore, David W -- Etchin, Sergey S -- Ewan, Mark R -- Fedurco, Milan -- Fraser, Louise J -- Fuentes Fajardo, Karin V -- Scott Furey, W -- George, David -- Gietzen, Kimberley J -- Goddard, Colin P -- Golda, George S -- Granieri, Philip A -- Green, David E -- Gustafson, David L -- Hansen, Nancy F -- Harnish, Kevin -- Haudenschild, Christian D -- Heyer, Narinder I -- Hims, Matthew M -- Ho, Johnny T -- Horgan, Adrian M -- Hoschler, Katya -- Hurwitz, Steve -- Ivanov, Denis V -- Johnson, Maria Q -- James, Terena -- Huw Jones, T A -- Kang, Gyoung-Dong -- Kerelska, Tzvetana H -- Kersey, Alan D -- Khrebtukova, Irina -- Kindwall, Alex P -- Kingsbury, Zoya -- Kokko-Gonzales, Paula I -- Kumar, Anil -- Laurent, Marc A -- Lawley, Cynthia T -- Lee, Sarah E -- Lee, Xavier -- Liao, Arnold K -- Loch, Jennifer A -- Lok, Mitch -- Luo, Shujun -- Mammen, Radhika M -- Martin, John W -- McCauley, Patrick G -- McNitt, Paul -- Mehta, Parul -- Moon, Keith W -- Mullens, Joe W -- Newington, Taksina -- Ning, Zemin -- Ling Ng, Bee -- Novo, Sonia M -- O'Neill, Michael J -- Osborne, Mark A -- Osnowski, Andrew -- Ostadan, Omead -- Paraschos, Lambros L -- Pickering, Lea -- Pike, Andrew C -- Pike, Alger C -- Chris Pinkard, D -- Pliskin, Daniel P -- Podhasky, Joe -- Quijano, Victor J -- Raczy, Come -- Rae, Vicki H -- Rawlings, Stephen R -- Chiva Rodriguez, Ana -- Roe, Phyllida M -- Rogers, John -- Rogert Bacigalupo, Maria C -- Romanov, Nikolai -- Romieu, Anthony -- Roth, Rithy K -- Rourke, Natalie J -- Ruediger, Silke T -- Rusman, Eli -- Sanches-Kuiper, Raquel M -- Schenker, Martin R -- Seoane, Josefina M -- Shaw, Richard J -- Shiver, Mitch K -- Short, Steven W -- Sizto, Ning L -- Sluis, Johannes P -- Smith, Melanie A -- Ernest Sohna Sohna, Jean -- Spence, Eric J -- Stevens, Kim -- Sutton, Neil -- Szajkowski, Lukasz -- Tregidgo, Carolyn L -- Turcatti, Gerardo -- Vandevondele, Stephanie -- Verhovsky, Yuli -- Virk, Selene M -- Wakelin, Suzanne -- Walcott, Gregory C -- Wang, Jingwen -- Worsley, Graham J -- Yan, Juying -- Yau, Ling -- Zuerlein, Mike -- Rogers, Jane -- Mullikin, James C -- Hurles, Matthew E -- McCooke, Nick J -- West, John S -- Oaks, Frank L -- Lundberg, Peter L -- Klenerman, David -- Durbin, Richard -- Smith, Anthony J -- B05823/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0701805/Medical Research Council/United Kingdom -- MOL04534/Biotechnology and Biological Sciences Research Council/United Kingdom -- Z01 HG200330-03/Intramural NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Nov 6;456(7218):53-9. doi: 10.1038/nature07517.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Illumina Cambridge Ltd. (Formerly Solexa Ltd), Chesterford Research Park, Little Chesterford, Nr Saffron Walden, Essex CB10 1XL, UK. dbentley@illumina.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18987734" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, X/genetics ; Consensus Sequence/genetics ; Genome, Human/*genetics ; Genomics/economics/*methods ; Genotype ; Humans ; Male ; Nigeria ; Polymorphism, Single Nucleotide/genetics ; Sensitivity and Specificity ; Sequence Analysis, DNA/economics/*methods
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    A variant associated with nicotine dependence, lung cancer and peripheral arterial disease (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-04
    Description: Smoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539558/" 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/PMC4539558/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorgeirsson, Thorgeir E -- Geller, Frank -- Sulem, Patrick -- Rafnar, Thorunn -- Wiste, Anna -- Magnusson, Kristinn P -- Manolescu, Andrei -- Thorleifsson, Gudmar -- Stefansson, Hreinn -- Ingason, Andres -- Stacey, Simon N -- Bergthorsson, Jon T -- Thorlacius, Steinunn -- Gudmundsson, Julius -- Jonsson, Thorlakur -- Jakobsdottir, Margret -- Saemundsdottir, Jona -- Olafsdottir, Olof -- Gudmundsson, Larus J -- Bjornsdottir, Gyda -- Kristjansson, Kristleifur -- Skuladottir, Halla -- Isaksson, Helgi J -- Gudbjartsson, Tomas -- Jones, Gregory T -- Mueller, Thomas -- Gottsater, Anders -- Flex, Andrea -- Aben, Katja K H -- de Vegt, Femmie -- Mulders, Peter F A -- Isla, Dolores -- Vidal, Maria J -- Asin, Laura -- Saez, Berta -- Murillo, Laura -- Blondal, Thorsteinn -- Kolbeinsson, Halldor -- Stefansson, Jon G -- Hansdottir, Ingunn -- Runarsdottir, Valgerdur -- Pola, Roberto -- Lindblad, Bengt -- van Rij, Andre M -- Dieplinger, Benjamin -- Haltmayer, Meinhard -- Mayordomo, Jose I -- Kiemeney, Lambertus A -- Matthiasson, Stefan E -- Oskarsson, Hogni -- Tyrfingsson, Thorarinn -- Gudbjartsson, Daniel F -- Gulcher, Jeffrey R -- Jonsson, Steinn -- Thorsteinsdottir, Unnur -- Kong, Augustine -- Stefansson, Kari -- R01 DA017932/DA/NIDA NIH HHS/ -- England -- Nature. 2008 Apr 3;452(7187):638-42. doi: 10.1038/nature06846.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉deCODE Genetics, 101 Reykjavik, Iceland. thorgeir@decode.is〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385739" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, Pair 15/*genetics ; Europe ; Female ; Genetic Predisposition to Disease/*genetics ; Genotype ; Humans ; Lung Neoplasms/*genetics ; Male ; Multigene Family/genetics ; New Zealand ; Odds Ratio ; Peripheral Vascular Diseases/*genetics ; Polymorphism, Single Nucleotide/*genetics ; Receptors, Nicotinic/*genetics ; Smoking/adverse effects/genetics ; Tobacco Use Disorder/*genetics
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  • 6
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    MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-02
    Description: MicroRNAs comprise a broad class of small non-coding RNAs that control expression of complementary target messenger RNAs. Dysregulation of microRNAs by several mechanisms has been described in various disease states including cardiac disease. Whereas previous studies of cardiac disease have focused on microRNAs that are primarily expressed in cardiomyocytes, the role of microRNAs expressed in other cell types of the heart is unclear. Here we show that microRNA-21 (miR-21, also known as Mirn21) regulates the ERK-MAP kinase signalling pathway in cardiac fibroblasts, which has impacts on global cardiac structure and function. miR-21 levels are increased selectively in fibroblasts of the failing heart, augmenting ERK-MAP kinase activity through inhibition of sprouty homologue 1 (Spry1). This mechanism regulates fibroblast survival and growth factor secretion, apparently controlling the extent of interstitial fibrosis and cardiac hypertrophy. In vivo silencing of miR-21 by a specific antagomir in a mouse pressure-overload-induced disease model reduces cardiac ERK-MAP kinase activity, inhibits interstitial fibrosis and attenuates cardiac dysfunction. These findings reveal that microRNAs can contribute to myocardial disease by an effect in cardiac fibroblasts. Our results validate miR-21 as a disease target in heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a cardiovascular disease setting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thum, Thomas -- Gross, Carina -- Fiedler, Jan -- Fischer, Thomas -- Kissler, Stephan -- Bussen, Markus -- Galuppo, Paolo -- Just, Steffen -- Rottbauer, Wolfgang -- Frantz, Stefan -- Castoldi, Mirco -- Soutschek, Jurgen -- Koteliansky, Victor -- Rosenwald, Andreas -- Basson, M Albert -- Licht, Jonathan D -- Pena, John T R -- Rouhanifard, Sara H -- Muckenthaler, Martina U -- Tuschl, Thomas -- Martin, Gail R -- Bauersachs, Johann -- Engelhardt, Stefan -- R01 CA059998/CA/NCI NIH HHS/ -- R01 CA78711/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 18;456(7224):980-4. doi: 10.1038/nature07511. Epub 2008 Nov 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine I, Interdisziplinares Zentrum fur Klinische Forschung (IZKF), University of Wuerzburg, 97080 Wuerzburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19043405" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathies/*genetics/*metabolism/pathology/therapy ; Cell Line ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibroblasts/*metabolism ; Gene Silencing ; Humans ; *MAP Kinase Signaling System ; Male ; Mice ; Mice, Transgenic ; MicroRNAs/*genetics ; Myocytes, Cardiac/cytology/metabolism ; Rats
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  • 7
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    The pluripotency factor Oct4 interacts with Ctcf and also controls X-chromosome pairing and counting (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-06-19
    Description: Pluripotency of embryonic stem (ES) cells is controlled by defined transcription factors. During differentiation, mouse ES cells undergo global epigenetic reprogramming, as exemplified by X-chromosome inactivation (XCI) in which one female X chromosome is silenced to achieve gene dosage parity between the sexes. Somatic XCI is regulated by homologous X-chromosome pairing and counting, and by the random choice of future active and inactive X chromosomes. XCI and cell differentiation are tightly coupled, as blocking one process compromises the other and dedifferentiation of somatic cells to induced pluripotent stem cells is accompanied by X chromosome reactivation. Recent evidence suggests coupling of Xist expression to pluripotency factors occurs, but how the two are interconnected remains unknown. Here we show that Oct4 (also known as Pou5f1) lies at the top of the XCI hierarchy, and regulates XCI by triggering X-chromosome pairing and counting. Oct4 directly binds Tsix and Xite, two regulatory noncoding RNA genes of the X-inactivation centre, and also complexes with XCI trans-factors, Ctcf and Yy1 (ref. 17), through protein-protein interactions. Depletion of Oct4 blocks homologous X-chromosome pairing and results in the inactivation of both X chromosomes in female cells. Thus, we have identified the first trans-factor that regulates counting, and ascribed new functions to Oct4 during X-chromosome reprogramming.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057664/" 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/PMC3057664/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Donohoe, Mary E -- Silva, Susana S -- Pinter, Stefan F -- Xu, Na -- Lee, Jeannie T -- GM58839/GM/NIGMS NIH HHS/ -- R01 GM058839/GM/NIGMS NIH HHS/ -- R01 GM058839-10/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 2;460(7251):128-32. doi: 10.1038/nature08098. Epub 2009 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536159" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Chromosome Pairing ; Female ; Humans ; Male ; Mice ; Octamer Transcription Factor-3/deficiency/genetics/*metabolism ; Protein Binding ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Repressor Proteins/*metabolism ; SOXB1 Transcription Factors ; Transcriptional Activation ; X Chromosome/*genetics/*metabolism ; X Chromosome Inactivation/*genetics ; YY1 Transcription Factor/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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    An anatomical signature for literacy (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-16
    Description: Language is a uniquely human ability that evolved at some point in the roughly 6,000,000 years since human and chimpanzee lines diverged. Even in the most linguistically impoverished environments, children naturally develop sophisticated language systems. In contrast, reading is a learnt skill that does not develop without intensive tuition and practice. Learning to read is likely to involve ontogenic structural brain changes, but these are nearly impossible to isolate in children owing to concurrent biological, environmental and social maturational changes. In Colombia, guerrillas are re-integrating into mainstream society and learning to read for the first time as adults. This presents a unique opportunity to investigate how literacy changes the brain, without the maturational complications present in children. Here we compare structural brain scans from those who learnt to read as adults (late-literates) with those from a carefully matched set of illiterates. Late-literates had more white matter in the splenium of the corpus callosum and more grey matter in bilateral angular, dorsal occipital, middle temporal, left supramarginal and superior temporal gyri. The importance of these brain regions for skilled reading was investigated in early literates, who learnt to read as children. We found anatomical connections linking the left and right angular and dorsal occipital gyri through the area of the corpus callosum where white matter was higher in late-literates than in illiterates; that reading, relative to object naming, increased the interhemispheric functional connectivity between the left and right angular gyri; and that activation in the left angular gyrus exerts top-down modulation on information flow from the left dorsal occipital gyrus to the left supramarginal gyrus. These findings demonstrate how the regions identified in late-literates interact during reading, relative to object naming, in early literates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carreiras, Manuel -- Seghier, Mohamed L -- Baquero, Silvia -- Estevez, Adelina -- Lozano, Alfonso -- Devlin, Joseph T -- Price, Cathy J -- 082420/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Oct 15;461(7266):983-6. doi: 10.1038/nature08461.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basque Center on Cognition Brain and Language, Donostia-San Sebastian 20009, Spain [2] IKERBASQUE, Basque Foundation for Science, Bilbao 48011, Spain. m.carreiras@bcbl.eu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19829380" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Brain/*anatomy & histology/*physiology ; Child ; Colombia ; Corpus Callosum/anatomy & histology/physiology ; Educational Status ; Female ; Humans ; Language ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Models, Neurological ; Neural Pathways/physiology ; *Reading ; Speech/physiology ; Young Adult
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-02-13
    Description: Multiple, complex molecular events characterize cancer development and progression. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724746/" 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/PMC2724746/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sreekumar, Arun -- Poisson, Laila M -- Rajendiran, Thekkelnaycke M -- Khan, Amjad P -- Cao, Qi -- Yu, Jindan -- Laxman, Bharathi -- Mehra, Rohit -- Lonigro, Robert J -- Li, Yong -- Nyati, Mukesh K -- Ahsan, Aarif -- Kalyana-Sundaram, Shanker -- Han, Bo -- Cao, Xuhong -- Byun, Jaeman -- Omenn, Gilbert S -- Ghosh, Debashis -- Pennathur, Subramaniam -- Alexander, Danny C -- Berger, Alvin -- Shuster, Jeffrey R -- Wei, John T -- Varambally, Sooryanarayana -- Beecher, Christopher -- Chinnaiyan, Arul M -- K99 CA129565/CA/NCI NIH HHS/ -- K99 CA129565-01A1/CA/NCI NIH HHS/ -- R01 CA133458/CA/NCI NIH HHS/ -- U01 CA111275/CA/NCI NIH HHS/ -- U01 CA111275-04/CA/NCI NIH HHS/ -- England -- Nature. 2009 Feb 12;457(7231):910-4. doi: 10.1038/nature07762.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Michigan Center for Translational Pathology, Ann Arbor, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19212411" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/physiology ; Cell Line ; Cell Line, Tumor ; *Disease Progression ; Gene Knockdown Techniques ; Glycine N-Methyltransferase/genetics/metabolism ; Humans ; Male ; *Metabolomics ; Prostatic Neoplasms/enzymology/genetics/*metabolism ; Sarcosine/analysis/*metabolism/urine ; Sarcosine Dehydrogenase/metabolism ; Signal Transduction
    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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