Adiponectin Hepatitis B Surface Antigen Growth Regulated
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Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897 -
Uncoupling Proteins: Functional Characteristics and Role in the Pathogenesis of Obesity and Type II Diabetes
Diabetologia 2001) 44: 946±965 Ó Springer-Verlag 2001 Uncoupling proteins: functional characteristics and role in the pathogenesis of obesity and Type II diabetes L. T.Dalgaard, O.Pedersen Steno Diabetes Center, Gentofte, Denmark Abstract obesity. The three uncoupling protein homologue genes UCP1, UCP2, and UCP3 have been investigat- Uncoupling proteins are mitochondrial carrier pro- ed for polymorphisms and mutations and their impact teins which are able to dissipate the proton gradient on Type II diabetes mellitus, obesity, and body weight of the inner mitochondrial membrane. This uncou- gain or BMI. The main conclusion is that variation in pling process reduces the amount of ATP generated the UCP1, UCP2 or UCP3 genes is not associated through an oxidation of fuels. The hypothesis that un- with major alterations of body weight gain. The con- coupling proteins UCPs) are candidate genes for hu- tribution of UCP genes towards polygenic obesity man obesity or Type II non-insulin-dependent) dia- and Type II diabetes is evaluated and discussed. [Dia- betes mellitus is based on the finding that a chemical betologia 2001) 44: 946±965] uncoupling of the mitochondrial membrane reduces body adiposity, and that lower metabolic rates predict Keywords Uncoupling proteins, Type II diabetes weight gain. It is straightforward to hypothesize that mellitus, obesity, genetics, body weight regulation, common polymorphisms of UCP1, UCP2 and UCP3 energy expenditure, metabolic rate, brown adipose genes lower metabolic rate by a more efficient energy tissue, white adipose tissue, reactive oxygen species, coupling in the mitochondria. Furthermore, geneti- polymorphism, mutation, transgenics, gene knock- cally engineered mice over expressing different UCP out. -
HMGB1 in Health and Disease R
Donald and Barbara Zucker School of Medicine Journal Articles Academic Works 2014 HMGB1 in health and disease R. Kang R. C. Chen Q. H. Zhang W. Hou S. Wu See next page for additional authors Follow this and additional works at: https://academicworks.medicine.hofstra.edu/articles Part of the Emergency Medicine Commons Recommended Citation Kang R, Chen R, Zhang Q, Hou W, Wu S, Fan X, Yan Z, Sun X, Wang H, Tang D, . HMGB1 in health and disease. 2014 Jan 01; 40():Article 533 [ p.]. Available from: https://academicworks.medicine.hofstra.edu/articles/533. Free full text article. This Article is brought to you for free and open access by Donald and Barbara Zucker School of Medicine Academic Works. It has been accepted for inclusion in Journal Articles by an authorized administrator of Donald and Barbara Zucker School of Medicine Academic Works. Authors R. Kang, R. C. Chen, Q. H. Zhang, W. Hou, S. Wu, X. G. Fan, Z. W. Yan, X. F. Sun, H. C. Wang, D. L. Tang, and +8 additional authors This article is available at Donald and Barbara Zucker School of Medicine Academic Works: https://academicworks.medicine.hofstra.edu/articles/533 NIH Public Access Author Manuscript Mol Aspects Med. Author manuscript; available in PMC 2015 December 01. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Mol Aspects Med. 2014 December ; 0: 1–116. doi:10.1016/j.mam.2014.05.001. HMGB1 in Health and Disease Rui Kang1,*, Ruochan Chen1, Qiuhong Zhang1, Wen Hou1, Sha Wu1, Lizhi Cao2, Jin Huang3, Yan Yu2, Xue-gong Fan4, Zhengwen Yan1,5, Xiaofang Sun6, Haichao Wang7, Qingde Wang1, Allan Tsung1, Timothy R. -
DNA Supercoiling with a Twist Edwin Kamau Louisiana State University and Agricultural and Mechanical College, [email protected]
Louisiana State University LSU Digital Commons LSU Doctoral Dissertations Graduate School 2005 DNA supercoiling with a twist Edwin Kamau Louisiana State University and Agricultural and Mechanical College, [email protected] Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_dissertations Recommended Citation Kamau, Edwin, "DNA supercoiling with a twist" (2005). LSU Doctoral Dissertations. 999. https://digitalcommons.lsu.edu/gradschool_dissertations/999 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Doctoral Dissertations by an authorized graduate school editor of LSU Digital Commons. For more information, please [email protected]. DNA SUPERCOILING WITH A TWIST A Dissertation Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Doctor of Philosophy in The Department of Biological Sciences By Edwin Kamau B.S. Horticulture, Egerton University, Kenya, 1996, May, 2005 DEDICATIONS I would like to dedicate this dissertation to my son, Ashford Kimani Kamau. Your age marks the life of my graduate school career. I have been a weekend dad, broke and with enormous financial responsibilities; it kills me to see how sometimes you cry your heart out on Sunday evening when our weekend time together is over. I miss you too every moment, you have encouraged me to be a better person, a better dad so that I can make you proud. At your tender age, I have learned a lot from you. We will soon spend all the time in the world we need together; travel, sports, music, pre-historic discoveries and adventures; the road is wide open. -
Nrg4 and Gpr120 Signalling in Brown Fat Anthony Chukunweike OKOLO
Nrg4 and Gpr120 Signalling in Brown Fat Anthony Chukunweike OKOLO Institute of Reproductive and Developmental Biology Department of Surgery and Cancer Faculty of Medicine Imperial College London A thesis submitted in fulfilment of the requirements for award of the degree of Doctor of Philosophy 1 Statement of Originality All experiments included in this thesis were performed by me unless otherwise stated in the text. 2 Copyright statement The copyright of this thesis rests with the author and is made available under a Creative Commons Attribution Non-Commercial No Directive Licence. Researchers are free to copy, distribute or transmit the thesis on the condition that they attribute it, and they do not use it for commercial purposes, and they do not alter, transform or build upon it. For any re-use or re-distribution, researchers must make clear to others the licence terms of this work. 3 Acknowledgments I would like to thank my supervisors Dr Aylin Hanyaloglu and Dr Mark Christian for giving me the great opportunity to work in their labs. Aylin put in a great deal of effort especially in area of Gpr120 signalling, including having to guide me through the critical imaging procedures. Aylin and Mark contributed a great deal towards the final edition of this thesis. I would also like to thank Dr Mark Christian for bringing me to Imperial College London to start off my PhD in his laboratory, and for being a great mentor and a continuous source of knowledge for me. I am grateful for your enduring patience in trying to bring out the best in me and ensuring that I develop the ‘critical thinking’ that is needed as a scientist. -
Perspectives in Diabetes Uncoupling Proteins 2 and 3 Potential Regulators of Mitochondrial Energy Metabolism Olivier Boss, Thilo Hagen, and Bradford B
Perspectives in Diabetes Uncoupling Proteins 2 and 3 Potential Regulators of Mitochondrial Energy Metabolism Olivier Boss, Thilo Hagen, and Bradford B. Lowell Mitochondria use energy derived from fuel combustion fuels and oxygen are converted into carbon dioxide, water, to create a proton electrochemical gradient across the and ATP (Fig. 1). The key challenge for the organism is to reg- mitochondrial inner membrane. This intermediate form ulate these many steps so that rates of ATP production are of energy is then used by ATP synthase to synthesize equal to rates of ATP utilization. This is not a small task given AT P. Uncoupling protein-1 (UCP1) is a brown fat–spe- that rates of ATP utilization can quickly increase severalfold cific mitochondrial inner membrane protein with proton (up to 100-fold in muscle during contraction). transport activity. UCP1 catalyzes a highly regulated proton leak, converting energy stored within the mito- Fuel metabolism and oxidative phosphorylation consist chondrial proton electrochemical potential gradient to of many tightly coupled enzymatic reactions (Fig. 1), which heat. This uncouples fuel oxidation from conversion of are regulated, in part, by ADP availability. Control by ADP is ADP to AT P. In rodents, UCP1 activity and brown fat accounted for by the chemiosmotic hypothesis of Mitchell (1). contribute importantly to whole-body energy expendi- Oxidation of fuels via the electron transport chain generates ture. Recently, two additional mitochondrial carriers a proton electrochemical potential gradient ( µH+) across with high similarity to UCP1 were molecularly cloned. the mitochondrial inner membrane. Protons reenter the In contrast to UCP1, UCP2 is expressed widely, and mitochondrial matrix via ATP synthase (F0F1-A TPase) in a UCP3 is expressed preferentially in skeletal muscle. -
Irisin As a Multifunctional Protein: Implications for Health and Certain Diseases
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Jagiellonian Univeristy Repository medicina Review Irisin as a Multifunctional Protein: Implications for Health and Certain Diseases Paulina Korta 1 , Ewa Poche´c 1,* and Agnieszka Mazur-Biały 2 1 Department of Glycoconjugate Biochemistry, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University, Gronostajowa 9, 30-387 Krakow, Poland 2 Department of Ergonomics and Exercise Physiology, Faculty of Health Sciences, Jagiellonian University, Medical College, Grzegorzecka 20, 31-531 Krakow, Poland * Correspondence: [email protected]; Tel.: +48-12-664-64-67 Received: 29 June 2019; Accepted: 12 August 2019; Published: 15 August 2019 Abstract: Sedentary life style is considered to be an independent risk factor for many disorders, including development of type 2 diabetes, obesity, immune dysfunction, asthma, and neurological or coronary heart disease. Irisin is released from myocytes during physical activity, and acts as a link between muscles and other tissues and organs. This myokine is produced as a result of proteolytic cleavage of FNDC5 protein present in the membrane of myocytes. Secretion of irisin is regulated by N-linked oligosaccharides attached to the protein molecule. The two N-glycan molecules, which constitute a significant part of the irisin glycoprotein, regulate the browning of adipocytes, which is the most important function of irisin. A receptor specific for irisin has still not been discovered. In some tissues irisin probably acts via integrins, which are widely expressed transmembrane receptors. Many studies have confirmed the multifunctional role of irisin and the beneficial effects of this molecule on body homeostasis. -
Exclusive Occurrence of Thermogenin Antigen in Brown Adipose Tissue
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Volume 150, number 1 FEBS LETTERS December 1982 Exclusive occurrence of thermogenin antigen in brown adipose tissue Barbara Cannon, Anders Hedin* and Jan Nedergaard Departments of Metabolic Research and *Immunology, The Wenner-Gren Institute, University of Stockholm, Norrtullsgatan 16, 113 45 Stockholm, Sweden Received 25 October 1982 Thermogenin is the purine-nucleotide binding polypeptide in brown adipose tissue mitochondria (Mr 32000) which confers upon these mitochondria the ability to produce heat. An enzyme-linked immunosorbent assay (ELISA) has been developed to demonstrate and quantitate the occurrence of thermogenin antigen in small amounts of tissue, and thus to characterize different depots of fat tissue as white or brown. The extreme sensitivity of the method allows determination of thermogenin in samples equivalent to < 1 mg tissue. The results indicate that thermogenin seems to be exclusively localised in brown fat mitochondria (as compared to white fat, liver or heart muscle mitochondria), and thermogenin antigen could only be found in brown adipocytes (as compared to white adipocytes). Thus, brown and white adipose tissue are probably ontogenetically different Brown adipose tissue ELISA Mitochondria Nonshivering thermogenesis Thermogenin White adipose tissue 1. INTRODUCTION form of white adipose tissue, or whether it should be considered as a bona fide organ in itself, with its The demonstration that the thermogenic func- own ontogeny [lo]. tion of brown adipose tissue is directly related to The present interest in the connection between the presence in the mitochondria of a specific poly- the activity of brown adipose tissue and the ten- peptide - thermogenin - with a subunit A4, 32000 dency to evolve obesity in animals and man (review has made it possible to study thermogenesis at the [l 11) has made it necessary to be able to charac- molecular level [1,2], (reviews [3-51). -
DNMT Inhibitors Increase Methylation at Subset of Cpgs in Colon
bioRxiv preprint doi: https://doi.org/10.1101/395467; this version posted August 25, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Title: DNMT inhibitors increase methylation at subset of CpGs in colon, bladder, lymphoma, 2 breast, and ovarian, cancer genome 3 Running title: Decitabine/azacytidine increases DNA methylation 4 Anil K Giri1, Tero Aittokallio1,2 5 1Institute for Molecular Medicine Finland, FIMM, University of Helsinki, Helsinki, Finland. 6 2Department of Mathematics and Statistics, University of Turku, Turku, Finland. 7 Correspondence to 8 Dr. Anil K Giri 9 Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, Finland. 10 Email: [email protected] 11 Financial disclosure: This work was funded by the Academy of Finland (grants 269862, 292611, 12 310507 and 313267), Cancer Society of Finland, and the Sigrid Juselius Foundation. 13 Ethical disclosure: This study is an independent analysis of existing data available in the public 14 domain and does not involve any animal or human samples that have been collected by the authors 15 themselves. 16 Author contribution: AKG conceptualized, analyzed the data and wrote the manuscript. TA 17 critically revised and edited the manuscript. The authors report no conflict of interest. 18 19 Word count: 20 Figure number: 5 21 Table number: 1 22 23 Abstract 24 Background: DNA methyltransferase inhibitors (DNMTi) decitabine and azacytidine are approved 25 therapies for acute myeloid leukemia and myelodysplastic syndrome. -
The Uncoupling Protein Homologues: UCP1, UCP2, UCP3, Stucp
Biochem. J. (2000) 345, 161–179 (Printed in Great Britain) 161 REVIEW ARTICLE The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP Daniel RICQUIER1 and Fre! de! ric BOUILLAUD Centre de Recherche sur l’Endocrinologie Mole! culaire et le De! veloppement (CEREMOD), Centre National de la recherche Scientifique (CNRS – Unit 9078), 9 rue Jules Hetzel, 92190 Meudon, France Animal and plant uncoupling protein (UCP) homologues form a energy expenditure in humans. The UCPs may also be involved subfamily of mitochondrial carriers that are evolutionarily re- in adaptation of cellular metabolism to an excessive supply of lated and possibly derived from a proton}anion transporter substrates in order to regulate the ATP level, the NAD+}NADH ancestor. The brown adipose tissue (BAT) UCP1 has a marked ratio and various metabolic pathways, and to contain superoxide and strongly regulated uncoupling activity, essential to the production. A major goal will be the analysis of mice that either maintenance of body temperature in small mammals. UCP lack the UCP2 or UCP3 gene or overexpress these genes. Other homologues identified in plants are induced in a cold environment aims will be to investigate the possible roles of UCP2 and UCP3 and may be involved in resistance to chilling. The biochemical in response to oxidative stress, lipid peroxidation, inflammatory activities and biological functions of the recently identified processes, fever and regulation of temperature in certain specific mammalian UCP2 and UCP3 are not well known. However, parts of the body. recent data support a role for these UCPs in State 4 respiration, respiration uncoupling and proton leaks in mitochondria. -
Energy Flow and Metabolic Efficiency Attributed to Brown Adipose Tissue
DWWULEXWHGWR ! ! " # $% &' ()*' ) % " $ + &,$( - + "$ . ,$" $ ! &/!() + ) ) $ 0 "/ ,$"1 + ) + /!) " 2 )2 ,$ "$ + /! " ,$ +) " 3 "4 ) /! /! - ) + + ) "$ /! "$ ) /! "1 + ) " ! ! 566 "" 6 7 8 55 5 5 !9 !: 2,*:;:!<9:=9 2,*:;:!<9:=> !"# )! <:! DOCTORAL THESIS Energy flow and metabolic efficiency attributed to brown adipose tissue Gabriella von Essen Energy flow and metabolic efficiency attributed to brown adipose tissue Gabriella von Essen The present thesis is based on the following enclosed papers: Paper I Adaptive Facultative Diet-induced Thermogenesis in Wild-type but not in UCP1-ablated Mice Gabriella von Essen, Erik Lindsund, Barbara Cannon and Jan Nedergaard Submitted for publication Paper II Highly recruited brown adipose tissue does not in itself protect against obesity Gabriella von Essen, Elaina Maldonado, Erik Lindsund, Barbara Cannon and Jan Nedergaard Under revision for Cell Metabolism Paper III At thermoneutrality, medium-chain fatty acids totally protect against diet-induced obesity in a UCP1-independent manner Gabriella von Essen, Petter Englund, Barbara Cannon and Jan Nedergaard Submitted for publication Paper IV No insulating -
Mitochondrial Uncoupling Proteins in the Central Nervous System Jeong Sook Kim-Han Washington University School of Medicine in St
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2005 Mitochondrial uncoupling proteins in the central nervous system Jeong Sook Kim-Han Washington University School of Medicine in St. Louis Laura L. Dugan Washington University School of Medicine in St. Louis Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Kim-Han, Jeong Sook and Dugan, Laura L., ,"Mitochondrial uncoupling proteins in the central nervous system." Antioxidants & Redox Signaling.7,9-10. 1173-1181. (2005). https://digitalcommons.wustl.edu/open_access_pubs/3159 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. 14024C09.pgs 8/11/05 10:32 AM Page 1173 ANTIOXIDANTS & REDOX SIGNALING Volume 7, Numbers 9 & 10, 2005 © Mary Ann Liebert, Inc. Forum Review Mitochondrial Uncoupling Proteins in the Central Nervous System JEONG SOOK KIM-HAN1 and LAURA L. DUGAN1,2,3 ABSTRACT Mitochondrial uncoupling proteins (UCPs), a subfamily of the mitochondrial transporter family, are related by sequence homology to UCP1. This protein, which is located in the inner mitochondrial membrane, dissi- pates the proton gradient between the intermembrane space and the mitochondrial matrix to uncouple elec- tron transport from ATP synthesis. UCP1 (thermogenin) was first discovered in brown adipose tissue and is responsible for non-shivering thermogenesis. Expression of mRNA for three other UCP isoforms, UCP2, UCP4, and BMCP1/UCP5, has been found at high levels in brain.