Changes in Pathogenicity and Immunogenicity of Mycoplasma Mycoides Subsp
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Universidade Estadual De Campinas Instituto De Biologia
UNIVERSIDADE ESTADUAL DE CAMPINAS INSTITUTO DE BIOLOGIA VERÔNICA APARECIDA MONTEIRO SAIA CEREDA O PROTEOMA DO CORPO CALOSO DA ESQUIZOFRENIA THE PROTEOME OF THE CORPUS CALLOSUM IN SCHIZOPHRENIA CAMPINAS 2016 1 VERÔNICA APARECIDA MONTEIRO SAIA CEREDA O PROTEOMA DO CORPO CALOSO DA ESQUIZOFRENIA THE PROTEOME OF THE CORPUS CALLOSUM IN SCHIZOPHRENIA Dissertação apresentada ao Instituto de Biologia da Universidade Estadual de Campinas como parte dos requisitos exigidos para a obtenção do Título de Mestra em Biologia Funcional e Molecular na área de concentração de Bioquímica. Dissertation presented to the Institute of Biology of the University of Campinas in partial fulfillment of the requirements for the degree of Master in Functional and Molecular Biology, in the area of Biochemistry. ESTE ARQUIVO DIGITAL CORRESPONDE À VERSÃO FINAL DA DISSERTAÇÃO DEFENDIDA PELA ALUNA VERÔNICA APARECIDA MONTEIRO SAIA CEREDA E ORIENTADA PELO DANIEL MARTINS-DE-SOUZA. Orientador: Daniel Martins-de-Souza CAMPINAS 2016 2 Agência(s) de fomento e nº(s) de processo(s): CNPq, 151787/2F2014-0 Ficha catalográfica Universidade Estadual de Campinas Biblioteca do Instituto de Biologia Mara Janaina de Oliveira - CRB 8/6972 Saia-Cereda, Verônica Aparecida Monteiro, 1988- Sa21p O proteoma do corpo caloso da esquizofrenia / Verônica Aparecida Monteiro Saia Cereda. – Campinas, SP : [s.n.], 2016. Orientador: Daniel Martins de Souza. Dissertação (mestrado) – Universidade Estadual de Campinas, Instituto de Biologia. 1. Esquizofrenia. 2. Espectrometria de massas. 3. Corpo caloso. -
| Hai Lui a Un Acutul Luniit Moonhiti
|HAI LUI AUN ACUTULUS010006055B2 LUNIIT MOONHITI (12 ) United States Patent (10 ) Patent No. : US 10 , 006 , 055 B2 Burk et al. (45 ) Date of Patent: Jun . 26 , 2018 ( 54 ) MICROORGANISMS FOR PRODUCING 2002/ 0168654 A1 11/ 2002 Maranas et al. 2003 / 0059792 Al 3 /2003 Palsson et al . BUTADIENE AND METHODS RELATED 2003 /0087381 A1 5 / 2003 Gokarn THERETO 2003 / 0224363 Al 12 /2003 Park et al . 2003 / 0233218 Al 12 /2003 Schilling (71 ) Applicant: Genomatica , Inc. , San Diego , CA (US ) 2004 / 0009466 AL 1 /2004 Maranas et al. 2004 / 0029149 Al 2 /2004 Palsson et al. ( 72 ) Inventors : Mark J . Burk , San Diego , CA (US ) ; 2004 / 0072723 A1 4 /2004 Palsson et al. Anthony P . Burgard , Bellefonte , PA 2004 / 0152159 Al 8 / 2004 Causey et al . 2005 /0042736 A1 2 / 2005 San et al . (US ) ; Robin E . Osterhout , San Diego , 2005 / 0079482 A1 4 / 2005 Maranas et al . CA (US ) ; Jun Sun , San Diego , CA 2006 / 0046288 Al 3 / 2006 Ka - Yiu et al. ( US ) ; Priti Pharkya , San Diego , CA 2006 / 0073577 A1 4 / 2006 Ka - Yiu et al . (US ) 2007 /0184539 Al 8 / 2007 San et al . 2009 / 0047718 Al 2 / 2009 Blaschek et al . 2009 / 0047719 Al 2 / 2009 Burgard et al . (73 ) Assignee : Genomatica , Inc ., San Diego , CA (US ) 2009 /0191593 A1 7 / 2009 Burk et al . 2010 / 0003716 A1 1 / 2010 Cervin et al. ( * ) Notice : Subject to any disclaimer , the term of this 2010 /0184171 Al 7 /2010 Jantama et al. patent is extended or adjusted under 35 2010 /0304453 Al 12 / 2010 Trawick et al . -
(12) Patent Application Publication (10) Pub. No.: US 2014/0155567 A1 Burk Et Al
US 2014O155567A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2014/0155567 A1 Burk et al. (43) Pub. Date: Jun. 5, 2014 (54) MICROORGANISMS AND METHODS FOR (60) Provisional application No. 61/331,812, filed on May THE BIOSYNTHESIS OF BUTADENE 5, 2010. (71) Applicant: Genomatica, Inc., San Diego, CA (US) Publication Classification (72) Inventors: Mark J. Burk, San Diego, CA (US); (51) Int. Cl. Anthony P. Burgard, Bellefonte, PA CI2P 5/02 (2006.01) (US); Jun Sun, San Diego, CA (US); CSF 36/06 (2006.01) Robin E. Osterhout, San Diego, CA CD7C II/6 (2006.01) (US); Priti Pharkya, San Diego, CA (52) U.S. Cl. (US) CPC ................. CI2P5/026 (2013.01); C07C II/I6 (2013.01); C08F 136/06 (2013.01) (73) Assignee: Genomatica, Inc., San Diego, CA (US) USPC ... 526/335; 435/252.3:435/167; 435/254.2: (21) Appl. No.: 14/059,131 435/254.11: 435/252.33: 435/254.21:585/16 (22) Filed: Oct. 21, 2013 (57) ABSTRACT O O The invention provides non-naturally occurring microbial Related U.S. Application Data organisms having a butadiene pathway. The invention addi (63) Continuation of application No. 13/101,046, filed on tionally provides methods of using Such organisms to produce May 4, 2011, now Pat. No. 8,580,543. butadiene. Patent Application Publication Jun. 5, 2014 Sheet 1 of 4 US 2014/O155567 A1 ?ueudos!SMS |?un61– Patent Application Publication Jun. 5, 2014 Sheet 2 of 4 US 2014/O155567 A1 VOJ OO O Z?un61– Patent Application Publication US 2014/O155567 A1 {}}} Hººso Patent Application Publication Jun. -
Primary Structure of Tektin Al
Proc. Nati. Acad. Sci. USA Vol. 89, pp. 8567-8571, September 1992 Cell Biology Primary structure of tektin Al: Comparison with intermediate- filament proteins and a model for its association with tubulin (basal body/centriole/dlia/flageila/microtubule) J. M. NORRANDER*, L. A. AMOSt, AND R. W. LINCK* *Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis, MN 55455; and tLaboratory of Molecular Biology, Medical Research Center, Hills Road, Cambridge, CB2 2QH, United Kingdom Communicated by M. F. Perutz, May 19, 1992 (receivedfor review January 22, 1992) ABSTRACT Tektins are proteins that form rilamentous MATERIALS AND METHODS polymers in the walls of ciliary and flagellar microtubules and that have biochemical and immunological properties similar to S. purpuratus gametes were collected, handled, and cultured those of intermediate-filament proteins. We report here the at 16'C, as described (14). At desired times, aliquots of sequence of a cDNA for tektin Al, one of the main tektins from eggs/embryos were isolated and frozen in liquid N2. Total Strongylocentrotus purpuratus sea urchin embryos. By hybrid- RNA and poly(A)+ mRNA were isolated (15). A Agtll cDNA ization analysis, tektin A mRNA appears maximally at cilio- expression library, constructed from blastulae (gift of T. L. genesis. The predicted structure of tektin Al (Mr 52,955) is a Thomas, Texas A & M, College Station, TX), was screened series of a-helical rod segments separated by nonhelical link- with polyclonal antibodies (16) against S. purpuratus sperm ers. The two halves of the rod appear homologous and are flagellar tektin A (11). The largest clone isolated, tekA10-2, probably related by gene duplication. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Leeds Thesis Template
Determining the Link Between Genome Integrity and Seed Quality Robbie Michael Gillett Submitted in accordance with the requirements for the degree of Doctor of Philosophy The University of Leeds Faculty of Biological Sciences School of Biology January, 2017 - ii - The candidate confirms that the work submitted is his own and that appropriate credit has been given where reference has been made to the work of others. This copy has been supplied on the understanding that it is copyright material and that no quotation from the thesis may be published without proper acknowledgement. The right of Robbie M. Gillett to be identified as Author of this work has been asserted by him in accordance with the Copyright, Designs and Patents Act 1988. © 2016 The University of Leeds and Robbie Michael Gillett - iii - Acknowledgements I would like to thank my supervisor Dr Christopher West and co-supervisor Dr. Wanda Waterworth for all of their support, expertise and incredible patience and for always being available to help. I would like to thank Aaron Barrett, James Cooper, Valérie Tennant, and all my other friends at university for their help throughout my PhD. Thanks to Vince Agboh and Grace Hoysteed for their combined disjointedness and to Ashley Hines, Daniel Johnston and Darryl Ransom for being a source of entertainment for many years. I would like to thank my international Sona friends, Lindsay Hoffman and Jan Maarten ten Katen. Finally unreserved thanks to my loving parents who supported me throughout the tough times and to my Grandma and Granddad, Jean and Dennis McCarthy, who were always very vocal with their love, support and pride. -
The Microbiota-Produced N-Formyl Peptide Fmlf Promotes Obesity-Induced Glucose
Page 1 of 230 Diabetes Title: The microbiota-produced N-formyl peptide fMLF promotes obesity-induced glucose intolerance Joshua Wollam1, Matthew Riopel1, Yong-Jiang Xu1,2, Andrew M. F. Johnson1, Jachelle M. Ofrecio1, Wei Ying1, Dalila El Ouarrat1, Luisa S. Chan3, Andrew W. Han3, Nadir A. Mahmood3, Caitlin N. Ryan3, Yun Sok Lee1, Jeramie D. Watrous1,2, Mahendra D. Chordia4, Dongfeng Pan4, Mohit Jain1,2, Jerrold M. Olefsky1 * Affiliations: 1 Division of Endocrinology & Metabolism, Department of Medicine, University of California, San Diego, La Jolla, California, USA. 2 Department of Pharmacology, University of California, San Diego, La Jolla, California, USA. 3 Second Genome, Inc., South San Francisco, California, USA. 4 Department of Radiology and Medical Imaging, University of Virginia, Charlottesville, VA, USA. * Correspondence to: 858-534-2230, [email protected] Word Count: 4749 Figures: 6 Supplemental Figures: 11 Supplemental Tables: 5 1 Diabetes Publish Ahead of Print, published online April 22, 2019 Diabetes Page 2 of 230 ABSTRACT The composition of the gastrointestinal (GI) microbiota and associated metabolites changes dramatically with diet and the development of obesity. Although many correlations have been described, specific mechanistic links between these changes and glucose homeostasis remain to be defined. Here we show that blood and intestinal levels of the microbiota-produced N-formyl peptide, formyl-methionyl-leucyl-phenylalanine (fMLF), are elevated in high fat diet (HFD)- induced obese mice. Genetic or pharmacological inhibition of the N-formyl peptide receptor Fpr1 leads to increased insulin levels and improved glucose tolerance, dependent upon glucagon- like peptide-1 (GLP-1). Obese Fpr1-knockout (Fpr1-KO) mice also display an altered microbiome, exemplifying the dynamic relationship between host metabolism and microbiota. -
Style Specifications Thesis
Structural Studies of Salvage Enzymes in Nucleotide Biosynthesis Martin Welin Faculty of Natural Resources and Agricultural Sciences Department of Molecular Biology Uppsala Doctoral thesis Swedish University of Agricultural Sciences Uppsala 2007 Acta Universitatis Agriculturae Sueciae 2007:21 ISSN 1652-6880 ISBN 978-91-576-7320-6 © 2007 Martin Welin, Uppsala Tryck: SLU Service/Repro, Uppsala 2007 Abstract Welin, M., 2007. Structural Studies of Salvage Enzymes in Nucleotide Biosynthesis. Doctoral dissertation. ISSN 1652-6880, ISBN 978-91-576-7320-6 There are two routes to produce deoxyribonucleoside triphosphates (dNTPs) precursors for DNA synthesis, the de novo and the salvage pathways. Deoxyribonucleoside kinases (dNKs) perform the initial phosphorylation of deoxyribonucleosides (dNs). Furthermore, they can act as activators for several medically important nucleoside analogs (NAs) for treatment against cancer or viral infections. Several disorders are characterized by mutations in enzymes involved in the nucleotide biosynthesis, such as Lesch-Nyhan disease that is linked to hypoxanthine guanine phosphoribosyltransferase (HPRT). In this thesis, the structures of human thymidine kinase 1 (TK1), a mycoplasmic deoxyadenosine kinase (Mm-dAK), and phosphoribosyltransferase domain containing 1 (PRTFDC1) are presented. Furthermore, a structural investigation of Drosophila melanogaster dNK (Dm-dNK) N64D mutant was carried out. The obtained structural information reveals the basis for substrate specificity for TKs and the bacterial dAKs. The TK1 revealed a structure different from other known dNK structures, containing an α/β domain similar to the RecA-F1ATPase family, and a lasso-like domain stabilized by a structural zinc. The Mm-dAK structure was similar to its human counterparts, but with some alterations in the proximity of the active site. -
Biochemical Basis for Differential Deoxyadenosine Toxicity To
Proc. Natl. Acad. Sci. USA Vol. 76, No. 5, pp. 2434-2437, May 1979 Medical Sciences Biochemical basis for differential deoxyadenosine toxicity to T and B lymphoblasts: Role for 5'-nucleotidase (deoxyadenosine kinase/deoxyadenylate kinase/immunodeficiency) ROBERT L. WORTMANN, BEVERLY S. MITCHELL, N. LAWRENCE EDWARDS, AND IRVING H. Fox Human Purine Research Center, Departments of Internal Medicine and Biological Chemistry, Clinical Research Center, University of Michigan Medical Center, Ann Arbor, Michigan 48109 Communicated by James B. Wyngaarden, March 7, 1979 ABSTRACT Deoxyadenosine metabolism was investigated tained from Calbiochem. Erythro-9-[3-(2-hydroxynonyl)]- in cultured human cells to elucidate the biochemical basis for adenine (EHNA) was a gift from G. B. Elion of Burroughs the sensitivity of T lymphoblasts and the resistance of B lym- Wellcome (Research Triangle Park, NC). Horse serum was phoblasts to deoxyadenosine toxicity. T lymphoblasts have a 20- to 45-fold greater capacity to synthesize deoxyadenosine nu- obtained from Flow Laboratories (Rockville, MD), and Eagle's cleotides than B lymphoblasts at deoxyadenosine concentrations minimal essential medium was purchased from GIBCO. From of 50-300 ,uM. During the synthesis of dATP, T lymphoblasts Amersham/Searle, [U-14C]deoxyadenosine (505 mCi/mmol), accumulate large quantities of dADP, whereas B lymphoblasts [8-14C]hypoxanthine (52.5 mCi/mmol), and [U-14C]deoxy- do not accumu ate dADP. Enzymes affecting deoxyadenosine adenosine monophosphate (574 mCi/mmol) were purchased; nucleotide synthesis were assayed in these cells. No substantial and, from ICN, [8-14C]adenosine monophosphate (34.4 mCi/ differences were evident in activities of deoxyadenosine kinase (ATP: deoxyadenosine 5'-phosphotransferase, EC 2.7.1.76) or mmol) was purchased (1 Ci = 3.7 X 1010 becquerels). -
Role of the Microtubule-Associated Protein ATIP3 in Cell Migration and Breast Cancer Metastasis Angie Molina Delgado
Role of the microtubule-associated protein ATIP3 in cell migration and breast cancer metastasis Angie Molina Delgado To cite this version: Angie Molina Delgado. Role of the microtubule-associated protein ATIP3 in cell migration and breast cancer metastasis. Molecular biology. Université René Descartes - Paris V, 2014. English. NNT : 2014PA05T022. tel-01068663 HAL Id: tel-01068663 https://tel.archives-ouvertes.fr/tel-01068663 Submitted on 26 Sep 2014 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Université Paris Descartes Ecole doctorale BioSPC Thesis submitted towards fulfillment of the requirement for the degree of DOCTOR of Health & Life Sciences Specialized in Cellular and Molecular Biology Role of the microtubule-associated protein ATIP3 in cell migration and breast cancer metastasis By Angie Molina Delgado Under supervision of Dr. Clara Nahmias Thesis defense 3 September, 2014 Members of jury: Dr. Ali BADACHE Reviewer Dr. Laurence LAFANECHERE Reviewer Dr. Franck PEREZ Examiner Dr. Stéphane HONORE Examiner Dr. Clara NAHMIAS Thesis Director Table of Contents List of abbreviations ....................................................................................................................... 9 “Rôle de la protéine associée aux microtubules ATIP3 dans la migration cellulaire et la formation de métastases du cancer du sein” ................................................................................................ 11 I. -
The Metabolic Building Blocks of a Minimal Cell Supplementary
The metabolic building blocks of a minimal cell Mariana Reyes-Prieto, Rosario Gil, Mercè Llabrés, Pere Palmer and Andrés Moya Supplementary material. Table S1. List of enzymes and reactions modified from Gabaldon et. al. (2007). n.i.: non identified. E.C. Name Reaction Gil et. al. 2004 Glass et. al. 2006 number 2.7.1.69 phosphotransferase system glc + pep → g6p + pyr PTS MG041, 069, 429 5.3.1.9 glucose-6-phosphate isomerase g6p ↔ f6p PGI MG111 2.7.1.11 6-phosphofructokinase f6p + atp → fbp + adp PFK MG215 4.1.2.13 fructose-1,6-bisphosphate aldolase fbp ↔ gdp + dhp FBA MG023 5.3.1.1 triose-phosphate isomerase gdp ↔ dhp TPI MG431 glyceraldehyde-3-phosphate gdp + nad + p ↔ bpg + 1.2.1.12 GAP MG301 dehydrogenase nadh 2.7.2.3 phosphoglycerate kinase bpg + adp ↔ 3pg + atp PGK MG300 5.4.2.1 phosphoglycerate mutase 3pg ↔ 2pg GPM MG430 4.2.1.11 enolase 2pg ↔ pep ENO MG407 2.7.1.40 pyruvate kinase pep + adp → pyr + atp PYK MG216 1.1.1.27 lactate dehydrogenase pyr + nadh ↔ lac + nad LDH MG460 1.1.1.94 sn-glycerol-3-phosphate dehydrogenase dhp + nadh → g3p + nad GPS n.i. 2.3.1.15 sn-glycerol-3-phosphate acyltransferase g3p + pal → mag PLSb n.i. 2.3.1.51 1-acyl-sn-glycerol-3-phosphate mag + pal → dag PLSc MG212 acyltransferase 2.7.7.41 phosphatidate cytidyltransferase dag + ctp → cdp-dag + pp CDS MG437 cdp-dag + ser → pser + 2.7.8.8 phosphatidylserine synthase PSS n.i. cmp 4.1.1.65 phosphatidylserine decarboxylase pser → peta PSD n.i. -
Q 297 Suppl USE
The following supplement accompanies the article Atlantic salmon raised with diets low in long-chain polyunsaturated n-3 fatty acids in freshwater have a Mycoplasma dominated gut microbiota at sea Yang Jin, Inga Leena Angell, Simen Rød Sandve, Lars Gustav Snipen, Yngvar Olsen, Knut Rudi* *Corresponding author: [email protected] Aquaculture Environment Interactions 11: 31–39 (2019) Table S1. Composition of high- and low LC-PUFA diets. Stage Fresh water Sea water Feed type High LC-PUFA Low LC-PUFA Fish oil Initial fish weight (g) 0.2 0.4 1 5 15 30 50 0.2 0.4 1 5 15 30 50 80 200 Feed size (mm) 0.6 0.9 1.3 1.7 2.2 2.8 3.5 0.6 0.9 1.3 1.7 2.2 2.8 3.5 3.5 4.9 North Atlantic fishmeal (%) 41 40 40 40 40 30 30 41 40 40 40 40 30 30 35 25 Plant meals (%) 46 45 45 42 40 49 48 46 45 45 42 40 49 48 39 46 Additives (%) 3.3 3.2 3.2 3.5 3.3 3.4 3.9 3.3 3.2 3.2 3.5 3.3 3.4 3.9 2.6 3.3 North Atlantic fish oil (%) 9.9 12 12 15 16 17 18 0 0 0 0 0 1.2 1.2 23 26 Linseed oil (%) 0 0 0 0 0 0 0 6.8 8.1 8.1 9.7 11 10 11 0 0 Palm oil (%) 0 0 0 0 0 0 0 3.2 3.8 3.8 5.4 5.9 5.8 5.9 0 0 Protein (%) 56 55 55 51 49 47 47 56 55 55 51 49 47 47 44 41 Fat (%) 16 18 18 21 22 22 22 16 18 18 21 22 22 22 28 31 EPA+DHA (% diet) 2.2 2.4 2.4 2.9 3.1 3.1 3.1 0.7 0.7 0.7 0.7 0.7 0.7 0.7 4 4.2 Table S2.