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DDAH I (C-19): Sc-26068
SANTA CRUZ BIOTECHNOLOGY, INC. DDAH I (C-19): sc-26068 The Power to Question BACKGROUND APPLICATIONS DDAH, a dimethylarginine dimethylaminohydrolase, hydrolyzes dimethyl DDAH I (C-19) is recommended for detection of DDAH I of mouse, rat and arginine (ADMA) and monomethyl arginine (MMA), both inhibitors of nitric human origin by Western Blotting (starting dilution 1:200, dilution range oxide synthases, and may be involved in in vivo modulation of nitric oxide 1:100-1:1000) and immunofluorescence (starting dilution 1:50, dilution production. Impairment of DDAH causes ADMA accumulation and a reduc- range 1:50-1:500). tion in cGMP generation. DDAH II, the predominant DDAH isoform in endothelial cells, facilitates the induction of nitric oxide synthesis by all- RECOMMENDED SECONDARY REAGENTS trans-Retinoic acid (atRA). DDAH proteins are highly expressed in colon, kid- To ensure optimal results, the following support (secondary) reagents are ney, stomach and liver tissues. recommended: 1) Western Blotting: use donkey anti-goat IgG-HRP: sc-2020 (dilution range: 1:2000-1:100,000) or Cruz Marker™ compatible donkey anti- REFERENCES goat IgG-HRP: sc-2033 (dilution range: 1:2000-1:5000), Cruz Marker™ 1. Nakagomi, S., et al. 1999. Dimethylarginine dimethylaminohydrolase Molecular Weight Standards: sc-2035, TBS Blotto A Blocking Reagent: (DDAH) as a nerve-injury-associated molecule: mRNA localization in the sc-2333 and Western Blotting Luminol Reagent: sc-2048. 2) Immunofluores- rat brain and its coincident up-regulation with neuronal NO synthase cence: use donkey anti-goat IgG-FITC: sc-2024 (dilution range: 1:100-1:400) (nNOS) in axotomized motoneurons. Eur. J. -
Enzymatic Encoding Methods for Efficient Synthesis Of
(19) TZZ__T (11) EP 1 957 644 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C12N 15/10 (2006.01) C12Q 1/68 (2006.01) 01.12.2010 Bulletin 2010/48 C40B 40/06 (2006.01) C40B 50/06 (2006.01) (21) Application number: 06818144.5 (86) International application number: PCT/DK2006/000685 (22) Date of filing: 01.12.2006 (87) International publication number: WO 2007/062664 (07.06.2007 Gazette 2007/23) (54) ENZYMATIC ENCODING METHODS FOR EFFICIENT SYNTHESIS OF LARGE LIBRARIES ENZYMVERMITTELNDE KODIERUNGSMETHODEN FÜR EINE EFFIZIENTE SYNTHESE VON GROSSEN BIBLIOTHEKEN PROCEDES DE CODAGE ENZYMATIQUE DESTINES A LA SYNTHESE EFFICACE DE BIBLIOTHEQUES IMPORTANTES (84) Designated Contracting States: • GOLDBECH, Anne AT BE BG CH CY CZ DE DK EE ES FI FR GB GR DK-2200 Copenhagen N (DK) HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI • DE LEON, Daen SK TR DK-2300 Copenhagen S (DK) Designated Extension States: • KALDOR, Ditte Kievsmose AL BA HR MK RS DK-2880 Bagsvaerd (DK) • SLØK, Frank Abilgaard (30) Priority: 01.12.2005 DK 200501704 DK-3450 Allerød (DK) 02.12.2005 US 741490 P • HUSEMOEN, Birgitte Nystrup DK-2500 Valby (DK) (43) Date of publication of application: • DOLBERG, Johannes 20.08.2008 Bulletin 2008/34 DK-1674 Copenhagen V (DK) • JENSEN, Kim Birkebæk (73) Proprietor: Nuevolution A/S DK-2610 Rødovre (DK) 2100 Copenhagen 0 (DK) • PETERSEN, Lene DK-2100 Copenhagen Ø (DK) (72) Inventors: • NØRREGAARD-MADSEN, Mads • FRANCH, Thomas DK-3460 Birkerød (DK) DK-3070 Snekkersten (DK) • GODSKESEN, -
Generated by SRI International Pathway Tools Version 25.0, Authors S
An online version of this diagram is available at BioCyc.org. Biosynthetic pathways are positioned in the left of the cytoplasm, degradative pathways on the right, and reactions not assigned to any pathway are in the far right of the cytoplasm. Transporters and membrane proteins are shown on the membrane. Periplasmic (where appropriate) and extracellular reactions and proteins may also be shown. Pathways are colored according to their cellular function. Gcf_000238675-HmpCyc: Bacillus smithii 7_3_47FAA Cellular Overview Connections between pathways are omitted for legibility. -
Association Between the Gut Microbiota and Blood Pressure in a Population Cohort of 6953 Individuals
Journal of the American Heart Association ORIGINAL RESEARCH Association Between the Gut Microbiota and Blood Pressure in a Population Cohort of 6953 Individuals Joonatan Palmu , MD; Aaro Salosensaari , MSc; Aki S. Havulinna , DSc (Tech); Susan Cheng , MD, MPH; Michael Inouye, PhD; Mohit Jain, MD, PhD; Rodolfo A. Salido , BSc; Karenina Sanders , BSc; Caitriona Brennan, BSc; Gregory C. Humphrey, BSc; Jon G. Sanders , PhD; Erkki Vartiainen , MD, PhD; Tiina Laatikainen , MD, PhD; Pekka Jousilahti, MD, PhD; Veikko Salomaa , MD, PhD; Rob Knight , PhD; Leo Lahti , DSc (Tech); Teemu J. Niiranen , MD, PhD BACKGROUND: Several small-scale animal studies have suggested that gut microbiota and blood pressure (BP) are linked. However, results from human studies remain scarce and conflicting. We wanted to elucidate the multivariable-adjusted as- sociation between gut metagenome and BP in a large, representative, well-phenotyped population sample. We performed a focused analysis to examine the previously reported inverse associations between sodium intake and Lactobacillus abun- dance and between Lactobacillus abundance and BP. METHODS AND RESULTS: We studied a population sample of 6953 Finns aged 25 to 74 years (mean age, 49.2±12.9 years; 54.9% women). The participants underwent a health examination, which included BP measurement, stool collection, and 24-hour urine sampling (N=829). Gut microbiota was analyzed using shallow shotgun metagenome sequencing. In age- and sex-adjusted models, the α (within-sample) and β (between-sample) diversities of taxonomic composition were strongly re- lated to BP indexes (P<0.001 for most). In multivariable-adjusted models, β diversity was only associated with diastolic BP (P=0.032). -
Links Among Neuronal Nitric Oxide Synthase, Oxidative Stress, and Asymmetric Dimethylarginine (Adma)
NITRIC OXIDE DEFICIENCY IN CHRONIC KIDNEY DISEASE: LINKS AMONG NEURONAL NITRIC OXIDE SYNTHASE, OXIDATIVE STRESS, AND ASYMMETRIC DIMETHYLARGININE (ADMA) By YOU-LIN TAIN A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2007 1 © 2007 You-Lin Tain 2 This dissertation is dedication to my family for their constant love 3 ACKNOWLEDGMENTS This dissertation would not have been possible without the support of many people. Many thanks go to my adviser: Dr. Chris Baylis gave me the chance to work on many projects and also gave me numerous valuable comments for my manuscripts. I would like to thank my committee members for their guidance and valuable comments: Dr. Richard Johnson, Dr. Mohan Raizada, and Dr. Mark Segal. I thanks also go to the Chang Gung Memorial Hospital for awarding me a fellowship, providing me with the financial means to complete this dissertation. I am grateful to many persons who shared their technical assistance and experience, especially Dr. Verlander and Dr. Chang (University of Florida), Dr. Muller and Dr. Szabo (Semmelweis University, Hungary), Dr. Griendling and Dr. Dikalova (Emory University), and Dr. Merchant and Dr. Klein (University of Louisville). Next, I would like to thank all of the members of Dr. Baylis lab, both past and present, with whom I have been fortunate enough to work: Dr. Aaron Erdely, Gerry Freshour, Kevin Engels, Lennie Samsell, Dr. Sarah Knight, Dr. Cheryl Smith, Dr. Jenny Sasser, Harold Snellen, Bruce Cunningham, Gin-Fu Chen, and Natasha Moningka. -
Circuits Regulating Superoxide and Nitric Oxide
antioxidants Article Circuits Regulating Superoxide and Nitric Oxide Production and Neutralization in Different Cell Types: Expression of Participating Genes and Changes Induced by Ionizing Radiation 1,2, 1,2, 1 1,2, Patryk Bil y, Sylwia Ciesielska y, Roman Jaksik and Joanna Rzeszowska-Wolny * 1 Department of Systems Biology and Engineering, Faculty of Automatic Control, Electronics and Computer Science, Silesian University of Technology, 44-100 Gliwice, Poland; [email protected] (P.B.); [email protected] (S.C.); [email protected] (R.J.) 2 Biotechnology Centre, Silesian University of Technology, 44-100 Gliwice, Poland * Correspondence: [email protected] These authors contributed equally. y Received: 30 June 2020; Accepted: 29 July 2020; Published: 3 August 2020 Abstract: Superoxide radicals, together with nitric oxide (NO), determine the oxidative status of cells, which use different pathways to control their levels in response to stressing conditions. Using gene expression data available in the Cancer Cell Line Encyclopedia and microarray results, we compared the expression of genes engaged in pathways controlling reactive oxygen species and NO production, neutralization, and changes in response to the exposure of cells to ionizing radiation (IR) in human cancer cell lines originating from different tissues. The expression of NADPH oxidases and NO synthases that participate in superoxide radical and NO production was low in all cell types. Superoxide dismutase, glutathione peroxidase, thioredoxin, and peroxiredoxins participating in radical neutralization showed high expression in nearly all cell types. Some enzymes that may indirectly influence superoxide radical and NO levels showed tissue-specific expression and differences in response to IR. -
Transcriptional Analysis of Sodium Valproate in a Serotonergic Cell Line Reveals Gene Regulation Through Both HDAC Inhibition-Dependent and Independent Mechanisms
bioRxiv preprint doi: https://doi.org/10.1101/837732; this version posted November 12, 2019. 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. Transcriptional analysis of sodium valproate in a serotonergic cell line reveals gene regulation through both HDAC inhibition-dependent and independent mechanisms Priyanka Sinha1,2, Simone Cree1,2, Allison L. Miller1,2, John F. Pearson1,2,3, Martin A. Kennedy1,2. 1Gene Structure and Function Laboratory, Department of Pathology and Biomedical Science, University of Otago, Christchurch, New Zealand. 2Carney Centre for Pharmacogenomics, University of Otago, Christchurch, New Zealand. 3Biostatistics and Computational Biology Unit, University of Otago, Christchurch, New Zealand. Correspondence to: Prof. M. A. Kennedy Department of Pathology and Biomedical Science University of Otago, Christchurch Christchurch, New Zealand Email: [email protected] Keywords: RNA-Seq, NanoString, lithium, valproate, HDAC inhibitor, mood stabilizer 1 bioRxiv preprint doi: https://doi.org/10.1101/837732; this version posted November 12, 2019. 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. Abstract Sodium valproate (VPA) is a histone deacetylase (HDAC) inhibitor, widely prescribed in the treatment of bipolar disorder, and yet the precise modes of therapeutic action for this drug are not fully understood. -
Gene Transfer As a Potential Treatment for Tetralujdrobiopterin Deficient States
Gene Transfer as a Potential Treatment for Tetralujdrobiopterin Deficient States Rickard F oxton Division of Neurochemistry Department of Molecular Neuroscience Institute of Neurology University College London Submitted November 2006 Funded by Brain Research Trust Thesis submitted for the degree of Doctor of Philosophy, University of London. I, Richard Hartas Foxton, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis.' 1 UMI Number: U592813 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. Dissertation Publishing UMI U592813 Published by ProQuest LLC 2013. Copyright in the Dissertation held by the Author. Microform Edition © ProQuest LLC. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code. ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 ABSTRACT Tetrahydrobiopterin (BH4) is an essential cofactor for dopamine (DA), noradrenaline (NA), serotonin and nitric oxide (NO) synthesis in the brain. Inborn errors of BH4 metabolism including GTP cyclohydrolase 1 (GTP-CH) deficiency are debilitating diseases in which BH4, DA, 5-HT and NO metabolism are impaired. Current treatment for these disorders is typically monoamine replacement +/- BH4. Whilst correction of the primary defect is the ideal, BH4 treatment is problematic as it is expensive and inefficacious. -
Copyright by Yun Wang 2010
Copyright by Yun Wang 2010 The Dissertation Committee for Yun Wang Certifies that this is the approved version of the following dissertation: Controlling Nitric Oxide (NO) Overproduction: Nω, Nω- Dimethylarginine Dimethylaminohydrolase (DDAH) as a Novel Drug Target Committee: Walter L. Fast, Supervisor Christian P. Whitman Jon D. Robertus George Georgiou Sean M. Kerwin Controlling Nitric Oxide (NO) Overproduction: Nω, Nω- Dimethylarginine Dimethylaminohydrolase (DDAH) as a Novel Drug Target by Yun Wang, B.S.; M.S. Dissertation Presented to the Faculty of the Graduate School of The University of Texas at Austin in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy The University of Texas at Austin August, 2010 Dedication To all people who have given me generous help when I am in Austin, including professors, colleagues and friends. To my beloved parents in P.R.China, who always motivate me to pursue my dream. Acknowledgements First and foremost, I would like to thank my supervisor, Dr. Walt Fast, for his generous support and for giving me an opportunity to work in his lab four years ago at the University of Texas at Austin. Walt gives me lots of freedom to explore scientific problems and provides a wonderful working environment along with my lovely colleagues. He always gives me useful directions when I meet difficulties. I appreciate every scientific conversation with him. They were especially important to me during the beginning of my Ph.D. study. I wouldn’t have accomplished as much as today without his help. In addition, I’d like to thank colleagues in Fast lab for their generous help during these years. -
(10) Patent No.: US 8119385 B2
US008119385B2 (12) United States Patent (10) Patent No.: US 8,119,385 B2 Mathur et al. (45) Date of Patent: Feb. 21, 2012 (54) NUCLEICACIDS AND PROTEINS AND (52) U.S. Cl. ........................................ 435/212:530/350 METHODS FOR MAKING AND USING THEMI (58) Field of Classification Search ........................ None (75) Inventors: Eric J. Mathur, San Diego, CA (US); See application file for complete search history. Cathy Chang, San Diego, CA (US) (56) References Cited (73) Assignee: BP Corporation North America Inc., Houston, TX (US) OTHER PUBLICATIONS c Mount, Bioinformatics, Cold Spring Harbor Press, Cold Spring Har (*) Notice: Subject to any disclaimer, the term of this bor New York, 2001, pp. 382-393.* patent is extended or adjusted under 35 Spencer et al., “Whole-Genome Sequence Variation among Multiple U.S.C. 154(b) by 689 days. Isolates of Pseudomonas aeruginosa” J. Bacteriol. (2003) 185: 1316 1325. (21) Appl. No.: 11/817,403 Database Sequence GenBank Accession No. BZ569932 Dec. 17. 1-1. 2002. (22) PCT Fled: Mar. 3, 2006 Omiecinski et al., “Epoxide Hydrolase-Polymorphism and role in (86). PCT No.: PCT/US2OO6/OOT642 toxicology” Toxicol. Lett. (2000) 1.12: 365-370. S371 (c)(1), * cited by examiner (2), (4) Date: May 7, 2008 Primary Examiner — James Martinell (87) PCT Pub. No.: WO2006/096527 (74) Attorney, Agent, or Firm — Kalim S. Fuzail PCT Pub. Date: Sep. 14, 2006 (57) ABSTRACT (65) Prior Publication Data The invention provides polypeptides, including enzymes, structural proteins and binding proteins, polynucleotides US 201O/OO11456A1 Jan. 14, 2010 encoding these polypeptides, and methods of making and using these polynucleotides and polypeptides. -
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. -
SET-Induced Calcium Signaling and MAPK/ERK Pathway Activation Mediate Dendritic Cell-Like Differentiation of U937 Cells
Leukemia (2005) 19, 1439–1445 & 2005 Nature Publishing Group All rights reserved 0887-6924/05 $30.00 www.nature.com/leu SET-induced calcium signaling and MAPK/ERK pathway activation mediate dendritic cell-like differentiation of U937 cells A Kandilci1 and GC Grosveld1 1Department of Genetics and Tumor Cell Biology, Mail Stop 331, St Jude Children’s Research Hospital, 332 N. Lauderdale, Memphis, TN 38105, USA Human SET, a target of chromosomal translocation in human G1/S transition by allowing cyclin E–CDK2 activity in the leukemia encodes a highly conserved, ubiquitously expressed, presence of p21.11 Second, SET interacts with cyclin B–CDK1.19 nuclear phosphoprotein. SET mediates many functions includ- ing chromatin remodeling, transcription, apoptosis and cell Overexpression of SET inhibits cyclin B-CDK1 activity, which in cycle control. We report that overexpression of SET directs turn, blocks the G2/M transition; this finding suggests a negative 13 differentiation of the human promonocytic cell line U937 along regulatory role for SET in G2/M transition. Overexpression of the dendritic cell (DC) pathway, as cells display typical cell division autoantigen-1 (CDA1), another member of the morphologic changes associated with DC fate and express NAP/SET family, inhibits proliferation and decreases bromo- the DC surface markers CD11b and CD86. Differentiation occurs deoxyuridine uptake in HeLa cells.20 Acidic and basic domains via a calcium-dependent mechanism involving the CaMKII and 20 MAPK/ERK pathways. Similar responses are elicited by inter- of CDA1 show 40% identity and 68% similarity to SET. feron-c (IFN-c) treatment with the distinction that IFN-c signaling We have recently shown that overexpression of SET in the activates the DNA-binding activity of STAT1 whereas SET human promonocytic cell line U937 causes G0/G1 arrest and overexpression does not.