Supplementary Table 1

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table 1 SUPPLEMENTARY DATA Supplementary Table 1. Mitochondrial and autophagy-focused post hoc analysis of islet cDNA expression microarrays from WT and Pdx1+/- mice. FC (Pdx1+/- NAME DESCRIPTION /Pdx1+/+) FDR Ndufs2 NADH dehydrogenase (ubiquinone) Fe-S protein 2 -1.769 5.48 Hspb7 heat shock protein family, member 7 (cardiovascular) -1.744 0 Got2 glutamate oxaloacetate transaminase 2, mitochondrial -1.695 26.38 Dhrs4 dehydrogenase/reductase (SDR family) member 4 -1.602 6.33 methylenetetrahydrofolate dehydrogenase (NAD+ dependent), methenyltetrahydrofolate Mthfd2 cyclohydrolase -1.597 20.72 Clec16a C-type lectin domain family 16, member A; KIAA0350 -1.583 6.33 Mrpl2 mitochondrial ribosomal protein L2 -1.487 40.08 Tomm20 translocase of outer mitochondrial membrane 20 homolog (yeast) -1.483 40.08 Hadh hydroxyacyl-Coenzyme A dehydrogenase -1.46 18.15 Pcx pyruvate carboxylase -1.448 7.18 Aldh1l2 aldehyde dehydrogenase 1 family, member L2 -1.434 5.48 Sars seryl-aminoacyl-tRNA synthetase -1.429 12.79 Rexo2 REX2, RNA exonuclease 2 homolog (S. cerevisiae) -1.427 40.08 Sars seryl-aminoacyl-tRNA synthetase -1.402 14.73 Bnip3l BCL2/adenovirus E1B interacting protein 3-like -1.398 31.02 Map1lc3b microtubule-associated protein 1 light chain 3 beta -1.394 31.02 Them2 thioesterase superfamily member 2 -1.389 8.77 Elac2 elaC homolog 2 (E. coli) -1.381 7.18 Pcx pyruvate carboxylase -1.377 8.77 Opa1 optic atrophy 1 homolog (human) -1.376 41.46 Acsl5 acyl-CoA synthetase long-chain family member 5 -1.375 41.46 Mrpl12 mitochondrial ribosomal protein L12 -1.363 31.02 Mrps24 mitochondrial ribosomal protein S24 -1.351 40.08 Aldh1b1 aldehyde dehydrogenase 1 family, member B1 -1.348 41.46 Vdac2 voltage-dependent anion channel 2 -1.334 41.46 Cox6c cytochrome c oxidase, subunit VIc -1.324 35.06 Brp44l brain protein 44-like -1.32 5.48 Hadh hydroxyacyl-Coenzyme A dehydrogenase -1.32 26.38 Cyb5r1 cytochrome b5 reductase 1 -1.314 41.46 2610524G07Rik RIKEN cDNA 2610524G07 gene -1.312 41.46 Gcat glycine C-acetyltransferase (2-amino-3-ketobutyrate-coenzyme A ligase) -1.309 41.46 Sars seryl-aminoacyl-tRNA synthetase -1.307 12.79 Acsm2 acyl-CoA synthetase medium-chain family member 2 -1.301 26.38 Vdac1 voltage-dependent anion channel 1 -1.301 41.46 Mrpl39 mitochondrial ribosomal protein L39 -1.295 5.48 Yars2 tyrosyl-tRNA synthetase 2 (mitochondrial) -1.274 7.18 Comt catechol-O-methyltransferase -1.272 20.72 Phb2 prohibitin 2 -1.268 35.06 Nme3 expressed in non-metastatic cells 3 -1.265 11.31 methylenetetrahydrofolate dehydrogenase (NADP+ dependent), methenyltetrahydrofolate Mthfd1 cyclohydrolase, formyltetrahydrofolate synthase -1.263 18.15 Mtch1 mitochondrial carrier homolog 1 (C. elegans) -1.259 7.18 Mrpl2 mitochondrial ribosomal protein L2 -1.257 40.08 Tdh L-threonine dehydrogenase -1.256 41.46 Nme3 expressed in non-metastatic cells 3 -1.254 11.31 Cox6a1 cytochrome c oxidase, subunit VI a, polypeptide 1 -1.253 20.72 Crot carnitine O-octanoyltransferase -1.245 40.08 Gfm2 G elongation factor, mitochondrial 2 -1.244 41.46 ©2015 American Diabetes Association. Published online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db15-0376/-/DC1 SUPPLEMENTARY DATA Pdss1 prenyl (solanesyl) diphosphate synthase, subunit 1 -1.244 41.46 Nt5c3 5'-nucleotidase, cytosolic III -1.242 20.72 Akr1b7 aldo-keto reductase family 1, member B7 -1.238 31.02 2310056P07Rik RIKEN cDNA 2310056P07 gene -1.234 41.46 Nt5c3 5'-nucleotidase, cytosolic III -1.226 7.18 Pitrm1 pitrilysin metallepetidase 1 -1.226 5.48 Gpx4 glutathione peroxidase 4 -1.223 5.48 Gpd2 glycerol phosphate dehydrogenase 2, mitochondrial -1.221 20.72 Mrps25 mitochondrial ribosomal protein S25 -1.221 48.24 Me3 malic enzyme 3, NADP(+)-dependent, mitochondrial -1.215 43.77 0610009O20Rik RIKEN cDNA 0610009O20 gene -1.213 48.24 Maoa monoamine oxidase A -1.213 43.77 Fth1 ferritin heavy chain 1 -1.212 18.15 Nme3 expressed in non-metastatic cells 3 -1.21 12.79 4432406C05Rik RIKEN cDNA 4432406C05 gene -1.209 41.46 Acadl acyl-Coenzyme A dehydrogenase, long-chain -1.207 43.77 Mrps26 mitochondrial ribosomal protein S26 -1.207 26.38 Acadm acyl-Coenzyme A dehydrogenase, medium chain -1.203 48.24 Hadh hydroxyacyl-Coenzyme A dehydrogenase -1.203 43.77 Fh1 fumarate hydratase 1 -1.193 43.77 2610524G07Rik RIKEN cDNA 2610524G07 gene -1.191 31.02 Hsd17b10 hydroxysteroid (17-beta) dehydrogenase 10 -1.191 41.46 Rdh14 retinol dehydrogenase 14 (all-trans and 9-cis) -1.189 35.06 Sqrdl sulfide quinone reductase-like (yeast) -1.189 11.31 Park7 Parkinson disease (autosomal recessive, early onset) 7 -1.188 31.02 Idh2 isocitrate dehydrogenase 2 (NADP+), mitochondrial -1.187 43.77 0610006I08Rik RIKEN cDNA 0610006I08 gene -1.186 40.08 Bax Bcl2-associated X protein -1.183 41.46 Cox5a cytochrome c oxidase, subunit Va -1.179 41.46 Mrps18b mitochondrial ribosomal protein S18B -1.177 31.02 A830073O21Rik RIKEN cDNA A830073O21 gene -1.174 48.24 methylenetetrahydrofolate dehydrogenase (NADP+ dependent), methenyltetrahydrofolate Mthfd1 cyclohydrolase, formyltetrahydrofolate synthase -1.174 12.79 Ldha lactate dehydrogenase A -1.17 40.08 Ldha lactate dehydrogenase A -1.168 31.02 H2-Ke6 H2-K region expressed gene 6 -1.167 40.08 Mrpl12 mitochondrial ribosomal protein L12 -1.167 20.72 Ndufab1 NADH dehydrogenase (ubiquinone) 1, alpha/beta subcomplex, 1 -1.167 26.38 Chchd4 coiled-coil-helix-coiled-coil-helix domain containing 4 -1.166 41.46 Triap1 TP53 regulated inhibitor of apoptosis 1 -1.164 40.08 Usmg5 upregulated during skeletal muscle growth 5 -1.164 41.46 Acaa1b acetyl-Coenzyme A acyltransferase 1B -1.163 8.77 Oxnad1 oxidoreductase NAD-binding domain containing 1 -1.163 41.46 Mrps7 mitchondrial ribosomal protein S7 -1.162 43.77 Cox7a2l cytochrome c oxidase subunit VIIa polypeptide 2-like -1.158 11.31 Hbld2 HESB like domain containing 2 -1.158 41.46 Slc25a25 solute carrier family 25 (mitochondrial carrier, phosphate carrier), member 25 -1.157 41.46 Ndufb4 NADH dehydrogenase (ubiquinone) 1 beta subcomplex 4 -1.154 40.08 Mtch1 mitochondrial carrier homolog 1 (C. elegans) -1.152 41.46 Gpx1 glutathione peroxidase 1 -1.151 41.46 Mrpl30 mitochondrial ribosomal protein L30 -1.151 40.08 2310056P07Rik RIKEN cDNA 2310056P07 gene -1.149 48.24 Crls1 cardiolipin synthase 1 -1.149 35.06 Hagh hydroxyacyl glutathione hydrolase -1.149 41.46 ©2015 American Diabetes Association. Published online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db15-0376/-/DC1 SUPPLEMENTARY DATA Nme2 expressed in non-metastatic cells 2, protein -1.149 41.46 Hagh hydroxyacyl glutathione hydrolase -1.148 40.08 Mrpl46 mitochondrial ribosomal protein L46 -1.148 26.38 Rab1b RAB1B, member RAS oncogene family -1.144 40.08 Gbas glioblastoma amplified sequence -1.143 40.08 Tfam transcription factor A, mitochondrial -1.143 41.46 0710008K08Rik RIKEN cDNA 0710008K08 gene -1.142 41.46 2010107E04Rik RIKEN cDNA 2010107E04 gene -1.142 40.08 Auh AU RNA binding protein/enoyl-coenzyme A hydratase -1.142 43.77 Cry1 cryptochrome 1 (photolyase-like) -1.142 48.24 Ndufb9 NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 9 -1.142 40.08 Ldha lactate dehydrogenase A -1.14 41.46 Tdh L-threonine dehydrogenase -1.14 43.77 1110001J03Rik RIKEN cDNA 1110001J03 gene -1.138 26.38 Cox7a2l cytochrome c oxidase subunit VIIa polypeptide 2-like -1.138 26.38 Rab1b RAB1B, member RAS oncogene family -1.138 40.08 Rhoa ras homolog gene family, member A -1.138 41.46 Zadh2 zinc binding alcohol dehydrogenase, domain containing 2 -1.136 35.06 Pnkd paroxysmal nonkinesiogenic dyskinesia -1.135 41.46 Brp44 brain protein 44 -1.133 48.24 Hint2 histidine triad nucleotide binding protein 2 -1.133 41.46 Mrrf mitochondrial ribosome recycling factor -1.133 35.06 Ndufa7 NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 7 (B14.5a) -1.133 41.46 Atpif1 ATPase inhibitory factor 1 -1.131 43.77 C1qbp complement component 1, q subcomponent binding protein -1.131 40.08 Guf1 GUF1 GTPase homolog (S. cerevisiae) -1.131 40.08 Idh3b isocitrate dehydrogenase 3 (NAD+) beta -1.131 26.38 Ndufa12l Ndufa12-like -1.131 41.46 Ndufs6 NADH dehydrogenase (ubiquinone) Fe-S protein 6 -1.13 20.72 Slc25a4 solute carrier family 25 (mitochondrial carrier, adenine nucleotide translocator), member 4 -1.129 43.77 Gpx1 glutathione peroxidase 1 -1.128 41.46 2010107E04Rik RIKEN cDNA 2010107E04 gene -1.125 41.46 Tspo translocator protein -1.124 43.77 Hmgcs2 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 2 -1.122 58.28 Hagh hydroxyacyl glutathione hydrolase -1.121 41.46 1110007M04Rik RIKEN cDNA 1110007M04 gene -1.12 43.77 mitochondria-associated protein involved in granulocyte-macrophage colony-stimulating factor Magmas signal transduction -1.12 40.08 Ndufa3 NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 3 -1.12 41.46 Rps14 ribosomal protein S14 -1.119 40.08 C1qbp complement component 1, q subcomponent binding protein -1.118 41.46 Auh AU RNA binding protein/enoyl-coenzyme A hydratase -1.117 35.06 Ict1 immature colon carcinoma transcript 1 -1.117 41.46 Nudt19 nudix (nucleoside diphosphate linked moiety X)-type motif 19 -1.117 43.77 Rab11b RAB11B, member RAS oncogene family -1.117 48.24 Cox7a2 cytochrome c oxidase, subunit VIIa 2 -1.115 40.08 Ndufb5 NADH dehydrogenase (ubiquinone) 1 beta subcomplex, 5 -1.115 40.08 Rab8b RAB8B, member RAS oncogene family -1.114 41.46 Yme1l1 YME1-like 1 (S. cerevisiae) -1.114 35.06 Nfxl1 nuclear transcription factor, X-box binding-like 1 -1.113 41.46 Rab8b RAB8B, member RAS oncogene family -1.113 41.46 Tomm20 translocase of outer mitochondrial membrane 20 homolog (yeast) -1.113 40.08 Mcart1 mitochondrial carrier triple repeat 1 -1.112 41.46 Mrpl15 mitochondrial ribosomal protein L15 -1.112 43.77 ©2015 American Diabetes Association.
Recommended publications
  • The Aldehyde Dehydrogenase ALDH2*2 Allele Exhibits Dominance Over ALDH2*1 in Transduced Hela Cells
    The aldehyde dehydrogenase ALDH2*2 allele exhibits dominance over ALDH2*1 in transduced HeLa cells. Q Xiao, … , T Johnston, D W Crabb J Clin Invest. 1995;96(5):2180-2186. https://doi.org/10.1172/JCI118272. Research Article Individuals heterozygous or homozygous for the variant aldehyde dehydrogenase (ALDH2) allele (ALDH2*2), which encodes a protein differing only at residue 487 from the normal protein, have decreased ALDH2 activity in liver extracts and experience cutaneous flushing when they drink alcohol. The mechanisms by which this allele exerts its dominant effect is unknown. To study this effect, the human ALDH2*1 cDNA was cloned and the ALDH2*2 allele was generated by site-directed mutagenesis. These cDNAs were transduced using retroviral vectors into HeLa and CV1 cells, which do not express ALDH2. The normal allele directed synthesis of immunoreactive ALDH2 protein (ALDH2E) with the expected isoelectric point. Extracts of these cells contained increased aldehyde dehydrogenase activity with low Km for the aldehyde substrate. The ALDH2*2 allele directed synthesis of mRNA and immunoreactive protein (ALDH2K), but the protein lacked enzymatic activity. When ALDH2*1-expressing cells were transduced with ALDH2*2 vectors, both mRNAs were expressed and immunoreactive proteins with isoelectric points ranging between those of ALDH2E and ALDH2K were present, indicating that the subunits formed heteromers. ALDH2 activity in these cells was reduced below that of the parental ALDH2*1-expressing cells. Thus, the ALDH2*2 allele is sufficient to cause ALDH2 deficiency in vitro. Find the latest version: https://jci.me/118272/pdf The Aldehyde Dehydrogenase ALDH2*2 Allele Exhibits Dominance over ALDH2*1 in Transduced HeLa Cells Qing Xiao, * Henry Weiner,* Timothy Johnston,* and David W.
    [Show full text]
  • Supplement 1 Overview of Dystonia Genes
    Supplement 1 Overview of genes that may cause dystonia in children and adolescents Gene (OMIM) Disease name/phenotype Mode of inheritance 1: (Formerly called) Primary dystonias (DYTs): TOR1A (605204) DYT1: Early-onset generalized AD primary torsion dystonia (PTD) TUBB4A (602662) DYT4: Whispering dystonia AD GCH1 (600225) DYT5: GTP-cyclohydrolase 1 AD deficiency THAP1 (609520) DYT6: Adolescent onset torsion AD dystonia, mixed type PNKD/MR1 (609023) DYT8: Paroxysmal non- AD kinesigenic dyskinesia SLC2A1 (138140) DYT9/18: Paroxysmal choreoathetosis with episodic AD ataxia and spasticity/GLUT1 deficiency syndrome-1 PRRT2 (614386) DYT10: Paroxysmal kinesigenic AD dyskinesia SGCE (604149) DYT11: Myoclonus-dystonia AD ATP1A3 (182350) DYT12: Rapid-onset dystonia AD parkinsonism PRKRA (603424) DYT16: Young-onset dystonia AR parkinsonism ANO3 (610110) DYT24: Primary focal dystonia AD GNAL (139312) DYT25: Primary torsion dystonia AD 2: Inborn errors of metabolism: GCDH (608801) Glutaric aciduria type 1 AR PCCA (232000) Propionic aciduria AR PCCB (232050) Propionic aciduria AR MUT (609058) Methylmalonic aciduria AR MMAA (607481) Cobalamin A deficiency AR MMAB (607568) Cobalamin B deficiency AR MMACHC (609831) Cobalamin C deficiency AR C2orf25 (611935) Cobalamin D deficiency AR MTRR (602568) Cobalamin E deficiency AR LMBRD1 (612625) Cobalamin F deficiency AR MTR (156570) Cobalamin G deficiency AR CBS (613381) Homocysteinuria AR PCBD (126090) Hyperphelaninemia variant D AR TH (191290) Tyrosine hydroxylase deficiency AR SPR (182125) Sepiaterine reductase
    [Show full text]
  • Crystal Structure of the Targeting Endonuclease of the Human LINE-1 Retrotransposon
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Structure, Vol. 12, 975–986, June, 2004, 2004 Elsevier Ltd. All rights reserved. DOI 10.1016/j.str.2004.04.011 Crystal Structure of the Targeting Endonuclease of the Human LINE-1 Retrotransposon Oliver Weichenrieder,1,* Kostas Repanas,1 transcriptase. Depending on the DNA integration mech- and Anastassis Perrakis* anism, two classes of retrotransposons are distin- The Netherlands Cancer Institute guished. The first class contains long terminal repeat Department of Molecular Carcinogenesis-H2 (LTR) retrotransposons and retroviruses. These retroele- Plesmanlaan 121 ments use an integrase that recognizes the LTRs of the 1066 CX Amsterdam double-stranded DNA copy. The second, much larger, The Netherlands and more ancient class includes all non-LTR retro- transposons. Those are thought to integrate via target- primed reverse transcription (TPRT), a process in which Summary reverse transcription and integration are coupled (Eick- bush and Malik, 2002; Kazazian, 2004). An endonuclease The human L1 endonuclease (L1-EN) is encoded by that is part of the same polypeptide chain as the reverse the non-LTR retrotransposon LINE-1 (L1). L1 is re- transcriptase nicks the genomic DNA and hands over sponsible for more than 1.5 million retrotransposition the resulting ribose 3Ј-hydroxyl end as a primer for re- events in the history of the human genome, contribut- verse transcription of associated template RNA (Cost ing more than a quarter to human genomic DNA (L1 et al., 2002; Luan et al., 1993). and Alu elements). L1-EN is related to the well-under- Most non-LTR retrotransposons encode an endonu- stood human DNA repair endonuclease APE1, and its clease located N-terminally of the reverse transcriptase.
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2013/0089535 A1 Yamashiro Et Al
    US 2013 0089535A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0089535 A1 Yamashiro et al. (43) Pub. Date: Apr. 11, 2013 (54) AGENT FOR REDUCING ACETALDEHYDE Publication Classification NORAL CAVITY (51) Int. Cl. (75) Inventors: Kan Yamashiro, Kakamigahara-shi (JP); A68/66 (2006.01) Takahumi Koyama, Kakamigahara-shi A638/51 (2006.01) (JP) A61O 11/00 (2006.01) A638/44 (2006.01) Assignee: AMANOENZYME INC., Nagoya-shi (52) U.S. Cl. (73) CPC. A61K 8/66 (2013.01); A61K 38/44 (2013.01); (JP) A61 K38/51 (2013.01); A61O II/00 (2013.01) (21) Appl. No.: 13/703,451 USPC .......... 424/94.4; 424/94.5; 435/191: 435/232 (22) PCT Fled: Jun. 7, 2011 (57) ABSTRACT Disclosed herein is a novel enzymatic agent effective in (86) PCT NO.: PCT/UP2011/062991 reducing acetaldehyde in the oral cavity. It has been found S371 (c)(1), that an aldehyde dehydrogenase derived from a microorgan (2), (4) Date: Dec. 11, 2012 ism belonging to the genus Saccharomyces and a threonine aldolase derived from Escherichia coli are effective in reduc (30) Foreign Application Priority Data ing low concentrations of acetaldehyde. Therefore, an agent for reducing acetaldehyde in the oral cavity is provided, Jun. 19, 2010 (JP) ................................. 2010-140O26 which contains these enzymes as active ingredients. Patent Application Publication Apr. 11, 2013 Sheet 1 of 2 US 2013/0089535 A1 FIG 1) 10.5 1 0 9.9.5 8. 5 CONTROL TA AD (BSA) ENZYME Patent Application Publication Apr. 11, 2013 Sheet 2 of 2 US 2013/0089535 A1 FIG 2) 110 the CONTROL (BSA) 100 354.
    [Show full text]
  • Downloaded from GEO
    bioRxiv preprint doi: https://doi.org/10.1101/2020.08.17.252007; this version posted November 3, 2020. 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 4.0 International license. Oxylipin metabolism is controlled by mitochondrial b-oxidation during bacterial inflammation. Mariya Misheva1, Konstantinos Kotzamanis1*, Luke C Davies1*, Victoria J Tyrrell1, Patricia R S Rodrigues1, Gloria A Benavides2, Christine Hinz1, Robert C Murphy3, Paul Kennedy4, Philip R Taylor1,5, Marcela Rosas1, Simon A Jones1, Sumukh Deshpande1, Robert Andrews1, Magdalena A Czubala1, Mark Gurney1, Maceler Aldrovandi1, Sven W Meckelmann1, Peter Ghazal1, Victor Darley-Usmar2, Daniel White1, and Valerie B O’Donnell1 1Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University, UK, 2Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA, 3Department of Pharmacology, University of Colorado Denver, Aurora, CO 80045, USA, 4Cayman Chemical 1180 E Ellsworth Rd, Ann Arbor, MI 48108, United States, 5UK Dementia Research Institute at Cardiff, Cardiff University, UK Address correspondence: Valerie O’Donnell, [email protected] or Daniel White, [email protected], Systems Immunity Research Institute, Cardiff University *Both authors contributed equally to the study 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.17.252007; this version posted November 3, 2020. 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.
    [Show full text]
  • Restriction Endonucleases
    Molecular Biology Problem Solver: A Laboratory Guide. Edited by Alan S. Gerstein Copyright © 2001 by Wiley-Liss, Inc. ISBNs: 0-471-37972-7 (Paper); 0-471-22390-5 (Electronic) 9 Restriction Endonucleases Derek Robinson, Paul R. Walsh, and Joseph A. Bonventre Background Information . 226 Which Restriction Enzymes Are Commercially Available? . 226 Why Are Some Enzymes More Expensive Than Others? . 227 What Can You Do to Reduce the Cost of Working with Restriction Enzymes? . 228 If You Could Select among Several Restriction Enzymes for Your Application, What Criteria Should You Consider to Make the Most Appropriate Choice? . 229 What Are the General Properties of Restriction Endonucleases? . 232 What Insight Is Provided by a Restriction Enzyme’s Quality Control Data? . 233 How Stable Are Restriction Enzymes? . 236 How Stable Are Diluted Restriction Enzymes? . 236 Simple Digests . 236 How Should You Set up a Simple Restriction Digest? . 236 Is It Wise to Modify the Suggested Reaction Conditions? . 237 Complex Restriction Digestions . 239 How Can a Substrate Affect the Restriction Digest? . 239 Should You Alter the Reaction Volume and DNA Concentration? . 241 Double Digests: Simultaneous or Sequential? . 242 225 Genomic Digests . 244 When Preparing Genomic DNA for Southern Blotting, How Can You Determine If Complete Digestion Has Been Obtained? . 244 What Are Your Options If You Must Create Additional Rare or Unique Restriction Sites? . 247 Troubleshooting . 255 What Can Cause a Simple Restriction Digest to Fail? . 255 The Volume of Enzyme in the Vial Appears Very Low. Did Leakage Occur during Shipment? . 259 The Enzyme Shipment Sat on the Shipping Dock for Two Days.
    [Show full text]
  • Organic & Biomolecular Chemistry
    Organic & Biomolecular Chemistry Accepted Manuscript This is an Accepted Manuscript, which has been through the Royal Society of Chemistry peer review process and has been accepted for publication. Accepted Manuscripts are published online shortly after acceptance, before technical editing, formatting and proof reading. Using this free service, authors can make their results available to the community, in citable form, before we publish the edited article. We will replace this Accepted Manuscript with the edited and formatted Advance Article as soon as it is available. You can find more information about Accepted Manuscripts in the Information for Authors. Please note that technical editing may introduce minor changes to the text and/or graphics, which may alter content. The journal’s standard Terms & Conditions and the Ethical guidelines still apply. In no event shall the Royal Society of Chemistry be held responsible for any errors or omissions in this Accepted Manuscript or any consequences arising from the use of any information it contains. www.rsc.org/obc Page 1 of 14 Organic & Biomolecular Chemistry Enantioselective imine reduction catalyzed by imine reductases and artificial metalloenzymes Daniela Gamenara a* , Pablo Domínguez de María b,c* Manuscript a: Organic Chemistry Department. Universidad de la República (UdelaR). Gral. Flores 2124. 11800 Montevideo, Uruguay. b: Institut für Technische und Makromolekulare Chemie (ITMC), Accepted RWTH Aachen University. Worringerweg 1. 52074 Aachen, Germany. c: Present address: Sustainable Momentum . Ap. Correos 3517. 35004, Las Palmas de Gran Canaria; Canary Islands; Spain. Chemistry Biomolecular & * Corresponding Authors: Dr. Daniela Gamenara. Tel.: +598 29247881; Fax: +598 29241906; E-mail: [email protected] ; Dr.
    [Show full text]
  • Inborn Errors of Metabolism Test Requisition
    LABORATORY OF GENETICS AND GENOMICS Mailing Address: For local courier service and/or inquiries, please contact 513-636-4474 • Fax: 513-636-4373 3333 Burnet Avenue, Room R1042 www.cincinnatichildrens.org/moleculargenetics • Email: [email protected] Cincinnati, OH 45229 INBORN ERRORS OF METABOLISM TEST REQUISITION All Information Must Be Completed Before Sample Can Be Processed PATIENT INFORMATION ETHNIC/RACIAL BACKGROUND (Choose All) Patient Name: ___________________ , ___________________ , ________ European American (White) African-American (Black) Last First MI Native American or Alaskan Asian-American Address: ____________________________________________________ Pacific Islander Ashkenazi Jewish ancestry ____________________________________________________ Latino-Hispanic _____________________________________________ Home Phone: ________________________________________________ (specify country/region of origin) MR# __________________ Date of Birth ________ / ________ / _______ Other ____________________________________________________ (specify country/region of origin) Gender: Male Female BILLING INFORMATION (Choose ONE method of payment) o REFERRING INSTITUTION o COMMERCIAL INSURANCE* Insurance can only be billed if requested at the time of service. Institution: ____________________________________________________ Policy Holder Name: _____________________________________________ Address: _____________________________________________________ Gender: ________________ Date of Birth ________ / ________ / _______
    [Show full text]
  • Genes Investigated
    BabyNEXTTM EXTENDED Investigated genes and associated diseases Gene Disease OMIM OMIM Condition RUSP gene Disease ABCC8 Familial hyperinsulinism 600509 256450 Metabolic disorder - ABCC8-related Inborn error of amino acid metabolism ABCD1 Adrenoleukodystrophy 300371 300100 Miscellaneous RUSP multisystem (C) * diseases ABCD4 Methylmalonic aciduria and 603214 614857 Metabolic disorder - homocystinuria, cblJ type Inborn error of amino acid metabolism ACAD8 Isobutyryl-CoA 604773 611283 Metabolic Disorder - RUSP dehydrogenase deficiency Inborn error of (S) ** organic acid metabolism ACAD9 acyl-CoA dehydrogenase-9 611103 611126 Metabolic Disorder - (ACAD9) deficiency Inborn error of fatty acid metabolism ACADM Acyl-CoA dehydrogenase, 607008 201450 Metabolic Disorder - RUSP medium chain, deficiency of Inborn error of fatty (C) acid metabolism ACADS Acyl-CoA dehydrogenase, 606885 201470 Metabolic Disorder - RUSP short-chain, deficiency of Inborn error of fatty (S) acid metabolism ACADSB 2-methylbutyrylglycinuria 600301 610006 Metabolic Disorder - RUSP Inborn error of (S) organic acid metabolism ACADVL very long-chain acyl-CoA 609575 201475 Metabolic Disorder - RUSP dehydrogenase deficiency Inborn error of fatty (C) acid metabolism ACAT1 Alpha-methylacetoacetic 607809 203750 Metabolic Disorder - RUSP aciduria Inborn error of (C) organic acid metabolism ACSF3 Combined malonic and 614245 614265 Metabolic Disorder - methylmalonic aciduria Inborn error of organic acid metabolism 1 ADA Severe combined 608958 102700 Primary RUSP immunodeficiency due
    [Show full text]
  • Health Effects Support Document for Perfluorooctanoic Acid (PFOA)
    United States Office of Water EPA 822-R-16-003 Environmental Protection Mail Code 4304T May 2016 Agency Health Effects Support Document for Perfluorooctanoic Acid (PFOA) Perfluorooctanoic Acid – May 2016 i Health Effects Support Document for Perfluorooctanoic Acid (PFOA) U.S. Environmental Protection Agency Office of Water (4304T) Health and Ecological Criteria Division Washington, DC 20460 EPA Document Number: 822-R-16-003 May 2016 Perfluorooctanoic Acid – May 2016 ii BACKGROUND The Safe Drinking Water Act (SDWA), as amended in 1996, requires the Administrator of the U.S. Environmental Protection Agency (EPA) to periodically publish a list of unregulated chemical contaminants known or anticipated to occur in public water systems and that may require regulation under SDWA. The SDWA also requires the Agency to make regulatory determinations on at least five contaminants on the Contaminant Candidate List (CCL) every 5 years. For each contaminant on the CCL, before EPA makes a regulatory determination, the Agency needs to obtain sufficient data to conduct analyses on the extent to which the contaminant occurs and the risk it poses to populations via drinking water. Ultimately, this information will assist the Agency in determining the most appropriate course of action in relation to the contaminant (e.g., developing a regulation to control it in drinking water, developing guidance, or deciding not to regulate it). The PFOA health assessment was initiated by the Office of Water, Office of Science and Technology in 2009. The draft Health Effects Support Document for Perfluoroctanoic Acid (PFOA) was completed in 2013 and released for public comment in February 2014.
    [Show full text]
  • CDH12 Cadherin 12, Type 2 N-Cadherin 2 RPL5 Ribosomal
    5 6 6 5 . 4 2 1 1 1 2 4 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 2 A A A A A A A A A A A A A A A A A A A A C C C C C C C C C C C C C C C C C C C C R R R R R R R R R R R R R R R R R R R R B , B B B B B B B B B B B B B B B B B B B , 9 , , , , 4 , , 3 0 , , , , , , , , 6 2 , , 5 , 0 8 6 4 , 7 5 7 0 2 8 9 1 3 3 3 1 1 7 5 0 4 1 4 0 7 1 0 2 0 6 7 8 0 2 5 7 8 0 3 8 5 4 9 0 1 0 8 8 3 5 6 7 4 7 9 5 2 1 1 8 2 2 1 7 9 6 2 1 7 1 1 0 4 5 3 5 8 9 1 0 0 4 2 5 0 8 1 4 1 6 9 0 0 6 3 6 9 1 0 9 0 3 8 1 3 5 6 3 6 0 4 2 6 1 0 1 2 1 9 9 7 9 5 7 1 5 8 9 8 8 2 1 9 9 1 1 1 9 6 9 8 9 7 8 4 5 8 8 6 4 8 1 1 2 8 6 2 7 9 8 3 5 4 3 2 1 7 9 5 3 1 3 2 1 2 9 5 1 1 1 1 1 1 5 9 5 3 2 6 3 4 1 3 1 1 4 1 4 1 7 1 3 4 3 2 7 6 4 2 7 2 1 2 1 5 1 6 3 5 6 1 3 6 4 7 1 6 5 1 1 4 1 6 1 7 6 4 7 e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e e l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l l p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p p m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m m
    [Show full text]
  • Targeting Glioblastoma Stem Cells Through Disruption of the Circadian Clock
    Published OnlineFirst August 27, 2019; DOI: 10.1158/2159-8290.CD-19-0215 RESEARCH ARTICLE Targeting Glioblastoma Stem Cells through Disruption of the Circadian Clock Zhen Dong1, Guoxin Zhang1, Meng Qu2, Ryan C. Gimple1,3, Qiulian Wu1, Zhixin Qiu1, Briana C. Prager1,3, Xiuxing Wang1, Leo J.Y. Kim1,3, Andrew R. Morton3, Deobrat Dixit1, Wenchao Zhou4, Haidong Huang4, Bin Li5, Zhe Zhu1, Shideng Bao4, Stephen C. Mack6, Lukas Chavez7, Steve A. Kay2, and Jeremy N. Rich1 Downloaded from cancerdiscovery.aacrjournals.org on September 24, 2021. © 2019 American Association for Cancer Research. Published OnlineFirst August 27, 2019; DOI: 10.1158/2159-8290.CD-19-0215 ABSTRACT Glioblastomas are highly lethal cancers, containing self-renewing glioblastoma stem cells (GSC). Here, we show that GSCs, differentiated glioblastoma cells (DGC), and nonmalignant brain cultures all displayed robust circadian rhythms, yet GSCs alone displayed exquisite dependence on core clock transcription factors, BMAL1 and CLOCK, for optimal cell growth. Downregulation of BMAL1 or CLOCK in GSCs induced cell-cycle arrest and apoptosis. Chromatin immu- noprecipitation revealed that BMAL1 preferentially bound metabolic genes and was associated with active chromatin regions in GSCs compared with neural stem cells. Targeting BMAL1 or CLOCK attenu- ated mitochondrial metabolic function and reduced expression of tricarboxylic acid cycle enzymes. Small-molecule agonists of two independent BMAL1–CLOCK negative regulators, the cryptochromes and REV-ERBs, downregulated stem cell factors and reduced GSC growth. Combination of cryp- tochrome and REV-ERB agonists induced synergistic antitumor effi cacy. Collectively, these fi ndings show that GSCs co-opt circadian regulators beyond canonical circadian circuitry to promote stemness maintenance and metabolism, offering novel therapeutic paradigms.
    [Show full text]