1 Supplementary Material Table S1. Acquired Salivary Proteins And
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Examples of Amino Acid Changes in Notothenioids Methods To
Supplementary Information S1 Candidate genes: examples of amino acid changes in notothenioids Methods To evaluate notothenioid amino acid changes in a cross‐section of genes, six candidates from a range of functional categories of interest were chosen for a more detailed examination. The selected genes comprised small, well‐characterised genes present in multiple fish species (mainly teleosts, but in some cases these analyses were extended to the Actinopterygii when sequences from the spotted gar (Lepisosteus oculatus) were available) and available in at least two notothenioids. The amino acid composition of a series of six candidate genes were further analysed in depth at the amino acid sequence level. These genes were superoxide dismutase 1 (SOD1), neuroglobin, dihydrofolate reductase (both paralogues), p53 and calmodulin. Clustal X alignments were constructed from orthologues identified in the four Notothenioid transcriptomes along with other fish orthologues extracted from either SwissProt (Bateman et al., 2017) or Ensembl release 91 (Aken et al., 2017). Alignment data were visualised and annotated in BoxShade version 3.21 (https://embnet.vital‐ it.ch/software/BOX_form.html). Notothenioid‐specific changes were noted and the type of substitution in terms of amino acid properties was noted. Results A range of amino acid changes were revealed, from virtually complete conservation between the notothenioids and other fish (calmodulin), to one amino acid substitution present in neuroglobin and SOD1, to more extensive changes in dihydrofolate reductase, dihydrofolate reductase‐like and p53. In the case of the latter three genes, notothenioid‐specific changes were at positions that were often highly variable in temperate fish species with up to six different amino acid substitutions and did not result in a definable pattern of directional substitution. -
C8cc08685k1.Pdf
Electronic Supplementary Material (ESI) for ChemComm. This journal is © The Royal Society of Chemistry 2018 Supporting Information Minimalist Linkers Suitable for Irreversible Inhibitors in Simultaneous Proteome Profiling, Live-Cell Imaging and Drug Screening Cuiping Guo,Yu Chang, Xin Wang, Chengqian Zhang, Piliang Hao*, Ke Ding and Zhengqiu Li* School of Pharmacy, Jinan University, Guangzhou, China 510632 *Corresponding author ([email protected]) 1. General Information All chemicals were purchased from commercial vendors and used without further purification, unless indicated otherwise. All reactions requiring anhydrous conditions were carried out under argon or nitrogen atmosphere using oven-dried glassware. AR-grade solvents were used for all reactions. Reaction progress was monitored by TLC on pre-coated silica plates (Merck 60 F254 nm, 0.25 µm) and spots were visualized by UV, iodine or other suitable stains. Flash column chromatography was carried out using silica gel (Qingdao Ocean). All NMR spectra (1H-NMR, 13C-NMR) were recorded on Bruker 300 MHz/400 MHz NMR spectrometers. Chemical shifts were reported in parts per million (ppm) referenced with respect to appropriate internal standards or residual solvent peaks (CDCl3 = 7.26 ppm, DMSO-d6 = 2.50 ppm). The following abbreviations were used in reporting spectra, br s (broad singlet), s (singlet), d (doublet), t (triplet), q (quartet), m (multiplet), dd (doublet of doublets). Mass spectra were obtained on Agilent LC-ESI-MS system. All analytical HPLC were carried out on Agilent system. Water with 0.1% TFA and acetonitrile with 0.1% TFA were used as eluents and the flow rate was 0.5 mL/min. -
Genome-Wide Association Studies Identify Genetic Loci Associated With
SUPPLEMENTARY DATA Genome-wide Association Studies Identify Genetic Loci Associated with Albuminuria in Diabetes SUPPLEMENTAL MATERIALS This work is dedicated to the memory of our colleague Dr. Wen Hong Linda Kao, a wonderful person, brilliant scientist and central member of the CKDGen Consortium. 1 ©2016 American Diabetes Association. Published online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db15-1313/-/DC1 SUPPLEMENTARY DATA Table of Contents SUPPLEMENTARY FIGURE 1: QQ PLOTS FOR ALL GWAS META-ANALYSES ............................................. 3 SUPPLEMENTARY FIGURE 2: MANHATTAN PLOTS FOR ALL GWAS META-ANALYSES ............................. 4 SUPPLEMENTARY FIGURE 3: REGIONAL ASSOCIATION PLOTS............................................................... 6 SUPPLEMENTARY FIGURE 4: EVALUATION OF GLOMERULOSCLEROSIS IN RAB38 KO, CONGENIC AND TRANSGENIC RATS. ........................................................................................................................... 17 SUPPLEMENTARY TABLE 1: CHARACTERISTICS OF THE STUDY POPULATIONS ..................................... 18 SUPPLEMENTARY TABLE 2: INFORMATION ABOUT STUDY DESIGN AND UACR MEASUREMENT .......... 20 SUPPLEMENTARY TABLE 3: STUDY-SPECIFIC INFORMATION ABOUT GENOTYPING, IMPUTATION AND DATA MANAGEMENT AND ANALYSIS ................................................................................................ 31 SUPPLEMENTARY TABLE 4: SNPS ASSOCIATED WITH UACR AMONG ALL INDIVIDUALS WITH A P-VALUE OF <1E-05. ....................................................................................................................................... -
Reprogramming of Trna Modifications Controls the Oxidative Stress Response by Codon-Biased Translation of Proteins
Reprogramming of tRNA modifications controls the oxidative stress response by codon-biased translation of proteins The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation Chan, Clement T.Y. et al. “Reprogramming of tRNA Modifications Controls the Oxidative Stress Response by Codon-biased Translation of Proteins.” Nature Communications 3 (2012): 937. As Published http://dx.doi.org/10.1038/ncomms1938 Publisher Nature Publishing Group Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/76775 Terms of Use Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use. Reprogramming of tRNA modifications controls the oxidative stress response by codon-biased translation of proteins Clement T.Y. Chan,1,2 Yan Ling Joy Pang,1 Wenjun Deng,1 I. Ramesh Babu,1 Madhu Dyavaiah,3 Thomas J. Begley3 and Peter C. Dedon1,4* 1Department of Biological Engineering, 2Department of Chemistry and 4Center for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139; 3College of Nanoscale Science and Engineering, University at Albany, SUNY, Albany, NY 12203 * Corresponding author: PCD, Department of Biological Engineering, NE47-277, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139; tel 617-253-8017; fax 617-324-7554; email [email protected] 2 ABSTRACT Selective translation of survival proteins is an important facet of cellular stress response. We recently demonstrated that this translational control involves a stress-specific reprogramming of modified ribonucleosides in tRNA. -
Protein Name Accession Number Molecular Weight Myovi-GTD
MyoVI-GTD MyoVI-GTD MyoVa-MGT MyoVa-MGT Molecular Spectral Unique Spectral Unique Protein Name Accession Number Weight Counts Peptides Counts Peptides Dync1h1 Cytoplasmic dynein 1 heavy chain 1 IPI00119876 532 kDa 310 121 515 182 Spna2 Spectrin alpha 2 IPI00757353 285 kDa 853 170 597 149 Myo5a 215 kDa protein IPI00875222 215 kDa 162 47 874 109 AU042671 hypothetical protein LOC269700 isoform 1 IPI00762814 453 kDa 2 2 231 104 Spnb2 Isoform 1 of Spectrin beta chain, brain 1 IPI00319830 274 kDa 505 122 347 100 Dmxl2 Isoform 1 of DmX-like protein 2 IPI00853932 338 kDa 63 38 251 100 Cltc Clathrin heavy chain 1 IPI00169916 (+1) 192 kDa 1994 138 565 90 Mtap2 12 days embryo spinal cord cDNA, RIKEN full-length enriched library, clone:C530026F16 product:microtubule-associated protein 2, full insert sequenceIPI00894724 199 kDa 229 82 258 74 Mtap1a Isoform 1 of Microtubule-associated protein 1A IPI00408909 (+1) 300 kDa 310 86 214 74 Itpr1 Isoform 4 of Inositol 1,4,5-trisphosphate receptor type 1 IPI00230019 (+3) 311 kDa 37 18 155 73 Huwe1 HECT, UBA and WWE domain containing 1 IPI00463909 (+1) 483 kDa 5 5 91 69 Fasn Fatty acid synthase IPI00113223 272 kDa 24 17 140 68 Usp9x Ubiquitin carboxyl-terminal hydrolase IPI00798468 291 kDa 68 45 98 65 Lrp1 Prolow-density lipoprotein receptor-related protein 1 precursor IPI00119063 505 kDa 92 53 109 62 Myh10 Myosin-10 IPI00515398 (+1) 229 kDa 65 40 98 59 Mical1 NEDD9-interacting protein with calponin homology and LIM domains IPI00116371 117 kDa 2 2 203 57 Plec1 Isoform PLEC-1I of Plectin-1 IPI00229509 (+10) -
Dysregulated Hepatic Methionine
Virginia Commonwealth University VCU Scholars Compass Internal Medicine Publications Dept. of Internal Medicine 2015 Dysregulated Hepatic Methionine Metabolism Drives Homocysteine Elevation in Diet-Induced Nonalcoholic Fatty Liver Disease Tommy Pacana Virginia Commonwealth University, [email protected] Sophie Cazanave Virginia Commonwealth University Aurora Verdianelli Virginia Commonwealth University See next page for additional authors Follow this and additional works at: http://scholarscompass.vcu.edu/intmed_pubs Part of the Medicine and Health Sciences Commons Copyright: © 2015 Pacana et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Downloaded from http://scholarscompass.vcu.edu/intmed_pubs/98 This Article is brought to you for free and open access by the Dept. of Internal Medicine at VCU Scholars Compass. It has been accepted for inclusion in Internal Medicine Publications by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Authors Tommy Pacana, Sophie Cazanave, Aurora Verdianelli, Viashali Patel, Hae-Ki Min, Faridoddin Mirshahi, Eoin Quinlavin, and Arun J. Sanyal This article is available at VCU Scholars Compass: http://scholarscompass.vcu.edu/intmed_pubs/98 RESEARCH ARTICLE Dysregulated Hepatic Methionine Metabolism Drives Homocysteine Elevation in Diet-Induced Nonalcoholic Fatty -
Table 1 Gene Name Increased Or Decreased in LTD
Table_1 gene_name increased or decreased in LTD protein_id description keep_supernatant keep_pellet comparison sample hit_annotation_methodpvalue fdr hit hit_annotation 2010300C02RIK increased E9Q3M9 Protein 2010300C02Rik OS=Mus musculus GN=2010300C02Rik PE=1 SV=1 TRUE TRUE NMDA - control pellet fdrtool 0,074667 0,584087 FALSE trend 2310035C23RIK|KIAA1468increased A0A087WSS1|E9QM90|Q148V7|Q148V7-2 Protein 2310035C23Rik OS=Mus musculus GN=2310035C23Rik PE=1 SV=1|Protein 2310035C23Rik OS=Mus musculusTRUE GN=2310035C23Rik PE=1 SV=2|LisH FALSE domain NMDAand HEAT - control repeat-containing protein KIAA1468 supernatant OS=Mus musculus GN=Kiaa1468 fdrtoolPE=1 SV=1|Isoform 0,080056 2 of 0,589077LisH domain FALSEand HEAT trend repeat-containing protein KIAA1468 OS=Mus musculus GN=Kiaa1468 ABR increased E9PUE7|Q5SSL4|Q5SSL4-2|Q5SSL4-3|Q5SSL4-4 Active breakpoint cluster region-related protein OS=Mus musculus GN=Abr PE=1 SV=1|Isoform 2 of Active breakpointTRUE cluster region-related protein TRUE OS=Mus musculus NMDA GN=Abr|Isoform - control 3 of Active breakpoint supernatant cluster region-related protein OS=Mus fdrtool musculus 0,08128 GN=Abr|Isoform 0,592743 4 of Active FALSE breakpoint trend cluster region-related protein OS=Mus musculus GN=Abr ADAM22 increased D3YUP9|Q9R1V6|Q9R1V6-10|Q9R1V6-11|Q9R1V6-12|Q9R1V6-13|Q9R1V6-14|Q9R1V6-15|Q9R1V6-17|Q9R1V6-4|Q9R1V6-5|Q9R1V6-6|Q9R1V6-7|Q9R1V6-8Disintegrin and metalloproteinase domain-containing protein 22 OS=Mus musculus GN=Adam22 PE=1 SV=1|DisintegrinFALSE and metalloproteinase domain-containing TRUE -
Propranolol-Mediated Attenuation of MMP-9 Excretion in Infants with Hemangiomas
Supplementary Online Content Thaivalappil S, Bauman N, Saieg A, Movius E, Brown KJ, Preciado D. Propranolol-mediated attenuation of MMP-9 excretion in infants with hemangiomas. JAMA Otolaryngol Head Neck Surg. doi:10.1001/jamaoto.2013.4773 eTable. List of All of the Proteins Identified by Proteomics This supplementary material has been provided by the authors to give readers additional information about their work. © 2013 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 eTable. List of All of the Proteins Identified by Proteomics Protein Name Prop 12 mo/4 Pred 12 mo/4 Δ Prop to Pred mo mo Myeloperoxidase OS=Homo sapiens GN=MPO 26.00 143.00 ‐117.00 Lactotransferrin OS=Homo sapiens GN=LTF 114.00 205.50 ‐91.50 Matrix metalloproteinase‐9 OS=Homo sapiens GN=MMP9 5.00 36.00 ‐31.00 Neutrophil elastase OS=Homo sapiens GN=ELANE 24.00 48.00 ‐24.00 Bleomycin hydrolase OS=Homo sapiens GN=BLMH 3.00 25.00 ‐22.00 CAP7_HUMAN Azurocidin OS=Homo sapiens GN=AZU1 PE=1 SV=3 4.00 26.00 ‐22.00 S10A8_HUMAN Protein S100‐A8 OS=Homo sapiens GN=S100A8 PE=1 14.67 30.50 ‐15.83 SV=1 IL1F9_HUMAN Interleukin‐1 family member 9 OS=Homo sapiens 1.00 15.00 ‐14.00 GN=IL1F9 PE=1 SV=1 MUC5B_HUMAN Mucin‐5B OS=Homo sapiens GN=MUC5B PE=1 SV=3 2.00 14.00 ‐12.00 MUC4_HUMAN Mucin‐4 OS=Homo sapiens GN=MUC4 PE=1 SV=3 1.00 12.00 ‐11.00 HRG_HUMAN Histidine‐rich glycoprotein OS=Homo sapiens GN=HRG 1.00 12.00 ‐11.00 PE=1 SV=1 TKT_HUMAN Transketolase OS=Homo sapiens GN=TKT PE=1 SV=3 17.00 28.00 ‐11.00 CATG_HUMAN Cathepsin G OS=Homo -
A Cell Line P53 Mutation Type UM
A Cell line p53 mutation Type UM-SCC 1 wt UM-SCC5 Exon 5, 157 GTC --> TTC Missense mutation by transversion (Valine --> Phenylalanine UM-SCC6 wt UM-SCC9 wt UM-SCC11A wt UM-SCC11B Exon 7, 242 TGC --> TCC Missense mutation by transversion (Cysteine --> Serine) UM-SCC22A Exon 6, 220 TAT --> TGT Missense mutation by transition (Tyrosine --> Cysteine) UM-SCC22B Exon 6, 220 TAT --> TGT Missense mutation by transition (Tyrosine --> Cysteine) UM-SCC38 Exon 5, 132 AAG --> AAT Missense mutation by transversion (Lysine --> Asparagine) UM-SCC46 Exon 8, 278 CCT --> CGT Missense mutation by transversion (Proline --> Alanine) B 1 Supplementary Methods Cell Lines and Cell Culture A panel of ten established HNSCC cell lines from the University of Michigan series (UM-SCC) was obtained from Dr. T. E. Carey at the University of Michigan, Ann Arbor, MI. The UM-SCC cell lines were derived from eight patients with SCC of the upper aerodigestive tract (supplemental Table 1). Patient age at tumor diagnosis ranged from 37 to 72 years. The cell lines selected were obtained from patients with stage I-IV tumors, distributed among oral, pharyngeal and laryngeal sites. All the patients had aggressive disease, with early recurrence and death within two years of therapy. Cell lines established from single isolates of a patient specimen are designated by a numeric designation, and where isolates from two time points or anatomical sites were obtained, the designation includes an alphabetical suffix (i.e., "A" or "B"). The cell lines were maintained in Eagle's minimal essential media supplemented with 10% fetal bovine serum and penicillin/streptomycin. -
An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Netwo
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis Sriram Devanathan Washington University School of Medicine in St. Louis Timothy Whitehead Washington University School of Medicine in St. Louis George G. Schweitzer Washington University School of Medicine in St. Louis Nicole Fettig Washington University School of Medicine in St. Louis Attila Kovacs Washington University School of Medicine in St. Louis See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Devanathan, Sriram; Whitehead, Timothy; Schweitzer, George G.; Fettig, Nicole; Kovacs, Attila; Korach, Kenneth S.; Finck, Brian N.; and Shoghi, Kooresh I., ,"An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis." PLoS One.9,7. e101900. (2014). https://digitalcommons.wustl.edu/open_access_pubs/3326 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]. Authors Sriram Devanathan, Timothy Whitehead, George G. Schweitzer, Nicole Fettig, Attila Kovacs, Kenneth S. Korach, Brian N. Finck, and Kooresh I. Shoghi This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/3326 An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Network Analysis Sriram Devanathan1, Timothy Whitehead1, George G. Schweitzer2, Nicole Fettig1, Attila Kovacs3, Kenneth S. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Steroid-Dependent Regulation of the Oviduct: a Cross-Species Transcriptomal Analysis
University of Kentucky UKnowledge Theses and Dissertations--Animal and Food Sciences Animal and Food Sciences 2015 Steroid-dependent regulation of the oviduct: A cross-species transcriptomal analysis Katheryn L. Cerny University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Cerny, Katheryn L., "Steroid-dependent regulation of the oviduct: A cross-species transcriptomal analysis" (2015). Theses and Dissertations--Animal and Food Sciences. 49. https://uknowledge.uky.edu/animalsci_etds/49 This Doctoral Dissertation is brought to you for free and open access by the Animal and Food Sciences at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Animal and Food Sciences by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known.