DOCSLIB.ORG

SUPPLEMENTAL DATA Apratoxin a Reversibly Inhibits the Secretory

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Liu Y, Law BK, Luesch H (2009) Apratoxin A reversibly inhibits the secretory pathway by preventing cotranslational translocation. Mol. Pharmacol. (manuscript number MOL 56085) SUPPLEMENTAL DATA Apratoxin A reversibly inhibits the secretory pathway by preventing cotranslational translocation Yanxia Liu, Brian K. Law, and Hendrik Luesch Department of Medicinal Chemistry, University of Florida, 1600 SW Archer Road, Gainesville, Florida 32610, USA (Y.L., H.L.); and Department of Pharmacology & Therapeutics, University of Florida, 1376 Mowry Road, Gainesville, Florida 32610, USA (B.K.L.) 1 Liu Y, Law BK, Luesch H (2009) Apratoxin A reversibly inhibits the secretory pathway by preventing cotranslational translocation. Mol. Pharmacol. (manuscript number MOL 56085) Supplementary Figure Supplementary Figure S1. Comparison of enzymatic deglycosylation (PNGase F), inhibition of glycosylation (tunicamycin) and apratoxin A treatment. Control U2OS cell lysates were deglycosylated with PNGase F (lane 1) and resulting PDGFR-β analyzed by immunoblot analysis and compared with lysates obtained from untreated U2OS cells and cells treated for 12 h with tunicamycin (500 ng/mL) or apratoxin A (50 nM). 2 Liu Y, Law BK, Luesch H (2009) Apratoxin A reversibly inhibits the secretory pathway by preventing cotranslational translocation. Mol. Pharmacol. (manuscript number MOL 56085) Supplementary Table S1 Apratoxin A (50 nM) induced fold changes in levels of proteins enriched after cell surface a biotinylation of U2OS cells (quantified by iTRAQ labeling) Gene Symbol Annotation Peptidesb 1 h 4 h 12 h 24 h Receptors/cell surface proteins LRPAP1 low density lipoprotein receptor-related protein 8 –1.13 –1.61 –4.06 –3.79 associated protein 1 M6PR mannose-6-phosphate receptor (cation dependent) 4 +1.02 –1.07 –2.70 –1.54 CD151 CD151 molecule (Raph blood group) 1 –1.01 +1.02 –2.63 –1.37 NPTN neuroplastin 5 –1.51 –1.15 –2.37 –1.92 GPC1 glypican 1 7 +1.36 +1.02 –2.21 –1.65 ITGAV integrin, alpha V (vitronectin receptor, alpha 21 +1.15 –1.03 –2.04 –1.76 polypeptide, antigen CD51) NRD1 nardilysin (N-arginine dibasic convertase) 16 –1.16 +1.24 –1.87 –2.22 TFRC transferrin receptor (p90, CD71) 28 +1.01 –1.25 –1.83 –2.79 DAG1 dystroglycan 1 (dystrophin-associated glycoprotein 1) 13 –1.09 –1.25 –1.71 –2.26 ITGB1 integrin, beta 1 (fibronectin receptor, beta 20 –1.06 –1.06 –1.56 –1.98 polypeptide, antigen CD29 includes MDF2, MSK12) NCAM1 neural cell adhesion molecule 1 12 –1.03 –1.06 –1.51 –2.16 Other membrane proteins TMED2 transmembrane emp24 domain trafficking protein 2 3 –1.31 +1.08 –2.36 –2.25 TMED10 transmembrane emp24-like trafficking protein 10 4 +1.20 –1.16 –1.82 –2.78 (yeast) VAPB VAMP (vesicle-associated membrane protein)- 2 +1.04 –2.35 –1.77 –1.73 associated protein B and C CCDC47 coiled-coil domain containing 47 4 +1.07 +1.38 –1.35 –13.87 ANXA1 annexin A1 5 +1.61 –1.12 +2.01 +1.81 Protein disulfide isomerases PDIA3 protein disulfide isomerase family A, member 3 23 +1.10 +1.15 –1.65 –3.02 PDIA4 protein disulfide isomerase family A, member 4 17 –1.04 +1.17 –1.93 –4.15 PDIA6 protein disulfide isomerase family A, member 6 12 –1.15 –1.04 –1.71 –2.86 TXNDC4 thioredoxin domain containing 4 (endoplasmic 7 +1.10 –1.13 –1.78 –2.14 reticulum) TXNDC5 thioredoxin domain containing 5 8 +1.13 +1.31 –1.88 –3.20 P4HB procollagen-proline, 2-oxoglutarate 4-dioxygenase 23 –1.02 +1.16 –1.87 –3.80 (proline 4-hydroxylase), beta polypeptide Other ER proteins CALU calumenin 8 –1.19 +1.11 –2.52 –5.08 RCN1 reticulocalbin 1, EF-hand calcium binding domain 8 –1.08 +1.04 –2.39 –5.87 RCN2 reticulocalbin 2, EF-hand calcium binding domain 5 –1.14 –1.15 –2.13 –2.14 P4HA1 procollagen-proline, 2-oxoglutarate 4-dioxygenase 11 –1.24 +1.01 –2.17 –2.68 (proline 4-hydroxylase), alpha polypeptide I PLOD2 procollagen-lysine, 2-oxoglutarate 5-dioxygenase 2 11 +1.05 –1.27 –1.69 –4.31 HSPA5 (BIP) heat shock 70kDa protein 5 (glucose-regulated 28 –1.02 +1.08 –2.08 –3.70 protein, 78kDa) PRKCSH protein kinase C substrate 80K-H (beta-subunit of 9 –1.11 +1.29 –2.08 –3.05 glucosidase II) LMAN1 lectin, mannose-binding, 1 11 –1.09 –1.13 –2.03 –2.67 HYOU1 hypoxia up-regulated 1 27 –1.14 +1.24 –2.02 –3.02 CANX calnexin 14 –1.08 –1.12 –2.02 –3.21 3 Liu Y, Law BK, Luesch H (2009) Apratoxin A reversibly inhibits the secretory pathway by preventing cotranslational translocation. Mol. Pharmacol. (manuscript number MOL 56085) HSP90B1 heat shock protein 90kDa beta (Grp94), member 1 38 ±1.00 +1.15 –1.95 –3.11 ERP29 endoplasmic reticulum protein 29 7 –1.03 +1.06 –1.80 –2.26 STT3A STT3, subunit of the oligosaccharyltransferase 8 +1.31 –1.11 –1.90 –1.99 complex, homolog A (S. cerevisiae) RPN1 ribophorin I 13 –1.06 –1.13 –1.77 –2.23 PPIB peptidylprolyl isomerase B (cyclophilin B) 14 –1.05 +1.36 –1.75 –3.32 CALR calreticulin 12 –1.15 +0.82 –1.69 –3.46 GANAB glucosidase, alpha; neutral AB 27 –1.06 +1.24 –1.64 –3.12 SERPINH1 serpin peptidase inhibitor, clade H (heat shock 15 +1.08 +1.09 –1.52 –2.00 protein 47), member 1, (collagen binding protein 1) UGCGL1 UDP-glucose ceramide glucosyltransferase-like 1 17 –1.28 –1.08 –1.06 –2.77 tRNA synthetases & protein biosynthesis RARS arginyl-tRNA synthetase 13 +1.04 –1.02 +1.43 +2.21 QARS glutaminyl-tRNA synthetase 15 –1.20 –1.15 +1.44 +1.47 DARS aspartyl-tRNA synthetase 9 –1.06 –1.15 +1.56 +1.85 KARS lysyl-tRNA synthetase 15 +1.06 +1.07 +1.59 +1.41 TARS threonyl-tRNA synthetase 11 –1.35 +1.13 +1.86 +1.29 IARS isoleucyl-tRNA synthetase 21 +1.63 –1.04 +2.02 +1.69 RPL12 ribosomal protein L12 3 +1.27 +1.66 +2.32 +2.15 EIF3D eukaryotic translation initiation factor 3, subunit D 3 –1.61 –1.43 +2.39 +1.11 SRP72 signal recognition particle 72kDa 12 +1.32 –1.08 +2.55 +1.50 Mitochondrial proteins GPD2 glycerol-3-phosphate dehydrogenase 2 10 +1.37 +1.08 –1.61 –2.55 (mitochondrial) HSD17B10 hydroxysteroid (17-beta) dehydrogenase 10 6 –1.25 –1.20 –1.47 –2.15 LOC647153 similar to voltage-dependent anion channel 2 6 –1.01 –1.02 –1.23 –2.06 Cytoskeletal proteins TPM1 tropomyosin 1 (alpha) 12 –3.65 –1.15 –1.40 –1.62 MYL6 myosin, light chain 6, alkali, smooth muscle and non- 5 –1.29 –1.14 +1.13 +2.44 muscle MYH9 myosin, heavy chain 9, non-muscle 53 +1.19 –1.19 +1.17 +3.15 Other proteins PSMA4 proteasome (prosome, macropain) subunit, alpha 6 –1.63 –1.04 –2.64 –4.00 type, 4 MESDC2 mesoderm development candidate 2 3 +2.71 +1.09 –2.13 –4.19 TBRG4 transforming growth factor beta regulator 4 8 –1.06 +1.22 –2.08 –1.42 PRDX4 peroxiredoxin 4 8 +1.01 +1.05 –1.84 –2.45 RAB1B RAB1B, member RAS oncogene family 9 –1.38 –1.02 –1.49 –2.26 RAB2A RAB2A, member RAS oncogene family 4 –1.40 +1.20 –1.09 –3.33 GNAI2 guanine nucleotide binding protein (G protein), alpha 11 +1.16 +1.08 –1.31 –2.00 inhibiting activity polypeptide 2 SCD stearoyl-CoA desaturase (delta-9-desaturase) 3 –1.22 –1.03 –1.29 –2.38 CDC42 cell division cycle 42 (GTP binding protein, 25kDa) 5 +1.08 –1.15 –1.22 –2.80 C14orf166 chromosome 14 open reading frame 166 5 +1.49 +2.10 +1.24 –1.16 PA2G4 proliferation-associated 2G4, 38kDa 6 +1.29 –2.31 –1.25 –1.31 PGAM1 phosphoglycerate mutase 1 (brain) 4 –1.17 –1.29 +1.39 +2.11 ALDOA aldolase A, fructose-bisphosphate 16 +1.10 –1.08 +1.53 +2.21 PRMT1 protein arginine methyltransferase 1 4 +1.14 +1.24 +2.09 –1.01 a 95% confidence level. b Used for protein identification. 4 .
Recommended publications
  • Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren A

    Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren A

    Virginia Commonwealth University VCU Scholars Compass Study of Biological Complexity Publications Center for the Study of Biological Complexity 2013 Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren A. Vanderlinden University of Colorado at Aurora Laura M. Saba University of Colorado at Aurora Katerina Kechris University of Colorado at Aurora See next page for additional authors Follow this and additional works at: http://scholarscompass.vcu.edu/csbc_pubs Part of the Life Sciences Commons © 2013 Vanderlinden 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/csbc_pubs/24 This Article is brought to you for free and open access by the Center for the Study of Biological Complexity at VCU Scholars Compass. It has been accepted for inclusion in Study of Biological Complexity Publications by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Authors Lauren A. Vanderlinden, Laura M. Saba, Katerina Kechris, Michael F. Miles, Paula L. Hoffman, and Boris Tabakoff This article is available at VCU Scholars Compass: http://scholarscompass.vcu.edu/csbc_pubs/24 Whole Brain and Brain Regional Coexpression Network Interactions Associated with Predisposition to Alcohol Consumption Lauren
  • Proteomic Analysis of the Venom of Jellyfishes Rhopilema Esculentum and Sanderia Malayensis

    Proteomic Analysis of the Venom of Jellyfishes Rhopilema Esculentum and Sanderia Malayensis

    marine drugs Article Proteomic Analysis of the Venom of Jellyfishes Rhopilema esculentum and Sanderia malayensis 1, 2, 2 2, Thomas C. N. Leung y , Zhe Qu y , Wenyan Nong , Jerome H. L. Hui * and Sai Ming Ngai 1,* 1 State Key Laboratory of Agrobiotechnology, School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China; [email protected] 2 Simon F.S. Li Marine Science Laboratory, State Key Laboratory of Agrobiotechnology, School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China; [email protected] (Z.Q.); [email protected] (W.N.) * Correspondence: [email protected] (J.H.L.H.); [email protected] (S.M.N.) Contributed equally. y Received: 27 November 2020; Accepted: 17 December 2020; Published: 18 December 2020 Abstract: Venomics, the study of biological venoms, could potentially provide a new source of therapeutic compounds, yet information on the venoms from marine organisms, including cnidarians (sea anemones, corals, and jellyfish), is limited. This study identified the putative toxins of two species of jellyfish—edible jellyfish Rhopilema esculentum Kishinouye, 1891, also known as flame jellyfish, and Amuska jellyfish Sanderia malayensis Goette, 1886. Utilizing nano-flow liquid chromatography tandem mass spectrometry (nLC–MS/MS), 3000 proteins were identified from the nematocysts in each of the above two jellyfish species. Forty and fifty-one putative toxins were identified in R. esculentum and S. malayensis, respectively, which were further classified into eight toxin families according to their predicted functions. Amongst the identified putative toxins, hemostasis-impairing toxins and proteases were found to be the most dominant members (>60%).
  • Transcriptional Regulation of RKIP in Prostate Cancer Progression

    Transcriptional Regulation of RKIP in Prostate Cancer Progression

    Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Sciences Transcriptional Regulation of RKIP in Prostate Cancer Progression Submitted by: Sandra Marie Beach In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences Examination Committee Major Advisor: Kam Yeung, Ph.D. Academic William Maltese, Ph.D. Advisory Committee: Sonia Najjar, Ph.D. Han-Fei Ding, M.D., Ph.D. Manohar Ratnam, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: May 16, 2007 Transcriptional Regulation of RKIP in Prostate Cancer Progression Sandra Beach University of Toledo ACKNOWLDEGMENTS I thank my major advisor, Dr. Kam Yeung, for the opportunity to pursue my degree in his laboratory. I am also indebted to my advisory committee members past and present, Drs. Sonia Najjar, Han-Fei Ding, Manohar Ratnam, James Trempe, and Douglas Pittman for generously and judiciously guiding my studies and sharing reagents and equipment. I owe extended thanks to Dr. William Maltese as a committee member and chairman of my department for supporting my degree progress. The entire Department of Biochemistry and Cancer Biology has been most kind and helpful to me. Drs. Roy Collaco and Hong-Juan Cui have shared their excellent technical and practical advice with me throughout my studies. I thank members of the Yeung laboratory, Dr. Sungdae Park, Hui Hui Tang, Miranda Yeung for their support and collegiality. The data mining studies herein would not have been possible without the helpful advice of Dr. Robert Trumbly. I am also grateful for the exceptional assistance and shared microarray data of Dr.
  • Toxicogenomics Applications of New Functional Genomics Technologies in Toxicology

    Toxicogenomics Applications of New Functional Genomics Technologies in Toxicology

    \-\w j Toxicogenomics Applications of new functional genomics technologies in toxicology Wilbert H.M. Heijne Proefschrift ter verkrijging vand egraa dva n doctor opgeza gva nd e rector magnificus vanWageninge n Universiteit, Prof.dr.ir. L. Speelman, in netopenbaa r te verdedigen op maandag6 decembe r200 4 des namiddagst e half twee ind eAul a - Table of contents Abstract Chapter I. page 1 General introduction [1] Chapter II page 21 Toxicogenomics of bromobenzene hepatotoxicity: a combined transcriptomics and proteomics approach[2] Chapter III page 48 Bromobenzene-induced hepatotoxicity atth etranscriptom e level PI Chapter IV page 67 Profiles of metabolites and gene expression in rats with chemically induced hepatic necrosis[4] Chapter V page 88 Liver gene expression profiles in relation to subacute toxicity in rats exposed to benzene[5] Chapter VI page 115 Toxicogenomics analysis of liver gene expression in relation to subacute toxicity in rats exposed totrichloroethylen e [6] Chapter VII page 135 Toxicogenomics analysis ofjoin t effects of benzene and trichloroethylene mixtures in rats m Chapter VII page 159 Discussion and conclusions References page 171 Appendices page 187 Samenvatting page 199 Dankwoord About the author Glossary Abbreviations List of genes Chapter I General introduction Parts of this introduction were publishedin : Molecular Biology in Medicinal Chemistry, Heijne etal., 2003 m NATO Advanced Research Workshop proceedings, Heijne eral., 2003 81 Chapter I 1. General introduction 1.1 Background /.1.1 Toxicologicalrisk
  • A Novel Pseudomonas Geniculata AGE Family Epimerase/Isomerase and Its Application in D-Mannose Synthesis

    A Novel Pseudomonas Geniculata AGE Family Epimerase/Isomerase and Its Application in D-Mannose Synthesis

    foods Article A Novel Pseudomonas geniculata AGE Family Epimerase/Isomerase and Its Application in d-Mannose Synthesis Zhanzhi Liu 1,2, Ying Li 1,2, Jing Wu 1,2 and Sheng Chen 1,2,* 1 State Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, China; [email protected] (Z.L.); [email protected] (Y.L.); [email protected] (J.W.) 2 School of Biotechnology and Key Laboratory of Industrial Biotechnology Ministry of Education, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, China * Correspondence: [email protected] Received: 29 September 2020; Accepted: 3 December 2020; Published: 6 December 2020 Abstract: d-mannose has exhibited excellent physiological properties in the food, pharmaceutical, and feed industries. Therefore, emerging attention has been applied to enzymatic production of d-mannose due to its advantage over chemical synthesis. The gene age of N-acetyl-d-glucosamine 2-epimerase family epimerase/isomerase (AGEase) derived from Pseudomonas geniculata was amplified, and the recombinant P. geniculata AGEase was characterized. The optimal temperature and pH of P. geniculata AGEase were 60 ◦C and 7.5, respectively. The Km, kcat, and kcat/Km of P. geniculata AGEase for d-mannose were 49.2 8.5 mM, 476.3 4.0 s 1, and 9.7 0.5 s 1 mM 1, respectively. ± ± − ± − · − The recombinant P. geniculata AGEase was classified into the YihS enzyme subfamily in the AGE enzyme family by analyzing its substrate specificity and active center of the three-dimensional (3D) structure. Further studies on the kinetics of different substrates showed that the P.
  • Mir-106B-Responsive Gene Landscape Identifies Regulation of Kruppel- Like Factor Family

    Mir-106B-Responsive Gene Landscape Identifies Regulation of Kruppel- Like Factor Family

    bioRxiv preprint doi: https://doi.org/10.1101/088229; this version posted November 17, 2016. 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. miR-106b-responsive gene landscape identifies regulation of Kruppel- like factor family Cody J. Wehrkamp Sathish Kumar Natarajan Ashley M. Mohr Mary Anne Phillippi Justin L. Mott Department of Biochemistry and Molecular Biology, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha Running title: miR-106b-responsive genes in cholangiocarcinoma Key words: Apoptosis, biliary tract cancer, KLF2, KLF4, KLF6, KLF10, KLF11, KLF13, LKLF, lung Kruppel-like factor, miR-106a, miRNA, next-generation sequencing Address for Correspondence: Justin L. Mott, MD, PhD Associate Professor Department of Biochemistry and Molecular Biology 985870 Nebraska Medical Center Omaha, NE 68198-5870 Tel: 402-559-3177 Fax: 402-559-6650 e-mail: [email protected] List of abbreviations: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, MTT; 4′,6-diamidine-2′- phenylindole dihydrochloride, DAPI; Crosslinking, ligation, and sequencing of hybrids, CLASH; Death receptor-5, DR5; Dulbecco’s Modified Eagle’s Medium, DMEM; False discovery rate, FDR; Fetal bovine serum, FBS; Kruppel-like factor, KLF; Locked-nucleic acid, LNA; Quantitative reverse-transcription PCR, qRT-PCR; Sodium dodecylsulfate-polyacrylamide gel electrophoresis, SDS-PAGE; Untranslated region, UTR; bioRxiv preprint doi: https://doi.org/10.1101/088229; this version posted November 17, 2016. 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.
  • Orlistat, a Novel Potent Antitumor Agent for Ovarian Cancer: Proteomic Analysis of Ovarian Cancer Cells Treated with Orlistat

    Orlistat, a Novel Potent Antitumor Agent for Ovarian Cancer: Proteomic Analysis of Ovarian Cancer Cells Treated with Orlistat

    INTERNATIONAL JOURNAL OF ONCOLOGY 41: 523-532, 2012 Orlistat, a novel potent antitumor agent for ovarian cancer: proteomic analysis of ovarian cancer cells treated with Orlistat HUI-QIONG HUANG1*, JING TANG1*, SHENG-TAO ZHOU1, TAO YI1, HONG-LING PENG1, GUO-BO SHEN2, NA XIE2, KAI HUANG2, TAO YANG2, JIN-HUA WU2, CAN-HUA HUANG2, YU-QUAN WEI2 and XIA ZHAO1,2 1Gynecological Oncology of Biotherapy Laboratory, Department of Gynecology and Obstetrics, West China Second Hospital, Sichuan University, Chengdu, Sichuan; 2State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China Received February 9, 2012; Accepted March 19, 2012 DOI: 10.3892/ijo.2012.1465 Abstract. Orlistat is an orally administered anti-obesity drug larly PKM2. These changes confirmed our hypothesis that that has shown significant antitumor activity in a variety of Orlistat is a potential inhibitor of ovarian cancer and can be tumor cells. To identify the proteins involved in its antitumor used as a novel adjuvant antitumor agent. activity, we employed a proteomic approach to reveal protein expression changes in the human ovarian cancer cell line Introduction SKOV3, following Orlistat treatment. Protein expression profiles were analyzed by 2-dimensional polyacrylamide In the 1920s, the Nobel Prize winner Otto Warburg observed gel electrophoresis (2-DE) and protein identification was a marked increase in glycolysis and enhanced lactate produc- performed on a MALDI-Q-TOF MS/MS instrument. More tion in tumor cells even when maintained in conditions of high than 110 differentially expressed proteins were visualized oxygen tension (termed Warburg effect), leading to widespread by 2-DE and Coomassie brilliant blue staining.
  • Tumor Suppressive Microrna-375 Regulates Oncogene AEG-1&Sol;MTDH in Head and Neck Squamous Cell Carcinoma (HNSCC)

    Tumor Suppressive Microrna-375 Regulates Oncogene AEG-1&Sol;MTDH in Head and Neck Squamous Cell Carcinoma (HNSCC)

    Journal of Human Genetics (2011) 56, 595–601 & 2011 The Japan Society of Human Genetics All rights reserved 1434-5161/11 $32.00 www.nature.com/jhg ORIGINAL ARTICLE Tumor suppressive microRNA-375 regulates oncogene AEG-1/MTDH in head and neck squamous cell carcinoma (HNSCC) Nijiro Nohata1,2, Toyoyuki Hanazawa2, Naoko Kikkawa1,2, Muradil Mutallip1,2, Daiju Sakurai2, Lisa Fujimura3, Kazumori Kawakami4, Takeshi Chiyomaru4, Hirofumi Yoshino4, Hideki Enokida4, Masayuki Nakagawa4, Yoshitaka Okamoto2 and Naohiko Seki1 Our microRNA (miRNA) expression signatures of hypopharyngeal squamous cell carcinoma, maxillary sinus squamous cell carcinoma and esophageal squamous cell carcinoma revealed that miR-375 was significantly reduced in cancer tissues compared with normal epithelium. In this study, we focused on the functional significance of miR-375 in cancer cells and identification of miR-375-regulated novel cancer networks in head and neck squamous cell carcinoma (HNSCC). Restoration of miR-375 showed significant inhibition of cell proliferation and induction of cell apoptosis in SAS and FaDu cell lines, suggesting that miR-375 functions as a tumor suppressor. We adopted genome-wide gene expression analysis to search for miR-375-regulated molecular targets. Gene expression data and luciferase reporter assays revealed that AEG-1/MTDH was directly regulated by miR-375. Cancer cell proliferation was significantly inhibited in HNSCC cells transfected with si-AEG-1/MTDH. In addition, expression levels of AEG-1/MTDH were significantly upregulated in cancer tissues. Therefore, AEG-1/MTDH may function as an oncogene in HNSCC. The identification of novel tumor suppressive miRNA and its regulated cancer pathways could provide new insights into potential molecular mechanisms of HNSCC oncogenesis.
  • New Approach for Untangling the Role of Uncommon Calcium-Binding Proteins in the Central Nervous System

    New Approach for Untangling the Role of Uncommon Calcium-Binding Proteins in the Central Nervous System

    brain sciences Review New Approach for Untangling the Role of Uncommon Calcium-Binding Proteins in the Central Nervous System Krisztina Kelemen * and Tibor Szilágyi Department of Physiology, Doctoral School, Faculty of Medicine, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, 540142 Târgu Mures, , Romania; [email protected] * Correspondence: [email protected]; Tel.: +40-746-248064 Abstract: Although Ca2+ ion plays an essential role in cellular physiology, calcium-binding proteins (CaBPs) were long used for mainly as immunohistochemical markers of specific cell types in different regions of the central nervous system. They are a heterogeneous and wide-ranging group of proteins. Their function was studied intensively in the last two decades and a tremendous amount of informa- tion was gathered about them. Girard et al. compiled a comprehensive list of the gene-expression profiles of the entire EF-hand gene superfamily in the murine brain. We selected from this database those CaBPs which are related to information processing and/or neuronal signalling, have a Ca2+- buffer activity, Ca2+-sensor activity, modulator of Ca2+-channel activity, or a yet unknown function. In this way we created a gene function-based selection of the CaBPs. We cross-referenced these findings with publicly available, high-quality RNA-sequencing and in situ hybridization databases (Human Protein Atlas (HPA), Brain RNA-seq database and Allen Brain Atlas integrated into the HPA) and created gene expression heat maps of the regional and cell type-specific expression levels of the selected CaBPs. This represents a useful tool to predict and investigate different expression patterns and functions of the less-known CaBPs of the central nervous system.
  • Masterarbeit / Master's Thesis

    Masterarbeit / Master's Thesis

    MASTERARBEIT / MASTER’S THESIS Titel der Masterarbeit / Title of the Master‘s Thesis „Physiology, Metabolism and Biohydrogen Production of Desulfurococcus fermentans“ verfasst von / submitted by Barbara Reischl, BSc angestrebter akademischer Grad / in partial fulfilment of the requirements for the degree of Master of Science (MSc) Wien, 2016 / Vienna 2016 Studienkennzahl lt. Studienblatt / A 066 830 degree programme code as it appears on the student record sheet: Studienrichtung lt. Studienblatt / Molecular Microbiology, Microbial Ecology degree programme as it appears on and Immunobiology the student record sheet: Betreut von / Supervisor: Univ.-Prof. Dipl.-Biol. Dr. Christa Schleper Mitbetreut von / Co-Supervisor: Mag. Mag. Dr. Simon Karl-Maria Rasso Rittmann, Bakk. 2 Table of Contents 1. Introduction .......................................................................................................... 5 1.1 Role of Biohydrogen ................................................................................................ 5 1.2 Hydrogenases ......................................................................................................... 6 1.3 Characteristics of Desulfurococcus fermentans ....................................................... 7 1.4 Aims of this Study ................................................................................................... 8 2. Material and Methods ............................................................................................ 9 2.1 Chemicals ..............................................................................................................
  • Production of Bulk Chemicals with Biocatalysis: Drivers and Challenges Reflected in Recent Industrial Granted Patents

    Production of Bulk Chemicals with Biocatalysis: Drivers and Challenges Reflected in Recent Industrial Granted Patents

    molecules Review Production of Bulk Chemicals with Biocatalysis: Drivers and Challenges Reflected in Recent Industrial Granted Patents (2015–2020) Nadia Guajardo 1,* and Pablo Domínguez de María 2 1 Programa Institucional de Fomento a la Investigación, Desarrollo e Innovación (PIDi), Universidad Tecnológica Metropolitana, Ignacio Valdivieso 2409, Santiago de Chile 8940000, Chile 2 Sustainable Momentum SL., Avenida Ansite 3, 4-6, 35011 Las Palmas de Gran Canaria, Spain; [email protected] * Correspondence: [email protected] Abstract: The application of biocatalysis and White Biotechnology tools in chemical areas concerning the production of bulk compounds and other related low-added value products (with high volumes) has been gaining importance in recent years. The expected drivers of biocatalysis for these sectors are energy savings, regioselectivity (leading to cleaner products), the possibility of using thermolabile substrates, as well as the generation of less by-products and manageable wastes. This paper explores some recent industrial granted patents related to biocatalysis and bulk chemicals. Several patents have been identified in fields such as biodiesel and esterification reactions, and sugar or furan chemistry. Overall, innovative strategies involve the identification of novel enzymes, the set-up of improved immobilization methods, as well as novel reactor designs that can offer improved performances and economics. The reported examples indicate that biocatalysis can certainly offer opportunities for Citation: Guajardo, N.; Domínguez these areas as well, far from the typical pharmaceutical and fine chemical applications often reported de María, P. Production of Bulk in the literature. Chemicals with Biocatalysis: Drivers and Challenges Reflected in Recent Keywords: biocatalysis; bulk compounds; sustainable processes; granted patents Industrial Granted Patents (2015–2020).
  • Genomic Approach in Idiopathic Intellectual Disability Maria De Fátima E Costa Torres

    Genomic Approach in Idiopathic Intellectual Disability Maria De Fátima E Costa Torres

    ESTUDOS DE 8 01 PDPGM 2 CICLO Genomic approach in idiopathic intellectual disability Maria de Fátima e Costa Torres D Autor. Maria de Fátima e Costa Torres D.ICBAS 2018 Genomic approach in idiopathic intellectual disability Genomic approach in idiopathic intellectual disability Maria de Fátima e Costa Torres SEDE ADMINISTRATIVA INSTITUTO DE CIÊNCIAS BIOMÉDICAS ABEL SALAZAR FACULDADE DE MEDICINA MARIA DE FÁTIMA E COSTA TORRES GENOMIC APPROACH IN IDIOPATHIC INTELLECTUAL DISABILITY Tese de Candidatura ao grau de Doutor em Patologia e Genética Molecular, submetida ao Instituto de Ciências Biomédicas Abel Salazar da Universidade do Porto Orientadora – Doutora Patrícia Espinheira de Sá Maciel Categoria – Professora Associada Afiliação – Escola de Medicina e Ciências da Saúde da Universidade do Minho Coorientadora – Doutora Maria da Purificação Valenzuela Sampaio Tavares Categoria – Professora Catedrática Afiliação – Faculdade de Medicina Dentária da Universidade do Porto Coorientadora – Doutora Filipa Abreu Gomes de Carvalho Categoria – Professora Auxiliar com Agregação Afiliação – Faculdade de Medicina da Universidade do Porto DECLARAÇÃO Dissertação/Tese Identificação do autor Nome completo _Maria de Fátima e Costa Torres_ N.º de identificação civil _07718822 N.º de estudante __ 198600524___ Email institucional [email protected] OU: [email protected] _ Email alternativo [email protected] _ Tlf/Tlm _918197020_ Ciclo de estudos (Mestrado/Doutoramento) _Patologia e Genética Molecular__ Faculdade/Instituto _Instituto de Ciências