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Supplemental Table S1
Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1 -
Association of Gene Ontology Categories with Decay Rate for Hepg2 Experiments These Tables Show Details for All Gene Ontology Categories
Supplementary Table 1: Association of Gene Ontology Categories with Decay Rate for HepG2 Experiments These tables show details for all Gene Ontology categories. Inferences for manual classification scheme shown at the bottom. Those categories used in Figure 1A are highlighted in bold. Standard Deviations are shown in parentheses. P-values less than 1E-20 are indicated with a "0". Rate r (hour^-1) Half-life < 2hr. Decay % GO Number Category Name Probe Sets Group Non-Group Distribution p-value In-Group Non-Group Representation p-value GO:0006350 transcription 1523 0.221 (0.009) 0.127 (0.002) FASTER 0 13.1 (0.4) 4.5 (0.1) OVER 0 GO:0006351 transcription, DNA-dependent 1498 0.220 (0.009) 0.127 (0.002) FASTER 0 13.0 (0.4) 4.5 (0.1) OVER 0 GO:0006355 regulation of transcription, DNA-dependent 1163 0.230 (0.011) 0.128 (0.002) FASTER 5.00E-21 14.2 (0.5) 4.6 (0.1) OVER 0 GO:0006366 transcription from Pol II promoter 845 0.225 (0.012) 0.130 (0.002) FASTER 1.88E-14 13.0 (0.5) 4.8 (0.1) OVER 0 GO:0006139 nucleobase, nucleoside, nucleotide and nucleic acid metabolism3004 0.173 (0.006) 0.127 (0.002) FASTER 1.28E-12 8.4 (0.2) 4.5 (0.1) OVER 0 GO:0006357 regulation of transcription from Pol II promoter 487 0.231 (0.016) 0.132 (0.002) FASTER 6.05E-10 13.5 (0.6) 4.9 (0.1) OVER 0 GO:0008283 cell proliferation 625 0.189 (0.014) 0.132 (0.002) FASTER 1.95E-05 10.1 (0.6) 5.0 (0.1) OVER 1.50E-20 GO:0006513 monoubiquitination 36 0.305 (0.049) 0.134 (0.002) FASTER 2.69E-04 25.4 (4.4) 5.1 (0.1) OVER 2.04E-06 GO:0007050 cell cycle arrest 57 0.311 (0.054) 0.133 (0.002) -
Amlexanox TBK1 & Ikke Inhibitor Catalog # Inh-Amx
Amlexanox TBK1 & IKKe inhibitor Catalog # inh-amx For research use only Version # 15I29-MM PRODUCT INFORMATION METHODS Contents: Preparation of 10 mg/ml (33.5 mM) stock solution • 50 mg Amlexanox 1- Weigh 10 mg of Amlexanox Storage and stability: 2- Add 1 ml of DMSO to 10 mg Amlexanox. Mix by vortexing. - Amlexanox is provided lyophilized and shipped at room temperature. 3- Prepare further dilutions using endotoxin-free water. Store at -20 °C. Lyophilized Amlexanox is stable for at least 2 years when properly stored. Working concentration: 1-300 μg/ml for cell culture assays - Upon resuspension, prepare aliquots of Amlexanox and store at -20 °C. Resuspended Amlexanox is stable for 6 months when properly stored. TBK1/IKKe inhibition: Quality control: Amlexanox can be used to assess the role of TBK1/IKKe using cellular - Purity ≥97% (UHPLC) assays, as described below in B16-Blue™ ISG cells. - The inhibitory activity of this product has been validated using cellular 1- Prepare a B16-Blue™ ISG cell suspension at ~500,000 cells/ml. assays. 2- Add 160 µl of cell suspension (~75,000 cells) per well. - The absence of bacterial contamination (e.g. lipoproteins and 3- Add 20 µl of Amlexanox 30-300 µg/ml (final concentration) and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK-Blue™ incubate at 37 °C for 1 hour. TLR4 cells. 4-Add 20 µl of sample per well of a flat-bottom 96-well plate. Note: We recommend using a positive control such as 5’ppp-dsRNA delivered intracellularly with LyoVec™ . DESCRIPTION 5- Incubate the plate at 37 °C in a 5% CO incubator for 18-24 hours. -
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Cr
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Crizotinib (PF-02341066) 1 4 55 Docetaxel 1 5 98 Anastrozole 1 6 25 Cladribine 1 7 23 Methotrexate 1 8 -187 Letrozole 1 9 65 Entecavir Hydrate 1 10 48 Roxadustat (FG-4592) 1 11 19 Imatinib Mesylate (STI571) 1 12 0 Sunitinib Malate 1 13 34 Vismodegib (GDC-0449) 1 14 64 Paclitaxel 1 15 89 Aprepitant 1 16 94 Decitabine 1 17 -79 Bendamustine HCl 1 18 19 Temozolomide 1 19 -111 Nepafenac 1 20 24 Nintedanib (BIBF 1120) 1 21 -43 Lapatinib (GW-572016) Ditosylate 1 22 88 Temsirolimus (CCI-779, NSC 683864) 1 23 96 Belinostat (PXD101) 1 24 46 Capecitabine 1 25 19 Bicalutamide 1 26 83 Dutasteride 1 27 68 Epirubicin HCl 1 28 -59 Tamoxifen 1 29 30 Rufinamide 1 30 96 Afatinib (BIBW2992) 1 31 -54 Lenalidomide (CC-5013) 1 32 19 Vorinostat (SAHA, MK0683) 1 33 38 Rucaparib (AG-014699,PF-01367338) phosphate1 34 14 Lenvatinib (E7080) 1 35 80 Fulvestrant 1 36 76 Melatonin 1 37 15 Etoposide 1 38 -69 Vincristine sulfate 1 39 61 Posaconazole 1 40 97 Bortezomib (PS-341) 1 41 71 Panobinostat (LBH589) 1 42 41 Entinostat (MS-275) 1 43 26 Cabozantinib (XL184, BMS-907351) 1 44 79 Valproic acid sodium salt (Sodium valproate) 1 45 7 Raltitrexed 1 46 39 Bisoprolol fumarate 1 47 -23 Raloxifene HCl 1 48 97 Agomelatine 1 49 35 Prasugrel 1 50 -24 Bosutinib (SKI-606) 1 51 85 Nilotinib (AMN-107) 1 52 99 Enzastaurin (LY317615) 1 53 -12 Everolimus (RAD001) 1 54 94 Regorafenib (BAY 73-4506) 1 55 24 Thalidomide 1 56 40 Tivozanib (AV-951) 1 57 86 Fludarabine -
Structural Basis of Sterol Recognition and Nonvesicular Transport by Lipid
Structural basis of sterol recognition and nonvesicular PNAS PLUS transport by lipid transfer proteins anchored at membrane contact sites Junsen Tonga, Mohammad Kawsar Manika, and Young Jun Ima,1 aCollege of Pharmacy, Chonnam National University, Bukgu, Gwangju, 61186, Republic of Korea Edited by David W. Russell, University of Texas Southwestern Medical Center, Dallas, TX, and approved December 18, 2017 (received for review November 11, 2017) Membrane contact sites (MCSs) in eukaryotic cells are hotspots for roidogenic acute regulatory protein-related lipid transfer), PITP lipid exchange, which is essential for many biological functions, (phosphatidylinositol/phosphatidylcholine transfer protein), Bet_v1 including regulation of membrane properties and protein trafficking. (major pollen allergen from birch Betula verrucosa), PRELI (pro- Lipid transfer proteins anchored at membrane contact sites (LAMs) teins of relevant evolutionary and lymphoid interest), and LAMs contain sterol-specific lipid transfer domains [StARkin domain (SD)] (LTPs anchored at membrane contact sites) (9). and multiple targeting modules to specific membrane organelles. Membrane contact sites (MCSs) are closely apposed regions in Elucidating the structural mechanisms of targeting and ligand which two organellar membranes are in close proximity, typically recognition by LAMs is important for understanding the interorga- within a distance of 30 nm (7). The ER, a major site of lipid bio- nelle communication and exchange at MCSs. Here, we determined synthesis, makes contact with almost all types of subcellular or- the crystal structures of the yeast Lam6 pleckstrin homology (PH)-like ganelles (10). Oxysterol-binding proteins, which are conserved domain and the SDs of Lam2 and Lam4 in the apo form and in from yeast to humans, are suggested to have a role in the di- complex with ergosterol. -
Fatty Liver Disease (Nafld/Nash)
CAYMANCURRENTS ISSUE 31 | WINTER 2019 FATTY LIVER DISEASE (NAFLD/NASH) Targeting Insulin Resistance for the Metabolic Homeostasis Targets Treatment of NASH Page 6 Page 1 Special Feature Inside: Tools to Study NAFLD/NASH A guide to PPAR function and structure Page 3 Pathophysiology of NAFLD Infographic Oxidative Stress, Inflammation, and Apoptosis Targets Page 5 Page 11 1180 EAST ELLSWORTH ROAD · ANN ARBOR, MI 48108 · (800) 364-9897 · WWW.CAYMANCHEM.COM Targeting Insulin Resistance for the Treatment of NASH Kyle S. McCommis, Ph.D. Washington University School of Medicine, St. Louis, MO The obesity epidemic has resulted in a dramatic escalation Defects in fat secretion do not appear to be a driver of in the number of individuals with hepatic fat accumulation hepatic steatosis, as NAFLD subjects display greater VLDL or steatosis. When not combined with excessive alcohol secretion both basally and after “suppression” by insulin.5 consumption, the broad term for this spectrum of disease Fatty acid β-oxidation is decreased in animal models and is referred to as non-alcoholic fatty liver disease (NAFLD). humans with NAFLD/NASH.6-8 A significant proportion of individuals with simple steatosis will progress to the severe form of the disease known as ↑ Hyperinsulinemia Insulin resistance non-alcoholic steatohepatitis (NASH), involving hepatocyte Hyperglycemia damage, inflammation, and fibrosis. If left untreated, Adipose lipolysis NASH can lead to more severe forms of liver disease such Steatosis as cirrhosis, hepatocellular carcinoma, liver failure, and De novo O ↑ lipogenesis HO eventually necessitate liver transplantation. Due to this large clinical burden, research efforts have greatly expanded Fatty acids to better understand NAFLD pathogenesis and the mechanisms underlying the transition to NASH. -
Perioperative Management of Patients Treated with Antithrombotics in Oral Surgery
SFCO/Perioperative management of patients treated with antithrombotic agents in oral surgery/Rationale/July 2015 SOCIÉTÉ FRANÇAISE DE CHIRURGIE ORALE [FRENCH SOCIETY OF ORAL SURGERY] IN COLLABORATION WITH THE SOCIÉTÉ FRANÇAISE DE CARDIOLOGIE [FRENCH SOCIETY OF CARDIOLOGY] AND THE PERIOPERATIVE HEMOSTASIS INTEREST GROUP Space Perioperative management of patients treated with antithrombotics in oral surgery. RATIONALE July 2015 P a g e 1 | 107 SFCO/Perioperative management of patients treated with antithrombotic agents in oral surgery/Rationale/July 2015 Abbreviations ACS Acute coronary syndrome(s) ADP Adenosine diphosphate Afib Atrial Fibrillation AHT Arterial hypertension Anaes Agence nationale d’accréditation et d’évaluation en santé [National Agency for Accreditation and Health Care Evaluation] APA Antiplatelet agent(s) aPTT Activated partial thromboplastin time ASA Aspirin BDMP Blood derived medicinal products BMI Body mass index BT Bleeding Time cAMP Cyclic adenosine monophosphate COX-1 Cyclooxygenase 1 CVA Cerebral vascular accident DIC Disseminated intravascular coagulation DOA Direct oral anticoagulant(s) DVT Deep vein thrombosis GEHT Study Group on Hemostasis and Thrombosis (groupe d’étude sur l’hémostase et la thrombose) GIHP Hemostasis and Thrombosis Interest Group (groupe d’intérêt sur l’hémostase et la thrombose) HAS Haute autorité de santé [French Authority for Health] HIT Heparin-induced thrombocytopenia IANB Inferior alveolar nerve block INR International normalized ratio IV Intravenous LMWH Low-molecular-weight heparin(s) -
Emerging Drug List AMLEXANOX
Emerging Drug List AMLEXANOX NO. 1 APRIL 2001 Trade Name (Generic): Amlexanox ( Apthera®) Manufacturer: Access Pharmaceuticals, Inc. / Paladin Labs Inc. Indication: For the treatment of aphthous ulcers (canker sores). Current Regulatory Amlexanox paste is currently marketed in the United States under the trademark Status (in Canada Apthasol™ and is also available in Japan in a tablet formulation for the treatment of and abroad): asthma. A Notice of Compliance was received from the Therapeutic Products Programme on December 11th, 2000. Paladin Labs Inc. would be the distributor of this product in Canada and they expect to launch the product early in the year 2001. Description: At this time, the exact mechanism of action by which amlexanox causes accelerated healing of aphthous ulcers is unknown. Amlexanox, an antiallergic agent, is a potent inhibitor of the formation and/or release of inflammatory mediators from cells including neutrophils and mast cells. As soon as a canker sore is discovered, a small amount of paste (i.e., 0.5 cm) is applied four times daily to each ulcer. Treatment is continued until the ulcer is healed. Should no significant healing or pain relief be apparent after 10 days of use, medical or dental advice should be sought. Apthera® is expected to be available as a 5% paste formulation in Canada. Current Treatment: Treating aphthous ulcers can be accomplished via topical and oral interventions. Medications are aimed at reducing secondary infection, controlling pain, reducing the duration of lesion presence, and possibly preventing recurrence. There have been numerous medications studied in the treatment of the lesions, both systemic and topical. -
Drug Formulary Effective October 1, 2021
Kaiser Permanente Hawaii QUEST Integration Drug Formulary Effective October 1, 2021 Kaiser Permanente Hawaii uses a drug formulary to ensure that the most appropriate and effective prescription drugs are available to you. The formulary is a list of drugs that have been approved by our Pharmacy and Therapeutics (P&T) Committee. Committee members include pharmacists, physicians, nurses, and other allied health care professionals. Our drug formulary allows us to select drugs that are safe, effective, and a good value for you. We review our formulary regularly so that we can add new drugs and remove drugs that can be replaced by newer, more effective drugs. The formulary also helps us restrict drugs that can be toxic or otherwise dangerous if. Our drug formulary is considered a closed formulary, which means that drugs on the list are usually covered under the prescription drug benefit, if you have one. However, drugs on our formulary may not be automatically covered under your prescription benefit because these benefits vary depending on your plan. Please check with your Kaiser Permanente pharmacist when you have questions about whether a drug is on our formulary or if there are any restrictions or limitations to obtaining a drug. NON-FORMULARY DRUGS Non-formulary drugs are those that are not included on our drug formulary. These include new drugs that haven’t been reviewed yet; drugs that our clinicians and pharmacists have decided to leave off the formulary, or a different strength or dosage of a formulary drug that we don’t stock in our Kaiser Permanente pharmacies. Even though non-formulary drugs are generally not covered under our prescription drug benefit options, your Kaiser Permanente doctor can request a non-formulary drug for you when formulary alternatives have failed and the non-formulary drug is medically necessary, provided the drug is not excluded under the prescription drug benefit. -
Malaysian STATISTICS on MEDICINE 2005
Malaysian STATISTICS ON MEDICINE 2005 Edited by: Sameerah S.A.R Sarojini S. With contributions from Goh A, Faridah A, Rosminah MD, Radzi H, Azuana R, Letchuman R, Muruga V, Zanariah H, Oiyammal C, Sim KH, Fong AYY, Tamil Selvan M, Basariah N, Hooi LS, Zaki Morad, Fadilah O, Lim V.K.E., Tan KK, Biswal BM, Lim YS, Lim GCC, Mohammad Anwar H.A, Ahmad Sabri O, Mary SC, Marzida M, Benjamin Chan TM, Suarn Singh, Zoriah A, Noor Ratna N , Abdul Razak M, Norzila Z, Shamsinah H A publication of the Pharmaceutical Services Division and the Clinical Research Centre Ministry of Health Malaysia Malaysian Statistics On Medicine 22005005 Edited by: Sameerah S.A.R Sarojini S. With contributions from Goh A, Faridah A, Rosminah MD, Radzi H, Azuana R, Letchuman R, Muruga V, Zanariah H, Oiyammal C, Sim KH, Fong AYY, Tamil Selvan M, Basariah N, Hooi LS, Zaki Morad, Fadilah O, Lim V.K.E., Tan KK, Biswal BM, Lim YS, Lim GCC, Mohammad Anwar H.A, Ahmad Sabri O, Mary SC, Marzida M, Benjamin Chan TM, Suarn Singh, Zoriah A, Noor Ratna N , Abdul Razak M, Norzila Z, Shamsinah H A publication of the Pharmaceutical Services Division and the Clinical Research Centre Ministry of Health Malaysia Malaysian Statistics On Medicine 2005 April 2007 © Ministry of Health Malaysia Published by: The National Medicines Use Survey Pharmaceutical Services Division Lot 36, Jalan Universiti 46350 Petaling Jaya Selangor, Malaysia Tel. : (603) 4043 9300 Fax : (603) 4043 9400 e-mail : [email protected] Web site : http://www.crc.gov.my/nmus This report is copyrighted. -
Pharmaceuticals As Environmental Contaminants
PharmaceuticalsPharmaceuticals asas EnvironmentalEnvironmental Contaminants:Contaminants: anan OverviewOverview ofof thethe ScienceScience Christian G. Daughton, Ph.D. Chief, Environmental Chemistry Branch Environmental Sciences Division National Exposure Research Laboratory Office of Research and Development Environmental Protection Agency Las Vegas, Nevada 89119 [email protected] Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada Why and how do drugs contaminate the environment? What might it all mean? How do we prevent it? Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada This talk presents only a cursory overview of some of the many science issues surrounding the topic of pharmaceuticals as environmental contaminants Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada A Clarification We sometimes loosely (but incorrectly) refer to drugs, medicines, medications, or pharmaceuticals as being the substances that contaminant the environment. The actual environmental contaminants, however, are the active pharmaceutical ingredients – APIs. These terms are all often used interchangeably Office of Research and Development National Exposure Research Laboratory, Environmental Sciences Division, Las Vegas, Nevada Office of Research and Development Available: http://www.epa.gov/nerlesd1/chemistry/pharma/image/drawing.pdfNational -
Vectorial Cholesterol Transport by the Protein OSBP Joelle Bigay, Bruno Mesmin, Bruno Antonny
A lipid exchange market : vectorial cholesterol transport by the protein OSBP Joelle Bigay, Bruno Mesmin, Bruno Antonny To cite this version: Joelle Bigay, Bruno Mesmin, Bruno Antonny. A lipid exchange market : vectorial cholesterol transport by the protein OSBP. médecine/sciences, EDP Sciences, 2020, 36 (2), pp.130 - 136. 10.1051/med- sci/2020009. hal-03001136 HAL Id: hal-03001136 https://hal.archives-ouvertes.fr/hal-03001136 Submitted on 12 Nov 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. médecine/sciences 2020 ; 36 : 130-6 médecine/sciences Un marché d’échange de lipides Transport vectoriel > Le cholestérol est synthétisé dans le réticu- lum endoplasmique (RE) puis transporté vers du cholestérol par les compartiments cellulaires dont la fonction la protéine OSBP en nécessite un taux élevé. Nous décrivons ici le Joëlle Bigay, Bruno Mesmin, Bruno Antonny mécanisme de transport du cholestérol du RE vers le réseau trans golgien (TGN) par la protéine OSBP (oxysterol binding protein). Celle-ci présente deux activités complémentaires : elle arrime les deux compartiments, RE et TGN, en formant un site de contact où les deux membranes sont à une vingtaine de nanomètres de distance ; puis elle Institut de Pharmacologie Moléculaire et Cellulaire, échange le cholestérol du RE avec un lipide pré- Université Côte d’Azur et CNRS, sent dans le TGN, le phosphatidylinositol 4-phos- UMR 7275, 660 route des lucioles, phate (PI4P).