Table SI. Differentially Expressed Genes. Gene Logfc Aveexpr T Value
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Anti-MYOZ2 (GW22350F)
3050 Spruce Street, Saint Louis, MO 63103 USA Tel: (800) 521-8956 (314) 771-5765 Fax: (800) 325-5052 (314) 771-5757 email: [email protected] Product Information Anti-MYOZ2 antibody produced in chicken, affinity isolated antibody Catalog Number GW22350F Formerly listed as GenWay Catalog Number 15-288-22350F, Myozenin-2 Antibody. – Storage Temperature Store at 20 °C The product is a clear, colorless solution in phosphate buffered saline, pH 7.2, containing 0.02% sodium azide. Synonyms: Myozenin 2, Calsarcin-1; FATZ-related protein 2 Species Reactivity: Human Product Description Myozenins may serve as intracellular binding proteins Tested Applications: WB involved in linking Z-disk proteins such as alpha-actinin. Recommended Dilutions: Recommended starting dilution gamma-filamin. TCAP/telethonin. LDB3/ZASP and localizing for Western blot analysis is 1:500, for tissue or cell staining calcineurin signaling to the sarcomere. Plays an important 1:200. role in the modulation of calcineurin signaling. May play a role in myofibrillogenesis. Note: Optimal concentrations and conditions for each application should be determined by the user. NCBI Accession number: NP_057683.1 Swiss Prot Accession number: Q9NPC6 Precautions and Disclaimer This product is for R&D use only, not for drug, household, or Gene Information: Human .. MYOZ2 (51778) other uses. Due to the sodium azide content a material Immunogen: Recombinant protein Myozenin 2 safety data sheet (MSDS) for this product has been sent to the attention of the safety officer of your institution. Please Immunogen Sequence: GI # 7706595, sequence 1 - 264 consult the Material Safety Data Sheet for information regarding hazards and safe handling practices. -
Oncostatin M Exhibit Elevated Responsiveness to IL-31 Receptor
IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M This information is current as Janine Bilsborough, Sherri Mudri, Eric Chadwick, Brandon of September 28, 2021. Harder and Stacey R. Dillon J Immunol 2010; 185:6023-6030; Prepublished online 18 October 2010; doi: 10.4049/jimmunol.0902769 http://www.jimmunol.org/content/185/10/6023 Downloaded from References This article cites 29 articles, 6 of which you can access for free at: http://www.jimmunol.org/content/185/10/6023.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 28, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M Janine Bilsborough,1 Sherri Mudri,1 Eric Chadwick,2 Brandon Harder,3 and Stacey R. Dillon IL-31 signals through the heterodimeric receptor IL-31RA and oncostatin M receptor (OSMR), and has been linked with the development of atopic dermatitis, a Th2 cytokine-associated disease in humans. -
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. -
1 Metabolic Dysfunction Is Restricted to the Sciatic Nerve in Experimental
Page 1 of 255 Diabetes Metabolic dysfunction is restricted to the sciatic nerve in experimental diabetic neuropathy Oliver J. Freeman1,2, Richard D. Unwin2,3, Andrew W. Dowsey2,3, Paul Begley2,3, Sumia Ali1, Katherine A. Hollywood2,3, Nitin Rustogi2,3, Rasmus S. Petersen1, Warwick B. Dunn2,3†, Garth J.S. Cooper2,3,4,5* & Natalie J. Gardiner1* 1 Faculty of Life Sciences, University of Manchester, UK 2 Centre for Advanced Discovery and Experimental Therapeutics (CADET), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Sciences Centre, Manchester, UK 3 Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK 4 School of Biological Sciences, University of Auckland, New Zealand 5 Department of Pharmacology, Medical Sciences Division, University of Oxford, UK † Present address: School of Biosciences, University of Birmingham, UK *Joint corresponding authors: Natalie J. Gardiner and Garth J.S. Cooper Email: [email protected]; [email protected] Address: University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom Telephone: +44 161 275 5768; +44 161 701 0240 Word count: 4,490 Number of tables: 1, Number of figures: 6 Running title: Metabolic dysfunction in diabetic neuropathy 1 Diabetes Publish Ahead of Print, published online October 15, 2015 Diabetes Page 2 of 255 Abstract High glucose levels in the peripheral nervous system (PNS) have been implicated in the pathogenesis of diabetic neuropathy (DN). However our understanding of the molecular mechanisms which cause the marked distal pathology is incomplete. Here we performed a comprehensive, system-wide analysis of the PNS of a rodent model of DN. -
The Role of Molecular Scaffolds at the Active Zone in Synaptic Vesicle Distribution and Release Probability
The Role of Molecular Scaffolds at the Active Zone in Synaptic Vesicle Distribution and Release Probability DISSERTATION To obtain the academic degree Doctor rerum naturalium (Dr. rer. nat.) submitted to the Department of Biology, Chemistry and Pharmacy Freie Universität Berlin Berlin, 2016 by Christina Beis (née Hollmann) This thesis was completed under the supervision of Prof. Dr. Stephan Sigrist from February 2011 to June 2016 at the Institute for Biology/ Genetics of Freie Universität Berlin, Germany. 1st reviewer: Prof. Dr. Stephan Sigrist 2nd reviewer: Prof. Dr. Hans-Joachim Pflüger Date of Defense: 21.11.2016 Statement of Authorship I hereby declare that the work presented in this thesis has been written independently and without inappropriate support. All sources of information are referenced. I hereby declare that this thesis has not been submitted, either in the same or in a different form, to this or any other university for a degree. ____________________________ Christina Beis Contents 1. Summary / Zusammenfassung .................................................................................................. 1 Summary....................................................................................................................................... 1 Zusammenfassung ........................................................................................................................ 3 2. Introduction .................................................................................................................................... -
System, Method and Software for Calculation of a Cannabis Drug Efficiency Index for the Reduction of Inflammation
International Journal of Molecular Sciences Article System, Method and Software for Calculation of a Cannabis Drug Efficiency Index for the Reduction of Inflammation Nicolas Borisov 1,† , Yaroslav Ilnytskyy 2,3,†, Boseon Byeon 2,3,4,†, Olga Kovalchuk 2,3 and Igor Kovalchuk 2,3,* 1 Moscow Institute of Physics and Technology, 9 Institutsky lane, Dolgoprudny, Moscow Region 141701, Russia; [email protected] 2 Department of Biological Sciences, University of Lethbridge, Lethbridge, AB T1K 3M4, Canada; [email protected] (Y.I.); [email protected] (B.B.); [email protected] (O.K.) 3 Pathway Rx., 16 Sandstone Rd. S., Lethbridge, AB T1K 7X8, Canada 4 Biomedical and Health Informatics, Computer Science Department, State University of New York, 2 S Clinton St, Syracuse, NY 13202, USA * Correspondence: [email protected] † First three authors contributed equally to this research. Abstract: There are many varieties of Cannabis sativa that differ from each other by composition of cannabinoids, terpenes and other molecules. The medicinal properties of these cultivars are often very different, with some being more efficient than others. This report describes the development of a method and software for the analysis of the efficiency of various cannabis extracts to detect the anti-inflammatory properties of the various cannabis extracts. The method uses high-throughput gene expression profiling data but can potentially use other omics data as well. According to the signaling pathway topology, the gene expression profiles are convoluted into the signaling pathway activities using a signaling pathway impact analysis (SPIA) method. The method was tested by inducing inflammation in human 3D epithelial tissues, including intestine, oral and skin, and then exposing these tissues to various extracts and then performing transcriptome analysis. -
Atrial Fibrillation (ATRIA) Study
European Journal of Human Genetics (2014) 22, 297–306 & 2014 Macmillan Publishers Limited All rights reserved 1018-4813/14 www.nature.com/ejhg REVIEW Atrial fibrillation: the role of common and rare genetic variants Morten S Olesen*,1,2,4, Morten W Nielsen1,2,4, Stig Haunsø1,2,3 and Jesper H Svendsen1,2,3 Atrial fibrillation (AF) is the most common cardiac arrhythmia affecting 1–2% of the general population. A number of studies have demonstrated that AF, and in particular lone AF, has a substantial genetic component. Monogenic mutations in lone and familial AF, although rare, have been recognized for many years. Presently, mutations in 25 genes have been associated with AF. However, the complexity of monogenic AF is illustrated by the recent finding that both gain- and loss-of-function mutations in the same gene can cause AF. Genome-wide association studies (GWAS) have indicated that common single-nucleotide polymorphisms (SNPs) have a role in the development of AF. Following the first GWAS discovering the association between PITX2 and AF, several new GWAS reports have identified SNPs associated with susceptibility of AF. To date, nine SNPs have been associated with AF. The exact biological pathways involving these SNPs and the development of AF are now starting to be elucidated. Since the first GWAS, the number of papers concerning the genetic basis of AF has increased drastically and the majority of these papers are for the first time included in a review. In this review, we discuss the genetic basis of AF and the role of both common and rare genetic variants in the susceptibility of developing AF. -
Insulin-Like Growth Factor Binding Protein-3 Exerts Its Anti-Metastatic Effect in Aerodigestive Tract Cancers by Disrupting the Protein Stability of Vimentin
cancers Article Insulin-Like Growth Factor Binding Protein-3 Exerts Its Anti-Metastatic Effect in Aerodigestive Tract Cancers by Disrupting the Protein Stability of Vimentin Huong Thuy Le 1,†,‡, Ho Jin Lee 1,†, Jaebeom Cho 1, Hye-Young Min 1, Ji-Sun Lee 1, Su-Jae Lee 2 and Ho-Young Lee 1,* 1 Creative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea; [email protected] (H.T.L.); [email protected] (H.J.L.); [email protected] (J.C.); [email protected] (H.-Y.M.); [email protected] (J.-S.L.) 2 Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul 04763, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-2-880-9277; Fax: +82-2-6280-5327 † These two authors contributed equally to this work and should be considered as first author. ‡ Current Address: Faculty of Pharmacy, Ton Duc Thang University, Ho Chi Minh City 700000, Vietnam. Simple Summary: Local invasion and distal metastasis are the main causes of cancer-related death and the poor prognosis of patients with aerodigestive tract cancers. Therefore, understanding the biology of invasion and metastasis is important for the development of effective therapeutic strategies. The present study shows that insulin-like growth factor binding protein-3 (IGFBP-3) inhibits the migration and invasion of non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC) cells in vitro and the development of metastasized tumors in vivo. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
Microrna Regulatory Pathways in the Control of the Actin–Myosin Cytoskeleton
cells Review MicroRNA Regulatory Pathways in the Control of the Actin–Myosin Cytoskeleton , , Karen Uray * y , Evelin Major and Beata Lontay * y Department of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary; [email protected] * Correspondence: [email protected] (K.U.); [email protected] (B.L.); Tel.: +36-52-412345 (K.U. & B.L.) The authors contributed equally to the manuscript. y Received: 11 June 2020; Accepted: 7 July 2020; Published: 9 July 2020 Abstract: MicroRNAs (miRNAs) are key modulators of post-transcriptional gene regulation in a plethora of processes, including actin–myosin cytoskeleton dynamics. Recent evidence points to the widespread effects of miRNAs on actin–myosin cytoskeleton dynamics, either directly on the expression of actin and myosin genes or indirectly on the diverse signaling cascades modulating cytoskeletal arrangement. Furthermore, studies from various human models indicate that miRNAs contribute to the development of various human disorders. The potentially huge impact of miRNA-based mechanisms on cytoskeletal elements is just starting to be recognized. In this review, we summarize recent knowledge about the importance of microRNA modulation of the actin–myosin cytoskeleton affecting physiological processes, including cardiovascular function, hematopoiesis, podocyte physiology, and osteogenesis. Keywords: miRNA; actin; myosin; actin–myosin complex; Rho kinase; cancer; smooth muscle; hematopoiesis; stress fiber; gene expression; cardiovascular system; striated muscle; muscle cell differentiation; therapy 1. Introduction Actin–myosin interactions are the primary source of force generation in mammalian cells. Actin forms a cytoskeletal network and the myosin motor proteins pull actin filaments to produce contractile force. All eukaryotic cells contain an actin–myosin network inferring contractile properties to these cells. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Inaugural Dissertation
Molecular Mechanisms that Regulate Neurotransmission and Establish Presynaptic Homeostasis at the Drosophila melanogaster Neuromuscular Junction Inaugural Dissertation to obtain the academic degree Doctor rerum naturalium (Dr. rer. nat.) submitted to the Department of Biology, Chemistry and Pharmacy of Freie Universität Berlin by Anthony William McCarthy from Dublin, Ireland February 2020 The experimental part of this thesis was conducted from September 2015 to November 2019 under the supervision of Dr. Alexander Walter at the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) and at the CharitéCrossOver, Charité Campus Berlin Mitte. 1st Reviewer: Dr. Alexander Walter 2nd Reviewer: Prof. Dr. Stephan Sigrist Date of Defence: Statement of Authorship I hereby declare that I am the sole author of this thesis and that I have not used any sources or tools other than those quoted. Use of work by any other author is identified as such and appropriately referenced. Berlin, February 2020 Anthony William McCarthy Acknowledgments I would like to take the opportunity to thank all the people who have been important and made an impact on me during my time in Berlin. I would first like to thank my supervisor, Dr. Alexander Walter, for his guidance and supervision over the years. His passion for science and expert knowledge as well as approachable nature made for insightful conversation, projecting me forward with my projects. I would also like to thank Prof. Dr. Stephan Sigrist for his valuable input during thesis committee meetings and for acting as a reviewer. I am grateful to Prof. Dr. Volker Haucke, the members of his lab and all those at the FMP in Buch for the plentiful feedback I received following thesis committee meetings and progress presentations.