Table SI. the Predicted Targets of Mir-221-3P with Targetscan Database

Total Page:16

File Type:pdf, Size:1020Kb

Table SI. the Predicted Targets of Mir-221-3P with Targetscan Database Table SI. The predicted targets of miR-221-3p with TargetScan database. Target gene Representative transcript Gene name VAPB ENST00000395802.3 VAMP (vesicle-associated membrane protein)-associated protein B and C TMSB15B ENST00000540220.1 Thymosin beta 15B TFG ENST00000240851.4 TRK-fused gene HECTD2 ENST00000371667.1 HECT domain containing E3 ubiquitin protein ligase 2 CLVS2 ENST00000275162.5 Clavesin 2 PAIP1 ENST00000514514.1 poly(A) binding protein interacting protein 1 MIDN ENST00000591446.2 Midnolin AGFG1 ENST00000310078.8 ArfGAP with FG repeats 1 HMBOX1 ENST00000397358.3 Homeobox containing 1 MYLIP ENST00000349606.4 Myosin regulatory light chain interacting protein SEC62 ENST00000337002.4 SEC62 homolog (S. cerevisiae) TMCC1 ENST00000432054.2 Transmembrane and coiled-coil domain family 1 PHACTR4 ENST00000373839.3 Phosphatase and actin regulator 4 AIDA ENST00000340020.6 Axin interactor, dorsalization associated BEAN1 ENST00000299694.8 Brain expressed, associated with NEDD4, 1 AMMECR1 ENST00000262844.5 Alport syndrome, midface hypoplasia and elliptocytosis chro- mosomal region gene 1 EIF3J ENST00000261868.5 Eukaryotic translation initiation factor 3, subunit J SMARCA5 ENST00000283131.3 SWI/SNF related, actin dependent regulator of chromatin, subfamily a, member 5 TCF12 ENST00000267811.5 Transcription factor 12 PNO1 ENST00000263657.2 Partner of NOB1 homolog (S. cerevisiae) ZBTB37 ENST00000367701.5 Zinc finger and BTB domain containing 37 FOS ENST00000303562.4 FBJ murine osteosarcoma viral oncogene homolog ZNF385A ENST00000551109.1 Zinc finger protein 385A ATAD2B ENST00000238789.5 ATPase family, AAA domain containing 2B NRK ENST00000243300.9 Nik related kinase IRF2 ENST00000393593.3 Interferon regulatory factor 2 PLCL2 ENST00000418129.2 Phospholipase C-like 2 SOCS3 ENST00000330871.2 Suppressor of cytokine signaling 3 MIER3 ENST00000381226.3 Mesoderm induction early response 1, family member 3 PIK3R1 ENST00000521381.1 Phosphoinositide-3-kinase, regulatory subunit 1 (alpha) SNCB ENST00000310112.3 Synuclein, beta RNF4 ENST00000511859.1 Ring finger protein 4 SYT10 ENST00000228567.3 Synaptotagmin X TOX ENST00000361421.1 Thymocyte selection-associated high mobility group box CRKL ENST00000354336.3 v-crk avian sarcoma virus CT10 oncogene homolog-like PTS ENST00000525803.1 6-pyruvoyltetrahydropterin synthase DDIT4 ENST00000307365.3 DNA-damage-inducible transcript 4 CHSY1 ENST00000254190.3 Chondroitin sulfate synthase 1 BBC3 ENST00000341983.4 BCL2 binding component 3 PCDHA2 ENST00000526136.1 Protocadherin alpha 2 DYNC1LI2 ENST00000258198.2 Dynein, cytoplasmic 1, light intermediate chain 2 DCAF7 ENST00000310827.4 DDB1 and CUL4 associated factor 7 CDKN1C ENST00000414822.3 Cyclin-dependent kinase inhibitor 1C (p57, Kip2) RBM24 ENST00000379052.5 RNA binding motif protein 24 KIF16B ENST00000354981.2 Kinesin family member 16B EMX2 ENST00000442245.4 Empty spiracles homeobox 2 FOXN2 ENST00000340553.3 Forkhead box N2 PDGFA ENST00000354513.5 Platelet-derived growth factor alpha polypeptide GTF2B ENST00000370500.5 General transcription factor IIB NLK ENST00000407008.3 Nemo-like kinase CASZ1 ENST00000377022.3 Castor zinc finger 1 ZFPM2 ENST00000407775.2 Zinc finger protein, FOG family member 2 WDR47 ENST00000400794.3 WD repeat domain 47 DMRT3 ENST00000190165.2 Doublesex and mab-3 related transcription factor 3 FAM199X ENST00000493442.1 Family with sequence similarity 199, X-linked NIPAL4 ENST00000311946.7 NIPA-like domain containing 4 Table SI. Continued. Target gene Representative transcript Gene name CD4 ENST00000011653.4 CD4 molecule ATXN1 ENST00000244769.4 Ataxin 1 THBS1 ENST00000260356.5 Thrombospondin 1 ARHGAP42 ENST00000524892.2 Rho GTPase activating protein 42 NDST3 ENST00000296499.5 N-deacetylase/N-sulfotransferase (heparan glucosaminyl) 3 CNOT2 ENST00000229195.3 CCR4-NOT transcription complex, subunit 2 GNAI3 ENST00000369851.4 Guanine nucleotide binding protein (G protein), alpha inhib- iting activity polypeptide 3 BEND4 ENST00000504360.1 BEN domain containing 4 KPNA1 ENST00000344337.6 Karyopherin alpha 1 (importin alpha 5) FLJ00388 ENST00000594280.1 CYR61 ENST00000451137.2 Cysteine-rich, angiogenic inducer, 61 C2orf91 ENST00000378711.2 Chromosome 2 open reading frame 91 ZSWIM4 ENST00000254323.2 Zinc finger, SWIM-type containing 4 MYO10 ENST00000513610.1 Myosin X PDE3A ENST00000359062.3 Phosphodiesterase 3A, cgmp-inhibited IPO7 ENST00000379719.3 Importin 7 H3F3A ENST00000366813.1 H3 histone, family 3A MYEF2 ENST00000324324.7 Myelin expression factor 2 DKK2 ENST00000285311.3 Dickkopf WNT signaling pathway inhibitor 2 PLCXD3 ENST00000377801.3 Phosphatidylinositol-specific phospholipase C, X domain containing 3 ADAM22 ENST00000398204.4 ADAM metallopeptidase domain 22 LHX8 ENST00000294638.5 LIM homeobox 8 CTCF ENST00000264010.4 CCCTC-binding factor (zinc finger protein) RFX3 ENST00000382004.3 Regulatory factor X, 3 (influences HLA class II expression) MARCKS ENST00000368635.4 Myristoylated alanine-rich protein kinase C substrate CAND1 ENST00000545606.1 Cullin-associated and neddylation-dissociated 1 TERF2 ENST00000254942.3 Telomeric repeat binding factor 2 PCDHA7 ENST00000525929.1 Protocadherin alpha 7 PCDHA5 ENST00000529859.1 Protocadherin alpha 5 PCDHA12 ENST00000398631.2 Protocadherin alpha 12 POGZ ENST00000392723.1 Pogo transposable element with ZNF domain IKZF4 ENST00000262032.5 IKAROS family zinc finger 4 (Eos) PCDHA1 ENST00000504120.2 Protocadherin alpha 1 PCDHA6 ENST00000529310.1 Protocadherin alpha 6 PCDHA4 ENST00000530339.1 Protocadherin alpha 4 PCDHA9 ENST00000532602.1 Protocadherin alpha 9 PCDHA10 ENST00000307360.5 Protocadherin alpha 10 PCDHA11 ENST00000398640.2 Protocadherin alpha 11 PCDHA3 ENST00000522353.2 Protocadherin alpha 3 PCDHA8 ENST00000531613.1 Protocadherin alpha 8 PCDHA13 ENST00000289272.2 Protocadherin alpha 13 PCDHAC1 ENST00000253807.2 Protocadherin alpha subfamily C, 1 MSL1 ENST00000398532.4 Male-specific lethal 1 homolog (Drosophila) SLC16A6 ENST00000327268.4 Solute carrier family 16, member 6 TRPS1 ENST00000395715.3 Trichorhinophalangeal syndrome I SH3BP4 ENST00000392011.2 SH3-domain binding protein 4 PCDHAC2 ENST00000289269.5 Protocadherin alpha subfamily C, 2 SEC23IP ENST00000369075.3 SEC23 interacting protein WASF2 ENST00000536657.1 WAS protein family, member 2 HNRNPA3 ENST00000411529.2 Heterogeneous nuclear ribonucleoprotein A3 HIPK1 ENST00000369558.1 Homeodomain interacting protein kinase 1 MITF ENST00000328528.6 Microphthalmia-associated transcription factor SLC25A37 ENST00000519973.1 Solute carrier family 25 (mitochondrial iron transporter), member 37 GPR12 ENST00000405846.3 G protein-coupled receptor 12 TIPARP ENST00000295924.7 TCDD-inducible poly(ADP-ribose) polymerase KDSR ENST00000406396.3 3-ketodihydrosphingosine reductase Table SI. Continued. Target gene Representative transcript Gene name RUNX2 ENST00000371432.3 Runt-related transcription factor 2 LRFN2 ENST00000338305.6 Leucine rich repeat and fibronectin type III domain containing 2 AMIGO1 ENST00000369864.4 Adhesion molecule with Ig-like domain 1 MEX3A ENST00000532414.2 Mex-3 RNA binding family member A ZFAND5 ENST00000237937.3 Zinc finger, AN1-type domain 5 CDH2 ENST00000269141.3 Cadherin 2, type 1, N-cadherin (neuronal) TTBK2 ENST00000267890.6 Tau tubulin kinase 2 AP3M1 ENST00000355264.4 Adaptor-related protein complex 3, mu 1 subunit HNRNPA0 ENST00000314940.4 Heterogeneous nuclear ribonucleoprotein A0 EIF1 ENST00000469257.1 Eukaryotic translation initiation factor 1 SOX11 ENST00000322002.3 SRY (sex determining region Y)-box 11 AGO4 ENST00000373210.3 Argonaute RISC catalytic component 4 BMI1 ENST00000376663.3 BMI1 polycomb ring finger oncogene HNRNPH3 ENST00000265866.7 Heterogeneous nuclear ribonucleoprotein H3 (2H9) WDR37 ENST00000358220.1 WD repeat domain 37 LYSMD1 ENST00000368908.5 LysM, putative peptidoglycan-binding, domain containing 1 PPP6C ENST00000373547.4 Protein phosphatase 6, catalytic subunit PKIA ENST00000396418.2 Protein kinase (camp-dependent, catalytic) inhibitor alpha C16orf45 ENST00000300006.4 Chromosome 16 open reading frame 45 GPBP1 ENST00000424459.3 GC-rich promoter binding protein 1 RNF44 ENST00000274811.4 Ring finger protein 44 COMMD3-BMI1 ENST00000602390.1 COMMD3-BMI1 readthrough PDIK1L ENST00000374271.4 PDLIM1 interacting kinase 1 like SOCS1 ENST00000332029.2 Suppressor of cytokine signaling 1 FRY ENST00000380250.3 Furry homolog (Drosophila) LPPR1 ENST00000374874.3 Lipid phosphate phosphatase-related protein type 1 PTPN3 ENST00000412145.1 Protein tyrosine phosphatase, non-receptor type 3 YTHDC1 ENST00000344157.4 YTH domain containing 1 FAM196B ENST00000377365.3 Family with sequence similarity 196, member B NANOS1 ENST00000425699.1 Nanos homolog 1 (Drosophila) NIPBL ENST00000448238.2 Nipped-B homolog (Drosophila) UBE2N ENST00000550657.1 Ubiquitin-conjugating enzyme E2N FNDC3A ENST00000492622.2 Fibronectin type III domain containing 3A PDZRN4 ENST00000298919.7 PDZ domain containing ring finger 4 GALNT18 ENST00000227756.4 UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase 18 FAM167A ENST00000284486.4 Family with sequence similarity 167, member A AGFG2 ENST00000262935.4 ArfGAP with FG repeats 2 CTIF ENST00000256413.3 CBP80/20-dependent translation initiation factor SRSF2 ENST00000392485.2 Serine/arginine-rich splicing factor 2 CXCR5 ENST00000292174.4 Chemokine (C-X-C motif) receptor 5 EIF4E3 ENST00000425534.3 Eukaryotic translation initiation factor 4E family member 3 ARHGAP28 ENST00000419673.2 Rho GTPase activating protein 28 MAGI1 ENST00000330909.8 Membrane associated guanylate kinase,
Recommended publications
  • The B Vitamins Nicotinamide (B3) and Riboflavin (B2)
    The B Vitamins Nicotinamide (B3) and Riboflavin (B2) Stimulate Metamorphosis in Larvae of the Deposit- Feeding Polychaete Capitella teleta: Implications for a Sensory Ligand-Gated Ion Channel Robert T. Burns1*, Jan A. Pechenik1, William J. Biggers2, Gia Scavo2, Christopher Lehman2 1 Department of Biology, Tufts University, Medford, Massachusetts, United States of America, 2 Department of Biology, Wilkes University, Wilkes-Barre, Pennsylvania, United States of America Abstract Marine sediments can contain B vitamins, presumably incorporated from settled, decaying phytoplankton and microorganisms associated with decomposition. Because B vitamins may be advantageous for the energetically intensive processes of metamorphosis, post-metamorphic growth, and reproduction, we tested several B vitamins to determine if they would stimulate larvae of the deposit-feeding polychaete Capitella teleta to settle and metamorphose. Nicotinamide and riboflavin individually stimulated larvae of C. teleta to settle and metamorphose, generally within 1–2 hours at nicotinamide concentrations as low as 3 mM and riboflavin concentrations as low as 50 mM. More than 80% of the larvae metamorphosed within 30 minutes at a nicotinamide concentration of 7 mM. The pyridine channel agonist pyrazinecarboxamide also stimulated metamorphosis at very low concentrations. In contrast, neither lumichrome, thiamine HCl, pyridoxine HCl, nor vitamin B12 stimulated larvae of C. teleta to metamorphose at concentrations as high as 500 mM. Larvae also did not metamorphose in response to either nicotinamide or pyrazinecarboxamide in calcium-free seawater or with the addition of 4-acetylpyridine, a competitive inhibitor of the pyridine receptor. Together, these results suggest that larvae of C. teleta are responding to nicotinamide and riboflavin via a chemosensory pyridine receptor similar to that previously reported to be present on crayfish chela and involved with food recognition.
    [Show full text]
  • Neural Stem Cell-Derived Exosomes Revert HFD-Dependent Memory Impairment Via CREB-BDNF Signalling
    International Journal of Molecular Sciences Article Neural Stem Cell-Derived Exosomes Revert HFD-Dependent Memory Impairment via CREB-BDNF Signalling Matteo Spinelli 1, Francesca Natale 1,2, Marco Rinaudo 1, Lucia Leone 1,2, Daniele Mezzogori 1, Salvatore Fusco 1,2,* and Claudio Grassi 1,2 1 Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; [email protected] (M.S.); [email protected] (F.N.); [email protected] (M.R.); [email protected] (L.L.); [email protected] (D.M.); [email protected] (C.G.) 2 Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy * Correspondence: [email protected] Received: 6 October 2020; Accepted: 25 November 2020; Published: 26 November 2020 Abstract: Overnutrition and metabolic disorders impair cognitive functions through molecular mechanisms still poorly understood. In mice fed with a high fat diet (HFD) we analysed the expression of synaptic plasticity-related genes and the activation of cAMP response element-binding protein (CREB)-brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signalling. We found that a HFD inhibited both CREB phosphorylation and the expression of a set of CREB target genes in the hippocampus. The intranasal administration of neural stem cell (NSC)-derived exosomes (exo-NSC) epigenetically restored the transcription of Bdnf, nNOS, Sirt1, Egr3, and RelA genes by inducing the recruitment of CREB on their regulatory sequences. Finally, exo-NSC administration rescued both BDNF signalling and memory in HFD mice. Collectively, our findings highlight novel mechanisms underlying HFD-related memory impairment and provide evidence of the potential therapeutic effect of exo-NSC against metabolic disease-related cognitive decline.
    [Show full text]
  • Genome-Wide Regulatory Roles of the C2H2-Type Zinc Finger Protein
    www.nature.com/scientificreports OPEN Genome-wide Regulatory Roles of the C2H2-type Zinc Finger Protein ZNF764 on the Glucocorticoid Received: 09 June 2016 Accepted: 23 December 2016 Receptor Published: 31 January 2017 Abeer Fadda1, Najeeb Syed2, Rafah Mackeh1, Anna Papadopoulou3, Shigeru Suzuki3,4, Puthen V. Jithesh2 & Tomoshige Kino1,3 The C2H2-type zinc finger protein ZNF764 acts as an enhancer for several steroid hormone receptors, and haploinsufficiency of this gene may be responsible for tissue resistance to multiple steroid hormones including glucocorticoids observed in a patient with 16p11.2 microdeletion. We examined genome-wide regulatory actions of ZNF764 on the glucocorticoid receptor (GR) in HeLa cells as a model system. ZNF764- and GR-binding sites demonstrated similar distribution in various genomic features. They positioned predominantly around 50–500 kbs from the transcription start sites of their nearby genes, and were closely localized with each other, overlapping in ~37% of them. ZNF764 demonstrated differential on/off effects on GR-binding and subsequent mRNA expression: some genes were highly dependent on the presence/absence of ZNF764, but others were not. Pathway analysis revealed that these 3 gene groups were involved in distinct cellular activities. ZNF764 physically interacted with GR at ligand-binding domain through its KRAB domain, and both its physical interaction to GR and zinc finger domain appear to be required for ZNF764 to regulate GR transcriptional activity. Thus, ZNF764 is a cofactor directing GR transcriptional activity toward specific biologic pathways by changing GR binding and transcriptional activity on the glucocorticoid-responsive genes. Steroid hormones exert diverse physiologic functions and play central roles in human physiology1,2.
    [Show full text]
  • Neurotransmitters-Drugs Andbrain Function.Pdf
    Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Neurotransmitters, Drugs and Brain Function Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Neurotransmitters, Drugs and Brain Function Edited by R. A. Webster Department of Pharmacology, University College London, UK JOHN WILEY & SONS, LTD Chichester Á New York Á Weinheim Á Brisbane Á Singapore Á Toronto Neurotransmitters, Drugs and Brain Function. Edited by Roy Webster Copyright & 2001 John Wiley & Sons Ltd ISBN: Hardback 0-471-97819-1 Paperback 0-471-98586-4 Electronic 0-470-84657-7 Copyright # 2001 by John Wiley & Sons Ltd. Bans Lane, Chichester, West Sussex PO19 1UD, UK National 01243 779777 International ++44) 1243 779777 e-mail +for orders and customer service enquiries): [email protected] Visit our Home Page on: http://www.wiley.co.uk or http://www.wiley.com All Rights Reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, scanning or otherwise, except under the terms of the Copyright, Designs and Patents Act 1988 or under the terms of a licence issued by the Copyright Licensing Agency Ltd, 90 Tottenham Court Road, London W1P0LP,UK, without the permission in writing of the publisher. Other Wiley Editorial Oces John Wiley & Sons, Inc., 605 Third Avenue, New York, NY 10158-0012, USA WILEY-VCH Verlag GmbH, Pappelallee 3, D-69469 Weinheim, Germany John Wiley & Sons Australia, Ltd.
    [Show full text]
  • 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.
    [Show full text]
  • Download Download
    Supplementary Figure S1. Results of flow cytometry analysis, performed to estimate CD34 positivity, after immunomagnetic separation in two different experiments. As monoclonal antibody for labeling the sample, the fluorescein isothiocyanate (FITC)- conjugated mouse anti-human CD34 MoAb (Mylteni) was used. Briefly, cell samples were incubated in the presence of the indicated MoAbs, at the proper dilution, in PBS containing 5% FCS and 1% Fc receptor (FcR) blocking reagent (Miltenyi) for 30 min at 4 C. Cells were then washed twice, resuspended with PBS and analyzed by a Coulter Epics XL (Coulter Electronics Inc., Hialeah, FL, USA) flow cytometer. only use Non-commercial 1 Supplementary Table S1. Complete list of the datasets used in this study and their sources. GEO Total samples Geo selected GEO accession of used Platform Reference series in series samples samples GSM142565 GSM142566 GSM142567 GSM142568 GSE6146 HG-U133A 14 8 - GSM142569 GSM142571 GSM142572 GSM142574 GSM51391 GSM51392 GSE2666 HG-U133A 36 4 1 GSM51393 GSM51394 only GSM321583 GSE12803 HG-U133A 20 3 GSM321584 2 GSM321585 use Promyelocytes_1 Promyelocytes_2 Promyelocytes_3 Promyelocytes_4 HG-U133A 8 8 3 GSE64282 Promyelocytes_5 Promyelocytes_6 Promyelocytes_7 Promyelocytes_8 Non-commercial 2 Supplementary Table S2. Chromosomal regions up-regulated in CD34+ samples as identified by the LAP procedure with the two-class statistics coded in the PREDA R package and an FDR threshold of 0.5. Functional enrichment analysis has been performed using DAVID (http://david.abcc.ncifcrf.gov/)
    [Show full text]
  • Investigation of Candidate Genes and Mechanisms Underlying Obesity
    Prashanth et al. BMC Endocrine Disorders (2021) 21:80 https://doi.org/10.1186/s12902-021-00718-5 RESEARCH ARTICLE Open Access Investigation of candidate genes and mechanisms underlying obesity associated type 2 diabetes mellitus using bioinformatics analysis and screening of small drug molecules G. Prashanth1 , Basavaraj Vastrad2 , Anandkumar Tengli3 , Chanabasayya Vastrad4* and Iranna Kotturshetti5 Abstract Background: Obesity associated type 2 diabetes mellitus is a metabolic disorder ; however, the etiology of obesity associated type 2 diabetes mellitus remains largely unknown. There is an urgent need to further broaden the understanding of the molecular mechanism associated in obesity associated type 2 diabetes mellitus. Methods: To screen the differentially expressed genes (DEGs) that might play essential roles in obesity associated type 2 diabetes mellitus, the publicly available expression profiling by high throughput sequencing data (GSE143319) was downloaded and screened for DEGs. Then, Gene Ontology (GO) and REACTOME pathway enrichment analysis were performed. The protein - protein interaction network, miRNA - target genes regulatory network and TF-target gene regulatory network were constructed and analyzed for identification of hub and target genes. The hub genes were validated by receiver operating characteristic (ROC) curve analysis and RT- PCR analysis. Finally, a molecular docking study was performed on over expressed proteins to predict the target small drug molecules. Results: A total of 820 DEGs were identified between
    [Show full text]
  • Modulating Hallmarks of Cholangiocarcinoma
    University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Fall 12-14-2018 Modulating Hallmarks of Cholangiocarcinoma Cody Wehrkamp University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Molecular Biology Commons Recommended Citation Wehrkamp, Cody, "Modulating Hallmarks of Cholangiocarcinoma" (2018). Theses & Dissertations. 337. https://digitalcommons.unmc.edu/etd/337 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. MODULATING HALLMARKS OF CHOLANGIOCARCINOMA by Cody J. Wehrkamp A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor Justin L. Mott University of Nebraska Medical Center Omaha, Nebraska November 2018 Supervisory Committee: Kaustubh Datta, Ph.D. Melissa Teoh‐Fitzgerald, Ph.D. Richard G. MacDonald, Ph.D. Acknowledgements This endeavor has led to scientific as well as personal growth for me. I am indebted to many for their knowledge, influence, and support along the way. To my mentor, Dr. Justin L. Mott, you have been an incomparable teacher and invaluable guide. You upheld for me the concept that science is intrepid, even when the experience is trying. Through my training, and now here at the end, I can say that it has been an honor to be your protégé. When you have shaped your future graduates to be and do great, I will be privileged to say that I was your first one.
    [Show full text]
  • Understanding Allergic Multimorbidity Within the Non-Eosinophilic
    University of Groningen Understanding allergic multimorbidity within the non-eosinophilic interactome Aguilar, Daniel; Lemonnier, Nathanael; Koppelman, Gerard H; Melén, Erik; Oliva, Baldo; Pinart, Mariona; Guerra, Stefano; Bousquet, Jean; Anto, Josep M Published in: PLoS ONE DOI: 10.1371/journal.pone.0224448 IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2019 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Aguilar, D., Lemonnier, N., Koppelman, G. H., Melén, E., Oliva, B., Pinart, M., Guerra, S., Bousquet, J., & Anto, J. M. (2019). Understanding allergic multimorbidity within the non-eosinophilic interactome. PLoS ONE, 14(11), [e0224448]. https://doi.org/10.1371/journal.pone.0224448 Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 26-12-2020 RESEARCH ARTICLE Understanding allergic multimorbidity within the non-eosinophilic interactome 1,2,3 4 5,6 7 Daniel AguilarID *, Nathanael LemonnierID , Gerard H.
    [Show full text]
  • Cellular and Molecular Signatures in the Disease Tissue of Early
    Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of
    [Show full text]
  • Serum Albumin OS=Homo Sapiens
    Protein Name Cluster of Glial fibrillary acidic protein OS=Homo sapiens GN=GFAP PE=1 SV=1 (P14136) Serum albumin OS=Homo sapiens GN=ALB PE=1 SV=2 Cluster of Isoform 3 of Plectin OS=Homo sapiens GN=PLEC (Q15149-3) Cluster of Hemoglobin subunit beta OS=Homo sapiens GN=HBB PE=1 SV=2 (P68871) Vimentin OS=Homo sapiens GN=VIM PE=1 SV=4 Cluster of Tubulin beta-3 chain OS=Homo sapiens GN=TUBB3 PE=1 SV=2 (Q13509) Cluster of Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 (P60709) Cluster of Tubulin alpha-1B chain OS=Homo sapiens GN=TUBA1B PE=1 SV=1 (P68363) Cluster of Isoform 2 of Spectrin alpha chain, non-erythrocytic 1 OS=Homo sapiens GN=SPTAN1 (Q13813-2) Hemoglobin subunit alpha OS=Homo sapiens GN=HBA1 PE=1 SV=2 Cluster of Spectrin beta chain, non-erythrocytic 1 OS=Homo sapiens GN=SPTBN1 PE=1 SV=2 (Q01082) Cluster of Pyruvate kinase isozymes M1/M2 OS=Homo sapiens GN=PKM PE=1 SV=4 (P14618) Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 Clathrin heavy chain 1 OS=Homo sapiens GN=CLTC PE=1 SV=5 Filamin-A OS=Homo sapiens GN=FLNA PE=1 SV=4 Cytoplasmic dynein 1 heavy chain 1 OS=Homo sapiens GN=DYNC1H1 PE=1 SV=5 Cluster of ATPase, Na+/K+ transporting, alpha 2 (+) polypeptide OS=Homo sapiens GN=ATP1A2 PE=3 SV=1 (B1AKY9) Fibrinogen beta chain OS=Homo sapiens GN=FGB PE=1 SV=2 Fibrinogen alpha chain OS=Homo sapiens GN=FGA PE=1 SV=2 Dihydropyrimidinase-related protein 2 OS=Homo sapiens GN=DPYSL2 PE=1 SV=1 Cluster of Alpha-actinin-1 OS=Homo sapiens GN=ACTN1 PE=1 SV=2 (P12814) 60 kDa heat shock protein, mitochondrial OS=Homo
    [Show full text]
  • WO 2019/079361 Al 25 April 2019 (25.04.2019) W 1P O PCT
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization I International Bureau (10) International Publication Number (43) International Publication Date WO 2019/079361 Al 25 April 2019 (25.04.2019) W 1P O PCT (51) International Patent Classification: CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, C12Q 1/68 (2018.01) A61P 31/18 (2006.01) DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, C12Q 1/70 (2006.01) HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, (21) International Application Number: MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, PCT/US2018/056167 OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, (22) International Filing Date: SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, 16 October 2018 (16. 10.2018) TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (26) Publication Language: English GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, TZ, (30) Priority Data: UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, 62/573,025 16 October 2017 (16. 10.2017) US TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, EE, ES, FI, FR, GB, GR, HR, HU, ΓΕ , IS, IT, LT, LU, LV, (71) Applicant: MASSACHUSETTS INSTITUTE OF MC, MK, MT, NL, NO, PL, PT, RO, RS, SE, SI, SK, SM, TECHNOLOGY [US/US]; 77 Massachusetts Avenue, TR), OAPI (BF, BJ, CF, CG, CI, CM, GA, GN, GQ, GW, Cambridge, Massachusetts 02139 (US).
    [Show full text]