DOCSLIB.ORG

Table SII. Differentially Expressed Micrornas in the Dataset from the Cancer Genome Atlas

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Table SII. Differentially Expressed Micrornas in the Dataset from the Cancer Genome Atlas Table SII. Differentially expressed microRNAs in the dataset from The Cancer Genome Atlas. Genesymbol LogFC P-value FDR A1CF -2.10229 2.084602×10^-3 7.08728×10^-3 A4GALT -3.52073 4.66×10^-28 2.42×10^-26 A4GNT -4.26856 3.96×10^-21 1.31×10^-19 AADAT 2.071161 1.88×10^-11 2.64×10^-10 ABCA12 2.015141 2.59912×10^-4 1.121563×10^-3 ABCA4 -5.49484 5.9×10^-61 1.29×10^-58 ABCA9 2.15609 7.66629×10^-3 2.1814238×10^-2 ABCA9-AS1 3.126405 8.61395×10^-4 3.253832×10^-3 ABCB1 -3.7445 6.92×10^-11 9.13×10^-10 ABCB10P1 2.984502 1.3629181×10^-2 3.5572807×10^-2 ABCB10P3 3.797105 1.7936677×10^-2 4.4878796×10^-2 ABCB4 2.732583 8.40693×10^-4 3.187454×10^-3 ABCC3 -3.89866 3.65×10^-28 1.91×10^-26 ABCC6P1 -2.13803 1.28×10^-6 8.98×10^-6 ABCC8 4.783716 4.87×10^-6 3.07×10^-5 ABCF2P2 3.646157 1.9174257×10^-2 4.7447767×10^-2 ABCG5 -2.23257 6.39×10^-17 1.5×10^-15 ABCG8 -3.03436 7.84×10^-14 1.41×10^-12 ABHD14B -2.08952 7.71×10^-22 2.69×10^-20 ABI3 -3.05056 9.76×10^-42 1.05×10^-39 ABO -3.74358 2.39×10^-24 9.89×10^-23 AC002127.2 4.687982 8.02447×10^-4 3.057116×10^-3 AC002310.2 2.024741 3.56781×10^-4 1.486288×10^-3 AC002351.1 4.648618 1.1547246×10^-2 3.0927155×10^-2 AC002368.1 3.130184 1.5645669×10^-2 3.9941757×10^-2 AC002401.4 -3.02059 7.25×10^-8 6.27×10^-7 AC002456.1 2.04042 2.31884×10^-3 7.775065×10^-3 AC002480.2 -3.4477 2.87×10^-13 4.87×10^-12 AC002480.3 -2.86235 4.84×10^-8 4.3×10^-7 AC002525.1 -2.16884 5.21×10^-6 3.26×10^-5 AC002563.1 -2.35933 1.97×10^-9 2.15×10^-8 AC003070.1 -2.11754 1.68×10^-7 1.38×10^-6 AC003070.2 -3.03071 2.53×10^-7 2.02×10^-6 AC003092.1 5.918868 3.94×10^-7 3.04×10^-6 AC003092.2 5.340477 1.98747×10^-4 8.80861×10^-4 AC003101.2 -2.33724 1.06×10^-5 6.22×10^-5 AC003659.1 3.749959 4.862572×10^-3 1.4804968×10^-2 AC003984.1 -6.75936 1.73×10^-38 1.63×10^-36 AC003985.2 5.811645 7.101381×10^-3 2.0468623×10^-2 AC004023.1 5.302541 1.76×10^-5 9.91×10^-5 AC004054.1 -2.15524 4.86×10^-5 2.47862×10^-4 AC004066.2 -2.76719 4.57×10^-5 2.3449×10^-4 AC004080.2 3.992392 2.9×10^-6 1.91×10^-5 AC004080.5 2.283856 5.311747×10^-3 1.5952964×10^-2 AC004080.6 3.169931 2.81×10^-5 1.51245×10^-4 AC004149.1 4.335929 9.28×10^-9 9.21×10^-8 AC004233.2 3.28088 1.1294353×10^-2 3.0371285×10^-2 AC004264.1 -2.74106 6.19×10^-11 8.21×10^-10 AC004408.2 4.931188 9.89×10^-6 5.84×10^-5 AC004453.2 2.356049 4.97122×10^-4 1.995655×10^-3 AC004466.1 -2.24489 6.2×10^-15 1.23×10^-13 AC004801.5 6.383665 2.76×10^-11 3.81×10^-10 AC004828.1 -2.13332 4.5629×10^-4 1.848223×10^-3 AC004836.1 2.181267 4.05637×10^-3 1.2648828×10^-2 AC004862.1 -2.08326 5.739777×10^-3 1.7053234×10^-2 AC004870.1 -4.226 5.39×10^-9 5.57×10^-8 AC004870.4 -2.40248 1.009005×10^-3 3.739164×10^-3 AC004917.1 -2.90511 6.74×10^-5 3.32892×10^-4 AC005009.1 2.705166 1.0865106×10^-2 2.9414819×10^-2 AC005009.2 2.620424 5.460372×10^-3 1.6319561×10^-2 AC005041.2 -3.46939 3.16×10^-12 4.84×10^-11 AC005041.3 3.180726 5.38×10^-6 3.36×10^-5 AC005050.1 -2.36774 3.48×10^-5 1.83256×10^-4 AC005062.1 -2.26603 3.11×10^-6 2.03×10^-5 AC005077.2 2.745935 5.498513×10^-3 1.6418339×10^-2 AC005077.4 2.796308 1.75275×10^-4 7.86866×10^-4 AC005082.1 -3.10576 8.12×10^-7 5.92×10^-6 AC005083.1 -5.34732 1.03×10^-27 5.26×10^-26 AC005208.1 -4.23282 3.77×10^-13 6.31×10^-12 AC005224.4 2.665221 8.388175×10^-3 2.357545×10^-2 AC005225.2 -3.46863 5.31×10^-21 1.73×10^-19 AC005237.1 -3.26347 5.13×10^-11 6.88×10^-10 AC005252.3 -3.72694 1.42189×10^-4 6.52329×10^-4 AC005274.1 -2.11342 1.72×10^-7 1.41×10^-6 AC005281.1 -5.89546 6.57×10^-20 1.97×10^-18 AC005291.2 3.38238 1.9432102×10^-2 4.800296×10^-2 AC005307.1 2.987792 1.7087×10^-4 7.68784×10^-4 AC005336.3 6.168811 5.82809×10^-4 2.297929×10^-3 AC005355.2 -2.03485 9.66×10^-5 4.60235×10^-4 AC005381.1 2.030927 2.400682×10^-3 8.016527×10^-3 AC005394.1 4.153471 6.147786×10^-3 1.8074006×10^-2 AC005487.1 -2.81741 1.1×10^-5 6.45×10^-5 AC005518.1 4.492284 1.387275×10^-3 4.954866×10^-3 AC005537.1 4.081751 2.03×10^-5 1.12688×10^-4 AC005550.2 5.328046 1.194205×10^-3 4.336626×10^-3 AC005609.1 3.911928 6.380732×10^-3 1.8666691×10^-2 AC005609.5 4.015418 8.73×10^-7 6.31×10^-6 AC005616.1 -5.29994 1.62×10^-35 1.28×10^-33 AC005746.2 -2.0237 4.25×10^-6 2.7×10^-5 AC005746.3 -2.12153 2.87×10^-6 1.89×10^-5 AC005753.1 -3.21577 2.63×10^-14 4.93×10^-13 AC005759.1 -2.46663 5.91×10^-11 7.87×10^-10 AC005821.1 -2.99749 1.28×10^-14 2.45×10^-13 AC005840.4 -2.38708 1.87×10^-9 2.06×10^-8 AC005912.2 -2.19802 7.37×10^-8 6.36×10^-7 AC005920.1 -4.28616 2.99×10^-24 1.23×10^-22 AC005920.3 -4.72388 6.85×10^-20 2.05×10^-18 AC006019.1 3.871232 1.453483×10^-3 5.160517×10^-3 AC006019.2 3.374852 1.23517×10^-4 5.74427×10^-4 AC006019.3 2.988347 1.2676475×10^-2 3.3520175×10^-2 AC006042.1 -3.12235 4.2×10^-16 9.27×10^-15 AC006206.1 6.883545 3.04968×10^-4 1.2942×10^-3 AC006206.2 10.22649 9.72×10^-7 6.97×10^-6 AC006238.1 -2.86008 9.16×10^-15 1.78×10^-13 AC006262.1 3.989411 1.651156×10^-2 4.1807002×10^-2 AC006273.1 -4.03391 2.74×10^-33 1.91×10^-31 AC006305.1 5.018016 8.91×10^-13 1.44×10^-11 AC006305.2 3.524275 1.8642008×10^-2 4.636883×10^-2 AC006329.2 3.247618 2.1×10^-5 1.16437×10^-4 AC006504.7 2.93004 5.56191×10^-4 2.204431×10^-3 AC006557.1 2.381601 1.85×10^-6 1.26×10^-5 AC006557.5 3.736473 1.22×10^-10 1.56×10^-9 AC006600.2 2.778197 1.535965×10^-3 5.418573×10^-3 AC006942.1 -2.39738 3.43×10^-23 1.33×10^-21 AC006994.2 -4.24761 8.01×10^-17 1.87×10^-15 AC007009.1 -2.05776 8.52×10^-6 5.1×10^-5 AC007014.1 -2.02222 2.3×10^-6 1.54×10^-5 AC007029.1 -2.16986 1.44×10^-6 1.01×10^-5 AC007036.1 -2.3336 5.01×10^-9 5.2×10^-8 AC007091.1 5.005086 1.8323549×10^-2 4.5704964×10^-2 AC007114.1 -2.61738 4.64×10^-21 1.52×10^-19 AC007128.1 4.018742 1.0226699×10^-2 2.7908691×10^-2 AC007128.2 4.895993 9.500858×10^-3 2.6174357×10^-2 AC007179.2 4.019319 1.0132081×10^-2 2.7692591×10^-2 AC007216.1 -2.59122 4.19×10^-10 5.07×10^-9 AC007255.1 -2.93772 3.85×10^-21 1.28×10^-19 AC007255.2 -2.60535 2.83×10^-5 1.52491×10^-4 AC007285.2 2.136946 8.32×10^-6 4.99×10^-5 AC007319.1 -2.0871 2.469112×10^-3 8.223361×10^-3 AC007336.1 -2.91326 1.22×10^-11 1.75×10^-10 AC007342.5 -2.81587 8.76×10^-7 6.34×10^-6 AC007342.9 -2.65832 1.42×10^-5 8.15×10^-5 AC007402.1 4.747235 1.1335105×10^-2 3.0451687×10^-2 AC007403.1 2.765346 1.7470499×10^-2 4.3891129×10^-2 AC007406.1 -4.50798 1.15×10^-17 2.91×10^-16 AC007406.2 -2.23247 2.65355×10^-4 1.142504×10^-3 AC007406.3 2.349801 1.53883×10^-4 7.0017×10^-4 AC007406.4 -2.40814 1.22×10^-9 1.38×10^-8 AC007422.2 4.308638 1.104649×10^-3 4.055549×10^-3 AC007424.1 2.696268 1.0919419×10^-2 2.9544105×10^-2 AC007490.1 -2.32388 6.89×10^-5 3.39501×10^-4 AC007495.1 2.48757 1.1382698×10^-2 3.0552056×10^-2 AC007546.1 -2.29885 5.48×10^-12 8.18×10^-11 AC007598.1 -2.40529 3.38×10^-8 3.09×10^-7 AC007598.2 -2.42376 2.85×10^-9 3.05×10^-8 AC007598.3 -2.32029 2.1×10^-12 3.28×10^-11 AC007601.1 -2.60758 2.12×10^-18 5.7×10^-17 AC007656.1 2.058266 7.313514×10^-3 2.0987856×10^-2 AC007728.2 -2.05328 1.2×10^-7 1×10^-6 AC007792.1 -2.81983 8.66×10^-7 6.27×10^-6 AC007834.1 -3.11891 7.38×10^-9 7.45×10^-8 AC007834.2 -2.06993 1.3×10^-6 9.15×10^-6 AC007848.1 8.343259 1.57×10^-5 8.88×10^-5 AC007848.2 7.381106 7.98×10^-11 1.04×10^-9 AC007849.1 -3.84593 1.51×10^-13 2.64×10^-12 AC007879.3 3.157692 1.8753739×10^-2 4.6603812×10^-2 AC007881.3 -2.01909 6.16×10^-7 4.6×10^-6 AC007906.2 -7.04153 1.63×10^-63 3.85×10^-61 AC007919.1 -3.78725 2.38×10^-13 4.09×10^-12 AC007919.2 -3.39599 2.68×10^-10 3.31×10^-9 AC007923.4 -2.97075 3.98×10^-7 3.06×10^-6 AC007938.2 2.77677 1.06×10^-5 6.23×10^-5 AC007938.3 2.641298 5×10^-6 3.14×10^-5 AC007953.2 6.962469 7.986023×10^-3 2.2597776×10^-2 AC007969.2 2.989799 1.56114×10^-4 7.08986×10^-4 AC007993.1 -3.18619 1.21×10^-14 2.33×10^-13 AC007993.2 -2.75756 6.27×10^-8 5.48×10^-7 AC008013.3 2.544322 5.162095×10^-3 1.5578452×10^-2 AC008033.3 -2.78088 9.51×10^-8 8.05×10^-7 AC008056.1 2.134005 1.9113321×10^-2 4.7345407×10^-2 AC008060.1 4.944455 6.387279×10^-3 1.8680925×10^-2 AC008060.4 5.78656 5.968412×10^-3 1.7628333×10^-2 AC008080.2 2.349709 1.2017539×10^-2 3.203601×10^-2 AC008105.2 -2.07826 8.37×10^-9 8.37×10^-8 AC008115.1 4.597 2.86294×10^-4 1.222592×10^-3 AC008115.2 3.196185 8.01309×10^-4 3.053383×10^-3 AC008268.1 3.696722 4.846393×10^-3 1.4766164×10^-2 AC008278.2 3.600756 2.48×10^-5 1.3499×10^-4 AC008392.1 2.986546 7.631857×10^-3 2.1733836×10^-2 AC008403.3 -2.50204 7.7×10^-9 7.76×10^-8 AC008415.1 2.14193 1.7477975×10^-2 4.3904212×10^-2 AC008432.1 3.75516 1.8961215×10^-2 4.7031833×10^-2 AC008448.1 4.981802 2.42761×10^-4 1.054844×10^-3 AC008464.1 4.35478 1.3047214×10^-2 3.4319981×10^-2 AC008539.1 4.508784 1.448011×10^-2 3.7410335×10^-2 AC008554.1 -5.05146 8.21×10^-32 5.28×10^-30 AC008555.3 3.855288 7.463121×10^-3 2.1342817×10^-2 AC008556.1 -2.58536 1.9×10^-10 2.39×10^-9 AC008588.1 2.860875 2.156055×10^-3 7.294968×10^-3 AC008591.1 3.99503 2.740058×10^-3 9.010997×10^-3 AC008592.3 -3.15256 6.16×10^-30 3.52×10^-28 AC008592.4 -3.82702 4.27×10^-18 1.12×10^-16 AC008649.1 3.930562 4.46278×10^-4 1.810891×10^-3 AC008649.2 -2.44333 9.93×10^-10 1.14×10^-8 AC008667.1 2.511317 1.51×10^-7 1.24×10^-6 AC008667.3 3.924527 2.67×10^-8 2.48×10^-7 AC008667.4 5.439898 3.5×10^-6 2.27×10^-5 AC008676.1 -3.24267 1.04×10^-33 7.56×10^-32 AC008738.1 -2.99087 1.86×10^-6 1.27×10^-5 AC008739.2 2.874794 1.72×10^-8 1.65×10^-7 AC008750.1 2.389907 7.9191×10^-4 3.021139×10^-3 AC008750.2 3.762549 1.8×10^-6 1.23×10^-5 AC008750.7 4.311419 1.32×10^-7 1.1×10^-6 AC008759.3 -2.04966 3.23499×10^-4 1.362681×10^-3 AC008760.1 -3.88194 6.74×10^-31 4.07×10^-29 AC008763.1 -2.2454 2.14×10^-7 1.73×10^-6 AC008781.1 -2.87236 1.11×10^-17 2.82×10^-16 AC008781.2 -2.18567 8.05×10^-9 8.09×10^-8 AC008870.3 2.184133 2.786662×10^-3 9.144834×10^-3 AC009005.1 2.710133 8.5×10^-6
Load more

Recommended publications
  • 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]
  • The Chondrocyte Channelome: a Novel Ion Channel Candidate in the Pathogenesis of Pectus Deformities
    Old Dominion University ODU Digital Commons Biological Sciences Theses & Dissertations Biological Sciences Summer 2017 The Chondrocyte Channelome: A Novel Ion Channel Candidate in the Pathogenesis of Pectus Deformities Anthony J. Asmar Old Dominion University, [email protected] Follow this and additional works at: https://digitalcommons.odu.edu/biology_etds Part of the Biology Commons, Molecular Biology Commons, and the Physiology Commons Recommended Citation Asmar, Anthony J.. "The Chondrocyte Channelome: A Novel Ion Channel Candidate in the Pathogenesis of Pectus Deformities" (2017). Doctor of Philosophy (PhD), Dissertation, Biological Sciences, Old Dominion University, DOI: 10.25777/pyha-7838 https://digitalcommons.odu.edu/biology_etds/19 This Dissertation is brought to you for free and open access by the Biological Sciences at ODU Digital Commons. It has been accepted for inclusion in Biological Sciences Theses & Dissertations by an authorized administrator of ODU Digital Commons. For more information, please contact [email protected]. THE CHONDROCYTE CHANNELOME: A NOVEL ION CHANNEL CANDIDATE IN THE PATHOGENESIS OF PECTUS DEFORMITIES by Anthony J. Asmar B.S. Biology May 2010, Virginia Polytechnic Institute M.S. Biology May 2013, Old Dominion University A Dissertation Submitted to the Faculty of Old Dominion University in Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY BIOMEDICAL SCIENCES OLD DOMINION UNIVERSITY August 2017 Approved by: Christopher Osgood (Co-Director) Michael Stacey (Co-Director) Lesley Greene (Member) Andrei Pakhomov (Member) Jing He (Member) ABSTRACT THE CHONDROCYTE CHANNELOME: A NOVEL ION CHANNEL CANDIDATE IN THE PATHOGENESIS OF PECTUS DEFORMITIES Anthony J. Asmar Old Dominion University, 2017 Co-Directors: Dr. Christopher Osgood Dr. Michael Stacey Costal cartilage is a type of rod-like hyaline cartilage connecting the ribs to the sternum.
    [Show full text]
  • Screening of 109 Neuropeptides on Asics Reveals No Direct Agonists
    www.nature.com/scientificreports OPEN Screening of 109 neuropeptides on ASICs reveals no direct agonists and dynorphin A, YFMRFamide and Received: 7 August 2018 Accepted: 14 November 2018 endomorphin-1 as modulators Published: xx xx xxxx Anna Vyvers, Axel Schmidt, Dominik Wiemuth & Stefan Gründer Acid-sensing ion channels (ASICs) belong to the DEG/ENaC gene family. While ASIC1a, ASIC1b and ASIC3 are activated by extracellular protons, ASIC4 and the closely related bile acid-sensitive ion channel (BASIC or ASIC5) are orphan receptors. Neuropeptides are important modulators of ASICs. Moreover, related DEG/ENaCs are directly activated by neuropeptides, rendering neuropeptides interesting ligands of ASICs. Here, we performed an unbiased screen of 109 short neuropeptides (<20 amino acids) on fve homomeric ASICs: ASIC1a, ASIC1b, ASIC3, ASIC4 and BASIC. This screen revealed no direct agonist of any ASIC but three modulators. First, dynorphin A as a modulator of ASIC1a, which increased currents of partially desensitized channels; second, YFMRFamide as a modulator of ASIC1b and ASIC3, which decreased currents of ASIC1b and slowed desensitization of ASIC1b and ASIC3; and, third, endomorphin-1 as a modulator of ASIC3, which also slowed desensitization. With the exception of YFMRFamide, which, however, is not a mammalian neuropeptide, we identifed no new modulator of ASICs. In summary, our screen confrmed some known peptide modulators of ASICs but identifed no new peptide ligands of ASICs, suggesting that most short peptides acting as ligands of ASICs are already known. Acid-sensing ion channels form a small family of proton-gated ion channels that belongs to the degenerin/epi- thelial Na+ channel (DEG/ENaC) gene family1.
    [Show full text]
  • 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
    [Show full text]
  • (P -Value<0.05, Fold Change≥1.4), 4 Vs. 0 Gy Irradiation
    Table S1: Significant differentially expressed genes (P -Value<0.05, Fold Change≥1.4), 4 vs. 0 Gy irradiation Genbank Fold Change P -Value Gene Symbol Description Accession Q9F8M7_CARHY (Q9F8M7) DTDP-glucose 4,6-dehydratase (Fragment), partial (9%) 6.70 0.017399678 THC2699065 [THC2719287] 5.53 0.003379195 BC013657 BC013657 Homo sapiens cDNA clone IMAGE:4152983, partial cds. [BC013657] 5.10 0.024641735 THC2750781 Ciliary dynein heavy chain 5 (Axonemal beta dynein heavy chain 5) (HL1). 4.07 0.04353262 DNAH5 [Source:Uniprot/SWISSPROT;Acc:Q8TE73] [ENST00000382416] 3.81 0.002855909 NM_145263 SPATA18 Homo sapiens spermatogenesis associated 18 homolog (rat) (SPATA18), mRNA [NM_145263] AA418814 zw01a02.s1 Soares_NhHMPu_S1 Homo sapiens cDNA clone IMAGE:767978 3', 3.69 0.03203913 AA418814 AA418814 mRNA sequence [AA418814] AL356953 leucine-rich repeat-containing G protein-coupled receptor 6 {Homo sapiens} (exp=0; 3.63 0.0277936 THC2705989 wgp=1; cg=0), partial (4%) [THC2752981] AA484677 ne64a07.s1 NCI_CGAP_Alv1 Homo sapiens cDNA clone IMAGE:909012, mRNA 3.63 0.027098073 AA484677 AA484677 sequence [AA484677] oe06h09.s1 NCI_CGAP_Ov2 Homo sapiens cDNA clone IMAGE:1385153, mRNA sequence 3.48 0.04468495 AA837799 AA837799 [AA837799] Homo sapiens hypothetical protein LOC340109, mRNA (cDNA clone IMAGE:5578073), partial 3.27 0.031178378 BC039509 LOC643401 cds. [BC039509] Homo sapiens Fas (TNF receptor superfamily, member 6) (FAS), transcript variant 1, mRNA 3.24 0.022156298 NM_000043 FAS [NM_000043] 3.20 0.021043295 A_32_P125056 BF803942 CM2-CI0135-021100-477-g08 CI0135 Homo sapiens cDNA, mRNA sequence 3.04 0.043389246 BF803942 BF803942 [BF803942] 3.03 0.002430239 NM_015920 RPS27L Homo sapiens ribosomal protein S27-like (RPS27L), mRNA [NM_015920] Homo sapiens tumor necrosis factor receptor superfamily, member 10c, decoy without an 2.98 0.021202829 NM_003841 TNFRSF10C intracellular domain (TNFRSF10C), mRNA [NM_003841] 2.97 0.03243901 AB002384 C6orf32 Homo sapiens mRNA for KIAA0386 gene, partial cds.
    [Show full text]
  • Insurance and Advance Pay Test Requisition
    Insurance and Advance Pay Test Requisition (2021) For Specimen Collection Service, Please Fax this Test Requisition to 1.610.271.6085 Client Services is available Monday through Friday from 8:30 AM to 9:00 PM EST at 1.800.394.4493, option 2 Patient Information Patient Name Patient ID# (if available) Date of Birth Sex designated at birth: 9 Male 9 Female Street address City, State, Zip Mobile phone #1 Other Phone #2 Patient email Language spoken if other than English Test and Specimen Information Consult test list for test code and name Test Code: Test Name: Test Code: Test Name: 9 Check if more than 2 tests are ordered. Additional tests should be checked off within the test list ICD-10 Codes (required for billing insurance): Clinical diagnosis: Age at Initial Presentation: Ancestral Background (check all that apply): 9 African 9 Asian: East 9 Asian: Southeast 9 Central/South American 9 Hispanic 9 Native American 9 Ashkenazi Jewish 9 Asian: Indian 9 Caribbean 9 European 9 Middle Eastern 9 Pacific Islander Other: Indications for genetic testing (please check one): 9 Diagnostic (symptomatic) 9 Predictive (asymptomatic) 9 Prenatal* 9 Carrier 9 Family testing/single site Relationship to Proband: If performed at Athena, provide relative’s accession # . If performed at another lab, a copy of the relative’s report is required. Please attach detailed medical records and family history information Specimen Type: Date sample obtained: __________ /__________ /__________ 9 Whole Blood 9 Serum 9 CSF 9 Muscle 9 CVS: Cultured 9 Amniotic Fluid: Cultured 9 Saliva (Not available for all tests) 9 DNA** - tissue source: Concentration ug/ml Was DNA extracted at a CLIA-certified laboratory or a laboratory meeting equivalent requirements (as determined by CAP and/or CMS)? 9 Yes 9 No 9 Other*: If not collected same day as shipped, how was sample stored? 9 Room temp 9 Refrigerated 9 Frozen (-20) 9 Frozen (-80) History of blood transfusion? 9 Yes 9 No Most recent transfusion: __________ /__________ /__________ *Please contact us at 1.800.394.4493, option 2 prior to sending specimens.
    [Show full text]
  • Liddle Syndrome
    Liddle syndrome Description Liddle syndrome is an inherited form of high blood pressure (hypertension). This condition is characterized by severe hypertension that begins unusually early in life, often in childhood, although some affected individuals are not diagnosed until adulthood. Some people with Liddle syndrome have no additional signs or symptoms, especially in childhood. Over time, however, untreated hypertension can lead to heart disease or stroke, which may be fatal. In addition to hypertension, affected individuals can have low levels of potassium in the blood (hypokalemia). Signs and symptoms of hypokalemia include muscle weakness or pain, fatigue, constipation, or heart palpitations. The shortage of potassium can also raise the pH of the blood, a condition known as metabolic alkalosis. Frequency Liddle syndrome is a rare condition, although its prevalence is unknown. The condition has been found in populations worldwide. Causes Liddle syndrome is caused by mutations in the SCNN1B or SCNN1G gene. Each of these genes provides instructions for making a piece (subunit) of a protein complex called the epithelial sodium channel (ENaC). These channels are found at the surface of certain cells called epithelial cells in many tissues of the body, including the kidneys, where the channels transport sodium into cells. In the kidney, ENaC channels open in response to signals that sodium levels in the blood are too low, which allows sodium to flow into cells. From the kidney cells, this sodium is returned to the bloodstream (a process called reabsorption) rather than being removed from the body in urine. Mutations in the SCNN1B or SCNN1G gene change the structure of the respective ENaC subunit.
    [Show full text]
  • Ion Channels
    UC Davis UC Davis Previously Published Works Title THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels. Permalink https://escholarship.org/uc/item/1442g5hg Journal British journal of pharmacology, 176 Suppl 1(S1) ISSN 0007-1188 Authors Alexander, Stephen PH Mathie, Alistair Peters, John A et al. Publication Date 2019-12-01 DOI 10.1111/bph.14749 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: Ion channels. British Journal of Pharmacology (2019) 176, S142–S228 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels Stephen PH Alexander1 , Alistair Mathie2 ,JohnAPeters3 , Emma L Veale2 , Jörg Striessnig4 , Eamonn Kelly5, Jane F Armstrong6 , Elena Faccenda6 ,SimonDHarding6 ,AdamJPawson6 , Joanna L Sharman6 , Christopher Southan6 , Jamie A Davies6 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 3Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 4Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, A-6020 Innsbruck, Austria 5School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 6Centre for Discovery Brain Science, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties.
    [Show full text]
  • Role of the Epithelial Sodium Channel in Salt-Sensitive Hypertension
    Acta Pharmacologica Sinica (2011) 32: 789–797 npg © 2011 CPS and SIMM All rights reserved 1671-4083/11 $32.00 www.nature.com/aps Review Role of the epithelial sodium channel in salt- sensitive hypertension Yan SUN1, Jia-ning ZHANG2, Dan ZHAO2, Qiu-shi WANG2, Yu-chun GU3, He-ping MA4, Zhi-ren ZHANG2, * 1Department of General Surgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China; 2Departments of Clini- cal Pharmacy and Cardiology, the 2nd Affiliated Hospital, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Harbin 150086, China; 3 Molecular Pharmacology, IMM, Peking University, Beijing 100871, China; 4Department of Physiology, Emory University, USA The epithelial sodium channel (ENaC) is a heteromeric channel composed of three similar but distinct subunits, α, β and γ. This chan- nel is an end-effector in the rennin-angiotensin-aldosterone system and resides in the apical plasma membrane of the renal cortical collecting ducts, where reabsorption of Na+ through ENaC is the final renal adjustment step for Na+ balance. Because of its regulation and function, the ENaC plays a critical role in modulating the homeostasis of Na+ and thus chronic blood pressure. The development of most forms of hypertension requires an increase in Na+ and water retention. The role of ENaC in developing high blood pressure is exemplified in the gain-of-function mutations in ENaC that cause Liddle’s syndrome, a severe but rare form of inheritable hypertension. The evidence obtained from studies using animal models and in human patients indicates that improper Na+ retention by the kidney elevates blood pressure and induces salt-sensitive hypertension.
    [Show full text]
  • Molecular Remodeling of Ion Channels, Exchangers and Pumps in Atrial and Ventricular Myocytes in Ischemic Cardiomyopathy Naomi Gronich National Institutes of Health
    Washington University School of Medicine Digital Commons@Becker Open Access Publications 2010 Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy Naomi Gronich National Institutes of Health Azad Kumar National Institutes of Health Yuwei Zhang National Institutes of Health Igor R. Efimov Washington University School of Medicine in St. Louis Nikolai M. Soldatov National Institutes of Health Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Gronich, Naomi; Kumar, Azad; Zhang, Yuwei; Efimov, Igor R.; and Soldatov, Nikolai M., ,"Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy." Channels.4,2. 101-107. (2010). https://digitalcommons.wustl.edu/open_access_pubs/2782 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. RESEarcH PAPER RESEarcH PaPER Channels 4:2, 101-107; March/April 2010; © 2010 Landes Bioscience Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy Naomi Gronich,1,‡,† Azad Kumar,1,§,† Yuwei Zhang,1,¥ Igor R. Efimov2 and Nikolai M. Soldatov1,* 1National Institute on Aging; National Institutes of Health; Baltimore, MD USA; 2Washington University in Saint Louis; St. Louis, MO USA Current addresses: ‡Internal Medicine and Department of Community Medicine and Epidemiology; Carmel Medical Center; Haifa, Israel; §Cell Biology and Gene Expression Unit; Laboratory of Neurogenetics; National Institute on Aging; National Institutes of Health; Bethesda, MD USA; ¥Surgery Branch; National Cancer Institute; National Institutes of Health; Bethesda, MD USA †These authors have contributed equally to this work.
    [Show full text]
  • Topography-Dependent Gene Expression and Function of Common Cell Archetypes in Large and Small Porcine Airways
    bioRxiv preprint doi: https://doi.org/10.1101/2021.03.16.435690; this version posted March 17, 2021. 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. Topography-dependent gene expression and function of common cell archetypes in large and small porcine airways Alejandro A. Pezzulo1,2,10*, Andrew L. Thurman1,10, Xiaopeng Li3, Raul Villacreses1, Wenjie Yu1, Steven E. Mather1, Guillermo S. Romano-Ibarra1, David K. Meyerholz4, David A. Stoltz1,2,5,6, Michael J. Welsh1,2,6,7,8, Ian M. Thornell1, Joseph Zabner1,2,9* Affiliations:: 1: Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA. 2: Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA. 3: Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University, Grand Rapids, MI. 4: Department of Pathology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 5: Department of Biomedical Engineering, University of Iowa, Iowa City, IA. 6: Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 7: Department of Neurology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 8: Howard Hughes Medical Institute, University of Iowa, Iowa City, IA Author List Footnotes: 9: Lead Contact 10: These authors contributed equally *Correspondence: [email protected], [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.16.435690; this version posted March 17, 2021.
    [Show full text]
  • A Variant of ASIC2 Mediates Sodium Retention in Nephrotic Syndrome
    A variant of ASIC2 mediates sodium retention in nephrotic syndrome Marc Fila, … , Gilles Crambert, Alain Doucet JCI Insight. 2021. https://doi.org/10.1172/jci.insight.148588. Research In-Press Preview Nephrology Graphical abstract Find the latest version: https://jci.me/148588/pdf 1 A variant of ASIC2 mediates sodium retention in nephrotic syndrome 1,2Marc Fila *, 1,2Ali Sassi*, 1,2Gaëlle Brideau, 1,2Lydie Cheval, 1,2 Luciana Morla, 1,2Pascal Houillier, 1,2Christine Walter, 1,2Michel Gennaoui, 1,2Laure Collignon L, 1,2Mathilde Keck, 1,2Gabrielle Planelles, 1,2Naziha Bakouh, 3Michel Peuchmaur, 4Georges Deschênes, 5Ignacio Anegon, 5Séverine Remy, 6Bruno Vogt, 1,2 Gilles Crambert#, 1,2Alain Doucet 1Centre de Recherche des Cordeliers, Sorbonne Universités, INSERM, Université de Paris, Laboratoire de Physiologie Rénale et Tubulopathies, F-75006, Paris, France 2CNRS, ERL8228, F-75006, Paris, France 3Cytology and Pathology DePartment, Robert Debré HosPital, F-75019, Paris, France 4Pediatric NePhrology DePartment, Robert Debré HosPital, F-75019, Paris, France 5INSERM UMR 1064, Centre de Recherches en TransPlantation et Immunologie (CRTI), Transgenic Rats ImmunoPhenomic facility, Nantes, France. 6DePartment of NePhrology and HyPertension, InselsPital, Bern University HosPital, CH- 3010, Bern, Switzerland Present address: Marc Fila, Pediatric NePhrology DePartment, HôPital Arnaud de Villeneuve Institut de Génomique Fonctionnelle UMR9023 CNRS U661 INSERM, MontPellier, France; Ali Sassi, DePartment of Cellular Physiology and Metabolism, University
    [Show full text]