DOCSLIB.ORG

No Cell Line Source 1 NCI-H28 ATCC 2 NCI-H2452 ATCC 3 NCI-H2052

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
No Cell Line Source 1 NCI-H28 ATCC 2 NCI-H2452 ATCC 3 NCI-H2052 SUPPLEMENTARY TABLE S1. List of 19 MM cell lines used in this study. No Cell line Source 1 NCI-H28 ATCC 2 NCI-H2452 ATCC 3 NCI-H2052 ATCC 4 MSTO-211H ATCC 5 ACC-MESO-1 RBCCB 6 ACC-MESO-4 RBCCB 7 HMMME RBCCB 8 ONE58 ECACC 9 NO36 ECACC 10 LO68 ECACC 11 Mero-14 ECACC 12 Mero-25 ECACC 13 Mero-41 ECACC 14 Mero-48a ECACC 15 Mero-82 ECACC 16 Mero-83 ECACC 17 Mero-84 ECACC 18 Mero-95 ECACC 19 NCI-H226 ATCC Abbreviations: ATCC, American Type Culture Collection (Manassas,VA); RBCCB, RIKEN BioResource Center Cell Bank (Tsukuba, Japan); ECACC, European Collection of Cell Cultures (Salisbury, UK). SUPPLEMENTARY TABLE S2. Clinicopathological characteristics of 23 MM cases subjected to targeted exon sequ Asbestos Pathological Sample Tumor / normal Gender Age Smoking Surgery exposure type CT-1T Tumor and normal F 40 no yes B panpleuropneumonectomy CT-2T Tumor and normal M 51 yes no E panpleuropneumonectomy CT-3T Tumor and normal M 50 yes no B panpleuropneumonectomy CT-4T Tumor and normal M 56 yes no E panpleuropneumonectomy CT-5T Tumor and normal M 67 yes no E panpleuropneumonectomy CT-6T Tumor and normal M 60 yes yes B panpleuropneumonectomy CT-7T Tumor and normal M 48 yes no E panpleuropneumonectomy CT-9T Tumor and normal M 46 no no B panpleuropneumonectomy CT-10T Tumor and normal M 54 yes yes E panpleuropneumonectomy CT-11T Tumor and normal M 61 yes yes B panpleuropneumonectomy CT-12T Tumor and normal M 50 yes no E panpleuropneumonectomy CT-13T Tumor and normal F 56 no no E panpleuropneumonectomy CT-14T Tumor and normal M 62 yes yes E panpleuropneumonectomy CT-15T Tumor and normal M 66 no yes B panpleuropneumonectomy CT-18T Tumor and normal M 61 yes unknown S panpleuropneumonectomy CT-19T Tumor and normal M 68 yes yes B panpleuropneumonectomy CT-20T Tumor and normal M 60 yes unknown E panpleuropneumonectomy CT-21T Tumor and normal M 71 yes yes S panpleuropneumonectomy CT-22T Tumor and normal M 58 yes no E panpleuropneumonectomy CT-23T Tumor and normal F 52 yes unknown E panpleuropneumonectomy CT-24T Tumor and normal M 65 yes yes B panpleuropneumonectomy CT-33T Tumor and normal M 55 yes yes B panpleuropneumonectomy CT-46T Tumor and normal M 41 yes unknown B panpleuropneumonectomy Abbreviations: B, Biphasic; E, Epithelial; S, Sarcomatous; F, Female; M, Male. SUPPLEMENTARY TABLE S3. Hippo pathway genes sequenced in this study. Gene symbol Target HGNC ID Function Location LATS1 exon + intron HGNC:6514 LATS, large tumor suppressor, homolog 1 (Drosophila) 6q25.1 LATS2 exon + intron HGNC:6515 LATS, large tumor suppressor, homolog 2 (Drosophila) 13q11-q12 FAT4 exon HGNC:23109 FAT tumor suppressor homolog 4 (Drosophila) 4q28.1 CRB1 exon HGNC:2343 crumbs homolog 1 (Drosophila) 1q31-q32.1 CRB2 exon HGNC:18688 crumbs homolog 2 (Drosophila) 9q33.2 CRB3 exon HGNC:20237 crumbs homolog 3 (Drosophila) 19p13.3 NF2 exon HGNC:7773 neurofibromin 2 (merlin) 22q12.2 FRMD1 exon HGNC:21240 FERM domain containing 1 6q27 RASSF2 exon HGNC:9883 Ras association (RalGDS/AF-6) domain family member 2 20p13 RASSF3 exon HGNC:14271 Ras association (RalGDS/AF-6) domain family member 3 12q14.2 RASSF4 exon HGNC:20793 Ras association (RalGDS/AF-6) domain family member 4 10q11.1 RASSF5 exon HGNC:17609 Ras association (RalGDS/AF-6) domain family member 5 1q31 RASSF6 exon HGNC:20796 Ras association (RalGDS/AF-6) domain family member 6 4q21.1 KIBRA exon HGNC:29435 WW and C2 domain containing 1 5q34 MST2 exon HGNC:11406 serine/threonine kinase 3 8q22.2 MST3 exon HGNC:11403 serine/threonine kinase 24 13q31.2-q32.3 MST4 exon Gene ID: 51765 Serine/threonine protein kinase MST4 Xq26.2 MOB3C exon HGNC:29800 MOB kinase activator 3C 1p34.1 MOB4 exon HGNC:17261 MOB family member 4, phocein 2q33.1 MOB1B exon HGNC:29801 MOB kinase activator 1B 4q13.3 MOB2 exon HGNC:24904 MOB kinase activator 2 11p15.5 MOB3A exon HGNC:29802 MOB kinase activator 3A 19p13.3 MOB3B exon HGNC:23825 MOB kinase activator 3B 9p21.1 FRMD6 exon HGNC:19839 FERM domain containing 6 14q22.1 RASSF1A exon HGNC:9882 Ras association (RalGDS/AF-6) domain family member 1 3p21.3 SAV1 exon HGNC:17795 salvador homolog 1 (Drosophila) 14q13-q23 MST1 exon HGNC:7380 macrophage stimulating 1 (hepatocyte growth factor-like) 3p21 MOB1A exon HGNC:16015 MOB kinase activator 1A 2p13.1 TAZ exon HGNC:11577 tafazzin Xq28 YWHAB exon HGNC:12849 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide 20q13.1 YWHAE exon HGNC:12851 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, epsilon polypeptide 17p13.3 YWHAG exon HGNC:12852 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide 7q11.23 YWHAH exon HGNC:12853 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, eta polypeptide 22q12.1-q13.1 YWHAQ exon HGNC:12854 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, theta polypeptide 2p25.2-p25.1 YWHAZ exon HGNC:12855 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide 8q22.3 YWHAS exon HGNC:10773 stratifin 1p36.11 TEAD1 exon HGNC:11714 TEA domain family member 1 (SV40 transcriptional enhancer factor) 11p15.4 TEAD2 exon HGNC:11715 TEA domain family member 2 19q13.3 TEAD3 exon HGNC:11716 TEA domain family member 3 6p21.2 TEAD4 exon HGNC:11717 TEA domain family member 4 12p13.3-p13.2 SUPPLEMENTARY TABLE S4. Whole-exon sequencing of 6 MM cell lines. No. Gene symbol Chr RefSeqb cDNA Amino acid Type 211H H2452 H28 MESO4 H2052 MESO1 1 EI24 11 NM_001007277 c.732_733insC p.R244fs frameshift insertion ○ ○ ○ ○ ○ ○ 2 KRTAP4-8 17 NM_031960 c.C204A p.S68R nonsynonymous SNV - - ○ - - ○ KRTAP4-8 17 NM_031960 c.2_3insA p.M1fs frameshift insertion ○ ○ ○ ○ ○ ○ 3 PRIM2 6 NM_000947 c.889_890insA p.E297fs frameshift insertion ○ ○ ○ ○ ○ ○ PRIM2 6 NM_000947 c.C916T p.R306X stopgain SNV - ○ - - - - 4 PRSS1 7 NM_002769 c.A508G p.K170E nonsynonymous SNV ○ ○ - - ○ ○ PRSS1 7 NM_002769 c.G512A p.C171Y nonsynonymous SNV ○ - - ○ - - PRSS1 7 NM_002769 c.G542A p.S181N nonsynonymous SNV ○ ○ ○ ○ ○ ○ 5 PRSS2 7 NM_002770 c.C10T p.P4S nonsynonymous SNV - - ○ ○ - - PRSS2 7 NM_002770 c.C47T p.T16I nonsynonymous SNV ○ ○ ○ ○ ○ ○ PRSS2 7 NM_002770 c.C95A p.S32Y nonsynonymous SNV ○ ○ ○ ○ ○ ○ 6 PRSS3 9 NM_001197098 c.284_285del p.95_95del frameshift deletion ○ - ○ - - - PRSS3 9 NM_001197098 c.A493G p.K165E nonsynonymous SNV - ○ - - - - PRSS3 9 NM_001197098 c.G524A p.S175N nonsynonymous SNV ○ ○ ○ ○ ○ ○ PRSS3 9 NM_001197098 c.639delT p.C213fs frameshift deletion - - ○ - - - 7 ZNF595 4 NM_182524 c.600_601insA p.Y200fs frameshift insertion ○ ○ ○ ○ ○ ○ 8 DDHD1 14 NM_001160148 c.337_338insGGCGGC p.S113delinsGGS nonframeshift insertion ○ ○ - ○ ○ ○ 9 KRT10 17 NM_000421 c.1637_1638del p.546_546del frameshift deletion - - ○ - - - KRT10 17 NM_000421 c.1468_1479del p.490_493del nonframeshift deletion ○ - - ○ ○ ○ KRT10 17 NM_000421 c.1473_1477del p.491_493del frameshift deletion - - ○ - - - 10 MLL3 7 NM_170606 c.A11405G p.D3802G nonsynonymous SNV - - - - ○ - MLL3 7 NM_170606 c.2448_2449insA p.Y816_I817delinsX stopgain SNV ○ ○ ○ - - ○ 11 OR1B1 9 NM_001004450 c.45_46insT p.L15fs frameshift insertion ○ ○ ○ ○ ○ - 12 ZAN 7 NM_173059 c.3290_3292del p.1097_1098del nonframeshift deletion - ○ - - ○ - ZAN 7 NM_003386 c.5767_5768insG p.F1923fs frameshift insertion ○ ○ - ○ - ○ 13 ALMS1 2 NM_015120 c.1570_1571insCTC p.S524delinsSP nonframeshift insertion ○ ○ - - ○ ○ 14 FZD1 7 NM_003505 c.264_265insCCG p.Q88delinsQP nonframeshift insertion ○ - ○ - ○ ○ 15 HOXD9 2 NM_014213 c.794_795insGCA p.P265delinsPQ nonframeshift insertion ○ ○ ○ ○ - - 16 KDM6B 17 NM_001080424 c.752_753insACCACC p.L251delinsLPP nonframeshift insertion - ○ - - ○ - KDM6B 17 NM_001080424 c.753_755del p.251_252del nonframeshift deletion - - - ○ - - KDM6B 17 NM_001080424 c.C1881G p.S627R nonsynonymous SNV - - ○ - - - 17 SLC9B1 4 NM_139173 c.1338_1339del p.446_447del frameshift deletion - - ○ ○ ○ ○ 18 AHNAK 11 NM_001620 c.C8897T p.P2966L nonsynonymous SNV ○ - - - - - AHNAK 11 NM_001620 c.C7225T p.P2409S nonsynonymous SNV - - - - ○ - AHNAK 11 NM_001620 c.C5565G p.I1855M nonsynonymous SNV - - - - - ○ 19 C15orf40 15 NM_001160113 c.396_397insT p.L132fs frameshift insertion ○ ○ - - - - C15orf40 15 NM_001160113 c.395delT p.L132X stopgain SNV - - - - - ○ 20 CDC27 17 NM_001114091 c.C818G p.A273G nonsynonymous SNV ○ - - ○ ○ - 21 COL6A6 3 NM_001102608 c.T3410C p.I1137T nonsynonymous SNV ○ - - - - - COL6A6 3 NM_001102608 c.C3883T p.R1295X stopgain SNV - - - - ○ - COL6A6 3 NM_001102608 c.T5542C p.F1848L nonsynonymous SNV - - ○ - - - 22 LOC388946 2 NM_001145051 c.462delG p.E154fs frameshift deletion ○ - - - ○ ○ 23 MAGEF1 3 NM_022149 c.477_478insGGA p.D159delinsED nonframeshift insertion ○ ○ ○ - - - 24 MCC 5 NM_001085377 c.64_65insGGC p.S22delinsGS nonframeshift insertion - ○ - ○ - ○ 25 MEGF9 9 NM_001080497 c.89_94del p.30_32del nonframeshift deletion - ○ ○ ○ - - 26 NBPF9 1 NM_001037675 c.116_117insAG p.K39fs frameshift insertion ○ ○ - ○ - - 27 NUDT11 X NM_018159 frameshift deletion ○ - - ○ - ○ 28 OVGP1 1 NM_002557 c.1560_1561insA p.G520fs frameshift insertion ○ - - - ○ ○ 29 RBMX X NM_002139 c.906_907insCC p.P302fs frameshift insertion ○ - - - ○ - RBMX X NM_002139 c.316_317insTT p.P106fs frameshift insertion ○ - ○ - ○ - 30 TDG 12 NM_003211 c.286_287insA p.E96fs frameshift insertion - ○ ○ ○ - - 31 ZFHX3 16 NM_001164766 c.2482_2483insCAA p.A828delinsQA nonframeshift insertion - - ○ - - - ZFHX3 16 NM_001164766 c.2476_2481del p.826_827del nonframeshift deletion - - - - - ○ ZFHX3 16 NM_006885 c.C1114G p.R372G nonsynonymous SNV - - - ○ - - 32 ABCA7 19 NM_019112 c.1180_1190del p.394_397del frameshift deletion
Load more

Recommended publications
  • Lats1/2 Regulate Yap/Taz to Control Nephron Progenitor Epithelialization and Inhibit Myofibroblast Formation
    BASIC RESEARCH www.jasn.org Lats1/2 Regulate Yap/Taz to Control Nephron Progenitor Epithelialization and Inhibit Myofibroblast Formation † † Helen McNeill* and Antoine Reginensi *Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada; and †Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada ABSTRACT In the kidney, formation of the functional filtration units, the nephrons, is essential for postnatal life. During development, mesenchymal progenitors tightly regulate the balance between self-renewal and differentia- tion to give rise to all nephron epithelia. Here, we investigated the functions of the Hippo pathway serine/ threonine-protein kinases Lats1 and Lats2, which phosphorylate and inhibit the transcriptional coactivators Yap and Taz, in nephron progenitor cells. Genetic deletion of Lats1 and Lats2 in nephron progenitors of mice led to disruption of nephrogenesis, with an accumulation of spindle-shaped cells in both cortical and medullary regions of the kidney. Lineage-tracing experiments revealed that the cells that accumulated in the interstitium derived from nephron progenitor cells and expressed E-cadherin as well as vimentin, a myofibroblastic marker not usually detected after mesenchymal-to-epithelial transition. The accumulation of these interstitial cells associated with collagen deposition and ectopic expression of the myofibroblastic markers vimentin and a-smooth-muscle actin in developing kidneys. Although these myofibroblastic cells had high Yap and Taz accumulation in the nucleus concomitant with a loss of phosphorylated Yap, reduction of Yap and/or Taz expression levels completely rescued the Lats1/2 phenotype. Taken together, our results demonstrate that Lats1/2 kinases restrict Yap/Taz activities to promote nephron progenitor cell differentiation in the mamma- lian kidney.
    [Show full text]
  • T2 and T17 Cytokines Alter the Cargo and Function of Airway Epithelium
    Ax et al. Respiratory Research (2020) 21:155 https://doi.org/10.1186/s12931-020-01402-3 RESEARCH Open Access T2 and T17 cytokines alter the cargo and function of airway epithelium-derived extracellular vesicles Elisabeth Ax1,2 , Zala Jevnikar2, Aleksander Cvjetkovic1 , Carina Malmhäll1 , Henric Olsson2, Madeleine Rådinger1*† and Cecilia Lässer1*† Abstract Background: Asthma is a common and heterogeneous disease that includes subgroups characterized by type 2 (T2) or type 17 (T17) immune responses for which there is a need to identify the underlying mechanisms and biomarkers in order to develop specific therapies. These subgroups can be defined by airway epithelium gene signatures and the airway epithelium has also been implicated to play a significant role in asthma pathology. Extracellular vesicles (EVs) carry functional biomolecules and participate in cell-to-cell communication in both health and disease, properties that are likely to be involved in airway diseases such as asthma. The aim of this study was to identify stimulus-specific proteins and functionality of bronchial epithelium-derived EVs following stimulation with T2 or T17 cytokines. Methods: EVs from cytokine-stimulated (T2: IL-4 + IL-13 or T17: IL-17A + TNFα) human bronchial epithelial cells cultured at air-liquid interface (HBEC-ALI) were isolated by density cushion centrifugation and size exclusion chromatography and characterized with Western blotting and electron microscopy. Transcriptomic (cells) and proteomic (EVs) profiling was also performed. Results: Our data shows that EVs are secreted and can be isolated from the apical side of HBEC-ALI and that cytokine stimulation increases EV release. Genes upregulated in cells stimulated with T2 or T17 cytokines were increased also on protein level in the EVs.
    [Show full text]
  • Viewed Under 23 (B) Or 203 (C) fi M M Male Cko Mice, and Largely Unaffected Magni Cation; Scale Bars, 500 M (B) and 50 M (C)
    BRIEF COMMUNICATION www.jasn.org Renal Fanconi Syndrome and Hypophosphatemic Rickets in the Absence of Xenotropic and Polytropic Retroviral Receptor in the Nephron Camille Ansermet,* Matthias B. Moor,* Gabriel Centeno,* Muriel Auberson,* † † ‡ Dorothy Zhang Hu, Roland Baron, Svetlana Nikolaeva,* Barbara Haenzi,* | Natalya Katanaeva,* Ivan Gautschi,* Vladimir Katanaev,*§ Samuel Rotman, Robert Koesters,¶ †† Laurent Schild,* Sylvain Pradervand,** Olivier Bonny,* and Dmitri Firsov* BRIEF COMMUNICATION *Department of Pharmacology and Toxicology and **Genomic Technologies Facility, University of Lausanne, Lausanne, Switzerland; †Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts; ‡Institute of Evolutionary Physiology and Biochemistry, St. Petersburg, Russia; §School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia; |Services of Pathology and ††Nephrology, Department of Medicine, University Hospital of Lausanne, Lausanne, Switzerland; and ¶Université Pierre et Marie Curie, Paris, France ABSTRACT Tight control of extracellular and intracellular inorganic phosphate (Pi) levels is crit- leaves.4 Most recently, Legati et al. have ical to most biochemical and physiologic processes. Urinary Pi is freely filtered at the shown an association between genetic kidney glomerulus and is reabsorbed in the renal tubule by the action of the apical polymorphisms in Xpr1 and primary fa- sodium-dependent phosphate transporters, NaPi-IIa/NaPi-IIc/Pit2. However, the milial brain calcification disorder.5 How- molecular identity of the protein(s) participating in the basolateral Pi efflux remains ever, the role of XPR1 in the maintenance unknown. Evidence has suggested that xenotropic and polytropic retroviral recep- of Pi homeostasis remains unknown. Here, tor 1 (XPR1) might be involved in this process. Here, we show that conditional in- we addressed this issue in mice deficient for activation of Xpr1 in the renal tubule in mice resulted in impaired renal Pi Xpr1 in the nephron.
    [Show full text]
  • Ubiquitination‑Deubiquitination in the Hippo Signaling Pathway (Review)
    ONCOLOGY REPORTS 41: 1455-1475, 2019 Ubiquitination‑deubiquitination in the Hippo signaling pathway (Review) YANTING LIU and JUN DENG Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China Received April 3, 2018; Accepted September 17, 2018 DOI: 10.3892/or.2019.6956 Abstract. The Hippo signaling pathway is considered to be Ubiquitin modifications are involved in regulating various a tissue growth regulator and tumor suppressor pathway that physiological processes and are counteracted by deubiquiti- controls cell proliferation, differentiation, survival, regen- nation. Imbalanced ubiquitination-deubiquitination is closely eration and tissue homeostasis. Defects in Hippo kinases associated with tumor initiation and progression. Therefore, and hyperactivation of transcriptional co-activator with the examination of the specific association between the Hippo PDZ-binding motif and Yes-associated protein (YAP) may pathway and ubiquitination is of interest. The present study contribute to the development of different types of cancer. reviews the modulatory mechanism of ubiquitination-deubiq- The Hippo pathway is regulated in a variety of way, of which uitination in the Hippo signaling pathway, the recent progress ubiquitination is of considerable importance. Ubiquitination is in identifying therapeutic targets and strategies, and the future a crucial post‑translational protein modification in cancer cells directions in the field that may contribute to better tumor and is an applicable target for pharmacological intervention. diagnosis and treatment. Contents Correspondence to: Dr Jun Deng, Department of Oncology, The First Affiliated Hospital of Nanchang University, 17 Yong Wai 1. Introduction Zheng Street, Nanchang, Jiangxi 330006, P.R. China 2. Overview of the Hippo pathway E-mail: [email protected] 3.
    [Show full text]
  • Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
    Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen,
    [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]
  • NICU Gene List Generator.Xlsx
    Neonatal Crisis Sequencing Panel Gene List Genes: A2ML1 - B3GLCT A2ML1 ADAMTS9 ALG1 ARHGEF15 AAAS ADAMTSL2 ALG11 ARHGEF9 AARS1 ADAR ALG12 ARID1A AARS2 ADARB1 ALG13 ARID1B ABAT ADCY6 ALG14 ARID2 ABCA12 ADD3 ALG2 ARL13B ABCA3 ADGRG1 ALG3 ARL6 ABCA4 ADGRV1 ALG6 ARMC9 ABCB11 ADK ALG8 ARPC1B ABCB4 ADNP ALG9 ARSA ABCC6 ADPRS ALK ARSL ABCC8 ADSL ALMS1 ARX ABCC9 AEBP1 ALOX12B ASAH1 ABCD1 AFF3 ALOXE3 ASCC1 ABCD3 AFF4 ALPK3 ASH1L ABCD4 AFG3L2 ALPL ASL ABHD5 AGA ALS2 ASNS ACAD8 AGK ALX3 ASPA ACAD9 AGL ALX4 ASPM ACADM AGPS AMELX ASS1 ACADS AGRN AMER1 ASXL1 ACADSB AGT AMH ASXL3 ACADVL AGTPBP1 AMHR2 ATAD1 ACAN AGTR1 AMN ATL1 ACAT1 AGXT AMPD2 ATM ACE AHCY AMT ATP1A1 ACO2 AHDC1 ANK1 ATP1A2 ACOX1 AHI1 ANK2 ATP1A3 ACP5 AIFM1 ANKH ATP2A1 ACSF3 AIMP1 ANKLE2 ATP5F1A ACTA1 AIMP2 ANKRD11 ATP5F1D ACTA2 AIRE ANKRD26 ATP5F1E ACTB AKAP9 ANTXR2 ATP6V0A2 ACTC1 AKR1D1 AP1S2 ATP6V1B1 ACTG1 AKT2 AP2S1 ATP7A ACTG2 AKT3 AP3B1 ATP8A2 ACTL6B ALAS2 AP3B2 ATP8B1 ACTN1 ALB AP4B1 ATPAF2 ACTN2 ALDH18A1 AP4M1 ATR ACTN4 ALDH1A3 AP4S1 ATRX ACVR1 ALDH3A2 APC AUH ACVRL1 ALDH4A1 APTX AVPR2 ACY1 ALDH5A1 AR B3GALNT2 ADA ALDH6A1 ARFGEF2 B3GALT6 ADAMTS13 ALDH7A1 ARG1 B3GAT3 ADAMTS2 ALDOB ARHGAP31 B3GLCT Updated: 03/15/2021; v.3.6 1 Neonatal Crisis Sequencing Panel Gene List Genes: B4GALT1 - COL11A2 B4GALT1 C1QBP CD3G CHKB B4GALT7 C3 CD40LG CHMP1A B4GAT1 CA2 CD59 CHRNA1 B9D1 CA5A CD70 CHRNB1 B9D2 CACNA1A CD96 CHRND BAAT CACNA1C CDAN1 CHRNE BBIP1 CACNA1D CDC42 CHRNG BBS1 CACNA1E CDH1 CHST14 BBS10 CACNA1F CDH2 CHST3 BBS12 CACNA1G CDK10 CHUK BBS2 CACNA2D2 CDK13 CILK1 BBS4 CACNB2 CDK5RAP2
    [Show full text]
  • Inferring the Progression of Multifocal Liver Cancer from Spatial and Temporal Genomic Heterogeneity
    Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Shi, J., Q. Xing, M. Duan, Z. Wang, L. Yang, Y. Zhao, X. Wang, et al. 2016. “Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity.” Oncotarget 7 (3): 2867-2877. doi:10.18632/oncotarget.6558. http:// dx.doi.org/10.18632/oncotarget.6558. Published Version doi:10.18632/oncotarget.6558 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27320297 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA www.impactjournals.com/oncotarget/ Oncotarget, Vol. 7, No. 3 Inferring the progression of multifocal liver cancer from spatial and temporal genomic heterogeneity Jie-Yi Shi1,†, Qingfeng Xing2,†, Meng Duan1,†, Zhi-Chao Wang1,†, Liu-Xiao Yang1, Ying-Jun Zhao3, Xiao-Ying Wang1, Yun Liu2, Minghua Deng2, Zhen-Bin Ding1, Ai-Wu Ke1, Jian Zhou1,4, Jia Fan1,4, Ya Cao5, Jiping Wang6, Ruibin Xi2, Qiang Gao1 1 Liver Cancer Institute, Zhongshan Hospital, and Key Laboratory of Carcinogenesis and Cancer Invasion (Ministry of Education), Fudan University, Shanghai, P. R. China 2School of Mathematical Sciences and Center for Statistical Science, Peking University, Beijing, P. R. China 3 Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shangai, P.
    [Show full text]
  • Essential Oil from Pinus Koraiensis Pinecones Inhibits Gastric Cancer Cells Via the HIPPO/YAP Signaling Pathway
    molecules Article Essential Oil from Pinus Koraiensis Pinecones Inhibits Gastric Cancer Cells via the HIPPO/YAP Signaling Pathway Yandong Zhang 1, Chao Xin 1, Junqiang Qiu 2 and Zhenyu Wang 1,* 1 Department of Food Science and Engineering, School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin 150090, China; [email protected] (Y.Z.); [email protected] (C.X.) 2 Department of Inorganic Chemistry and Analytical Chemistry, School of Pharmacy, Hainan Medical University, Haikou 570100, China; [email protected] * Correspondence: [email protected] Received: 17 September 2019; Accepted: 22 October 2019; Published: 25 October 2019 Abstract: Pinecone is a traditional folk herb, which has been used in China for many years. In this paper, the essential oil from Pinus koraiensis pinecones (PEO) was obtained by hydrodistillation and 41 compounds were identified by gas chromatography–mass spectrometry (GC-MS), mainly including α-Pinene (40.91%), Limonene (24.82%), and β-Pinene (7.04%). The purpose of this study was to investigate the anti-tumor activity of PEO on MGC-803 cells and its mechanism. Anti-tumor experiments in vitro showed PEO could significantly inhibit the proliferation and migration of MGC-803 cells, and it also could arrest the cell cycle in the G2/M phase, decrease the mitochondrial membrane potential, and induce apoptosis. Finally, the effects of PEO on genes expression on MGC-803 cells were analyzed by RNA sequencing, and results showed that after treatment with PEO, 100 genes were up-regulated, and 57 genes were down-regulated. According to the KEGG pathway and GSEA, FAT4, STK3, LATS2, YAP1, and AJUBA were down-regulated, which were related to HIPPO signaling pathway.
    [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]
  • Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
    Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A.
    [Show full text]
  • This Thesis Has Been Submitted in Fulfilment of the Requirements for a Postgraduate Degree (E.G
    This thesis has been submitted in fulfilment of the requirements for a postgraduate degree (e.g. PhD, MPhil, DClinPsychol) at the University of Edinburgh. Please note the following terms and conditions of use: This work is protected by copyright and other intellectual property rights, which are retained by the thesis author, unless otherwise stated. A copy can be downloaded for personal non-commercial research or study, without prior permission or charge. This thesis cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author. The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author. When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given. The CX3CR1/CX3CL1 Axis Drives the Migration and Maturation of Oligodendroglia in the Central Nervous System Catriona Ford Thesis Submitted for the Degree of Doctor of Philosophy The University of Edinburgh 2017 Abstract In the central nervous system, the axons of neurons are protected from damage and aided in electrical conductivity by the myelin sheath, a complex of proteins and lipids formed by oligodendrocytes. Loss or damage to the myelin sheath may result in impairment of electrical axonal conduction and eventually to neuronal death. Such demyelination is responsible, at least in part, for the disabling neurodegeneration observed in pathologies such as Multiple Sclerosis (MS) and Spinal Cord Injury. In the regenerative process of remyelination, oligodendrocyte precursor cells (OPCs), the resident glial stem cell population of the adult CNS, migrate toward the injury site, proliferate and differentiate into adult oligodendrocytes which subsequently reform the myelin sheath.
    [Show full text]