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Supplementary Table S4. FGA Co-Expressed Gene List in LUAD

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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 2 BMP6 0.405 6p24-p23 bone morphogenetic protein 6 TTC39C 0.402 18q11.2 tetratricopeptide repeat domain 39C CATSPERB 0.401 14q32.12 catsper channel auxiliary subunit beta XBP1 0.401 22q12.1|22q12X-box binding protein 1 PIM3 0.398 22q13 Pim-3 proto-oncogene, serine/threonine kinase ID1 0.396 20q11 inhibitor of DNA binding 1, dominant negative helix-loop-helix protein AKR1C2 0.396 10p15-p14 aldo-keto reductase family 1, member C2 ATP2A2 0.395 12q24.11 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 EPAS1 0.395 2p21-p16 endothelial PAS domain protein 1 C2CD4D 0.393 1q21.3 C2 calcium-dependent domain containing 4D SHTN1 0.391 10q25.3 shootin 1 GK 0.391 Xp21.3 glycerol kinase PDIA3P1 0.385 1q21.1 protein disulfide isomerase family A, member 3 pseudogene 1 CHMP1B 0.385 18p11.21 charged multivesicular body protein 1B PCSK9 0.384 1p32.3 proprotein convertase subtilisin/kexin type 9 PDIA3 0.384 15q15 protein disulfide isomerase family A, member 3 DACT2 0.381 6q27 dishevelled-binding antagonist of beta-catenin 2 HSP90B1 0.38 12q24.2-q24.3heat shock protein 90kDa beta (Grp94), member 1 PRR26 0.379 10p15.3 proline rich 26 MISP 0.378 19p13.3 mitotic spindle positioning KSR1 0.375 17q11.2 kinase suppressor of ras 1 TC2N 0.375 14q32.12 tandem C2 domains, nuclear CPE 0.374 4q32.3 carboxypeptidase E SCARB1 0.372 12q24.31 scavenger receptor class B, member 1 SPINK1 0.372 5q32 serine peptidase inhibitor, Kazal type 1 LGSN 0.371 6pter-q22.33lengsin, lens protein with glutamine synthetase domain FRAT2 0.37 10q24.1 frequently rearranged in advanced T-cell lymphomas 2 GK3P 0.369 4q32.1 glycerol kinase 3 pseudogene AKR1C1 0.369 10p15-p14 aldo-keto reductase family 1, member C1 MSMB 0.367 10q11.2 microseminoprotein, beta- FAAH2 0.366 Xp11.21 fatty acid amide hydrolase 2 SEMA4G 0.366 10q24.31 sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4G HHIPL2 0.364 1q41 HHIP-like 2 LINC00319 0.363 21q22.3 long intergenic non-protein coding RNA 319 PPP1R3B 0.363 8p23.1 protein phosphatase 1, regulatory subunit 3B SLC7A11 0.361 4q28.3 solute carrier family 7 (anionic amino acid transporter light chain, xc- system), member 11 NR4A1 0.361 12q13 nuclear receptor subfamily 4, group A, member 1 MAP2K6 0.359 17q24.3 mitogen-activated protein kinase kinase 6 BASP1 0.358 5p15.1 brain abundant, membrane attached signal protein 1 CARD14 0.357 17q25 caspase recruitment domain family, member 14 ITIH2 0.357 10p15 inter-alpha-trypsin inhibitor heavy chain 2 GABARAPL10.355 12p13.2 GABA(A) receptor-associated protein like 1 MAPK4 0.355 18q21.1 mitogen-activated protein kinase 4 MTMR7 0.355 8p22 myotubularin related protein 7 RASD1 0.353 17p11.2 RAS, dexamethasone-induced 1 PLEKHG2 0.352 19q13.2 pleckstrin homology domain containing, family G (with RhoGef domain) member 2 PITPNC1 0.352 17q24.2 phosphatidylinositol transfer protein, cytoplasmic 1 CLPX 0.352 15q22.31 caseinolytic mitochondrial matrix peptidase chaperone subunit HNF1A 0.351 12q24.2 HNF1 homeobox A FXR2 0.35 17p13.1 fragile X mental retardation, autosomal homolog 2 BHLHA15 0.349 7q21.3 basic helix-loop-helix family, member a15 CHML 0.349 1q43 choroideremia-like (Rab escort protein 2) PDE3B 0.348 11p15.1 phosphodiesterase 3B, cGMP-inhibited CABYR 0.348 18q11.2 calcium binding tyrosine-(Y)-phosphorylation regulated TRIM31 0.348 6p21.3 tripartite motif containing 31 AVPI1 0.347 10q24.2 arginine vasopressin-induced 1 RFK 0.347 9q21.13 riboflavin kinase TMEM254 0.347 10q22.3 transmembrane protein 254 NNMT 0.345 11q23.1 nicotinamide N-methyltransferase NARS 0.344 18q21.31 asparaginyl-tRNA synthetase KCTD3 0.343 1q41 potassium channel tetramerization domain containing 3 RDH10 0.343 8q21.11 retinol dehydrogenase 10 (all-trans) CSGALNACT10.342 8p21.3 chondroitin sulfate N-acetylgalactosaminyltransferase 1 THPO 0.341 3q27 thrombopoietin DLGAP1-AS10.341 18p11.31 DLGAP1 antisense RNA 1 KIAA1549 0.341 7q34 KIAA1549 ATP8B1 0.34 18q21.31 ATPase, aminophospholipid transporter, class I, type 8B, member 1 FAM46A 0.339 6q14 family with sequence similarity 46, member A ZBED1 0.338 Xp22.33;Yp11zinc finger, BED-type containing 1 WDR72 0.337 15q21.3 WD repeat domain 72 RPH3AL 0.337 17p13.3 rabphilin 3A-like (without C2 domains) CNPY2 0.337 12q15 canopy FGF signaling regulator 2 AMBP 0.336 9q32-q33 alpha-1-microglobulin/bikunin precursor PRKAA2 0.335 1p31 protein kinase, AMP-activated, alpha 2 catalytic subunit KIT 0.335 4q12 v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog GPT2 0.335 16q12.1 glutamic pyruvate transaminase (alanine aminotransferase) 2 CYP24A1 0.335 20q13 cytochrome P450, family 24, subfamily A, polypeptide 1 DHTKD1 0.335 10p14 dehydrogenase E1 and transketolase domain containing 1 FECH 0.335 18q21.3 ferrochelatase PNKD 0.334 2q35 paroxysmal nonkinesigenic dyskinesia BPIFA1 0.334 20q11.2 BPI fold containing family A, member 1 CCDC64 0.334 12q24.23 coiled-coil domain containing 64 PDE3A 0.334 12p12 phosphodiesterase 3A, cGMP-inhibited FAM222A 0.333 12q24.11 family with sequence similarity 222, member A PCSK1 0.332 5q15-q21 proprotein convertase subtilisin/kexin type 1 DOCK5 0.332 8p21.2 dedicator of cytokinesis 5 PPIB 0.331 15q21-q22 peptidylprolyl isomerase B (cyclophilin B) SMOC1 0.331 14q24.2 SPARC related modular calcium binding 1 FKBP11 0.331 12q13.12 FK506 binding protein 11, 19 kDa LARP4 0.33 12q13.12 La ribonucleoprotein domain family, member 4 CHL1 0.33 3p26.1 cell adhesion molecule L1-like MCF2L 0.33 13q34 MCF.2 cell line derived transforming sequence-like TMED6 0.33 16q22.1 transmembrane emp24 protein transport domain containing 6 SUDS3 0.329 12q24.23 suppressor of defective silencing 3 homolog (S. cerevisiae) GLCE 0.329 15q23 glucuronic acid epimerase CDH17 0.329 8q22.1 cadherin 17, LI cadherin (liver-intestine) SPTSSA 0.329 14q13.1 serine palmitoyltransferase, small subunit A DNAJC12 0.329 10q22.1 DnaJ (Hsp40) homolog, subfamily C, member 12 MPDU1 0.328 17p13.1-p12mannose-P-dolichol utilization defect 1 TAT 0.327 16q22.1 tyrosine aminotransferase VIMP 0.327 15q26.3 VCP-interacting membrane selenoprotein GLDC 0.327 9p22 glycine dehydrogenase (decarboxylating) AIFM2 0.326 10q22.1 apoptosis-inducing factor, mitochondrion-associated, 2 KCNK3 0.326 2p23 potassium channel, two pore domain subfamily K, member 3 GSTP1 0.324 11q13 glutathione S-transferase pi 1 AKR1C3 0.324 10p15-p14 aldo-keto reductase family 1, member C3 SLC45A4 0.324 8q24.3 solute carrier family 45, member 4 ATP2A3 0.324 17p13.3 ATPase, Ca++ transporting, ubiquitous KIF21A 0.323 12q12 kinesin family member 21A HYAL1 0.322 3p21.31 hyaluronoglucosaminidase 1 MCCC2 0.322 5q12-q13 methylcrotonoyl-CoA carboxylase 2 (beta) ODC1 0.322 2p25 ornithine decarboxylase 1 RIMKLB 0.321 12p13.31 ribosomal modification protein rimK-like family member B CHD1L 0.321 1q12 chromodomain helicase DNA binding protein 1-like COL25A1 0.32 4q25 collagen, type XXV, alpha 1 STARD10 0.32 11q13 StAR-related lipid transfer (START) domain containing 10 AACS 0.32 12q24.31 acetoacetyl-CoA synthetase VAPA 0.319 18p11.22 VAMP (vesicle-associated membrane protein)-associated protein A, 33kDa IFT81 0.319 12q24.13 intraflagellar transport 81 CA8 0.318 8q12.1 carbonic anhydrase VIII ENO3 0.317 17p13.2 enolase 3 (beta, muscle) ISG20 0.317 15q26 interferon stimulated exonuclease gene 20kDa DCTN6 0.317 8p12 dynactin 6 ETS2 0.316 21q22.2 v-ets avian erythroblastosis virus E26 oncogene homolog 2 DECR1 0.314 8q21.3 2,4-dienoyl CoA reductase 1, mitochondrial PCSK6 0.313 15q26.3 proprotein convertase subtilisin/kexin type 6 TRAF2 0.313 9q34 TNF receptor-associated factor 2 MUC5B 0.313 11p15.5 mucin 5B, oligomeric mucus/gel-forming PITX2 0.313 4q25 paired-like homeodomain 2 F7 0.312 13q34 coagulation factor VII (serum prothrombin conversion accelerator) GRAMD1A 0.312 19q13.13 GRAM domain containing 1A BTG1 0.312 12q22 B-cell translocation gene 1, anti-proliferative NOSTRIN 0.311 2q31.1 nitric oxide synthase trafficking ADSSL1 0.311 14q32.33 adenylosuccinate synthase like 1 BAG1 0.311
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  • Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-Cell Leukemia

    Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-Cell Leukemia

    Author Manuscript Published OnlineFirst on March 27, 2020; DOI: 10.1158/1078-0432.CCR-19-3519 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Constitutive activation of RAS/MAPK pathway cooperates with trisomy 21 and is therapeutically exploitable in Down syndrome B-cell Leukemia Anouchka P. Laurent1,2, Aurélie Siret1, Cathy Ignacimouttou1, Kunjal Panchal3, M’Boyba K. Diop4, Silvia Jenny5, Yi-Chien Tsai5, Damien Ross-Weil1, Zakia Aid1, Naïs Prade6, Stéphanie Lagarde6, Damien Plassard7, Gaelle Pierron8, Estelle Daudigeos-Dubus4, Yann Lecluse4, Nathalie Droin1, Beat Bornhauser5, Laurence C. Cheung3,9, John D. Crispino10, Muriel Gaudry1, Olivier A. Bernard1, Elizabeth Macintyre11, Carole Barin Bonnigal12, Rishi S. Kotecha3,9,13, Birgit Geoerger4, Paola Ballerini14, Jean-Pierre Bourquin5, Eric Delabesse6, Thomas Mercher1,15 and Sébastien Malinge1,3 1INSERM U1170, Gustave Roussy Institute, Université Paris Saclay, Villejuif, France 2Université Paris Diderot, Paris, France 3Telethon Kids Cancer Centre, Telethon Kids Institute, University of Western Australia, Perth, Australia 4Gustave Roussy Institute Cancer Campus, Department of Pediatric and Adolescent Oncology, INSERM U1015, Equipe Labellisée Ligue Nationale contre le Cancer, Université Paris-Saclay, Villejuif, France 5Department of Pediatric Oncology, Children’s Research Centre, University Children’s Hospital Zurich, Zurich, Switzerland 6Centre of Research on Cancer of Toulouse (CRCT), CHU Toulouse, Université Toulouse III, Toulouse, France 7IGBMC, Plateforme GenomEast, UMR7104 CNRS, Ilkirch, France 8Service de Génétique, Institut Curie, Paris, France 9School of Pharmacy and Biomedical Sciences, Curtin University, Bentley, Australia 10Division of Hematology/Oncology, Northwestern University, Chicago, USA 11Hematology, Université de Paris, Institut Necker-Enfants Malades and Assistance Publique – Hopitaux de Paris, Paris, France 12Centre Hospitalier Universitaire de Tours, Tours, France 1 Downloaded from clincancerres.aacrjournals.org on September 30, 2021.
  • The Role of the Mtor Pathway in Developmental Reprogramming Of

    The Role of the Mtor Pathway in Developmental Reprogramming Of

    THE ROLE OF THE MTOR PATHWAY IN DEVELOPMENTAL REPROGRAMMING OF HEPATIC LIPID METABOLISM AND THE HEPATIC TRANSCRIPTOME AFTER EXPOSURE TO 2,2',4,4'- TETRABROMODIPHENYL ETHER (BDE-47) An Honors Thesis Presented By JOSEPH PAUL MCGAUNN Approved as to style and content by: ________________________________________________________** Alexander Suvorov 05/18/20 10:40 ** Chair ________________________________________________________** Laura V Danai 05/18/20 10:51 ** Committee Member ________________________________________________________** Scott C Garman 05/18/20 10:57 ** Honors Program Director ABSTRACT An emerging hypothesis links the epidemic of metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD) and diabetes with chemical exposures during development. Evidence from our lab and others suggests that developmental exposure to environmentally prevalent flame-retardant BDE47 may permanently reprogram hepatic lipid metabolism, resulting in an NAFLD-like phenotype. Additionally, we have demonstrated that BDE-47 alters the activity of both mTOR complexes (mTORC1 and 2) in hepatocytes. The mTOR pathway integrates environmental information from different signaling pathways, and regulates key cellular functions such as lipid metabolism, innate immunity, and ribosome biogenesis. Thus, we hypothesized that the developmental effects of BDE-47 on liver lipid metabolism are mTOR-dependent. To assess this, we generated mice with liver-specific deletions of mTORC1 or mTORC2 and exposed these mice and their respective controls perinatally to
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus

    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.
  • Evidence for Differential Alternative Splicing in Blood of Young Boys With

    Evidence for Differential Alternative Splicing in Blood of Young Boys With

    Stamova et al. Molecular Autism 2013, 4:30 http://www.molecularautism.com/content/4/1/30 RESEARCH Open Access Evidence for differential alternative splicing in blood of young boys with autism spectrum disorders Boryana S Stamova1,2,5*, Yingfang Tian1,2,4, Christine W Nordahl1,3, Mark D Shen1,3, Sally Rogers1,3, David G Amaral1,3 and Frank R Sharp1,2 Abstract Background: Since RNA expression differences have been reported in autism spectrum disorder (ASD) for blood and brain, and differential alternative splicing (DAS) has been reported in ASD brains, we determined if there was DAS in blood mRNA of ASD subjects compared to typically developing (TD) controls, as well as in ASD subgroups related to cerebral volume. Methods: RNA from blood was processed on whole genome exon arrays for 2-4–year-old ASD and TD boys. An ANCOVA with age and batch as covariates was used to predict DAS for ALL ASD (n=30), ASD with normal total cerebral volumes (NTCV), and ASD with large total cerebral volumes (LTCV) compared to TD controls (n=20). Results: A total of 53 genes were predicted to have DAS for ALL ASD versus TD, 169 genes for ASD_NTCV versus TD, 1 gene for ASD_LTCV versus TD, and 27 genes for ASD_LTCV versus ASD_NTCV. These differences were significant at P <0.05 after false discovery rate corrections for multiple comparisons (FDR <5% false positives). A number of the genes predicted to have DAS in ASD are known to regulate DAS (SFPQ, SRPK1, SRSF11, SRSF2IP, FUS, LSM14A). In addition, a number of genes with predicted DAS are involved in pathways implicated in previous ASD studies, such as ROS monocyte/macrophage, Natural Killer Cell, mTOR, and NGF signaling.