Toxicogenomics of A375 Human Malignant Melanoma Cells Treated with Arbutin

Total Page:16

File Type:pdf, Size:1020Kb

Toxicogenomics of A375 Human Malignant Melanoma Cells Treated with Arbutin Journal of Biomedical Science (2007) 14:87–105 DOI 10.1007/s11373-006-9130-6 Toxicogenomics of A375 human malignant melanoma cells treated with arbutin Sun-Long Cheng1, Rosa Huang Liu2, Jin-Nan Sheu1, Shui-Tein Chen3,4, Supachok Sinchaikul3 & Gregory Jiazer Tsay5,* 1Institute of Medicine, Chung Shan Medical University, Taichung, 40242, Taiwan; 2School of Nutrition, Chung Shan Medical University, Taichung, 40242, Taiwan; 3Institute of Biological Chemistry and Genomics Research Center, Academia Sinica, Taipei, 11529, Taiwan; 4Institute of Biochemical Sciences, College of Life Science, National Taiwan University, Taipei, 10617, Taiwan; 5Institute of Immunology, Chung Shan Medical University, 110 Sec. 1, Chien-Kuo N. Road, Taichung, 40242, Taiwan Received 17 August 2006; accepted 10 October 2006 Ó 2006 National Science Council, Taipei Key words: arbutin, A375 cells, toxicogenomics, DNA microarray, gene expression Summary Although arbutin is a natural product and widely used as an ingredient in skin care products, its effect on the gene expression level of human skin with malignant melanoma cells is rarely reported. We aim to investigate the genotoxic effect of arbutin on the differential gene expression profiling in A375 human malignant melanoma cells through its effect on tumorigenesis and related side-effect. The DNA microarray analysis provided the differential gene expression pattern of arbutin-treated A375 cells with the significant changes of 324 differentially expressed genes, containing 88 up-regulated genes and 236 down-regulated genes. The gene ontology of differentially expressed genes was classified as belonging to cellular component, molecular function and biological process. In addition, four down-regulated genes of AKT1, CLECSF7, FGFR3, and LRP6 served as candidate genes and correlated to suppress the biological processes in the cell cycle of cancer progression and in the downstream signaling pathways of malignancy of melanocytic tumorigenesis. Introduction study of its biological effect on human genomics level in the regulation of malignant melanogenesis Arbutin, a natural compound of beta-D-glucopyr- through the functional effect on carcinogenesis is anoside of hydroquinone, is widely used as an not clear and rarely reported. ingredient in skin care products [1]. It is effective in Recently, the high throughput technology of the treatment of various cutaneous hyperpigmen- DNA microarray has become important in geneo- tations and has the inhibitory effects on the mic research and used to analyze gene expression melanogenesis in melanoma cells [2–4]. However, profiling of human melanomas [5–7]. Since the recent findings have raised serious questions of study of gene expression profiling in human concern regarding both the safety and side-effect melanoma cells treated with arbutin has never of arbutin. Although some inhibitory effects of been reported, it would be very challenging to use arbutin on melanogenesis in melanoma cells and the DNA microarray in studying the biological its mechanism have been elucidated, the intensive effect of arbutin on malignant melanoma cells through its action on anti-cancer property. In this *To whom correspondence should be addressed. Tel: +886-4- study, we aim to investigate the genotoxic effect of 24738170; Fax: +886-4-23248172; E-mail: [email protected] arbutin on the differential gene expression profiling 88 in A375 human malignant melanoma cells through bicarbonate, 1 mM sodium pyruvate and 1% its effect on melanocytic tumorigenesis for cancer antibiotic-antimycotic in a humidified incubator therapy and other related side-effects. We used the with 5% CO2 and 95% air at 37 °C. Upon DNA microarray technology and bioinformatic confluence, the cells were detached by treatment tools to explore the differential gene expression with 0.05% trypsin and 0.53 mM EDTA. During profiling in arbutin-treated A375 cells and to subculture, the medium was replaced every classify the differentially expressed genes by Gene 2–3 days. Oncology, which provided more understanding of the genetic basis of metabolic and cellular Treatment with arbutin and cell viability test responses in tumergenesis of human skin cancer. In addition, we compared the biological effects To perform cell attachment, the cells were seeded of arbutin and kojic acid on differentially at 5.0 Â 103 cells/well in 96-well tissue culture- expressed genes in A375 cells and also proposed treated plates (NUNCTM, Roskilde, Denmark) in the hypothetical pathway of arbutin-responsive 100 ll of culture media. They were then washed genes correlated in the suppression of tumorigen- with PBS and were cultured either alone or in the esis. These candidate genes may lead to conse- presence of various concentrations of arbutin quently aid for early diagnostic and therapeutic (0.32, 1.6, 8, 40, 200 and 1000 lg/ml) for 72 h. applications. Arbutin was suspended in 0.01% DMSO, and the control was added with the same concentration of DMSO in order to reduce the variation of cell Materials and methods growth inhibition. Triplicate experiments were done for each pair group of arbutin concentration Materials and control. The cell viability was determined by MTT assay [8]. The percentage of cell growth Human malignant melanoma cell line, A375 inhibition was calculated as follows: Inhibition (CRL-1619), was obtained from the ATCC (Rock- (%) = [1-A550 nm (arbutin)/A550 nm (con- ville, MD, USA). Dulbecco’s Modified Eagle’s trol)] Â 100%. Medium (DMEM), D-PBS and Trypsin-EDTA were purchased from Atlanta Biologicals (Nor- RNA preparation and quantitative measurement cross, GA, USA). Fetal bovine serum, sodium pyruvate, antibiotic-antimycotic and TRIzol re- After the cells were treated with 8 lg/ml arbutin agent were purchased from Invitrogen (Carlsbad, for 24 h, RNA was extracted by a modified CA, USA). Arbutin, MTT (methylthiazoletetrazo- method using TRIzol combined with the RNeasy lium) and sodium bicarbonate were purchased Mini Kit. The total RNA was quantified by a UV from Sigma (St. Louis, MO, USA). RNeasy Mini spectrophotometer and RNA quality was evalu- Kit was purchased from Qiagen (Valencia, CA, ated by capillary electrophoresis on an Agilent USA). Cyanine 3- and 5-labeled CTP were pur- 2100 Bioanalyzer using RNA 6000 Nano LabChip chased from Perkin-Elemer/NEN Life Science Kit. For each paired sample, the number of (Boston, MS, USA). RNA 6000 Nano LabChip independent paired samples of cultured cells that Kit, Low RNA Input Fluorescent Linear Ampli- were treated with arbutin either present or absent fication Kit, Human 1A Oligo Microarray Kit was done in triplicate. (V2), in situ Hybridization Kit Plus, and Stabil- ization and Drying Solution were purchased from RNA amplification and labeling Agilent Technologies (Palo Alto, CA, USA). All other chemicals were purchased from Sigma Targets of cRNA were amplified and fluorescently (St. Loius, MO, USA). labeled from 0.5 lg total RNA in each reaction using the Agilent Low RNA Input Fluorescent Cell culture Linear Amplification kit. For each sample pair, the control sample was labeled with Cy3 and the A375 cells were cultured in DMEM supplemented treated sample was labeled with Cy5. After puri- with 10% fetal bovine serum, 1.5 g/l sodium fication using Qiagen’s RNeasy mini-spin 89 columns, the quantification, quality and size databases: NCBI (http://www.ncbi.nlm.nih.gov), distribution of the labeled cRNA targets were Ensembl (http://www.ensembl.org), TIGR (http:// then determined by ultraviolet (UV) spectropho- www.tigr.org) and GeneCards (http://www.gene tometry and RNA 6000 Nano LabChip Assay. cards.org). In addition, the category classification of gene expression was done by in-house Bulk Microarray hybridization Gene Search System for Java (BGSSJ) program that is a searching system accomplished by open Hybridization was performed following the Agi- database connectivity, UniGene database and lent oligonucleotide microarray hybridization Gene Ontology knowledgebase, and is available user’s manual and Agilent in situ Hybridization at http://servx8.sinica.edu.tw/bgss-cgi-bin/gene.pl. Kit Plus. Briefly, 2 lg of the labeled cRNA per On the other hand, the protein search program channel was mixed with 50 ll10Â control targets used the Swiss-Prot/TrEMBL (http://www.exp- and nuclease-free water to a final volume of 240 ll. asy.ch/sprot), Proteome (http://www.prote- Each sample tube was added with 10 llof ome.com/databases/HumanPD/reports) and 25Â fragmentation buffer and was incubated at PubMed (http://www.ncbi.nl.nih.gov/PubMed). 60 °C in a water bath in the dark for 30 min. The Moreover, the combining pathway databases of reaction was then terminated by adding 250 llof Biocarta (http://www.biocarta.com), KEGG 2Â hybridization buffer. A volume of 500 llof (http://www.genome.ad.jp/kegg/pathway.html) hybridization mix was applied to Agilent’s Human and the PubMed literature were used to search the 1A Oligonucleotide Microarray, containing 20,173 correlated signaling pathways and mechanisms in (60 mer) oligonucleotide probes, and hybridized in the malignant melanogenesis of A375 cells. a hybridization rotation oven at 60 °C for 17 h. The slides which disassembled in 6Â SSPE and Real-time quantitative PCR (RT-qPCR) 0.005% N-Lauroylsarcosine were washed with 6Â SSPE, 0.005% N-Lauroylsarcosine for 1 min at Specific oligonucleotide primer pairs were room temperature, then with 0.06Â SSPE, 0.005% designed using the analysis Beacon designer 4.00 N-Lauroylsarcosine for 1 min and with Stabiliza- (Premier Biosoft International) and were then used tion and Drying Solution for 30 s. for real-time quantitative PCR. The sequences of the primers used are: (1) AKT1 (NM_005163, Data analysis and bioinformatics 150 bp): forward 5¢-ACCATCACACCACCTG- ACCAAG-3¢ and reverse 5¢-CGCCTCTCCATC- The microarray chip was scanned using an Agilent CCTCCAAG-3¢; (2) CLECSF7 (NM_130441, G2565BA Microarray Scanner System, and the 184 bp): forward 5¢-ATCAACACCAGGGAAG- Agilent Feature Extraction software 7.5 used AACAGG-3¢ and reverse 5¢-TCGCACAACGCT- defaults for all parameters including a parameter- CAT CAAGG-3¢; (3) FGFR3 (NM_000142, ized error model to compute the significance 102 bp): forward 5¢-CTGCCAGCCGAGGAG- (p-values) of log ratios.
Recommended publications
  • Proteomic Profile of Human Spermatozoa in Healthy And
    Cao et al. Reproductive Biology and Endocrinology (2018) 16:16 https://doi.org/10.1186/s12958-018-0334-1 REVIEW Open Access Proteomic profile of human spermatozoa in healthy and asthenozoospermic individuals Xiaodan Cao, Yun Cui, Xiaoxia Zhang, Jiangtao Lou, Jun Zhou, Huafeng Bei and Renxiong Wei* Abstract Asthenozoospermia is considered as a common cause of male infertility and characterized by reduced sperm motility. However, the molecular mechanism that impairs sperm motility remains unknown in most cases. In the present review, we briefly reviewed the proteome of spermatozoa and seminal plasma in asthenozoospermia and considered post-translational modifications in spermatozoa of asthenozoospermia. The reduction of sperm motility in asthenozoospermic patients had been attributed to factors, for instance, energy metabolism dysfunction or structural defects in the sperm-tail protein components and the differential proteins potentially involved in sperm motility such as COX6B, ODF, TUBB2B were described. Comparative proteomic analysis open a window to discover the potential pathogenic mechanisms of asthenozoospermia and the biomarkers with clinical significance. Keywords: Proteome, Spermatozoa, Sperm motility, Asthenozoospermia, Infertility Background fertilization failure [4] and it has become clear that iden- Infertility is defined as the lack of ability to achieve a tifying the precise proteins and the pathways involved in clinical pregnancy after one year or more of unprotected sperm motility is needed [5]. and well-timed intercourse with the same partner [1]. It is estimated that around 15% of couples of reproductive age present with infertility, and about half of the infertil- Application of proteomic techniques in male ity is associated with male partner [2, 3].
    [Show full text]
  • Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-Like Mouse Models: Tracking the Role of the Hairless Gene
    University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 5-2006 Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene Yutao Liu University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Liu, Yutao, "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino- like Mouse Models: Tracking the Role of the Hairless Gene. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1824 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yutao Liu entitled "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, with a major in Life Sciences. Brynn H. Voy, Major Professor We have read this dissertation and recommend its acceptance: Naima Moustaid-Moussa, Yisong Wang, Rogert Hettich Accepted for the Council: Carolyn R.
    [Show full text]
  • Table 2. Significant
    Table 2. Significant (Q < 0.05 and |d | > 0.5) transcripts from the meta-analysis Gene Chr Mb Gene Name Affy ProbeSet cDNA_IDs d HAP/LAP d HAP/LAP d d IS Average d Ztest P values Q-value Symbol ID (study #5) 1 2 STS B2m 2 122 beta-2 microglobulin 1452428_a_at AI848245 1.75334941 4 3.2 4 3.2316485 1.07398E-09 5.69E-08 Man2b1 8 84.4 mannosidase 2, alpha B1 1416340_a_at H4049B01 3.75722111 3.87309653 2.1 1.6 2.84852656 5.32443E-07 1.58E-05 1110032A03Rik 9 50.9 RIKEN cDNA 1110032A03 gene 1417211_a_at H4035E05 4 1.66015788 4 1.7 2.82772795 2.94266E-05 0.000527 NA 9 48.5 --- 1456111_at 3.43701477 1.85785922 4 2 2.8237185 9.97969E-08 3.48E-06 Scn4b 9 45.3 Sodium channel, type IV, beta 1434008_at AI844796 3.79536664 1.63774235 3.3 2.3 2.75319499 1.48057E-08 6.21E-07 polypeptide Gadd45gip1 8 84.1 RIKEN cDNA 2310040G17 gene 1417619_at 4 3.38875643 1.4 2 2.69163229 8.84279E-06 0.0001904 BC056474 15 12.1 Mus musculus cDNA clone 1424117_at H3030A06 3.95752801 2.42838452 1.9 2.2 2.62132809 1.3344E-08 5.66E-07 MGC:67360 IMAGE:6823629, complete cds NA 4 153 guanine nucleotide binding protein, 1454696_at -3.46081884 -4 -1.3 -1.6 -2.6026947 8.58458E-05 0.0012617 beta 1 Gnb1 4 153 guanine nucleotide binding protein, 1417432_a_at H3094D02 -3.13334396 -4 -1.6 -1.7 -2.5946297 1.04542E-05 0.0002202 beta 1 Gadd45gip1 8 84.1 RAD23a homolog (S.
    [Show full text]
  • Seq2pathway Vignette
    seq2pathway Vignette Bin Wang, Xinan Holly Yang, Arjun Kinstlick May 19, 2021 Contents 1 Abstract 1 2 Package Installation 2 3 runseq2pathway 2 4 Two main functions 3 4.1 seq2gene . .3 4.1.1 seq2gene flowchart . .3 4.1.2 runseq2gene inputs/parameters . .5 4.1.3 runseq2gene outputs . .8 4.2 gene2pathway . 10 4.2.1 gene2pathway flowchart . 11 4.2.2 gene2pathway test inputs/parameters . 11 4.2.3 gene2pathway test outputs . 12 5 Examples 13 5.1 ChIP-seq data analysis . 13 5.1.1 Map ChIP-seq enriched peaks to genes using runseq2gene .................... 13 5.1.2 Discover enriched GO terms using gene2pathway_test with gene scores . 15 5.1.3 Discover enriched GO terms using Fisher's Exact test without gene scores . 17 5.1.4 Add description for genes . 20 5.2 RNA-seq data analysis . 20 6 R environment session 23 1 Abstract Seq2pathway is a novel computational tool to analyze functional gene-sets (including signaling pathways) using variable next-generation sequencing data[1]. Integral to this tool are the \seq2gene" and \gene2pathway" components in series that infer a quantitative pathway-level profile for each sample. The seq2gene function assigns phenotype-associated significance of genomic regions to gene-level scores, where the significance could be p-values of SNPs or point mutations, protein-binding affinity, or transcriptional expression level. The seq2gene function has the feasibility to assign non-exon regions to a range of neighboring genes besides the nearest one, thus facilitating the study of functional non-coding elements[2]. Then the gene2pathway summarizes gene-level measurements to pathway-level scores, comparing the quantity of significance for gene members within a pathway with those outside a pathway.
    [Show full text]
  • Molecular Subtypes of Diffuse Large B-Cell Lymphoma Arise by Distinct Genetic Pathways
    Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways Georg Lenza, George W. Wrightb, N. C. Tolga Emrea, Holger Kohlhammera, Sandeep S. Davea, R. Eric Davisa, Shannon Cartya, Lloyd T. Lama, A. L. Shaffera, Wenming Xiaoc, John Powellc, Andreas Rosenwaldd, German Ottd,e, Hans Konrad Muller-Hermelinkd, Randy D. Gascoynef, Joseph M. Connorsf, Elias Campog, Elaine S. Jaffeh, Jan Delabiei, Erlend B. Smelandj,k, Lisa M. Rimszal, Richard I. Fisherm,n, Dennis D. Weisenburgero, Wing C. Chano, and Louis M. Staudta,q aMetabolism Branch, bBiometric Research Branch, cCenter for Information Technology, and hLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892; dDepartment of Pathology, University of Wu¨rzburg, 97080 Wu¨rzburg, Germany; eDepartment of Clinical Pathology, Robert-Bosch-Krankenhaus, 70376 Stuttgart, Germany; fBritish Columbia Cancer Agency, Vancouver, British Columbia, Canada V5Z 4E6; gHospital Clinic, University of Barcelona, 08036 Barcelona, Spain; iPathology Clinic and jInstitute for Cancer Research, Rikshospitalet Hospital, Oslo, Norway; kCentre for Cancer Biomedicine, Faculty Division the Norwegian Radium Hospital, N-0310, Oslo, Norway; lDepartment of Pathology, University of Arizona, Tucson, AZ 85724; mSouthwest Oncology Group, 24 Frank Lloyd Wright Drive, Ann Arbor, MI 48106 ; nJames P. Wilmot Cancer Center, University of Rochester, Rochester, NY 14642; and oDepartments of Pathology and Microbiology, University of Nebraska, Omaha, NE 68198 Edited by Ira
    [Show full text]
  • Genome-Wide Approach to Identify Risk Factors for Therapy-Related Myeloid Leukemia
    Leukemia (2006) 20, 239–246 & 2006 Nature Publishing Group All rights reserved 0887-6924/06 $30.00 www.nature.com/leu ORIGINAL ARTICLE Genome-wide approach to identify risk factors for therapy-related myeloid leukemia A Bogni1, C Cheng2, W Liu2, W Yang1, J Pfeffer1, S Mukatira3, D French1, JR Downing4, C-H Pui4,5,6 and MV Relling1,6 1Department of Pharmaceutical Sciences, The University of Tennessee, Memphis, TN, USA; 2Department of Biostatistics, The University of Tennessee, Memphis, TN, USA; 3Hartwell Center, The University of Tennessee, Memphis, TN, USA; 4Department of Pathology, The University of Tennessee, Memphis, TN, USA; 5Department of Hematology/Oncology St Jude Children’s Research Hospital, The University of Tennessee, Memphis, TN, USA; and 6Colleges of Medicine and Pharmacy, The University of Tennessee, Memphis, TN, USA Using a target gene approach, only a few host genetic risk therapy increases, the importance of identifying host factors for factors for treatment-related myeloid leukemia (t-ML) have been secondary neoplasms increases. defined. Gene expression microarrays allow for a more 4 genome-wide approach to assess possible genetic risk factors Because DNA microarrays interrogate multiple ( 10 000) for t-ML. We assessed gene expression profiles (n ¼ 12 625 genes in one experiment, they allow for a ‘genome-wide’ probe sets) in diagnostic acute lymphoblastic leukemic cells assessment of genes that may predispose to leukemogenesis. from 228 children treated on protocols that included leukemo- DNA microarray analysis of gene expression has been used to genic agents such as etoposide, 13 of whom developed t-ML. identify distinct expression profiles that are characteristic of Expression of 68 probes, corresponding to 63 genes, was different leukemia subtypes.13,14 Studies using this method have significantly related to risk of t-ML.
    [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]
  • Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
    Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7
    [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]
  • ZNF41 Antibody (N-Term) Blocking Peptide Synthetic Peptide Catalog # Bp17581a
    10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 ZNF41 Antibody (N-term) Blocking Peptide Synthetic peptide Catalog # BP17581a Specification ZNF41 Antibody (N-term) Blocking Peptide ZNF41 Antibody (N-term) Blocking Peptide - - Background Product Information This gene product is a likely zinc finger Primary Accession P51814 familytranscription factor. It contains KRAB-A and KRAB-B domains thatact as transcriptional repressors in related proteins, and multiplezinc ZNF41 Antibody (N-term) Blocking Peptide - Additional Information finger DNA binding motifs and finger linking regionscharacteristic of the Kruppel family. This gene is part of a genecluster on Gene ID 7592 chromosome Xp11.23. Several alternatively splicedtranscript variants have been described, Other Names however, the full-lengthnature of only some of Zinc finger protein 41, ZNF41 them is known. Format ZNF41 Antibody (N-term) Blocking Peptide Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in - References solution using the appropriate buffer as needed. Ross, M.T., et al. Nature 434(7031):325-337(2005)Colland, F., et al. Storage Genome Res. 14(7):1324-1332(2004)Shoichet, Maintain refrigerated at 2-8°C for up to 6 S.A., et al. Am. J. Hum. Genet. months. For long term storage store at 73(6):1341-1354(2003)Rosati, M., et al. -20°C. Cytogenet. Cell Genet. 85 (3-4), 291-296 (1999) :Knight, J.C., et al. Genomics Precautions 21(1):180-187(1994) This product is for research use only. Not for use in diagnostic or therapeutic procedures. ZNF41 Antibody (N-term) Blocking Peptide - Protein Information Name ZNF41 Function May be involved in transcriptional regulation.
    [Show full text]
  • Transcriptional and Post-Transcriptional Regulation of ATP-Binding Cassette Transporter Expression
    Transcriptional and Post-transcriptional Regulation of ATP-binding Cassette Transporter Expression by Aparna Chhibber DISSERTATION Submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in Pharmaceutical Sciences and Pbarmacogenomies in the Copyright 2014 by Aparna Chhibber ii Acknowledgements First and foremost, I would like to thank my advisor, Dr. Deanna Kroetz. More than just a research advisor, Deanna has clearly made it a priority to guide her students to become better scientists, and I am grateful for the countless hours she has spent editing papers, developing presentations, discussing research, and so much more. I would not have made it this far without her support and guidance. My thesis committee has provided valuable advice through the years. Dr. Nadav Ahituv in particular has been a source of support from my first year in the graduate program as my academic advisor, qualifying exam committee chair, and finally thesis committee member. Dr. Kathy Giacomini graciously stepped in as a member of my thesis committee in my 3rd year, and Dr. Steven Brenner provided valuable input as thesis committee member in my 2nd year. My labmates over the past five years have been incredible colleagues and friends. Dr. Svetlana Markova first welcomed me into the lab and taught me numerous laboratory techniques, and has always been willing to act as a sounding board. Michael Martin has been my partner-in-crime in the lab from the beginning, and has made my days in lab fly by. Dr. Yingmei Lui has made the lab run smoothly, and has always been willing to jump in to help me at a moment’s notice.
    [Show full text]
  • Next-MP50 Status Report
    The neXt-50 Challenge The neXt-50 Challenge September 16, 2017 status report of next-50 Challenge by individual Chromosome groups. PI MPs Silver MPs JPR SI JPR SI JPR SI Other Papers Ch Submitted In press In revision 1 Ping Xu 2 1 1 0 2 Lydie Lane 12 3 2 2 0 2 3 Takeshi Kawamura 0 4 0 0 0 1 4 Yu-Ju Chen 26 in progress 86 1 0 1 0 5 6 7 Ed Nice 0 0 1 8 9 10 Jin Park 0 1 0 0 0 0 11 Jong Shin 2 in progress 2 1 0 1 0 12 Ravi Sirdeshmukh 0 0 0 0 0 0 13 Young-Ki Paik 0 5 2 1 1 0 14 CharLes Pineau 12 3 15 GiLberto Domont 0 2 1 0 1 0 16 Fernando CorraLes 2 (+ 9) 165 2 0 2 5 17 GiL Omenn 0 0 3 1 2 8 18 Andrey Archakov 0 0 1 0 1 3 19 20 Siqi Liu 1 0 1 21 Albert Sickmann 0 0 0 0 0 22 X Tadashi Yamamoto 1 0 1 0 Y Hosseini SaLekdeh 1 2 1 1 0 Mt TOTAL 15 268 19 6 13 20 (in progress) 37 C-HPP 2017-09-16 1 The neXt-50 Challenge Chromosome 1 (Ping Xu) PIC Leaders: Ping Xu, Fuchu He Contributing labs: Ping Xu, Beijing Proteome Research Center Fuchu He, Beijing Proteome Research Center Dong Yang, Beijing Proteome Research Center Wantao Ying, Beijing Proteome Research Center Pengyuan Yang, Fudan University Siqi Liu, Beijing Genome Institute Qinyu He, Jinan University Major lab members or partners contributing to the neXt50: Yao Zhang (Beijing Proteome Research Center), Yihao Wang (Beijing Proteome Research Center), Cuitong He (Beijing Proteome Research Center), Wei Wei (Beijing Proteome Research Center), Yanchang Li (Beijing Proteome Research Center), Feng Xu (Beijing Proteome Research Center), Xuehui Peng (Beijing Proteome Research Center).
    [Show full text]