DOCSLIB.ORG

Supplementary Table S1. List of Mirnas on Human Chromosome 3P and the Changes of Their Genome Copies Determined by Genomic Real-Time PCR

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Supplementary Table S1. List of miRNAs on human chromosome 3p and the changes of their genome copies determined by genomic real-time PCR. Change of frequency, ID Accession Chromosome Start End Strand genome copy % hsa-mir-378b MI0014154 3p25.3 10371913 10371969 + No difference hsa-mir-885 MI0005560 3p25.3 10436173 10436246 - Deletion 25% hsa-mir-4270 MI0015878 3p25.1 15537746 15537815 - Amplification 80% hsa-mir-3134 MI0014155 3p25.1 15738805 15738878 - No difference hsa-mir-563 MI0003569 3p25.1 15915278 15915356 + No difference hsa-mir-3714 MI0016135 3p24.3 16974688 16974752 + No difference hsa-mir-4791 MI0017438 3p24.3 19356340 19356423 - No difference hsa-mir-3135a MI0014156 3p24.3 20179057 20179133 + No difference hsa-mir-4792 MI0017439 3p24.2 24562853 24562926 - Deletion 35% hsa-mir-4442 MI0016785 3p24.2 25706364 25706430 - No difference hsa-mir-466 MI0014157 3p23 31203196 31203279 - No difference hsa-mir-128-2 MI0000727 3p22.3 35785968 35786051 + Deletion 75% hsa-mir-26a-1 MI0000083 3p22.2 38010895 38010971 + Deletion 35% hsa-mir-138-1 MI0000476 3p21.32 44155704 44155802 + Deletion 25% hsa-mir-564 MI0003570 3p21.31 44903380 44903473 + Deletion 25% hsa-mir-1226 MI0006313 3p21.31 47891045 47891119 + No difference hsa-mir-4443 MI0016786 3p21.31 48238054 48238106 + No difference hsa-mir-2115 MI0010634 3p21.31 48357850 48357949 - No difference hsa-mir-711 MI0012488 3p21.31 48616335 48616410 - No difference hsa-mir-4793 MI0017440 3p21.31 48681627 48681713 - No difference hsa-mir-425 MI0001448 3p21.31 49057581 49057667 - Amplification 65% hsa-mir-191 MI0000465 3p21.31 49058051 49058142 - Amplification 65% hsa-mir-4271 MI0015879 3p21.31 49311553 49311619 + No difference hsa-mir-5193 MI0018172 3p21.31 49843570 49843678 - Deletion 35% hsa-mir-566 MI0003572 3p21.31 50210759 50210852 + No difference hsa-mir-4787 MI0017434 3p21.2 50712511 50712594 + No difference hsa-let-7g MI0000433 3p21.1 52302294 52302377 - Deletion 60% hsa-mir-135a-1 MI0000452 3p21.1 52328235 52328324 - Deletion 20% hsa-mir-3938 MI0016594 3p14.3 55886520 55886622 - Deletion 35% hsa-mir-4444-2 MI0019111 3p12.3 75263627 75263700 + Amplification 70% hsa-mir-1324 MI0006657 3p12.3 75679914 75680009 + No difference hsa-mir-4273 MI0015881 3p12.3 75787431 75787514 + Deletion 20% hsa-mir-3923 MI0016430 3p12.3 79557037 79557119 + No difference hsa-mir-5688 MI0019292 3p12.1 85434860 85434942 + Amplification 25% Supplementary Table S2. Clinical significance of the expression of miR-128 in breast cancer patients. Parameter n miR-128 expression (+), n (%) p value Age (years) ≤ 35 5 3 (60.0) 0.149 35-55 50 23 (46.0) > 55 30 8 (26.7) Tumor size (cm) ≤ 2 4 3 (75.0) 0.302 2-5 65 24 (36.9) > 5 16 7 (43.8) Lymph node metastasis Absent 30 21 (70.0) 0.020 Present 55 24 (43.6) Histology Ductual 80 20 (25) 0.206 Lobular 2 1 (50) Other types 3 2 (67) Grade I 3 1 (33.3) 0.810 II 54 23 (42.6) III 28 10 (35.7) Stage I -II 49 29 (59.2) 0.036 III-IV 36 13 (36.1) Estrogen receptor － 48 20 (41.7) 0.721 ＋ 37 14 (37.8) Progesterone receptor － 50 18 (36.0) 0.368 ＋ 35 16 (45.7) c-erbB-2 low 63 22 (34.9) 0.106 high 22 12 (54.5) Ki-67 + 19 10(52.6) 0.027 ++ 22 12 (54.5) +++ 31 10 (32.3) ++++ 13 2 (15.4) Note: Estrogen and progesterone receptor, HER2/Neu and Ki67 data were obtained from patients’ pathology records. Scoring stained sections (Supplement) The Ki67 labeling index (LI) was scored by counting 500 cells and determining the percentage of cells that stained positively for Ki67: score +, 0~25%; score ++, 26%~50%; score +++, 51%~75%; score ++++, > 75%. (Brown et al., 2002) REFERENCE: Brown DC, Gatter KC. Ki67 protein: the immaculate deception. Histopathology 2002; 40:2-11. Supplementary Table S3. Invariable analysis of clinical outcome according to the expression of miR-128 in breast cancer patients (85 cases) miR-128 expression 5-yr survival Positive Negative P Survival Time (months) (95% CL) 59.1(55.7-62.5) 52.9(48.8-57.2) 0.017 Overall survival Survival Rate (%) 76.5 52.0 Survival Time (months) (95% CL) 55.2(50.1-60.4) 44.8(38.7-50.9) 0.023 Relapse-free survival Survival Rate (%) 70.6 48.0 Supplementary Table S4. List of mRNAs predicted to be targeted by miR-128 by all the three programs: MiRanda, Pictar and TargetScan. Target gene Gene Name ABCB9 ATP-binding cassette, sub-family B (MDR/TAP), member 9 ADCY2 adenylate cyclase 2 (brain) ADCY3 adenylate cyclase 3 ARID1B AT rich interactive domain 1B (SWI1-like) BAZ2B bromodomain adjacent to zinc finger domain, 2B BMI1 BMI1 polycomb ring finger oncogene BTG2 BTG family, member 2 C5orf13 chromosome 5 open reading frame 13 C9orf97 chromosome 9 open reading frame 97 CA12 carbonic anhydrase XII CABP1 calcium binding protein 1 CASC3 cancer susceptibility candidate 3 CDH24 cadherin-like 24 CNR1 cannabinoid receptor 1 (brain) CORO1C coronin, actin binding protein, 1C CPEB3 cytoplasmic polyadenylation element binding protein 3 CRKL v-crk sarcoma virus CT10 oncogene homolog (avian)-like CSF1 colony stimulating factor 1 (macrophage) CTDSP2 CTD (carboxy-terminal domain, RNA polymerase II, polypeptide A) small phosphatase 2 DCX doublecortex; lissencephaly, X-linked (doublecortin) DIRAS2 DIRAS family, GTP-binding RAS-like 2 DTX1 deltex homolog 1 (Drosophila) E2F3 E2F transcription factor 3 ECE2 endothelin converting enzyme 2 ELMO1 engulfment and cell motility 1 EPHB2 EPH receptor B2 EVI5 ecotropic viral integration site 5 FBXO33 F-box protein 33 FLRT3 fibronectin leucine rich transmembrane protein 3 FOXP4 forkhead box P4 FOXQ1 forkhead box Q1 FXR2 fragile X mental retardation, autosomal homolog 2 GCC1 GRIP and coiled-coil domain containing 1 GNS glucosamine (N-acetyl)-6-sulfatase (Sanfilippo disease IIID) HAO1 hydroxyacid oxidase (glycolate oxidase) 1 HMGB3 high-mobility group box 3 HOXA13 homeobox A13 HOXB8 homeobox B8 ING5 inhibitor of growth family, member 5 ISL1 ISL LIM homeobox 1 ITPKC inositol 1,4,5-trisphosphate 3-kinase C KCNK10 potassium channel, subfamily K, member 10 KLF4 Kruppel-like factor 4 (gut) LIN28 lin-28 homolog (C. elegans) MAP2K4 mitogen-activated protein kinase kinase 4 MAP2K7 mitogen-activated protein kinase kinase 7 MAP4K5 mitogen-activated protein kinase kinase kinase kinase 5 MAPK14 mitogen-activated protein kinase 14 MGAT1 mannosyl (alpha-1,3-)-glycoprotein beta-1,2-N-acetylglucosaminyltransferase MOSPD3 motile sperm domain containing 3 MPP2 membrane protein, palmitoylated 2 (MAGUK p55 subfamily member 2) NANOG homeobox transcription factor Nanog NGFR nerve growth factor receptor (TNFR superfamily, member 16) NHS Nance-Horan syndrome (congenital cataracts and dental anomalies) NPTX1 neuronal pentraxin I NRBF2 nuclear receptor binding factor 2 NXF1 nuclear RNA export factor 1 NXT2 nuclear transport factor 2-like export factor 2 ORC5L origin recognition complex, subunit 5-like (yeast) PAIP2 poly(A) binding protein interacting protein 2 PDE3A phosphodiesterase 3A, cGMP-inhibited PDE7B phosphodiesterase 7B PHB prohibitin PLAGL2 pleiomorphic adenoma gene-like 2 PLK2 polo-like kinase 2 (Drosophila) PPP1CC protein phosphatase 1, catalytic subunit, gamma isoform PPP4C protein phosphatase 4 (formerly X), catalytic subunit PRDM16 PR domain containing 16 PTPN5 protein tyrosine phosphatase, non-receptor type 5 (striatum-enriched) PTPN9 protein tyrosine phosphatase, non-receptor type 9 RARA retinoic acid receptor, alpha RERE arginine-glutamic acid dipeptide (RE) repeats RNF38 ring finger protein 38 RPS6KA5 ribosomal protein S6 kinase, 90kDa, polypeptide 5 RYBP RING1 and YY1 binding protein SASH1 SAM and SH3 domain containing 1 SEC61A1 Sec61 alpha 1 subunit (S. cerevisiae) SH2D3C SH2 domain containing 3C SIRT1 sirtuin (silent mating type information regulation 2 homolog) 1 (S. cerevisiae) SLC35F3 solute carrier family 35, member F3 SLC39A13 solute carrier family 39 (zinc transporter), member 13 SLC6A1 solute carrier family 6 (neurotransmitter transporter, GABA), member 1 SNAI1 snail homolog 1 (Drosophila) SP1 Sp1 transcription factor SP2 Sp2 transcription factor SPATA2 spermatogenesis associated 2 STK24 serine/threonine kinase 24 (STE20 homolog, yeast) SYT1 synaptotagmin I TLK2 tousled-like kinase 2 TMEFF1 transmembrane protein with EGF-like and two follistatin-like domains 1 TMSB10 thymosin beta 10 TNPO3 transportin 3 UBE2E2 ubiquitin-conjugating enzyme E2E 2 (UBC4/5 homolog, yeast) ULK1 unc-51-like kinase 1 (C. elegans) WDTC1 WD and tetratricopeptide repeats 1 XPR1 xenotropic and polytropic retrovirus receptor YWHAB tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, beta polypeptide ZNF24 zinc finger protein 24 Supplementary Table S5. qRT-PCR analysis of the effect of forced expression of miR-128 in MDA-MB-231 cells or depleted expression of miR-128 in MCF-10A cells on mRNA levels of several key genes functionally involved in oncogenicity and neoplastic progression. Fold change with transfection Fold change with Functional gene by miR-128 mimics in transfection by miR-128 grouping Gene MDA-MB-231§ p-value ASO in MCF-10A& p-value CCND1 0.13 1.16E-04 3.08 6.83E-04 ATM 0.36 4.76E-04 4.76 4.25E-03 BRCA1 0.12 6.32E-04 1.73 1.64E-02 CCNE1 0.05 2.61E-03 6.73 2.54E-03 Cell cycle CDC25A 0.15 1.54E-03 1.20 6.72E-03 control and CDK2 0.45 1.45E-03 1.54 4.70E-02 DNA damage CDK4 0.53 1.62E-04 3.28 2.45E-04 repair CDKN1A 0.25 6.77E-04 2.64 1.06E-03 CDKN2A 9.43 3.87E-04 6.22 5.35E-04 CDKN1B 0.53 3.42E-03 3.95 4.73E-03 CHEK2 0.58 1.19E-02 1.59 2.32E-03 E2F1 0.04 1.31E-03 16.62 6.23E-05 MDM2 33.00 4.44E-04 0.34 5.02E-05 RB1 0.67 4.33E-04 1.52 7.17E-03 S100A4 0.76 2.96E-02 0.87 8.77E-02 TP53 36.08 4.51E-04 0.11 1.60E-04 APAF1 0.58 8.50E-03
Recommended publications
  • Essential Genes and Their Role in Autism Spectrum Disorder

    Essential Genes and Their Role in Autism Spectrum Disorder

    University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2017 Essential Genes And Their Role In Autism Spectrum Disorder Xiao Ji University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Bioinformatics Commons, and the Genetics Commons Recommended Citation Ji, Xiao, "Essential Genes And Their Role In Autism Spectrum Disorder" (2017). Publicly Accessible Penn Dissertations. 2369. https://repository.upenn.edu/edissertations/2369 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/2369 For more information, please contact [email protected]. Essential Genes And Their Role In Autism Spectrum Disorder Abstract Essential genes (EGs) play central roles in fundamental cellular processes and are required for the survival of an organism. EGs are enriched for human disease genes and are under strong purifying selection. This intolerance to deleterious mutations, commonly observed haploinsufficiency and the importance of EGs in pre- and postnatal development suggests a possible cumulative effect of deleterious variants in EGs on complex neurodevelopmental disorders. Autism spectrum disorder (ASD) is a heterogeneous, highly heritable neurodevelopmental syndrome characterized by impaired social interaction, communication and repetitive behavior. More and more genetic evidence points to a polygenic model of ASD and it is estimated that hundreds of genes contribute to ASD. The central question addressed in this dissertation is whether genes with a strong effect on survival and fitness (i.e. EGs) play a specific oler in ASD risk. I compiled a comprehensive catalog of 3,915 mammalian EGs by combining human orthologs of lethal genes in knockout mice and genes responsible for cell-based essentiality.
  • Supplementary Table S2

    Supplementary Table S2

    1-high in cerebrotropic Gene P-value patients Definition BCHE 2.00E-04 1 Butyrylcholinesterase PLCB2 2.00E-04 -1 Phospholipase C, beta 2 SF3B1 2.00E-04 -1 Splicing factor 3b, subunit 1 BCHE 0.00022 1 Butyrylcholinesterase ZNF721 0.00028 -1 Zinc finger protein 721 GNAI1 0.00044 1 Guanine nucleotide binding protein (G protein), alpha inhibiting activity polypeptide 1 GNAI1 0.00049 1 Guanine nucleotide binding protein (G protein), alpha inhibiting activity polypeptide 1 PDE1B 0.00069 -1 Phosphodiesterase 1B, calmodulin-dependent MCOLN2 0.00085 -1 Mucolipin 2 PGCP 0.00116 1 Plasma glutamate carboxypeptidase TMX4 0.00116 1 Thioredoxin-related transmembrane protein 4 C10orf11 0.00142 1 Chromosome 10 open reading frame 11 TRIM14 0.00156 -1 Tripartite motif-containing 14 APOBEC3D 0.00173 -1 Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3D ANXA6 0.00185 -1 Annexin A6 NOS3 0.00209 -1 Nitric oxide synthase 3 SELI 0.00209 -1 Selenoprotein I NYNRIN 0.0023 -1 NYN domain and retroviral integrase containing ANKFY1 0.00253 -1 Ankyrin repeat and FYVE domain containing 1 APOBEC3F 0.00278 -1 Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3F EBI2 0.00278 -1 Epstein-Barr virus induced gene 2 ETHE1 0.00278 1 Ethylmalonic encephalopathy 1 PDE7A 0.00278 -1 Phosphodiesterase 7A HLA-DOA 0.00305 -1 Major histocompatibility complex, class II, DO alpha SOX13 0.00305 1 SRY (sex determining region Y)-box 13 ABHD2 3.34E-03 1 Abhydrolase domain containing 2 MOCS2 0.00334 1 Molybdenum cofactor synthesis 2 TTLL6 0.00365 -1 Tubulin tyrosine ligase-like family, member 6 SHANK3 0.00394 -1 SH3 and multiple ankyrin repeat domains 3 ADCY4 0.004 -1 Adenylate cyclase 4 CD3D 0.004 -1 CD3d molecule, delta (CD3-TCR complex) (CD3D), transcript variant 1, mRNA.
  • Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene

    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.
  • The Transition from Primary Colorectal Cancer to Isolated Peritoneal Malignancy

    The Transition from Primary Colorectal Cancer to Isolated Peritoneal Malignancy

    medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . The transition from primary colorectal cancer to isolated peritoneal malignancy is associated with a hypermutant, hypermethylated state Sally Hallam1, Joanne Stockton1, Claire Bryer1, Celina Whalley1, Valerie Pestinger1, Haney Youssef1, Andrew D Beggs1 1 = Surgical Research Laboratory, Institute of Cancer & Genomic Science, University of Birmingham, B15 2TT. Correspondence to: Andrew Beggs, [email protected] KEYWORDS: Colorectal cancer, peritoneal metastasis ABBREVIATIONS: Colorectal cancer (CRC), Colorectal peritoneal metastasis (CPM), Cytoreductive surgery and heated intraperitoneal chemotherapy (CRS & HIPEC), Disease free survival (DFS), Differentially methylated regions (DMR), Overall survival (OS), TableFormalin fixed paraffin embedded (FFPE), Hepatocellular carcinoma (HCC) ARTICLE CATEGORY: Research article NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2020.02.24.20027318; this version posted February 25, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license . NOVELTY AND IMPACT: Colorectal peritoneal metastasis (CPM) are associated with limited and variable survival despite patient selection using known prognostic factors and optimal currently available treatments.
  • Overexpression of RNF38 Facilitates TGF-Β Signaling by Ubiquitinating

    Overexpression of RNF38 Facilitates TGF-Β Signaling by Ubiquitinating

    Peng et al. Journal of Experimental & Clinical Cancer Research (2019) 38:113 https://doi.org/10.1186/s13046-019-1113-3 RESEARCH Open Access Overexpression of RNF38 facilitates TGF-β signaling by Ubiquitinating and degrading AHNAK in hepatocellular carcinoma Rui Peng1,2†, Peng-Fei Zhang1,3†, Xuan Yang1†, Chuan-Yuan Wei1†, Xiao-Yong Huang1, Jia-Bin Cai1, Jia-Cheng Lu1, Chao Gao1, Hai-Xiang Sun1, Qiang Gao1, Dou-Sheng Bai2, Guo-Ming Shi1*, Ai-Wu Ke1* and Jia Fan1,4* Abstract Background: RING finger protein 38 (RNF38), a member of the RNF protein family, has just emerged as a vital driver of cancer progression. However, the oncogenic mechanisms of RNF38 remain unexplored. Methods: Using frozen tumor tissue and tissue microarray from hepatocellular carcinoma (HCC) patients, we tried to probe the expression of RNF38 in HCC and its clinical value. Then the biological functions of RNF38 were analyzed in vivo and vitro. Stable isotope labeling with amino acids (SILAC) in cell culture and co-immunoprecipitation proteomic analyses were combined to reveal the potential mechanism of RNF38 in HCC progression. Results: We report that RNF38 expression was markedly higher in HCC tissues than in peritumor tissues. Correspondingly, RNF38 overexpression promoted the HCC cell migration and invasion and inhibited apoptosis both in vitro and in vivo. And elevated RNF38 expression induced HCC cell epithelial-mesenchymal transition by facilitating transforming growth factor-β (TGF-β) signaling via ubiquitinating and degrading neuroblast differentiation-associated protein (AHNAK), a well-established inhibitor of TGF-β signaling. Furthermore, AHNAK interference restored the HCC cell invasion and metastasis deprived by RNF38 downregulation.
  • Region Based Gene Expression Via Reanalysis of Publicly Available Microarray Data Sets

    Region Based Gene Expression Via Reanalysis of Publicly Available Microarray Data Sets

    University of Louisville ThinkIR: The University of Louisville's Institutional Repository Electronic Theses and Dissertations 5-2018 Region based gene expression via reanalysis of publicly available microarray data sets. Ernur Saka University of Louisville Follow this and additional works at: https://ir.library.louisville.edu/etd Part of the Bioinformatics Commons, Computational Biology Commons, and the Other Computer Sciences Commons Recommended Citation Saka, Ernur, "Region based gene expression via reanalysis of publicly available microarray data sets." (2018). Electronic Theses and Dissertations. Paper 2902. https://doi.org/10.18297/etd/2902 This Doctoral Dissertation is brought to you for free and open access by ThinkIR: The University of Louisville's Institutional Repository. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of ThinkIR: The University of Louisville's Institutional Repository. This title appears here courtesy of the author, who has retained all other copyrights. For more information, please contact [email protected]. REGION BASED GENE EXPRESSION VIA REANALYSIS OF PUBLICLY AVAILABLE MICROARRAY DATA SETS By Ernur Saka B.S. (CEng), University of Dokuz Eylul, Turkey, 2008 M.S., University of Louisville, USA, 2011 A Dissertation Submitted To the J. B. Speed School of Engineering in Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Computer Science and Engineering Department of Computer Engineering and Computer Science University of Louisville Louisville, Kentucky May 2018 Copyright 2018 by Ernur Saka All rights reserved REGION BASED GENE EXPRESSION VIA REANALYSIS OF PUBLICLY AVAILABLE MICROARRAY DATA SETS By Ernur Saka B.S. (CEng), University of Dokuz Eylul, Turkey, 2008 M.S., University of Louisville, USA, 2011 A Dissertation Approved On April 20, 2018 by the following Committee __________________________________ Dissertation Director Dr.
  • Clathrin Heavy and Light Chain Isoforms Originated by Independent Mechanisms of Gene Duplication During Chordate Evolution

    Clathrin Heavy and Light Chain Isoforms Originated by Independent Mechanisms of Gene Duplication During Chordate Evolution

    Clathrin heavy and light chain isoforms originated by independent mechanisms of gene duplication during chordate evolution Diane E. Wakeham†‡, Laurent Abi-Rached‡§, Mhairi C. Towler†¶, Jeremy D. Wilbur†ʈ, Peter Parham§, and Frances M. Brodsky†,†† †The G. W. Hooper Foundation and Departments of Biopharmaceutical Sciences, Pharmaceutical Chemistry, and Microbiology and Immunology and ʈBiophysics Program, University of California, San Francisco, CA 94143-0552; and §Department of Structural Biology and Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305 Communicated by J. Michael Bishop, University of California, San Francisco, CA, March 22, 2005 (received for review January 14, 2005) In humans, there are two isoforms each of clathrin heavy chain biogenesis. CHC17 is expressed ubiquitously in vertebrate tissues (CHC17 and CHC22) and light chain (LCa and LCb) subunits, all and a functional orthologue is present in all eukaryotic organ- encoded by separate genes. CHC17 forms the ubiquitous clathrin- isms analyzed. The CHC22 isoform is highly expressed in human coated vesicles that mediate membrane traffic. CHC22 is implicated skeletal muscle, with a low level detected in other tissues. CHC22 in specialized membrane organization in skeletal muscle. CHC17 is is concentrated at neuromuscular and myotendinous junctions, bound and regulated by LCa and LCb, whereas CHC22 does not and its expression increases during myogenesis and muscle functionally interact with either light chain. The imbalanced inter- regeneration (10, 11). Thus, CHC22 appears to have a role actions between clathrin subunit isoforms suggest a distinct evo- distinct from CHC17 in specialized muscle membrane organi- lutionary history for each isoform pair. Phylogenetic and sequence zation. CHC17 and CHC22 have a remarkably high protein sequence identity (85%), despite their evident differences in analysis placed both heavy and light chain gene duplications function.
  • Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation

    Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation

    BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
  • Clinical Impact of Copy Number Variation Changes in Bladder Cancer Samples

    Clinical Impact of Copy Number Variation Changes in Bladder Cancer Samples

    EXPERIMENTAL AND THERAPEUTIC MEDICINE 22: 901, 2021 Clinical impact of copy number variation changes in bladder cancer samples VICTORIA SPASOVA1, BORIS MLADENOV2, SIMEON RANGELOV3, ZORA HAMMOUDEH1, DESISLAVA NESHEVA1, DIMITAR SERBEZOV1, RADA STANEVA1,4, SAVINA HADJIDEKOVA1,4, MIHAIL GANEV1, LUBOMIR BALABANSKI1,5, RADOSLAVA VAZHAROVA5,6, CHAVDAR SLAVOV3, DRAGA TONCHEVA1 and OLGA ANTONOVA1 1Department of Medical Genetics, Medical University‑Sofia, 1431 Sofia;2 Department of Urology, UMBALSM N.I. Pirogov, 1606 Sofia; 3Department of Urology, Tsaritsa Yoanna University Hospital, 1527 Sofia; 4Medical Genetics Laboratory, Nadezhda Women's Health Hospital, 1373 Sofia; 5Medical Genetics Laboratory, GARH Malinov, 1680 Sofia; 6Department of Biology, Medical Genetics and Microbiology, Faculty of Medicine, Sofia University St. Kliment Ohridski, 1407 Sofia, Bulgaria Received November 30, 2019; Accepted February 18, 2021 DOI: 10.3892/etm.2021.10333 Abstract. The aim of the present study was to detect copy uroepithelial tumours may lay a foundation for implementing number variations (CNVs) related to tumour progression and molecular CNV profiling of bladder tumours as part of a metastasis of urothelial carcinoma through whole‑genome routine progression risk estimation strategy, thus expanding scanning. A total of 30 bladder cancer samples staged from the personalized therapeutic approach. pTa to pT4 were included in the study. DNA was extracted from freshly frozen tissue via standard phenol‑chloroform extraction Introduction and CNV analysis was performed on two alternative platforms (CytoChip Oligo aCGH, 4x44K and Infinium OncoArray‑500K The most successful approach to treating a disease has BeadChip; Illumina, Inc.). Data were analysed with BlueFuse always been etiological therapy. In the case of bladder Multi software and Karyostudio, respectively.
  • Supplementary Table 1

    Supplementary Table 1

    Supplementary Table 1. 492 genes are unique to 0 h post-heat timepoint. The name, p-value, fold change, location and family of each gene are indicated. Genes were filtered for an absolute value log2 ration 1.5 and a significance value of p ≤ 0.05. Symbol p-value Log Gene Name Location Family Ratio ABCA13 1.87E-02 3.292 ATP-binding cassette, sub-family unknown transporter A (ABC1), member 13 ABCB1 1.93E-02 −1.819 ATP-binding cassette, sub-family Plasma transporter B (MDR/TAP), member 1 Membrane ABCC3 2.83E-02 2.016 ATP-binding cassette, sub-family Plasma transporter C (CFTR/MRP), member 3 Membrane ABHD6 7.79E-03 −2.717 abhydrolase domain containing 6 Cytoplasm enzyme ACAT1 4.10E-02 3.009 acetyl-CoA acetyltransferase 1 Cytoplasm enzyme ACBD4 2.66E-03 1.722 acyl-CoA binding domain unknown other containing 4 ACSL5 1.86E-02 −2.876 acyl-CoA synthetase long-chain Cytoplasm enzyme family member 5 ADAM23 3.33E-02 −3.008 ADAM metallopeptidase domain Plasma peptidase 23 Membrane ADAM29 5.58E-03 3.463 ADAM metallopeptidase domain Plasma peptidase 29 Membrane ADAMTS17 2.67E-04 3.051 ADAM metallopeptidase with Extracellular other thrombospondin type 1 motif, 17 Space ADCYAP1R1 1.20E-02 1.848 adenylate cyclase activating Plasma G-protein polypeptide 1 (pituitary) receptor Membrane coupled type I receptor ADH6 (includes 4.02E-02 −1.845 alcohol dehydrogenase 6 (class Cytoplasm enzyme EG:130) V) AHSA2 1.54E-04 −1.6 AHA1, activator of heat shock unknown other 90kDa protein ATPase homolog 2 (yeast) AK5 3.32E-02 1.658 adenylate kinase 5 Cytoplasm kinase AK7
  • Rabbit Anti-Phospho-BCAR1-SL12575R

    Rabbit Anti-Phospho-BCAR1-SL12575R

    SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-phospho-BCAR1 SL12575R-FITC Product Name: Anti-phospho-BCAR1 (Tyr751)/FITC Chinese Name: FITC标记的磷酸化乳腺癌抗雌激素耐药蛋白1抗体 BCAR1 (phospho Y751); BCAR1(phospho Y751); p-BCAR1(p-Tyr751); Breast cancer anti estrogen resistance 1 protein; BCAR 1; Bcar1; BCAR1_HUMAN; Breast cancer Alias: anti estrogen resistance 1; Breast cancer anti-estrogen resistance protein 1; CAS; Cas scaffolding protein family member 1; Crk associated substrate; Crk associated substrate p130Cas; CRK-associated substrate; CRKAS; P130CAS. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 93kDa Cellular localization: The cell membrane Form: Lyophilized or Liquid Concentration: 1mg/mlwww.sunlongbiotech.com KLH conjugated synthesised phosphopeptide derived from human BCAR1 around the immunogen: phosphorylation site of Tyr751 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: Product Detail: p130 represents one of several known substrates for v-Crk encoded p47. p130 Cas (for Crk-associated substrate) exhibits a high level of tyrosine phosphorylation and is tightly associated with v-Crk, suggesting a role in v-Crk-mediated cell signaling.
  • Comparative Analysis of the Ubiquitin-Proteasome System in Homo Sapiens and Saccharomyces Cerevisiae

    Comparative Analysis of the Ubiquitin-Proteasome System in Homo Sapiens and Saccharomyces Cerevisiae

    Comparative Analysis of the Ubiquitin-proteasome system in Homo sapiens and Saccharomyces cerevisiae Inaugural-Dissertation zur Erlangung des Doktorgrades der Mathematisch-Naturwissenschaftlichen Fakultät der Universität zu Köln vorgelegt von Hartmut Scheel aus Rheinbach Köln, 2005 Berichterstatter: Prof. Dr. R. Jürgen Dohmen Prof. Dr. Thomas Langer Dr. Kay Hofmann Tag der mündlichen Prüfung: 18.07.2005 Zusammenfassung I Zusammenfassung Das Ubiquitin-Proteasom System (UPS) stellt den wichtigsten Abbauweg für intrazelluläre Proteine in eukaryotischen Zellen dar. Das abzubauende Protein wird zunächst über eine Enzym-Kaskade mit einer kovalent gebundenen Ubiquitinkette markiert. Anschließend wird das konjugierte Substrat vom Proteasom erkannt und proteolytisch gespalten. Ubiquitin besitzt eine Reihe von Homologen, die ebenfalls posttranslational an Proteine gekoppelt werden können, wie z.B. SUMO und NEDD8. Die hierbei verwendeten Aktivierungs- und Konjugations-Kaskaden sind vollständig analog zu der des Ubiquitin- Systems. Es ist charakteristisch für das UPS, daß sich die Vielzahl der daran beteiligten Proteine aus nur wenigen Proteinfamilien rekrutiert, die durch gemeinsame, funktionale Homologiedomänen gekennzeichnet sind. Einige dieser funktionalen Domänen sind auch in den Modifikations-Systemen der Ubiquitin-Homologen zu finden, jedoch verfügen diese Systeme zusätzlich über spezifische Domänentypen. Homologiedomänen lassen sich als mathematische Modelle in Form von Domänen- deskriptoren (Profile) beschreiben. Diese Deskriptoren können wiederum dazu verwendet werden, mit Hilfe geeigneter Verfahren eine gegebene Proteinsequenz auf das Vorliegen von entsprechenden Homologiedomänen zu untersuchen. Da die im UPS involvierten Homologie- domänen fast ausschließlich auf dieses System und seine Analoga beschränkt sind, können domänen-spezifische Profile zur Katalogisierung der UPS-relevanten Proteine einer Spezies verwendet werden. Auf dieser Basis können dann die entsprechenden UPS-Repertoires verschiedener Spezies miteinander verglichen werden.