RNA-Sequencing Analysis of Hepg2 Cells Treated with Atorvastatin
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Kids First Pediatric Research Program (Kids First) Poster Session at ASHG Accelerating Pediatric Genomics Research Through Collaboration October 15Th, 2019
The Gabriella Miller Kids First Pediatric Research Program (Kids First) Poster Session at ASHG Accelerating Pediatric Genomics Research through Collaboration October 15th, 2019 Background The Gabriella Miller Kids First Pediatric Research Program (Kids First) is a trans- NIH Common Fund program initiated in response to the 2014 Gabriella Miller Kids First Research Act. The program’s vision is to alleviate suffering from childhood cancer and structural birth defects by fostering collaborative research to uncover the etiology of these diseases and support data sharing within the pediatric research community. This is implemented through developing the Gabriella Miller Kids First Data Resource (Kids First Data Resource) and populating this resource with whole genome sequence datasets and associated clinical and phenotypic information. Both childhood cancers and structural birth defects are critical and costly conditions associated with substantial morbidity and mortality. Elucidating the underlying genetic etiology of these diseases has the potential to profoundly improve preventative measures, diagnostics, and therapeutic interventions. Purpose During this evening poster session, attendees will gain a broad understanding of the utility of the genomic data generated by Kids First, learn about the progress of Kids First X01 cohort projects, and observe demonstrations of the tools and functionalities of the recently launched Kids First Data Resource Portal. The session is an opportunity for the scientific community and public to engage with Kids First investigators, collaborators, and a growing community of researchers, patient foundations, and families. Several other NIH and external data efforts will present posters and be available to discuss collaboration opportunities as we work together to accelerate pediatric research. -
Derivation of Hypermethylated Pluripotent Embryonic Stem Cells with High Potency
Cell Research (2018) 28:22-34. ORIGINAL ARTICLE www.nature.com/cr Derivation of hypermethylated pluripotent embryonic stem cells with high potency Siqin Bao1, 2, Walfred WC Tang3, Baojiang Wu2, Shinseog Kim3, 8, Jingyun Li4, Lin Li4, Toshihiro Kobayashi3, Caroline Lee3, Yanglin Chen2, Mengyi Wei2, Shudong Li5, Sabine Dietmann6, Fuchou Tang4, Xihe Li1, 2, 7, M Azim Surani3 1The State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, Inner Mongolia University, Hohhot 010070, China; 2Research Center for Animal Genetic Resources of Mongolia Plateau, College of Life Sciences, Inner Mongolia University, Hohhot 010070, China; 3Wellcome Trust Cancer Research UK Gurdon Institute, Tennis Court Road, University of Cam- bridge, Cambridge CB2 1QN, UK; 4BIOPIC, School of Life Sciences, Peking University, Beijing 100871, China; 5Cancer Research UK and Medical Research Council Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Ox- ford OX3 7DQ, UK; 6Wellcome Trust-Medical Research Council Stem Cell Institute, Tennis Court Road, University of Cambridge, Cambridge CB2 3EG, UK; 7Inner Mongolia Saikexing Institute of Breeding and Reproductive Biotechnology in Domestic Animal, Hohhot 011517, China Naive hypomethylated embryonic pluripotent stem cells (ESCs) are developmentally closest to the preimplanta- tion epiblast of blastocysts, with the potential to contribute to all embryonic tissues and the germline, excepting the extra-embryonic tissues in chimeric embryos. By contrast, epiblast stem cells (EpiSCs) resembling postimplantation epiblast are relatively more methylated and show a limited potential for chimerism. Here, for the first time, we re- veal advanced pluripotent stem cells (ASCs), which are developmentally beyond the pluripotent cells in the inner cell mass but with higher potency than EpiSCs. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Identification of Novel Y Chromosome Encoded Transcripts by Testis Transcriptome Analysis of Mice with Deletions of the Y Chromo
Open Access Research2005TouréetVolume al. 6, Issue 12, Article R102 Identification of novel Y chromosome encoded transcripts by testis comment transcriptome analysis of mice with deletions of the Y chromosome long arm Aminata Touré¤*, Emily J Clemente¤†, Peter JI Ellis†, Shantha K Mahadevaiah*, Obah A Ojarikre*, Penny AF Ball‡, Louise Reynard*, Kate L Loveland‡, Paul S Burgoyne* and Nabeel A Affara† reviews Addresses: *Division of Developmental Genetics, MRC National Institute for Medical Research, Mill Hill, London, NW7 1AA, UK. †University of Cambridge, Department of Pathology, Tennis Court Road, Cambridge, CB2 1QP, UK. ‡Monash Institute of Medical Research, Monash University, and The Australian Research Council Centre of Excellence in Biotechnology and Development, Melbourne, Victoria 3168 Australia. ¤ These authors contributed equally to this work. Correspondence: Paul S Burgoyne. E-mail: [email protected] reports Published: 2 December 2005 Received: 17 June 2005 Revised: 19 September 2005 Genome Biology 2005, 6:R102 (doi:10.1186/gb-2005-6-12-r102) Accepted: 27 October 2005 The electronic version of this article is the complete one and can be found online at http://genomebiology.com/2005/6/12/R102 deposited research © 2005 Touré et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Y<p>Microarraymosome chromosome long arm -analysis encoded (MSYq) of mouse identifiedthe changes testis novel transcripts in the Y chromosome-encoded testis transcriptome resulting transcripts.</p> from deletions of the male-specific region on the mouse chro- Abstract Background: The male-specific region of the mouse Y chromosome long arm (MSYq) is research refereed comprised largely of repeated DNA, including multiple copies of the spermatid-expressed Ssty gene family. -
Investigation of the Underlying Hub Genes and Molexular Pathogensis in Gastric Cancer by Integrated Bioinformatic Analyses
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Investigation of the underlying hub genes and molexular pathogensis in gastric cancer by integrated bioinformatic analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 22, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract The high mortality rate of gastric cancer (GC) is in part due to the absence of initial disclosure of its biomarkers. The recognition of important genes associated in GC is therefore recommended to advance clinical prognosis, diagnosis and and treatment outcomes. The current investigation used the microarray dataset GSE113255 RNA seq data from the Gene Expression Omnibus database to diagnose differentially expressed genes (DEGs). Pathway and gene ontology enrichment analyses were performed, and a proteinprotein interaction network, modules, target genes - miRNA regulatory network and target genes - TF regulatory network were constructed and analyzed. Finally, validation of hub genes was performed. The 1008 DEGs identified consisted of 505 up regulated genes and 503 down regulated genes. -
Molecular Effects of Isoflavone Supplementation Human Intervention Studies and Quantitative Models for Risk Assessment
Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis committee Promotors Prof. Dr Pieter van ‘t Veer Professor of Nutritional Epidemiology Wageningen University Prof. Dr Evert G. Schouten Emeritus Professor of Epidemiology and Prevention Wageningen University Co-promotors Dr Anouk Geelen Assistant professor, Division of Human Nutrition Wageningen University Dr Lydia A. Afman Assistant professor, Division of Human Nutrition Wageningen University Other members Prof. Dr Jaap Keijer, Wageningen University Dr Hubert P.J.M. Noteborn, Netherlands Food en Consumer Product Safety Authority Prof. Dr Yvonne T. van der Schouw, UMC Utrecht Dr Wendy L. Hall, King’s College London This research was conducted under the auspices of the Graduate School VLAG (Advanced studies in Food Technology, Agrobiotechnology, Nutrition and Health Sciences). Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis submitted in fulfilment of the requirements for the degree of doctor at Wageningen University by the authority of the Rector Magnificus Prof. Dr M.J. Kropff, in the presence of the Thesis Committee appointed by the Academic Board to be defended in public on Friday 20 June 2014 at 13.30 p.m. in the Aula. Vera van der Velpen Molecular effects of isoflavone supplementation: Human intervention studies and quantitative models for risk assessment 154 pages PhD thesis, Wageningen University, Wageningen, NL (2014) With references, with summaries in Dutch and English ISBN: 978-94-6173-952-0 ABSTRact Background: Risk assessment can potentially be improved by closely linked experiments in the disciplines of epidemiology and toxicology. -
Supplementary Materials
Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine -
Downregulation of Rap1gap Through Epigenetic Silencing and Loss of Heterozygosity Promotes Invasion and Progression of Thyroid Tumors
Published OnlineFirst February 2, 2010; DOI: 10.1158/0008-5472.CAN-09-2812 Published Online First on February 2, 2010 as 10.1158/0008-5472.CAN-09-2812 Molecular and Cellular Pathobiology Cancer Research Downregulation of Rap1GAP through Epigenetic Silencing and Loss of Heterozygosity Promotes Invasion and Progression of Thyroid Tumors Hui Zuo1, Manoj Gandhi1, Martin M. Edreira2, Daniel Hochbaum2, Vishwajit L. Nimgaonkar3, Ping Zhang1, James DiPaola1, Viktoria Evdokimova1, Daniel L. Altschuler2, and Yuri E. Nikiforov1 Abstract Thyroid cancer is the most common type of endocrine malignancy, encompassing tumors with various levels of invasive growth and aggressiveness. Rap1GAP, a Rap1 GTPase-activating protein, inhibits the RAS superfamily protein Rap1 by facilitating hydrolysis of GTP to GDP. In this study, we analyzed 197 thyroid tumor samples and showed that Rap1GAP was frequently lost or downregulated in various types of tumors, particularly in the most invasive and aggressive forms of thyroid cancer. The downregulation was due to pro- moter hypermethylation and/or loss of heterozygosity, found in the majority of thyroid tumors. Treatment with demethylating agent 5-aza-deoxycytidine and/or histone deacetylation inhibitor trichostatin A induced gene reexpression in thyroid cells. A genetic polymorphism, Y609C, was seen in 7% of thyroid tumors but was not related to gene downregulation. Loss of Rap1GAP expression correlated with tumor invasiveness but not with specific mutations activating the mitogen-activated protein kinase pathway. Rap1GAP downregulation was required in vitro for cell migration and Matrigel invasion. Recovery of Rap1GAP expression inhibited thy- roid cell proliferation and colony formation. Overall, our findings indicate that epigenetic or genetic loss of Rap1GAP is very common in thyroid cancer, where these events are sufficient to promote cell proliferation and invasion. -
A Set of Regulatory Genes Co-Expressed in Embryonic Human Brain Is Implicated in Disrupted Speech Development
Molecular Psychiatry https://doi.org/10.1038/s41380-018-0020-x ARTICLE A set of regulatory genes co-expressed in embryonic human brain is implicated in disrupted speech development 1 1 1 2 3 Else Eising ● Amaia Carrion-Castillo ● Arianna Vino ● Edythe A. Strand ● Kathy J. Jakielski ● 4,5 6 7 8 9 Thomas S. Scerri ● Michael S. Hildebrand ● Richard Webster ● Alan Ma ● Bernard Mazoyer ● 1,10 4,5 6,11 6,12 13 Clyde Francks ● Melanie Bahlo ● Ingrid E. Scheffer ● Angela T. Morgan ● Lawrence D. Shriberg ● Simon E. Fisher 1,10 Received: 22 September 2017 / Revised: 3 December 2017 / Accepted: 2 January 2018 © The Author(s) 2018. This article is published with open access Abstract Genetic investigations of people with impaired development of spoken language provide windows into key aspects of human biology. Over 15 years after FOXP2 was identified, most speech and language impairments remain unexplained at the molecular level. We sequenced whole genomes of nineteen unrelated individuals diagnosed with childhood apraxia of speech, a rare disorder enriched for causative mutations of large effect. Where DNA was available from unaffected parents, CHD3 SETD1A WDR5 fi 1234567890();,: we discovered de novo mutations, implicating genes, including , and . In other probands, we identi ed novel loss-of-function variants affecting KAT6A, SETBP1, ZFHX4, TNRC6B and MKL2, regulatory genes with links to neurodevelopment. Several of the new candidates interact with each other or with known speech-related genes. Moreover, they show significant clustering within a single co-expression module of genes highly expressed during early human brain development. This study highlights gene regulatory pathways in the developing brain that may contribute to acquisition of proficient speech. -
Stroke Genetics and Genomics
Faculdade de Medicina da Universidade de Lisboa Unidade Neurológica de Investigação Clínica PhD Thesis Stroke Genetics and Genomics Tiago Krug Coelho Host Institution: Instituto Gulbenkian de Ciência Supervisor at Instituto Gulbenkian de Ciência: Doctor Sofia Oliveira Supervisor at Faculdade de Medicina da Universidade de Lisboa: Professor José Ferro PhD in Biomedical Sciences Specialization in Neurosciences 2010 Stroke Genetics and Genomics A ciência tem, de facto, um único objectivo: a verdade. Não esgota perfeitamente a sua tarefa se não descobre a causa do todo. Chiara Lubich i Stroke Genetics and Genomics ii Stroke Genetics and Genomics A impressão desta dissertação foi aprovada pela Comissão Coordenadora do Conselho Científico da Faculdade de Medicina de Lisboa em reunião de 28 de Setembro de 2010. iii Stroke Genetics and Genomics iv Stroke Genetics and Genomics As opiniões expressas são da exclusiva responsabilidade do seu autor. v Stroke Genetics and Genomics vi Stroke Genetics and Genomics Abstract ABSTRACT This project presents a comprehensive approach to the identification of new genes that influence the risk for developing stroke. Stroke is the leading cause of death in Portugal and the third leading cause of death in the developed world. It is even more disabling than lethal, and the persistent neurological impairment and physical disability caused by stroke have a very high socioeconomic cost. Moreover, the number of affected individuals is expected to increase with the current aging of the population. Stroke is a “brain attack” cutting off vital blood and oxygen to the brain cells and it is a complex disease resulting from environmental and genetic factors. -
Mouse REC114 Is Essential for Meiotic DNA Double-Strand Break Formation and Forms a Complex with MEI4
Published Online: 10 December, 2018 | Supp Info: http://doi.org/10.26508/lsa.201800259 Downloaded from life-science-alliance.org on 26 September, 2021 Research Article Mouse REC114 is essential for meiotic DNA double-strand break formation and forms a complex with MEI4 Rajeev Kumar2,*, Cecilia Oliver1,*, Christine Brun1,*, Ariadna B Juarez-Martinez3, Yara Tarabay1, Jan Kadlec3, Bernard de Massy1 Programmed formation of DNA double-strand breaks (DSBs) during meiotic prophase to allow homologues to find each other initiates the meiotic homologous recombination pathway. This and to be connected by reciprocal products of recombination (i.e., pathway is essential for proper chromosome segregation at the crossovers) (Hunter, 2015). This homologous recombination path- first meiotic division and fertility. Meiotic DSBs are catalyzed by way is initiated by the formation of DNA double-strand breaks Spo11. Several other proteins are essential for meiotic DSB for- (DSBs) (de Massy, 2013) that are preferentially repaired using the mation, including three evolutionarily conserved proteins first homologous chromatid as a template. Meiotic DSB formation and identified in Saccharomyces cerevisiae (Mer2, Mei4, and Rec114). repair are expected to be tightly regulated because improper DSB These three S. cerevisiae proteins and their mouse orthologs repair is a potential threat to genome integrity (Sasaki et al, 2010; (IHO1, MEI4, and REC114) co-localize on the axes of meiotic Keeney et al, 2014). In Saccharomyces cerevisiae, several genes chromosomes, and mouse IHO1 and MEI4 are essential for meiotic are essential for their formation and at least five of them are Rec114 DSB formation. Here, we show that mouse is required for evolutionarily conserved. -
Patterns and Mechanisms of Sex Ratio Distortion in the Collaborative
bioRxiv preprint doi: https://doi.org/10.1101/2021.06.23.449644; this version posted June 23, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Patterns and Mechanisms of Sex Ratio Distortion in the 2 Collaborative Cross Mouse Mapping Population 3 4 5 Brett A. Haines*, Francesca Barradale†, Beth L. Dumont*,‡ 6 7 8 * The Jackson Laboratory, 600 Main Street, Bar Harbor ME 04609 9 † Department of Biology, Williams College, 59 Lab Campus Drive, Williamstown, MA 01267 10 11 ‡ Tufts University, Graduate School of Biomedical Sciences, 136 Harrison Ave, Boston MA 12 02111 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.06.23.449644; this version posted June 23, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 13 Running Title: Sex Ratio Distortion in House Mice 14 15 Key words: sex ratio distortion, Collaborative Cross, intergenomic conflict, sex chromosomes, 16 ampliconic genes, Slx, Slxl1, Sly, Diversity Outbred, house mouse 17 18 Address for Correspondence: 19 20 Beth Dumont 21 The Jackson Laboratory 22 600 Main Street 23 Bar Harbor, ME 04609 24 25 P: 207-288-6647 26 E: [email protected] 2 bioRxiv preprint doi: https://doi.org/10.1101/2021.06.23.449644; this version posted June 23, 2021.