Mouse Plekhg2 Knockout Project (CRISPR/Cas9)
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Open Data for Differential Network Analysis in Glioma
International Journal of Molecular Sciences Article Open Data for Differential Network Analysis in Glioma , Claire Jean-Quartier * y , Fleur Jeanquartier y and Andreas Holzinger Holzinger Group HCI-KDD, Institute for Medical Informatics, Statistics and Documentation, Medical University Graz, Auenbruggerplatz 2/V, 8036 Graz, Austria; [email protected] (F.J.); [email protected] (A.H.) * Correspondence: [email protected] These authors contributed equally to this work. y Received: 27 October 2019; Accepted: 3 January 2020; Published: 15 January 2020 Abstract: The complexity of cancer diseases demands bioinformatic techniques and translational research based on big data and personalized medicine. Open data enables researchers to accelerate cancer studies, save resources and foster collaboration. Several tools and programming approaches are available for analyzing data, including annotation, clustering, comparison and extrapolation, merging, enrichment, functional association and statistics. We exploit openly available data via cancer gene expression analysis, we apply refinement as well as enrichment analysis via gene ontology and conclude with graph-based visualization of involved protein interaction networks as a basis for signaling. The different databases allowed for the construction of huge networks or specified ones consisting of high-confidence interactions only. Several genes associated to glioma were isolated via a network analysis from top hub nodes as well as from an outlier analysis. The latter approach highlights a mitogen-activated protein kinase next to a member of histondeacetylases and a protein phosphatase as genes uncommonly associated with glioma. Cluster analysis from top hub nodes lists several identified glioma-associated gene products to function within protein complexes, including epidermal growth factors as well as cell cycle proteins or RAS proto-oncogenes. -
Proteomic Identification of Potential Cancer Markers in Human Urine Using Subtractive Analysis
INTERNATIONAL JOURNAL OF ONCOLOGY 48: 1921-1932, 2016 Proteomic identification of potential cancer markers in human urine using subtractive analysis HOLGER HUSI1, RICHARD J.E. SKipworth2, ANDREW Cronshaw3, KENNETH C.H. FEARON2* and JAMES A. ROSS2* 1Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, G12 8QQ; 2School of Clinical Sciences, 3School of Biological Sciences, University of Edinburgh, Edinburgh, EH16 4SB, UK Received November 21, 2015; Accepted December 27, 2015 DOI: 10.3892/ijo.2016.3424 Abstract. Urine is an ideal medium in which to focus diag- Introduction nostic cancer research due to the non-invasive nature and ease of sampling. Many large-scale proteomic studies have Screening of human tissues for cancer biomarkers is an impor- shown that urine is unexpectedly complex. We hypothesised tant task in cancer diagnosis and treatment, which is hindered that novel diagnostic cancer biomarkers could be discovered by the complexity of the sample systems studied. A less using a comparative proteomic analysis of pre-existing data. complex system such as urine is a preferred medium to screen We assembled a database of 100 published datasets of 5,620 for protein or peptide biomarkers due to the non-invasive urinary proteins, as well as 46 datasets of 8,620 non-redundant sampling of patients, ease of sampling and the unrestricted proteins derived from kidney and blood proteome analyses. quantities obtainable. Urine is relatively stable in terms of The data were then used to either subtract or compare mole- protein/peptide composition and fragmentation compared cules from a novel urinary proteome profiling dataset that we with other bodily fluids such as serum, where proteolytic generated. -
Based on Network Pharmacology and RNA Sequencing Techniques to Explore the Molecular Mechanism of Huatan Jiangzhuo Decoction for Treating Hyperlipidemia
Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2021, Article ID 9863714, 16 pages https://doi.org/10.1155/2021/9863714 Research Article Based on Network Pharmacology and RNA Sequencing Techniques to Explore the Molecular Mechanism of Huatan Jiangzhuo Decoction for Treating Hyperlipidemia XiaowenZhou ,1 ZhenqianYan ,1 YaxinWang ,1 QiRen ,1 XiaoqiLiu ,2 GeFang ,3 Bin Wang ,4 and Xiantao Li 1 1Laboratory of TCM Syndrome Essence and Objectification, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China 2Guangzhou Sagene Tech Co., Ltd., Guangzhou 510006, China 3College of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha 410208, China 4Shenzhen Traditional Chinese Medicine Hospital, Shenzhen 518000, China Correspondence should be addressed to Xiantao Li; [email protected] Received 22 May 2020; Revised 12 March 2021; Accepted 18 March 2021; Published 12 April 2021 Academic Editor: Jianbo Wan Copyright © 2021 Xiaowen Zhou et al. +is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Hyperlipidemia, due to the practice of unhealthy lifestyles of modern people, has been a disturbance to a large portion of population worldwide. Recently, several scholars have turned their attention to Chinese medicine (CM) to seek out a lipid-lowering approach with high efficiency and low toxicity. +is study aimed to explore the mechanism of Huatan Jiangzhuo decoction (HTJZD, a prescription of CM) in the treatment of hyperlipidemia and to determine the major regulation pathways and potential key targets involved in the treatment process. -
A High-Throughput Approach to Uncover Novel Roles of APOBEC2, a Functional Orphan of the AID/APOBEC Family
Rockefeller University Digital Commons @ RU Student Theses and Dissertations 2018 A High-Throughput Approach to Uncover Novel Roles of APOBEC2, a Functional Orphan of the AID/APOBEC Family Linda Molla Follow this and additional works at: https://digitalcommons.rockefeller.edu/ student_theses_and_dissertations Part of the Life Sciences Commons A HIGH-THROUGHPUT APPROACH TO UNCOVER NOVEL ROLES OF APOBEC2, A FUNCTIONAL ORPHAN OF THE AID/APOBEC FAMILY A Thesis Presented to the Faculty of The Rockefeller University in Partial Fulfillment of the Requirements for the degree of Doctor of Philosophy by Linda Molla June 2018 © Copyright by Linda Molla 2018 A HIGH-THROUGHPUT APPROACH TO UNCOVER NOVEL ROLES OF APOBEC2, A FUNCTIONAL ORPHAN OF THE AID/APOBEC FAMILY Linda Molla, Ph.D. The Rockefeller University 2018 APOBEC2 is a member of the AID/APOBEC cytidine deaminase family of proteins. Unlike most of AID/APOBEC, however, APOBEC2’s function remains elusive. Previous research has implicated APOBEC2 in diverse organisms and cellular processes such as muscle biology (in Mus musculus), regeneration (in Danio rerio), and development (in Xenopus laevis). APOBEC2 has also been implicated in cancer. However the enzymatic activity, substrate or physiological target(s) of APOBEC2 are unknown. For this thesis, I have combined Next Generation Sequencing (NGS) techniques with state-of-the-art molecular biology to determine the physiological targets of APOBEC2. Using a cell culture muscle differentiation system, and RNA sequencing (RNA-Seq) by polyA capture, I demonstrated that unlike the AID/APOBEC family member APOBEC1, APOBEC2 is not an RNA editor. Using the same system combined with enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analyses I showed that, unlike the AID/APOBEC family member AID, APOBEC2 does not act as a 5-methyl-C deaminase. -
Supplementary Information – Postema Et Al., the Genetics of Situs Inversus Totalis Without Primary Ciliary Dyskinesia
1 Supplementary information – Postema et al., The genetics of situs inversus totalis without primary ciliary dyskinesia Table of Contents: Supplementary Methods 2 Supplementary Results 5 Supplementary References 6 Supplementary Tables and Figures Table S1. Subject characteristics 9 Table S2. Inbreeding coefficients per subject 10 Figure S1. Multidimensional scaling to capture overall genomic diversity 11 among the 30 study samples Table S3. Significantly enriched gene-sets under a recessive mutation model 12 Table S4. Broader list of candidate genes, and the sources that led to their 13 inclusion Table S5. Potential recessive and X-linked mutations in the unsolved cases 15 Table S6. Potential mutations in the unsolved cases, dominant model 22 2 1.0 Supplementary Methods 1.1 Participants Fifteen people with radiologically documented SIT, including nine without PCD and six with Kartagener syndrome, and 15 healthy controls matched for age, sex, education and handedness, were recruited from Ghent University Hospital and Middelheim Hospital Antwerp. Details about the recruitment and selection procedure have been described elsewhere (1). Briefly, among the 15 people with radiologically documented SIT, those who had symptoms reminiscent of PCD, or who were formally diagnosed with PCD according to their medical record, were categorized as having Kartagener syndrome. Those who had no reported symptoms or formal diagnosis of PCD were assigned to the non-PCD SIT group. Handedness was assessed using the Edinburgh Handedness Inventory (EHI) (2). Tables 1 and S1 give overviews of the participants and their characteristics. Note that one non-PCD SIT subject reported being forced to switch from left- to right-handedness in childhood, in which case five out of nine of the non-PCD SIT cases are naturally left-handed (Table 1, Table S1). -
Transdifferentiation of Human Mesenchymal Stem Cells
Transdifferentiation of Human Mesenchymal Stem Cells Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Julius-Maximilians-Universität Würzburg vorgelegt von Tatjana Schilling aus San Miguel de Tucuman, Argentinien Würzburg, 2007 Eingereicht am: Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Martin J. Müller Gutachter: PD Dr. Norbert Schütze Gutachter: Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am: Hiermit erkläre ich ehrenwörtlich, dass ich die vorliegende Dissertation selbstständig angefertigt und keine anderen als die von mir angegebenen Hilfsmittel und Quellen verwendet habe. Des Weiteren erkläre ich, dass diese Arbeit weder in gleicher noch in ähnlicher Form in einem Prüfungsverfahren vorgelegen hat und ich noch keinen Promotionsversuch unternommen habe. Gerbrunn, 4. Mai 2007 Tatjana Schilling Table of contents i Table of contents 1 Summary ........................................................................................................................ 1 1.1 Summary.................................................................................................................... 1 1.2 Zusammenfassung..................................................................................................... 2 2 Introduction.................................................................................................................... 4 2.1 Osteoporosis and the fatty degeneration of the bone marrow..................................... 4 2.2 Adipose and bone -
Supplementary Table S2. List of Genes with Expression That Is Positively Correlated (Pearson Correlation Coefficient P>0.3)
Supplementary Table S2. List of genes with expression that is positively correlated (Pearson correlation coefficient p>0.3) with HOXA9 expression in the study by Sun et al (1). Most HOXA genes (indicated by bold face) show highly significant positive correlation with HOXA9 expression, except for HOXA6 and HOXA13, similar to our findings in the UCSF and MDA tumor sets. Note that HOXA11, which did not demonstrate a statistically significant positive correlation with HOXA9 expression in both the UCSF and MDA tumor sets, demonstrates a substantially lower correlation coefficient relative to the other HOXA genes that positively correlate with HOXA9 expression in the study by Sun et al. These data were obtained from the online ONCOMINE database (www.oncomine.org) (2) searching for transcripts positively correlated with HOXA9 expression. Gene Name Gene Symbol Reporter ID Correlation (p) homeobox A9 HOXA9 214651_s_at .7682 homeobox A9 HOXA9 209905_at .7682 homeobox A10 HOXA10 213150_at .6058 homeobox A7 HOXA7 235753_at .6058 homeobox A10 HOXA10 213147_at .6058 homeobox A7 HOXA7 206847_s_at .6058 homeobox A4 HOXA4 206289_at .5741 homeobox A2 HOXA2 1557051_s_at .5379 homeobox A1 HOXA1 214639_s_at .5379 homeobox A3 HOXA3 235521_at .5379 homeobox B2 HOXB2 205453_at .5379 homeobox B3 HOXB3 228904_at .5379 EST EST 1555907_at .5379 homeobox A4 HOXA4 230080_at .5379 homeobox A2 HOXA2 228642_at .5379 homeobox A2 HOXA2 1557050_at .5379 homeobox A5 HOXA5 213844_at .5379 homeobox A2 HOXA2 214457_at .5113 homeobox B7 HOXB7 204778_x_at .5042 homeobox C6 HOXC6 -
Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein -
Integrated Transcriptome and in Vitro Analysis Revealed Anti-Proliferative
www.nature.com/scientificreports OPEN Integrated transcriptome and in vitro analysis revealed anti-proliferative efect of citral Received: 26 November 2018 Accepted: 5 March 2019 in human stomach cancer through Published: xx xx xxxx apoptosis Sri Renukadevi Balusamy1, Sivasubramanian Ramani 1, Sathishkumar Natarajan 2, Yeon Ju Kim3 & Haribalan Perumalsamy3 Cancer is the second leading cause of death globally, particularly stomach cancer is third most common causes of cancer death worldwide. Citral possesses anti-tumor activity in various cancer cell lines, However its efect toward stomach cancer and its mechanism of action is have yet to be elucidated. The goal of the present study is to elucidate the role of citral in stomach cancer using transcriptome and in vitro approaches. We performed transcriptome analysis using RNA-seq and explored its capability to persuade apoptosis in AGS human stomach cancer cell lines in vitro. Furthermore, the enrichment and KEGG pathway results suggested that there are several genes involved to induce apoptosis pathway. Furthermore, our study also demonstrated that citral arrested colony formation and migration of cancer cells signifcantly than that of untreated cells. RNA-seq revealed a total of 125 million trimmed reads obtained from both control and citral treated groups respectively. A total number of 612 diferentially expressed genes (DEGs) were identifed which includes 216 genes up-regulated and 396 genes down- regulated genes after treatment. The enrichment analysis identifed DEGs genes from transcriptome libraries including cell death, cell cycle, apoptosis and cell growth. The present study showed the signifcant inhibition efect upon citral by regulating various genes involved in signaling pathways, inhibits metastasis, colony formation and induced apoptosis both in silico and in vitro. -
Network Reconstruction and Significant Pathway Extraction
Network Reconstruction and Significant Pathway Extraction Using Phosphoproteomic Data from Cancer Cells Marion Buffard, Aurélien Naldi, Ovidiu Radulescu, Peter Coopman, Romain Larive, Gilles Freiss To cite this version: Marion Buffard, Aurélien Naldi, Ovidiu Radulescu, Peter Coopman, Romain Larive, et al..Net- work Reconstruction and Significant Pathway Extraction Using Phosphoproteomic Data from Cancer Cells. Proteomics, Wiley-VCH Verlag, 2019, 19 (21-22), pp.1800450. 10.1002/pmic.201800450. hal- 03049205 HAL Id: hal-03049205 https://hal.archives-ouvertes.fr/hal-03049205 Submitted on 9 Dec 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Network reconstruction and significant pathway extraction using phosphoproteomic data from cancer cells BUFFARD Marion1,2, NALDI Aurélien3, RADULESCU Ovidiu2,#, COOPMAN Peter J1,#, LARIVE 5 Romain Maxime4,#,¶ and FREISS Gilles1,#,¶ # Equal contributing authors 1 IRCM, Univ Montpellier, ICM, INSERM, Montpellier, France. 10 2 DIMNP, Univ Montpellier, CNRS, Montpellier, France. 3 Computational Systems Biology Team, Institut de Biologie de l'École Normale Supérieure, Centre National de la Recherche Scientifique UMR8197, INSERM U1024, École Normale Supérieure, PSL Université, Paris, France. 4 IBMM, Univ Montpellier, CNRS, ENSCM, Montpellier, France. 15 ¶ To whom correspondence should be addressed at: Gilles FREISS, IRCM, INSERM U1194, 208 rue des Apothicaires, F-34298 Montpellier cedex 5, France. -
Biomedical Informatics
BIOMEDICAL INFORMATICS Abstract GENE LIST AUTOMATICALLY DERIVED FOR YOU (GLAD4U): DERIVING AND PRIORITIZING GENE LISTS FROM PUBMED LITERATURE JEROME JOURQUIN Thesis under the direction of Professor Bing Zhang Answering questions such as ―Which genes are related to breast cancer?‖ usually requires retrieving relevant publications through the PubMed search engine, reading these publications, and manually creating gene lists. This process is both time-consuming and prone to errors. We report GLAD4U (Gene List Automatically Derived For You), a novel, free web-based gene retrieval and prioritization tool. The quality of gene lists created by GLAD4U for three Gene Ontology terms and three disease terms was assessed using ―gold standard‖ lists curated in public databases. We also compared the performance of GLAD4U with that of another gene prioritization software, EBIMed. GLAD4U has a high overall recall. Although precision is generally low, its prioritization methods successfully rank truly relevant genes at the top of generated lists to facilitate efficient browsing. GLAD4U is simple to use, and its interface can be found at: http://bioinfo.vanderbilt.edu/glad4u. Approved ___________________________________________ Date _____________ GENE LIST AUTOMATICALLY DERIVED FOR YOU (GLAD4U): DERIVING AND PRIORITIZING GENE LISTS FROM PUBMED LITERATURE By Jérôme Jourquin Thesis Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE in Biomedical Informatics May, 2010 Nashville, Tennessee Approved: Professor Bing Zhang Professor Hua Xu Professor Daniel R. Masys ACKNOWLEDGEMENTS I would like to express profound gratitude to my advisor, Dr. Bing Zhang, for his invaluable support, supervision and suggestions throughout this research work. -
PLEKHG2 CRISPR/Cas9 KO Plasmid (H): Sc-413048
SANTA CRUZ BIOTECHNOLOGY, INC. PLEKHG2 CRISPR/Cas9 KO Plasmid (h): sc-413048 BACKGROUND APPLICATIONS The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and PLEKHG2 CRISPR/Cas9 KO Plasmid (h) is recommended for the disruption of CRISPR-associated protein (Cas9) system is an adaptive immune response gene expression in human cells. defense mechanism used by archea and bacteria for the degradation of foreign genetic material (4,6). This mechanism can be repurposed for other 20 nt non-coding RNA sequence: guides Cas9 functions, including genomic engineering for mammalian systems, such as to a specific target location in the genomic DNA gene knockout (KO) (1,2,3,5). CRISPR/Cas9 KO Plasmid products enable the U6 promoter: drives gRNA scaffold: helps Cas9 identification and cleavage of specific genes by utilizing guide RNA (gRNA) expression of gRNA bind to target DNA sequences derived from the Genome-scale CRISPR Knock-Out (GeCKO) v2 library developed in the Zhang Laboratory at the Broad Institute (3,5). Termination signal Green Fluorescent Protein: to visually REFERENCES verify transfection CRISPR/Cas9 Knockout Plasmid CBh (chicken β-Actin 1. Cong, L., et al. 2013. Multiplex genome engineering using CRISPR/Cas hybrid) promoter: drives expression of Cas9 systems. Science 339: 819-823. 2A peptide: allows production of both Cas9 and GFP from the 2. Mali, P., et al. 2013. RNA-guided human genome engineering via Cas9. same CBh promoter Science 339: 823-826. Nuclear localization signal 3. Ran, F.A., et al. 2013. Genome engineering using the CRISPR-Cas9 system. Nuclear localization signal SpCas9 ribonuclease Nat. Protoc. 8: 2281-2308.