Table S5.1 HUVEC Co-Culture Vs Worm-Free Up-Regulated Genes
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Insights from Conventional and Unconventional Myosins A
Structure-Function Analysis of Motor Proteins: Insights from Conventional and Unconventional Myosins A Thesis SUBMITTED TO THE FACULTY OF UNIVERSITY OF MINNESOTA BY Karl J. Petersen IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY Margaret A. Titus, Advisor David D. Thomas, Co-Advisor December 2016 © Karl J. Petersen 2016 Acknowledgements This thesis would not exist without the patient support of my advisors, Meg Titus and Dave Thomas. Any shortcomings are my own. Collaborators Holly Goodson, Anne Houdusse, and Gant Luxton also provided invaluable training and support. I am also grateful for essential services provided by departmental staff: Sarah Blakely Anderson, Octavian Cornea, Sarah Dittrich, Karen Hawkinson, Michelle Lewis, Mary Muwahid, Laurie O’Neill, Darlene Toedter, with apologies to others not listed. Thanks to friends and colleagues at the University of Minnesota: Ashley Arthur, Kelly Bower, Brett Colson, Sinziana Cornea, Chi Meng Fong, Greg Gillispie, Piyali Guhathakurta, Tejas Gupte, Tom Hays, Norma Jiménez Ramírez, Dawn Lowe, Allison MacLean, Santiago Martínez Cifuentes, Jared Matzke, Megan McCarthy, Joachim Mueller, Joe Muretta, Kurt Peterson, Mary Porter, Ewa Prochniewicz, Mike Ritt, Cosmo Saunders, Shiv Sivaramakrishnan, Ruth Sommese, Doug Tritschler, Brian Woolums. i Abstract Myosin motor proteins play fundamental roles in a multitude of cellular processes. Myosin generates force on cytoskeletal actin filaments to control cell shape, most dramatically during cytokinesis, and has a conserved role in defining cell polarity. Myosin contracts the actin cytoskeleton, ensuring prompt turnover of cellular adhesion sites, retracting the cell body during migration and development, and contracting muscle among diverse other functions. How myosins work, and why force generation is essential for their function, is in many cases an open question. -
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 -
Transcriptional Profiling Identifies the Lncrna PVT1 As a Novel Regulator of the Asthmatic Phenotype in Human Airway Smooth Muscle
Accepted Manuscript Transcriptional profiling identifies the lncRNA PVT1 as a novel regulator of the asthmatic phenotype in human airway smooth muscle Philip J. Austin, MSc, Eleni Tsitsiou, PhD, Charlotte Boardman, MD, Simon W. Jones, PhD, Mark A. Lindsay, PhD, Ian M. Adcock, PhD, Kian Fan Chung, MD PhD, Mark M. Perry, PhD PII: S0091-6749(16)30571-1 DOI: 10.1016/j.jaci.2016.06.014 Reference: YMAI 12203 To appear in: Journal of Allergy and Clinical Immunology Received Date: 5 April 2016 Revised Date: 24 May 2016 Accepted Date: 13 June 2016 Please cite this article as: Austin PJ, Tsitsiou E, Boardman C, Jones SW, Lindsay MA, Adcock IM, Chung KF, Perry MM, Transcriptional profiling identifies the lncRNA PVT1 as a novel regulator of the asthmatic phenotype in human airway smooth muscle, Journal of Allergy and Clinical Immunology (2016), doi: 10.1016/j.jaci.2016.06.014. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT 1 Transcriptional profiling identifies the lncRNA PVT1 as a novel 2 regulator of the asthmatic phenotype in human airway smooth muscle 3 4 Philip J. Austin MSc 1, Eleni Tsitsiou PhD 2, Charlotte Boardman MD 1, Simon W. -
Molecular Evolutionary Analysis of Plastid Genomes in Nonphotosynthetic Angiosperms and Cancer Cell Lines
The Pennsylvania State University The Graduate School Department or Biology MOLECULAR EVOLUTIONARY ANALYSIS OF PLASTID GENOMES IN NONPHOTOSYNTHETIC ANGIOSPERMS AND CANCER CELL LINES A Dissertation in Biology by Yan Zhang 2012 Yan Zhang Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Dec 2012 The Dissertation of Yan Zhang was reviewed and approved* by the following: Schaeffer, Stephen W. Professor of Biology Chair of Committee Ma, Hong Professor of Biology Altman, Naomi Professor of Statistics dePamphilis, Claude W Professor of Biology Dissertation Adviser Douglas Cavener Professor of Biology Head of Department of Biology *Signatures are on file in the Graduate School iii ABSTRACT This thesis explores the application of evolutionary theory and methods in understanding the plastid genome of nonphotosynthetic parasitic plants and role of mutations in tumor proliferations. We explore plastid genome evolution in parasitic angiosperms lineages that have given up the primary function of plastid genome – photosynthesis. Genome structure, gene contents, and evolutionary dynamics were analyzed and compared in both independent and related parasitic plant lineages. Our studies revealed striking similarities in changes of gene content and evolutionary dynamics with the loss of photosynthetic ability in independent nonphotosynthetic plant lineages. Evolutionary analysis suggests accelerated evolution in the plastid genome of the nonphotosynthetic plants. This thesis also explores the application of phylogenetic and evolutionary analysis in cancer biology. Although cancer has often been likened to Darwinian process, very little application of molecular evolutionary analysis has been seen in cancer biology research. In our study, phylogenetic approaches were used to explore the relationship of several hundred established cancer cell lines based on multiple sequence alignments constructed with variant codons and residues across 494 and 523 genes. -
Proteomic Expression Profile in Human Temporomandibular Joint
diagnostics Article Proteomic Expression Profile in Human Temporomandibular Joint Dysfunction Andrea Duarte Doetzer 1,*, Roberto Hirochi Herai 1 , Marília Afonso Rabelo Buzalaf 2 and Paula Cristina Trevilatto 1 1 Graduate Program in Health Sciences, School of Medicine, Pontifícia Universidade Católica do Paraná (PUCPR), Curitiba 80215-901, Brazil; [email protected] (R.H.H.); [email protected] (P.C.T.) 2 Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru 17012-901, Brazil; [email protected] * Correspondence: [email protected]; Tel.: +55-41-991-864-747 Abstract: Temporomandibular joint dysfunction (TMD) is a multifactorial condition that impairs human’s health and quality of life. Its etiology is still a challenge due to its complex development and the great number of different conditions it comprises. One of the most common forms of TMD is anterior disc displacement without reduction (DDWoR) and other TMDs with distinct origins are condylar hyperplasia (CH) and mandibular dislocation (MD). Thus, the aim of this study is to identify the protein expression profile of synovial fluid and the temporomandibular joint disc of patients diagnosed with DDWoR, CH and MD. Synovial fluid and a fraction of the temporomandibular joint disc were collected from nine patients diagnosed with DDWoR (n = 3), CH (n = 4) and MD (n = 2). Samples were subjected to label-free nLC-MS/MS for proteomic data extraction, and then bioinformatics analysis were conducted for protein identification and functional annotation. The three Citation: Doetzer, A.D.; Herai, R.H.; TMD conditions showed different protein expression profiles, and novel proteins were identified Buzalaf, M.A.R.; Trevilatto, P.C. -
Apoptotic Cells Inflammasome Activity During the Uptake of Macrophage
Downloaded from http://www.jimmunol.org/ by guest on September 29, 2021 is online at: average * The Journal of Immunology , 26 of which you can access for free at: 2012; 188:5682-5693; Prepublished online 20 from submission to initial decision 4 weeks from acceptance to publication April 2012; doi: 10.4049/jimmunol.1103760 http://www.jimmunol.org/content/188/11/5682 Complement Protein C1q Directs Macrophage Polarization and Limits Inflammasome Activity during the Uptake of Apoptotic Cells Marie E. Benoit, Elizabeth V. Clarke, Pedro Morgado, Deborah A. Fraser and Andrea J. Tenner J Immunol cites 56 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2012/04/20/jimmunol.110376 0.DC1 This article http://www.jimmunol.org/content/188/11/5682.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 29, 2021. The Journal of Immunology Complement Protein C1q Directs Macrophage Polarization and Limits Inflammasome Activity during the Uptake of Apoptotic Cells Marie E. -
Egfr Activates a Taz-Driven Oncogenic Program in Glioblastoma
EGFR ACTIVATES A TAZ-DRIVEN ONCOGENIC PROGRAM IN GLIOBLASTOMA by Minling Gao A thesis submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland March 2020 ©2020 Minling Gao All rights reserved Abstract Hyperactivated EGFR signaling is associated with about 45% of Glioblastoma (GBM), the most aggressive and lethal primary brain tumor in humans. However, the oncogenic transcriptional events driven by EGFR are still incompletely understood. We studied the role of the transcription factor TAZ to better understand master transcriptional regulators in mediating the EGFR signaling pathway in GBM. The transcriptional coactivator with PDZ- binding motif (TAZ) and its paralog gene, the Yes-associated protein (YAP) are two transcriptional co-activators that play important roles in multiple cancer types and are regulated in a context-dependent manner by various upstream signaling pathways, e.g. the Hippo, WNT and GPCR signaling. In GBM cells, TAZ functions as an oncogene that drives mesenchymal transition and radioresistance. This thesis intends to broaden our understanding of EGFR signaling and TAZ regulation in GBM. In patient-derived GBM cell models, EGF induced TAZ and its known gene targets through EGFR and downstream tyrosine kinases (ERK1/2 and STAT3). In GBM cells with EGFRvIII, an EGF-independent and constitutively active mutation, TAZ showed EGF- independent hyperactivation when compared to EGFRvIII-negative cells. These results revealed a novel EGFR-TAZ signaling axis in GBM cells. The second contribution of this thesis is that we performed next-generation sequencing to establish the first genome-wide map of EGF-induced TAZ target genes. -
Temporal Endogenous Gene Expression Profiles in Response to Polymer-Mediated Transfection and Profile Comparison to Lipid-Mediated Transfection Timothy M
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Biological Systems Engineering: Papers and Biological Systems Engineering Publications 2015 Temporal endogenous gene expression profiles in response to polymer-mediated transfection and profile comparison to lipid-mediated transfection Timothy M. Martin University of Nebraska Medical Center, [email protected] Sarah A. Plautz University of Nebraska-Lincoln, [email protected] Angela K. Pannier University of Nebraska-Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/biosysengfacpub Part of the Bioresource and Agricultural Engineering Commons, Environmental Engineering Commons, and the Other Civil and Environmental Engineering Commons Martin, Timothy M.; Plautz, Sarah A.; and Pannier, Angela K., "Temporal endogenous gene expression profiles in response to polymer-mediated transfection and profile comparison to lipid-mediated transfection" (2015). Biological Systems Engineering: Papers and Publications. 518. https://digitalcommons.unl.edu/biosysengfacpub/518 This Article is brought to you for free and open access by the Biological Systems Engineering at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Biological Systems Engineering: Papers and Publications by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Published in The Journal of Gene Medicine 17 (2015), pp. 33–53. doi 10.1002/jgm.2822 PMID: 25663627 Copyright © 2015 John Wiley & Sons, Ltd. Used by permission Submitted 17 November 2014; revised 1 February 2015; accepted 3 February 2015 digitalcommons.unl.edu Temporal endogenous gene expression profiles in response to polymer-mediated transfection and profile comparison to lipid-mediated transfection Timothy M. Martin,1 Sarah A. Plautz,2 and Angela K. -
Cultivado Com Queratinócitos Humanos Hacat Utilizando RNA-Seq
UNIVERSIDADE DE RIBEIRÃO PRETO- UNAERP PROGRAMA DE PÓS-GRADUAÇÃO EM BIOTECNOLOGIA UNIDADE DE BIOTECNOLOGIA Avaliação do perfil transcricional de Trichophyton rubrum co- cultivado com queratinócitos humanos HaCat utilizando RNA-Seq. MESTRANDA : Monise Fazolin Petrucelli ORIENTADORA: Profa. Dra. Ana Lúcia Fachin Saltoratto RIBEIRÃO PRETO- SP 2017 Mestranda: Monise Fazolin Petrucelli AVALIAÇÃO DO PERFIL TRANSCRICIONAL DE Trichophyton rubrum CO-CULTIVADO COM QUERATINÓCITOS HUMANOS HaCat UTILIZANDO RNA-SEQ. Dissertação de mestrado apresentada à Universidade de Ribeirão Preto UNAERP, como requisito para obtenção do título de Mestre em Biotecnologia. Orientadora: Profª. Drª. Ana Lúcia Fachin Saltoratto Ribeirão Preto 2017 Ficha catalográfica preparada pelo Centro de Processamento Técnico da Biblioteca Central da UNAERP - Universidade de Ribeirão Preto - AGRADECIMENTOS Primeiramente a Deus por permitir a realização desta conquista. Aos meus pais por todo o apoio, carinho e incentivo em todos os momentos e que foram fundamentais para que eu pudesse acreditar e vencer as etapas de maiores dificuldades. À minha orientadora, Prof. Drª. Ana Lúcia por todo o ensinamento proporcionado que contribuíram tanto para meu desenvolvimento pessoal e profissional além do apoio, incentivo, amizade e confiança depositada em mim para a realização deste trabalho. Ao Prof.Dr. Mozart Marins pelos conselhos e discussões que também nos auxiliaram durante a execução deste projeto. À colaboração oferecida pelo Prof. Dr. Wilson e pela técnica Kamila Peroni do Laboratório de Genética Molecular e Bioinformática do Hemocentro de Ribeirão Preto para a realização do sequenciamento e ao Prof. Dr. Pablo do Departamento de Genética da Faculdade de Medicina de Ribeirão Preto- USP pela colaboração e orientação nas análises de bioinformática. -
Genome-Wide Profiling of Druggable Active Tumor Defense Mechanisms to Enhance Cancer Immunotherapy
bioRxiv preprint doi: https://doi.org/10.1101/843185; this version posted November 15, 2019. 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. Genome-wide profiling of druggable active tumor defense mechanisms to enhance cancer immunotherapy Rigel J. Kishton1,2,*,#, Shashank J. Patel1,2,†,*, Suman K. Vodnala1,2, Amy E. Decker3, Yogin Patel1,2, Madhusudhanan Sukumar1,2, Tori N. Yamamoto1,2,4, Zhiya Yu1,2, Michelle Ji1,2, Amanda N. Henning1,2, Devikala Gurusamy1,2, Douglas C. Palmer1,2, Winifred Lo1, Anna Pasetto1, Parisa Malekzadeh1, Drew C. Deniger1, Kris C. Wood3, Neville E. Sanjana5,6, Nicholas P. Restifo1,2, #, § 1Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA 2Center for Cell-Based Therapy, National Cancer Institute, Bethesda, MD 20892, USA 3Department of Pharmacology & Cancer Biology, Duke University School of Medicine, Durham, NC, USA 4Immunology Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA 5New York Genome Center, New York, NY 10013 USA 6Department of Biology, New York University, New York, NY 10003, USA *These authors contributed equally to this work. †Present address: NextCure Inc., Beltsville, MD 20705, USA §Present address: Lyell Immunopharma, South San Francisco, CA 94080, USA #Corresponding authors. NPR: [email protected]. RJK: [email protected]. bioRxiv preprint doi: https://doi.org/10.1101/843185; this version posted November 15, 2019. 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. -
Running Head: MYH16 CORRELATIONAL STUDY 1
Running Head: MYH16 CORRELATIONAL STUDY 1 A Novel Correlational Study of Myosin Heavy Chain 16 and Skull Shape Evolution Running Head: MYH16 CORRELATIONAL STUDY 2 Abstract: Myosin Heavy Chain 16 (MYH16) is a super fast-twitch masticatory muscle protein expressed in most organisms. In 2004, Dr. Hansel Stedman’s lab discovered a mutation in MYH16 in the human lineage, and hypothesized that it led to the increased brain size in humans relative to non-human primates. Due to the lack of modern bioinformatics tools at their disposal at the time, Dr. Stedman could not fully prove or disprove this hypothesis, leading to intense debate. In an attempt to provide more information on this subject, this project seeks for a relationship between the presence/absence of MYH16 and brain size relative to the organism’s body. This study found that for organisms with mutated MYH16, there was a correlation between mutation and brain size, but for organisms with deleted MYH16, there was no such correlation. Though not a definitive answer, the results of this study provide an intriguing modification to Dr. Stedman’s original theory. Running Head: MYH16 CORRELATIONAL STUDY 3 1. Introduction: Evolution, at its most basic level, is the origination of a new species from an existing species. Organisms evolve as their genes change due to mutations of any kind, and within the broad scope of evolution, one can focus on the evolution of genes to understand how exactly one species evolved from another (Reece, 2014). Genes evolve through the process of molecular evolution, in which DNA is mutated in some manner and a new protein comes into existence (Reece, 2014). -
Figure S1. 17-Mer Distribution in the Yangtze Finless Porpoise Genome
Figure S1. 17-mer distribution in the Yangtze finless porpoise genome. The x-axis is 17-mer depth (X); the y-axis is the number of sequencing reads at that depth. Figure S2. Sequence depth distribution of the assembly data. The x-axis shows the sequencing depth (X) and the y-axis shows the number of bases at a given depth. The results demonstrate that 99% of bases sequencing depth is more than 20. Figure S3. Comparison of gene structure characteristics of Yangtze finless porpoise and other cetaceans. The x-axis represents the length of corresponding genetic element of exon number and the y-axis represents gene density. Figure S4. Phylogeny relationships between the Yangtze finless porpoise and other mammals reconstructed by RAxML with the GTR+G+I model. Table S1. Summary of sequenced reads Raw Reads Qualified Reads1 Total Read Sequence Physical Total Read Sequence Physical Library SRA Data Length Coverage2 Coverage2 Data Length Coverage2 Coverage2 Insert Size (bp) Number (Gb) (bp) (×) (×) (Gb) (bp) (×) (×) 289 58.94 150.00 23.67 22.80 57.84 149.75 23.23 22.41 SRR6923836 462 71.33 150.00 28.65 44.12 70.12 149.74 28.16 43.44 SRR6923837 624 67.47 150.00 27.10 56.36 63.90 149.67 25.66 53.50 SRR6923834 791 57.58 150.00 23.12 60.97 55.39 149.67 22.24 58.78 SRR6923835 4,000 108.73 150.00 43.67 582.22 70.74 150.00 28.41 378.80 SRR6923832 7,000 115.4 150.00 46.35 1,081.39 84.76 150.00 34.04 794.27 SRR6923833 11,000 107.37 150.00 43.12 1,581.08 79.78 150.00 32.04 1,174.81 SRR6923830 18,000 127.46 150.00 51.19 3,071.33 97.75 150.00 39.26 2,355.42 SRR6923831 Total 714.28 - 286.87 6,500.27 580.28 - 233.04 4,881.43 - 1Raw reads in mate-paired libraries were filtered to remove duplicates and reads with low quality and/or adapter contamination, raw reads in paired-end libraries were filtered in the same manner then subjected to k-mer-based correction.