Mouse Tmem120a Knockout Project (CRISPR/Cas9)
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A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
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. -
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BioMed Research International Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data Guest Editors: Julia Tzu-Ya Weng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data BioMed Research International Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data Guest Editors: Julia Tzu-Ya Weng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Copyright © 2014 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “BioMed Research International.” All articles are open access articles distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Contents Novel Bioinformatics Approaches for Analysis of High-Throughput Biological Data,JuliaTzu-YaWeng, Li-Ching Wu, Wen-Chi Chang, Tzu-Hao Chang, Tatsuya Akutsu, and Tzong-Yi Lee Volume2014,ArticleID814092,3pages Evolution of Network Biomarkers from Early to Late Stage Bladder Cancer Samples,Yung-HaoWong, Cheng-Wei Li, and Bor-Sen Chen Volume 2014, Article ID 159078, 23 pages MicroRNA Expression Profiling Altered by Variant Dosage of Radiation Exposure,Kuei-FangLee, Yi-Cheng Chen, Paul Wei-Che Hsu, Ingrid Y. Liu, and Lawrence Shih-Hsin Wu Volume2014,ArticleID456323,10pages EXIA2: Web Server of Accurate and Rapid Protein Catalytic Residue Prediction, Chih-Hao Lu, Chin-Sheng -
WO 2014/205555 Al 31 December 2014 (31.12.2014) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2014/205555 Al 31 December 2014 (31.12.2014) P O P C T (51) International Patent Classification: British Columbia V5Y 2G1 (CA). WATAHIKI, Akira; A61K 31/713 (2006.01) G01N 33/48 (2006.01) 15-5 Takakura-cho, Nishinomiya, 62-0872 (JP). LIU, Hui A61K 31/7088 (2006.01) G01N 33/50 (2006.01) Hsuan; 207 - 5770 Oak Street, Vancouver, British A61P 35/00 (2006.01) CI2N 15/113 (2010.01) Columbia V6M 4M5 (CA). PAROLIA, Abhijit; 505 C12Q 1/68 (2006.01) Mumfordganj, 2 11002 Allahabad U.P. (IN). (21) International Application Number: (74) Agents: SECHLEY, Konrad et al; Gowling Lafleur PCT/CA2014/000538 Henderson LLP, 2300, 550 Burrard Street, Vancouver, British Columbia V6C 2B5 (CA). (22) International Filing Date: 27 June 2014 (27.06.2014) (81) Designated States (unless otherwise indicated, for every kind of national protection available): AE, AG, AL, AM, (25) Filing Language: English AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (26) Publication Language: English BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (30) Priority Data: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 61/841,225 28 June 2013 (28.06.2013) US KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, (71) Applicant: BRITISH COLUMBIA CANCER AGENCY MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, BRANCH [CA/CA]; 675 West 10th Avenue, Vancouver, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, British Columbia V5Z 1L3 (CA). -
Capturing Epidermal Stemness
Capturing epidermal stemness THÈSE NO 6975 (2016) PRÉSENTÉE LE 28 OCTOBRE 2016 À LA FACULTÉ DES SCIENCES DE LA VIE LABORATOIRE DE DYNAMIQUE DES CELLULES SOUCHES PROGRAMME DOCTORAL EN APPROCHES MOLÉCULAIRES DU VIVANT ÉCOLE POLYTECHNIQUE FÉDÉRALE DE LAUSANNE POUR L'OBTENTION DU GRADE DE DOCTEUR ÈS SCIENCES PAR Andrea ZAFFALON acceptée sur proposition du jury: Prof. D. Constam, président du jury Prof. Y. Barrandon, directeur de thèse Prof. G. Cossu, rapporteur Prof. S. Nishikawa, rapporteur Prof. B. Deplancke, rapporteur Suisse 2016 Acknowledgements First of all, I would like to thank my thesis supervisor, Yann Barrandon, for giving me the opportunity to work in his laboratory and for supporting me to develop my ideas. I am very grateful that he provided me the tools and the environment to grow as a scientist and to explore very interesting questions at the interface between clinical and basic stem cell research. I warmly thank the members of my thesis jury, Prof. Giulio Cossu, Prof. Bart Deplancke, Prof. Shinichi Nishikawa and Prof. Daniel Constam for taking the time to evaluate and discuss my work. I would like to acknowledge Ariane Rochat for her help and contribution to this thesis. The project on the 3T3-J2 cells would not have been possible without her teaching and critical work to maintain the culture system in stellar conditions. Thanks to her, I was able to perform experiments on precious human skin biopsies. She also contributed in preparing the cell samples for the telomere experiment. I also would like to thank the team of the Biomolecular Screening Facility (BSF). -
Dual Specificity Phosphatases from Molecular Mechanisms to Biological Function
International Journal of Molecular Sciences Dual Specificity Phosphatases From Molecular Mechanisms to Biological Function Edited by Rafael Pulido and Roland Lang Printed Edition of the Special Issue Published in International Journal of Molecular Sciences www.mdpi.com/journal/ijms Dual Specificity Phosphatases Dual Specificity Phosphatases From Molecular Mechanisms to Biological Function Special Issue Editors Rafael Pulido Roland Lang MDPI • Basel • Beijing • Wuhan • Barcelona • Belgrade Special Issue Editors Rafael Pulido Roland Lang Biocruces Health Research Institute University Hospital Erlangen Spain Germany Editorial Office MDPI St. Alban-Anlage 66 4052 Basel, Switzerland This is a reprint of articles from the Special Issue published online in the open access journal International Journal of Molecular Sciences (ISSN 1422-0067) from 2018 to 2019 (available at: https: //www.mdpi.com/journal/ijms/special issues/DUSPs). For citation purposes, cite each article independently as indicated on the article page online and as indicated below: LastName, A.A.; LastName, B.B.; LastName, C.C. Article Title. Journal Name Year, Article Number, Page Range. ISBN 978-3-03921-688-8 (Pbk) ISBN 978-3-03921-689-5 (PDF) c 2019 by the authors. Articles in this book are Open Access and distributed under the Creative Commons Attribution (CC BY) license, which allows users to download, copy and build upon published articles, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. The book as a whole is distributed by MDPI under the terms and conditions of the Creative Commons license CC BY-NC-ND. Contents About the Special Issue Editors .................................... -
Dynamics of Dual Specificity Phosphatases and Their Interplay with Protein Kinases in Immune Signaling Yashwanth Subbannayya1,2, Sneha M
bioRxiv preprint doi: https://doi.org/10.1101/568576; this version posted March 5, 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. Dynamics of dual specificity phosphatases and their interplay with protein kinases in immune signaling Yashwanth Subbannayya1,2, Sneha M. Pinto1,2, Korbinian Bösl1, T. S. Keshava Prasad2 and Richard K. Kandasamy1,3,* 1Centre of Molecular Inflammation Research (CEMIR), and Department of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology, N-7491 Trondheim, Norway 2Center for Systems Biology and Molecular Medicine, Yenepoya (Deemed to be University), Mangalore 575018, India 3Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo and Oslo University Hospital, N-0349 Oslo, Norway *Correspondence: Richard K. Kandasamy ([email protected]) Abstract Dual specificity phosphatases (DUSPs) have a well-known role as regulators of the immune response through the modulation of mitogen activated protein kinases (MAPKs). Yet the precise interplay between the various members of the DUSP family with protein kinases is not well understood. Recent multi-omics studies characterizing the transcriptomes and proteomes of immune cells have provided snapshots of molecular mechanisms underlying innate immune response in unprecedented detail. In this study, we focused on deciphering the interplay between members of the DUSP family with protein kinases in immune cells using publicly available omics datasets. Our analysis resulted in the identification of potential DUSP- mediated hub proteins including MAPK7, MAPK8, AURKA, and IGF1R. Furthermore, we analyzed the association of DUSP expression with TLR4 signaling and identified VEGF, FGFR and SCF-KIT pathway modules to be regulated by the activation of TLR4 signaling. -
An Evaluation of Cancer Subtypes and Glioma Stem Cell Characterisation Unifying Tumour Transcriptomic Features with Cell Line Expression and Chromatin Accessibility
An evaluation of cancer subtypes and glioma stem cell characterisation Unifying tumour transcriptomic features with cell line expression and chromatin accessibility Ewan Roderick Johnstone EMBL-EBI, Darwin College University of Cambridge This dissertation is submitted for the degree of Doctor of Philosophy Darwin College December 2016 Dedicated to Klaudyna. Declaration • I hereby declare that except where specific reference is made to the work of others, the contents of this dissertation are original and have not been submitted in whole or in part for consideration for any other degree or qualification in this, or any other university. • This dissertation is my own work and contains nothing which is the outcome of work done in collaboration with others, except as specified in the text and Acknowledge- ments. • This dissertation is typeset in LATEX using one-and-a-half spacing, contains fewer than 60,000 words including appendices, footnotes, tables and equations and has fewer than 150 figures. Ewan Roderick Johnstone December 2016 Acknowledgements This work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC, Ref:1112564) and supported by the European Molecular Biology Laboratory (EMBL) and its outstation, the European Bioinformatics Institute (EBI). I have many people to thank for assistance in preparing this thesis. First and foremost I must thank my supervisor, Paul Bertone for his support and willingness to take me on as a student. My thanks are also extended to present and past members of the Bertone group, particularly Pär Engström and Remco Loos who have provided a great deal of guidance over the course of my studentship. -
A Biochemical Landscape of A-To-I RNA Editing in the Human Brain Transcriptome
Downloaded from genome.cshlp.org on October 3, 2021 - Published by Cold Spring Harbor Laboratory Press Resource A biochemical landscape of A-to-I RNA editing in the human brain transcriptome Masayuki Sakurai,1,4 Hiroki Ueda,1,4 Takanori Yano,1 Shunpei Okada,1 Hideki Terajima,1 Toutai Mitsuyama,2 Atsushi Toyoda,3 Asao Fujiyama,3 Hitomi Kawabata,1 and Tsutomu Suzuki1,5 1Department of Chemistry and Biotechnology, Graduate School of Engineering, University of Tokyo, Tokyo 113-8656, Japan; 2Computational Biology Research Center (CBRC), National Institute of Advanced Industrial Science and Technology (AIST), Tokyo 135-0064, Japan; 3Comparative Genomics Laboratory, Center for Genetic Resource Information, National Institute of Genetics, Shizuoka 411-8540, Japan Inosine is an abundant RNA modification in the human transcriptome and is essential for many biological processes in modulating gene expression at the post-transcriptional level. Adenosine deaminases acting on RNA (ADARs) catalyze the hydrolytic deamination of adenosines to inosines (A-to-I editing) in double-stranded regions. We previously established a biochemical method called ‘‘inosine chemical erasing’’ (ICE) to directly identify inosines on RNA strands with high reliability. Here, we have applied the ICE method combined with deep sequencing (ICE-seq) to conduct an unbiased genome-wide screening of A-to-I editing sites in the transcriptome of human adult brain. Taken together with the sites identified by the conventional ICE method, we mapped 19,791 novel sites and newly found 1258 edited mRNAs, including 66 novel sites in coding regions, 41 of which cause altered amino acid assignment. ICE-seq detected novel editing sites in various repeat elements as well as in short hairpins. -
Full Disclosures
ARTICLE OPEN ACCESS Critical exon indexing improves clinical interpretation of copy number variants in neurodevelopmental disorders E. Robert Wassman, MD,* Karen S. Ho, PhD,* Diana Bertrand, MS, Kyle W. Davis, ScM, Megan M. Martin, MS, Correspondence Stephanie Page, BS, Andreas Peiffer, MD, PhD, Aparna Prasad, PhD, Moises A. Serrano, PhD, Hope Twede, BS, Dr. Wassman [email protected] Rena Vanzo, MS, Stephen W. Scherer, PhD, Mohammed Uddin, PhD, and Charles H. Hensel, PhD* Neurol Genet 2019;5:e378. doi:10.1212/NXG.0000000000000378 Abstract Objective To evaluate a new tool to aid interpretation of copy number variants (CNVs) in individuals with neurodevelopmental disabilities. Methods Critical exon indexing (CEI) was used to identify genes with critical exons (CEGs) from clinically reported CNVs, which may contribute to neurodevelopmental disorders (NDDs). The 742 pathogenic CNVs and 1,363 variants of unknown significance (VUS) identified by chromosomal microarray analysis in 5,487 individuals with NDDs were subjected to CEI to identify CEGs. CEGs identified in a subsequent random series of VUS were evaluated for relevance to CNV interpretation. Results CEI identified a total of 2,492 unique CEGs in pathogenic CNVs and 953 in VUS compared with 259 CEGs in 6,965 CNVs from 873 controls. These differences are highly significant (p < 0.00001) whether compared as frequency, average, or normalized by CNV size. Twenty-one percent of VUS CEGs were not represented in Online Mendelian Inheritance in Man, high- lighting limitations of existing resources for identifying potentially impactful genes within CNVs. CEGs were highly correlated with other indices and known pathways of relevance. -
HHS Public Access Provided by Iupuischolarworks Author Manuscript
View metadata, citation and similar papers at core.ac.uk brought to you by CORE HHS Public Access provided by IUPUIScholarWorks Author manuscript Author Manuscript Author ManuscriptPharmacol Author Manuscript Biochem Behav Author Manuscript . Author manuscript; available in PMC 2015 July 27. Published in final edited form as: Pharmacol Biochem Behav. 2008 June ; 89(4): 481–498. doi:10.1016/j.pbb.2008.01.023. Differential gene expression in the nucleus accumbens with ethanol self-administration in inbred alcohol-preferring rats Zachary A. Rodd1,6, Mark W. Kimpel1,6, Howard J. Edenberg2,4,5, Richard L. Bell1,6, Wendy N. Strother1,6, Jeanette N. McClintick2,5, Lucinda G. Carr3, Tiebing Liang3, and William J. McBride1,6 1Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN 46202-4887 2Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202-4887 3Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202-4887 4Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202-4887 5Center for Medical Genomics, Indiana University School of Medicine, Indianapolis, IN 46202-4887 6Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN 46202-4887 Abstract The current study examined the effects of operant ethanol (EtOH) self-administration on gene expression in the nucleus accumbens (ACB) and amygdala (AMYG) of inbred alcohol-preferring (iP) rats. Rats self-trained on a standard two-lever operant paradigm to administer either water- water, EtOH (15% v/v)-water, or saccharin (SAC; 0.0125% g/v)-water. Animals were killed 24 hr after the last operant session, and the ACB and AMYG dissected; RNA was extracted and purified for microarray analysis. -
Affymetrix Probe ID Gene Symbol 1007 S at DDR1 1494 F At
Affymetrix Probe ID Gene Symbol 1007_s_at DDR1 1494_f_at CYP2A6 1552312_a_at MFAP3 1552368_at CTCFL 1552396_at SPINLW1 /// WFDC6 1552474_a_at GAMT 1552486_s_at LACTB 1552586_at TRPV3 1552619_a_at ANLN 1552628_a_at HERPUD2 1552680_a_at CASC5 1552928_s_at MAP3K7IP3 1552978_a_at SCAMP1 1553099_at TIGD1 1553106_at C5orf24 1553530_a_at ITGB1 1553997_a_at ASPHD1 1554127_s_at MSRB3 1554152_a_at OGDH 1554168_a_at SH3KBP1 1554217_a_at CCDC132 1554279_a_at TRMT2B 1554334_a_at DNAJA4 1554480_a_at ARMC10 1554510_s_at GHITM 1554524_a_at OLFM3 1554600_s_at LMNA 1555021_a_at SCARF1 1555058_a_at LPGAT1 1555197_a_at C21orf58 1555282_a_at PPARGC1B 1555460_a_at SLC39A6 1555559_s_at USP25 1555564_a_at CFI 1555594_a_at MBNL1 1555729_a_at CD209 1555733_s_at AP1S3 1555906_s_at C3orf23 1555945_s_at FAM120A 1555947_at FAM120A 1555950_a_at CD55 1557137_at TMEM17 1557910_at HSP90AB1 1558027_s_at PRKAB2 1558680_s_at PDE1A 1559136_s_at FLJ44451 /// IDS 1559490_at LRCH3 1562378_s_at PROM2 1562443_at RLBP1L2 1563522_at DDX10 /// LOC401533 1563834_a_at C1orf62 1566509_s_at FBXO9 1567214_a_at PNN 1568678_s_at FGFR1OP 1569629_x_atLOC389906 /// LOC441528 /// LOC728687 /// LOC729162 1598_g_at GAS6 /// LOC100133684 200064_at HSP90AB1 200596_s_at EIF3A 200597_at EIF3A 200604_s_at PRKAR1A 200621_at CSRP1 200638_s_at YWHAZ 200640_at YWHAZ 200641_s_at YWHAZ 200702_s_at DDX24 200742_s_at TPP1 200747_s_at NUMA1 200762_at DPYSL2 200872_at S100A10 200878_at EPAS1 200931_s_at VCL 200965_s_at ABLIM1 200998_s_at CKAP4 201019_s_at EIF1AP1 /// EIF1AX 201028_s_at CD99 201036_s_at HADH