Relevance Network Between Chemosensitivity and Transcriptome in Human Hepatoma Cells1
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METACYC ID Description A0AR23 GO:0004842 (Ubiquitin-Protein Ligase
Electronic Supplementary Material (ESI) for Integrative Biology This journal is © The Royal Society of Chemistry 2012 Heat Stress Responsive Zostera marina Genes, Southern Population (α=0. -
FK506-Binding Protein 12.6/1B, a Negative Regulator of [Ca2+], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. A link to any extended data will be provided when the final version is posted online. Research Articles: Neurobiology of Disease FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats John C. Gant1, Eric M. Blalock1, Kuey-Chu Chen1, Inga Kadish2, Olivier Thibault1, Nada M. Porter1 and Philip W. Landfield1 1Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536 2Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294 DOI: 10.1523/JNEUROSCI.2234-17.2017 Received: 7 August 2017 Revised: 10 October 2017 Accepted: 24 November 2017 Published: 18 December 2017 Author contributions: J.C.G. and P.W.L. designed research; J.C.G., E.M.B., K.-c.C., and I.K. performed research; J.C.G., E.M.B., K.-c.C., I.K., and P.W.L. analyzed data; J.C.G., E.M.B., O.T., N.M.P., and P.W.L. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. NIH grants AG004542, AG033649, AG052050, AG037868 and McAlpine Foundation for Neuroscience Research Corresponding author: Philip W. Landfield, [email protected], Department of Pharmacology & Nutritional Sciences, University of Kentucky, 800 Rose Street, UKMC MS 307, Lexington, KY 40536 Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2234-17.2017 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published. -
Lineage-Specific Evolution of the Vertebrate Otopetrin Gene Family Revealed by Comparative Genomic Analyses
Hurle et al. BMC Evolutionary Biology 2011, 11:23 http://www.biomedcentral.com/1471-2148/11/23 RESEARCHARTICLE Open Access Lineage-specific evolution of the vertebrate Otopetrin gene family revealed by comparative genomic analyses Belen Hurle1, Tomas Marques-Bonet2,3, Francesca Antonacci3, Inna Hughes4, Joseph F Ryan1, NISC Comparative Sequencing Program1,5, Evan E Eichler3, David M Ornitz6, Eric D Green1,5* Abstract Background: Mutations in the Otopetrin 1 gene (Otop1) in mice and fish produce an unusual bilateral vestibular pathology that involves the absence of otoconia without hearing impairment. The encoded protein, Otop1, is the only functionally characterized member of the Otopetrin Domain Protein (ODP) family; the extended sequence and structural preservation of ODP proteins in metazoans suggest a conserved functional role. Here, we use the tools of sequence- and cytogenetic-based comparative genomics to study the Otop1 and the Otop2-Otop3 genes and to establish their genomic context in 25 vertebrates. We extend our evolutionary study to include the gene mutated in Usher syndrome (USH) subtype 1G (Ush1g), both because of the head-to-tail clustering of Ush1g with Otop2 and because Otop1 and Ush1g mutations result in inner ear phenotypes. Results: We established that OTOP1 is the boundary gene of an inversion polymorphism on human chromosome 4p16 that originated in the common human-chimpanzee lineage more than 6 million years ago. Other lineage- specific evolutionary events included a three-fold expansion of the Otop genes in Xenopus tropicalis and of Ush1g in teleostei fish. The tight physical linkage between Otop2 and Ush1g is conserved in all vertebrates. -
Genome-Wide Rnai Screening Identifies Human Proteins with A
RESOURCES Genome-wide RNAi screening identifies human proteins with a regulatory function in the early secretory pathway Jeremy C. Simpson1,7, Brigitte Joggerst2, Vibor Laketa2, Fatima Verissimo2, Cihan Cetin2, Holger Erfle2,6, Mariana G. Bexiga1, Vasanth R. Singan1, Jean-Karim Hériché3, Beate Neumann3, Alvaro Mateos2, Jonathon Blake4, Stephanie Bechtel5, Vladimir Benes4, Stefan Wiemann5, Jan Ellenberg2,3 and Rainer Pepperkok2,7 The secretory pathway in mammalian cells has evolved to facilitate the transfer of cargo molecules to internal and cell surface membranes. Use of automated microscopy-based genome-wide RNA interference screens in cultured human cells allowed us to identify 554 proteins influencing secretion. Cloning, fluorescent-tagging and subcellular localization analysis of 179 of these proteins revealed that more than two-thirds localize to either the cytoplasm or membranes of the secretory and endocytic pathways. The depletion of 143 of them resulted in perturbations in the organization of the COPII and/or COPI vesicular coat complexes of the early secretory pathway, or the morphology of the Golgi complex. Network analyses revealed a so far unappreciated link between early secretory pathway function, small GTP-binding protein regulation, actin cytoskeleton organization and EGF-receptor-mediated signalling. This work provides an important resource for an integrative understanding of global cellular organization and regulation of the secretory pathway in mammalian cells. Within higher eukaryotic cells membrane traffic pathways connect the Extensive efforts over many years have revealed a significant number various membrane-bounded organelles, thereby ensuring that they of regulators associated with the secretory pathway. Early biochemical retain the correct complement of proteins and lipids to maintain approaches to identify individual machinery components have started cellular homeostasis. -
Title Second-Line Chemotherapy for Small-Cell Lung Cancer
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Kyoto University Research Information Repository Second-line chemotherapy for small-Cell Lung Cancer Title (SCLC). Author(s) Kim, Young Hak; Mishima, Michiaki Citation Cancer treatment reviews (2011), 37(2): 143-150 Issue Date 2011-04 URL http://hdl.handle.net/2433/137220 Right © 2010 Elsevier Ltd Type Journal Article Textversion author Kyoto University Second-line Chemotherapy for Small-Cell Lung Cancer (SCLC) Young Hak Kim and Michiaki Mishima Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto 606-8507, Japan For reprints and all correspondence: Young Hak Kim Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawaharacho, Sakyo-ku, Kyoto 606-8507, Japan Phone: +81-75-751-3830; Fax: +81-75-751-4643; E-mail: [email protected] Running title: Second-line Chemotherapy for SCLC Key words: small-cell lung cancer, relapsed, chemotherapy, second line, sensitive, refractory 1 Abstract Although small-cell lung cancer (SCLC) generally shows an excellent response to initial chemotherapy, most patients finally relapse and salvage chemotherapy is considered. Usually, the response to salvage chemotherapy significantly differs between sensitive and refractory relapse. Sensitive relapse is relatively chemosensitive and re-challenge with the same drugs as used in the initial chemotherapy has been used historically, while refractory relapse is extremely chemoresistant and its prognosis has been abysmal. To date, a number of clinical trials have been carried out for relapsed SCLC; however, the number of randomized trials is quite limited. -
Genome-Wide Enrichment Analysis Between Endometriosis and Obesity-Related Traits Reveals Novel Susceptibility Loci
Human Molecular Genetics, 2015, Vol. 24, No. 4 1185–1199 doi:10.1093/hmg/ddu516 Advance Access published on October 8, 2014 Genome-wide enrichment analysis between endometriosis and obesity-related traits reveals novel susceptibility loci Nilufer Rahmioglu1, Stuart Macgregor2, Alexander W. Drong1,A˚ sa K. Hedman1,5, Holly R. Harris6,7, Joshua C. Randall8, Inga Prokopenko1,9,10, The International Endogene Consortium (IEC), The GIANT Consortium, Dale R. Nyholt3, Andrew P. Morris1,11,{, Grant W. Montgomery4,{, Downloaded from https://academic.oup.com/hmg/article/24/4/1185/617584 by guest on 05 February 2021 Stacey A. Missmer6,{, Cecilia M. Lindgren1,12,{ and Krina T. Zondervan1,13,∗,{ 1Wellcome Trust Center for Human Genetics, University of Oxford, Oxford OX3 7BN, UK, 2Statistical Genetics, 3Neurogenetics, 4Molecular Epidemiology, QIMR Berghofer Medical Research Institute, Brisbane, QLD 4029, Australia, 5Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden, 6Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA, 7Unit of Nutritional Epidemiology, Institute for Environmental Medicine, Karolinska Institutet, PO Box 210, SE-171 77 Stockholm, Sweden, 8Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK, 9Department of Genomics of Common Disease, Imperial College London, London W12 0NN, UK, 10Oxford Centre for Diabetes, Endocrinology and Metabolism, University -
Supplementary Information Genomice and Transcriptomic Analysis
Supplementary Information Genomice and Transcriptomic Analysis for Identification of Genes and Interlinked Pathways Mediating Artemisinin Resistance in Leishmania donovani Sushmita Ghosh1,2, Aditya Verma1, Vinay Kumar1, Dibyabhaba Pradhan3, Angamuthu Selvapandiyan 2, Poonam Salotra1, Ruchi Singh1* 1. ICMR- National Institute of Pathology, Safdarjung Hospital Campus, New Delhi-110029, India 2. Jamia Hamdard University-Institute of Molecular Medicine, New Delhi-110062, India 3. ICMR-AIIMS Computational Genomics Centre, Indian Council of Medical Research, New Delhi- 110029 *Correspondence: [email protected] Supplementary Figures and Tables: Figure S1. Figure S1: Comparative transcriptional responses following ART adaptation in L. donovani. Overlap of log2 transformed K133 AS-R and K133 WT expression ratio plotted as a function of chromosomal location of probes representing the full genome microarray. The plot represents the average values of three independent hybridizations for each isolate. Table S1: List of genes validated for their modulated expression by Quantitative real time- PCR S.N Primer Gene Name/ Function/relevance Primer Sequence o. Name Gene ID 1 AQP1 Aquaglyceropor Metal ion F- in (LinJ.31.0030) transmembrane 5’CAGGGACAGCTCGAGGGTAA transporter activity, AA3’ integral to membrane; transmembrane R- transport; transporter 5’GTTACCGGCGTGAAAGACAG activity; water TG3’ transport. 2 A2 A2 protein Cellular response to F- (LinJ.22.0670) stress 5’GTTGGCCCGCTTTCTGTTGG3’ R- 5’ACCAACGTCAACAGAGAGA GGG3’ 3 ABCG1 ATP-binding ATP binding, ATPase -
The Abundance of Cis-Acting Loci Leading to Differential Allele
Yeo et al. BMC Genomics (2016) 17:620 DOI 10.1186/s12864-016-2922-9 RESEARCH ARTICLE Open Access The abundance of cis-acting loci leading to differential allele expression in F1 mice and their relationship to loci harboring genes affecting complex traits Seungeun Yeo1, Colin A. Hodgkinson1, Zhifeng Zhou1, Jeesun Jung2, Ming Leung1, Qiaoping Yuan1 and David Goldman1* Abstract Background: Genome-wide surveys have detected cis-acting quantitative trait loci altering levels of RNA transcripts (RNA-eQTLs) by associating SNV alleles to transcript levels. However, the sensitivity and specificity of detection of cis- expression quantitative trait loci (eQTLs) by genetic approaches, reliant as it is on measurements of transcript levels in recombinant inbred strains or offspring from arranged crosses, is unknown, as is their relationship to QTL’s for complex phenotypes. Results: We used transcriptome-wide differential allele expression (DAE) to detect cis-eQTLs in forebrain and kidney from reciprocal crosses between three mouse inbred strains, 129S1/SvlmJ, DBA/2J, and CAST/EiJ and C57BL/6 J. Two of these crosses were previously characterized for cis-eQTLs and QTLs for various complex phenotypes by genetic analysis of recombinant inbred (RI) strains. 5.4 %, 1.9 % and 1.5 % of genes assayed in forebrain of B6/ 129SF1, B6/DBAF1, and B6/CASTF1 mice, respectively, showed differential allelic expression, indicative of cis-acting alleles at these genes. Moreover, the majority of DAE QTLs were observed to be tissue-specific with only a small fraction showing cis-effects in both tissues. Comparing DAE QTLs in F1 mice to cis-eQTLs previously mapped in RI strains we observed that many of the cis-eQTLs were not confirmed by DAE. -
Nimustine Induces DNA Breaks and Crosslinks in NIH/3T3 Cells
International Journal of Bioscience, Biochemistry and Bioinformatics, Vol. 3, No. 3, May 2013 Nimustine Induces DNA Breaks and Crosslinks in NIH/3T3 Cells Lin-Na Zhao, Xue-Chai Chen, Yan-Yan Zhong, Qin-Xia Hou, and Ru-Gang Zhong study of drug-induced DNA cross-linking to reveal the Abstract—The relationship between carcinogenicity and difference between the nitrosourea anticancer mechanism DNA interstrand cross-links of nitrosoureas is poorly defined. and carcinogenic role. 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3- (2-chloroethyl)- ACNU was discovered in 1974 as the first water-soluble 3- nitrosourea (ACNU, nimustine) is one of nitrosoureas used in nitrosourea compound [11], and mainly used in the clinic of the treatment of high-grade gliomas. It has the capability of causing DNA interstrand cross-links (ICLs) to kill cancer cells. glioblastoma patients before the introduction of But it can also cause the generation of secondary tumors with 8-carbamoyl-3-methylimidazo [5, 1-d]-1, 2, 3, carcinogenic side effects. In present study, we investigated DNA 5-tetrazin-4(3H) -one (temozolomide, TMZ) because of its interstrand cross-links, DNA double-strand breaks and cell high permeability across blood-brain barrier (BBB) and good cycle phase in NIH/3T3 cells from the primary mouse cytotoxic activity for gliomas [12]-[13]. BCNU always embryonic fibroblast cells induced by ACNU. This result induces two major types of genotoxic damage to the cell: indicated that the concentration of 60 and 75μg/ml of ACNU could be detected significantly ICLs, and the γ-H2AX has the DNA mono adducts and DNA interstrand cross-links. -
Long Non-Coding RNA Lncshgl Recruits Hnrnpa1 to Suppress Hepatic Gluconeogenesis and Lipogenesis
Page 1 of 60 Diabetes Long non-coding RNA LncSHGL recruits hnRNPA1 to suppress hepatic gluconeogenesis and lipogenesis Junpei Wang1,2#, Weili Yang1,2#, Zhenzhen Chen1, Ji Chen1, Yuhong Meng1, Biaoqi Feng1, Libo Sun3, Lin Dou4, Jian Li4, Qinghua Cui2*, Jichun Yang1* 1Department of Physiology and Pathophysiology, School of Basic Medical Sciences Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education Center for Non-coding RNA Medicine Peking University Health Science Center Beijing 100191, China 2Department of Biomedical Informatics, School of Basic Medical Sciences Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Center for Non-coding RNA Medicine Peking University Health Science Center, Beijing 100191, China 3Beijing You An Hospital,Capital Medical University, Beijing 100069, China 4Key Laboratory of Geriatrics, Beijing Institute of Geriatrics & Beijing Hospital, Ministry of Health, Beijing 100730, China #These authors contributed equally to this work *Correspondence to: Jichun Yang, Ph.D. Department of Physiology and Pathophysiology, School of Basic Medical Sciences Peking University Health Science Center, Beijing 100191, China Email: [email protected]; Tel: (+86) 10-82801403 Or to: Qinghua Cui, Ph.D. Department of Biomedical Informatics, School of Basic Medical Sciences Peking University Health Science Center, Beijing 100191, China Email:[email protected]; Tel:(+86)10-82801585 1 Diabetes Publish Ahead of Print, published online January 30, 2018 Diabetes Page 2 of 60 Abstract Mammalian genomes encode a huge number of LncRNAs with unknown functions. This study determined the role and mechanism of a new LncRNA, LncRNA Suppressor of Hepatic Gluconeogenesis and Lipogenesis (LncSHGL), in regulating hepatic glucose/lipid metabolism. -
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing -
Nanoconjugates Able to Cross the Blood-Brain Barrier Alexander H Stegh, Janina Paula Luciano, Samuel A
(12) STANDARD PATENT (11) Application No. AU 2017216461 B2 (19) AUSTRALIAN PATENT OFFICE (54) Title Nanoconjugates Able To Cross The Blood-Brain Barrier (51) International Patent Classification(s) A61K 31/7088 (2006.01) A61K 48/00 (2006.0 1) A61K 9/00 (2006.01) A61P 35/00 (2006.01) (21) Application No: 2017216461 (22) Date of Filing: 2017.08.15 (43) Publication Date: 2017.08.31 (43) Publication Journal Date: 2017.08.31 (44) Accepted Journal Date: 2019.10.17 (62) Divisional of: 2012308302 (71) Applicant(s) NorthwesternUniversity (72) Inventor(s) Mirkin, Chad A.;Ko, Caroline H.;Stegh, Alexander;Giljohann, David A.;Luciano, Janina;Jensen, Sam (74) Agent / Attorney WRAYS PTY LTD, L7 863 Hay St, Perth, WA, 6000, AU (56) Related Art US 2010/0233084 Al LJUBIMOVA et al. "Nanoconjugate based on polymalic acid for tumor targeting", Chemico-Biological Interactions, 2008, Vol. 171, Pages 195-203. WO 2011/028847 Al BONOU et al. "Nanotechnology approach for drug addiction therapy: Gene silencing using delivery of gold nanorod-siRNA nanoplex in dopaminergic neurons", PNAS, 2009, Vol. 106, No. 14, Pages 5546-5550. PATIL et al. "Temozolomide Delivery to Tumor Cells by a Multifunctional Nano Vehicle Based on Poly(#-L-malic acid)", Pharmaceutical Research, 2010, Vol. 27, Pages 2317-2329. ABSTRACT Polyvalent nanoconjugates address the critical challenges in therapeutic use. The single-entity, targeted therapeutic is able to cross the blood-brain barrier (BBB) and is thus effective in the treatment of central nervous system (CNS) disorders. Further, despite the tremendously high 5 cellular uptake of nanoconjugates, they exhibit no toxicity in the cell types tested thus far.