Suppementary Table 9. Predicted Targets of Hsa-Mir-181A by Targetscan 6.2
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(12) Patent Application Publication (10) Pub. No.: US 2016/0237501 A1 SHARP Et Al
US 2016O23750 1A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2016/0237501 A1 SHARP et al. (43) Pub. Date: Aug. 18, 2016 (54) BIOMARKERS FOR DIAGNOSIS OF Related U.S. Application Data TRANSIENT SCHEMICATTACKS (62) Division of application No. 13/182,630, filed on Jul. (71) Applicant: The Regents of the University of 14, 2011, now abandoned. California, Oakland, CA (US) (60) Provisional application No. 61/364.334, filed on Jul. 14, 2010. (72) Inventors: Frank SHARP, Davis, CA (US); Xinhua ZHAN. Vacaville, CA (US); Publication Classification Glen C. JICKLING, Sacramento, CA (US): S. Claiborne JOHNSTON, San (51) Int. Cl. Francisco, CA (US) CI2O I/68 (2006.01) (52) U.S. Cl. (73) Assignee: The Regents of the University of CPC ........ CI2O 1688 (2013.0); CI2O 2600/158 California, Oakland, CA (US) (2013.01); C12O 2600/1 18 (2013.01) (57) ABSTRACT (21) Appl. No.: 15/043,577 The present invention provides methods and compositions for diagnosing and predicting the risk and cause of transient (22) Filed: Feb. 14, 2016 ischemic attacks (TIA). Patent Application Publication Aug. 18, 2016 Sheet 1 of 4 US 2016/0237SO1 A1 Standardized intensity s sis: iagnosis Controls xIA Figure IA-B Patent Application Publication Aug. 18, 2016 Sheet 2 of 4 US 2016/0237SO1 A1 & TA Cross-validated Probabilities (Thresholds 0.89) * Controls Controls TA ----------------------------------------------------------------------------------------------------------------------------------------- ... 0.9 O.8 O O 20 Subjects30 40 SO 50 Figure 2 Patent Application Publication Aug. 18, 2016 Sheet 3 of 4 US 2016/0237SO1 A1 Cross-validated Probabilities (Threshold=3.97) & TIA1 & A2 TIA1 T1A2 . -
Mechanical Forces Induce an Asthma Gene Signature in Healthy Airway Epithelial Cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T
www.nature.com/scientificreports OPEN Mechanical forces induce an asthma gene signature in healthy airway epithelial cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T. Kho4, Kelan Tantisira1, Marc Santolini 1,5, Feixiong Cheng6,7,8, Jennifer A. Mitchel3, Maureen McGill3, Michael J. O’Sullivan3, Margherita De Marzio1,3, Amitabh Sharma1, Scott H. Randell9, Jefrey M. Drazen3, Jefrey J. Fredberg3 & Scott T. Weiss1,3* Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufcient to induce infammatory, late repair, and fbrotic pathways. Remarkably, this molecular profle of non-asthmatic cells after compression recapitulated the profle of asthmatic cells before compression. Together, these results show that even in the absence of any infammatory stimulus, mechanical compression alone is sufcient to induce an asthma-like molecular signature. Bronchial epithelial cells (BECs) form a physical barrier that protects pulmonary airways from inhaled irritants and invading pathogens1,2. Moreover, environmental stimuli such as allergens, pollutants and viruses can induce constriction of the airways3 and thereby expose the bronchial epithelium to compressive mechanical stress. In BECs, this compressive stress induces structural, biophysical, as well as molecular changes4,5, that interact with nearby mesenchyme6 to cause epithelial layer unjamming1, shedding of soluble factors, production of matrix proteins, and activation matrix modifying enzymes, which then act to coordinate infammatory and remodeling processes4,7–10. -
Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-Cell Leukemia
Author Manuscript Published OnlineFirst on March 27, 2020; DOI: 10.1158/1078-0432.CCR-19-3519 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Constitutive activation of RAS/MAPK pathway cooperates with trisomy 21 and is therapeutically exploitable in Down syndrome B-cell Leukemia Anouchka P. Laurent1,2, Aurélie Siret1, Cathy Ignacimouttou1, Kunjal Panchal3, M’Boyba K. Diop4, Silvia Jenny5, Yi-Chien Tsai5, Damien Ross-Weil1, Zakia Aid1, Naïs Prade6, Stéphanie Lagarde6, Damien Plassard7, Gaelle Pierron8, Estelle Daudigeos-Dubus4, Yann Lecluse4, Nathalie Droin1, Beat Bornhauser5, Laurence C. Cheung3,9, John D. Crispino10, Muriel Gaudry1, Olivier A. Bernard1, Elizabeth Macintyre11, Carole Barin Bonnigal12, Rishi S. Kotecha3,9,13, Birgit Geoerger4, Paola Ballerini14, Jean-Pierre Bourquin5, Eric Delabesse6, Thomas Mercher1,15 and Sébastien Malinge1,3 1INSERM U1170, Gustave Roussy Institute, Université Paris Saclay, Villejuif, France 2Université Paris Diderot, Paris, France 3Telethon Kids Cancer Centre, Telethon Kids Institute, University of Western Australia, Perth, Australia 4Gustave Roussy Institute Cancer Campus, Department of Pediatric and Adolescent Oncology, INSERM U1015, Equipe Labellisée Ligue Nationale contre le Cancer, Université Paris-Saclay, Villejuif, France 5Department of Pediatric Oncology, Children’s Research Centre, University Children’s Hospital Zurich, Zurich, Switzerland 6Centre of Research on Cancer of Toulouse (CRCT), CHU Toulouse, Université Toulouse III, Toulouse, France 7IGBMC, Plateforme GenomEast, UMR7104 CNRS, Ilkirch, France 8Service de Génétique, Institut Curie, Paris, France 9School of Pharmacy and Biomedical Sciences, Curtin University, Bentley, Australia 10Division of Hematology/Oncology, Northwestern University, Chicago, USA 11Hematology, Université de Paris, Institut Necker-Enfants Malades and Assistance Publique – Hopitaux de Paris, Paris, France 12Centre Hospitalier Universitaire de Tours, Tours, France 1 Downloaded from clincancerres.aacrjournals.org on September 30, 2021. -
Gentaur Products List
Chapter 2 : Gentaur Products List • Rabbit Anti LAMR1 Polyclonal Antibody Cy5 Conjugated Conjugated • Rabbit Anti Podoplanin gp36 Polyclonal Antibody Cy5 • Rabbit Anti LAMR1 CT Polyclonal Antibody Cy5 • Rabbit Anti phospho NFKB p65 Ser536 Polyclonal Conjugated Conjugated Antibody Cy5 Conjugated • Rabbit Anti CHRNA7 Polyclonal Antibody Cy5 Conjugated • Rat Anti IAA Monoclonal Antibody Cy5 Conjugated • Rabbit Anti EV71 VP1 CT Polyclonal Antibody Cy5 • Rabbit Anti Connexin 40 Polyclonal Antibody Cy5 • Rabbit Anti IAA Indole 3 Acetic Acid Polyclonal Antibody Conjugated Conjugated Cy5 Conjugated • Rabbit Anti LHR CGR Polyclonal Antibody Cy5 Conjugated • Rabbit Anti Integrin beta 7 Polyclonal Antibody Cy5 • Rabbit Anti Natrexone Polyclonal Antibody Cy5 Conjugated • Rabbit Anti MMP 20 Polyclonal Antibody Cy5 Conjugated Conjugated • Rabbit Anti Melamine Polyclonal Antibody Cy5 Conjugated • Rabbit Anti BCHE NT Polyclonal Antibody Cy5 Conjugated • Rabbit Anti NAP1 NAP1L1 Polyclonal Antibody Cy5 • Rabbit Anti Acetyl p53 K382 Polyclonal Antibody Cy5 • Rabbit Anti BCHE CT Polyclonal Antibody Cy5 Conjugated Conjugated Conjugated • Rabbit Anti HPV16 E6 Polyclonal Antibody Cy5 Conjugated • Rabbit Anti CCP Polyclonal Antibody Cy5 Conjugated • Rabbit Anti JAK2 Polyclonal Antibody Cy5 Conjugated • Rabbit Anti HPV18 E6 Polyclonal Antibody Cy5 Conjugated • Rabbit Anti HDC Polyclonal Antibody Cy5 Conjugated • Rabbit Anti Microsporidia protien Polyclonal Antibody Cy5 • Rabbit Anti HPV16 E7 Polyclonal Antibody Cy5 Conjugated • Rabbit Anti Neurocan Polyclonal -
Seq2pathway Vignette
seq2pathway Vignette Bin Wang, Xinan Holly Yang, Arjun Kinstlick May 19, 2021 Contents 1 Abstract 1 2 Package Installation 2 3 runseq2pathway 2 4 Two main functions 3 4.1 seq2gene . .3 4.1.1 seq2gene flowchart . .3 4.1.2 runseq2gene inputs/parameters . .5 4.1.3 runseq2gene outputs . .8 4.2 gene2pathway . 10 4.2.1 gene2pathway flowchart . 11 4.2.2 gene2pathway test inputs/parameters . 11 4.2.3 gene2pathway test outputs . 12 5 Examples 13 5.1 ChIP-seq data analysis . 13 5.1.1 Map ChIP-seq enriched peaks to genes using runseq2gene .................... 13 5.1.2 Discover enriched GO terms using gene2pathway_test with gene scores . 15 5.1.3 Discover enriched GO terms using Fisher's Exact test without gene scores . 17 5.1.4 Add description for genes . 20 5.2 RNA-seq data analysis . 20 6 R environment session 23 1 Abstract Seq2pathway is a novel computational tool to analyze functional gene-sets (including signaling pathways) using variable next-generation sequencing data[1]. Integral to this tool are the \seq2gene" and \gene2pathway" components in series that infer a quantitative pathway-level profile for each sample. The seq2gene function assigns phenotype-associated significance of genomic regions to gene-level scores, where the significance could be p-values of SNPs or point mutations, protein-binding affinity, or transcriptional expression level. The seq2gene function has the feasibility to assign non-exon regions to a range of neighboring genes besides the nearest one, thus facilitating the study of functional non-coding elements[2]. Then the gene2pathway summarizes gene-level measurements to pathway-level scores, comparing the quantity of significance for gene members within a pathway with those outside a pathway. -
An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Netwo
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis Sriram Devanathan Washington University School of Medicine in St. Louis Timothy Whitehead Washington University School of Medicine in St. Louis George G. Schweitzer Washington University School of Medicine in St. Louis Nicole Fettig Washington University School of Medicine in St. Louis Attila Kovacs Washington University School of Medicine in St. Louis See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Devanathan, Sriram; Whitehead, Timothy; Schweitzer, George G.; Fettig, Nicole; Kovacs, Attila; Korach, Kenneth S.; Finck, Brian N.; and Shoghi, Kooresh I., ,"An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis." PLoS One.9,7. e101900. (2014). https://digitalcommons.wustl.edu/open_access_pubs/3326 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Sriram Devanathan, Timothy Whitehead, George G. Schweitzer, Nicole Fettig, Attila Kovacs, Kenneth S. Korach, Brian N. Finck, and Kooresh I. Shoghi This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/3326 An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Network Analysis Sriram Devanathan1, Timothy Whitehead1, George G. Schweitzer2, Nicole Fettig1, Attila Kovacs3, Kenneth S. -
Chromosomal Assignment of the Genes for Human Aldehyde Dehydrogenase-1 and Aldehyde Dehydrogenase-2 LILY C
Am J Hum Genet 38:641-648, 1986 Chromosomal Assignment of the Genes for Human Aldehyde Dehydrogenase-1 and Aldehyde Dehydrogenase-2 LILY C. Hsu,', AKIRA YOSHIDA,' AND T. MOHANDAS2 SUMMARY Chromosomal assignment of the genes for two major human aldehyde dehydrogenase isozymes, that is, cytosolic aldehyde dehydrogenase-1 (ALDH1) and mitochondrial aldehyde dehydrogenase-2 (ALDH2) were determined. Genomic DNA, isolated from a panel of mouse- human and Chinese hamster-human hybrid cell lines, was digested by restriction endonucleases and subjected to Southern blot hybridiza- tion using cDNA probes for ALDH1 and for ALDH2. Based on the distribution pattern of ALDH1 and ALDH2 in cell hybrids, ALDHI was assigned to the long arm of human chromosome 9 and ALDH2 to chromosome 12. INTRODUCTION Two major and at least two minor aldehyde dehydrogenase isozymes exist in human and other mammalian livers. One of the major isozymes, designated as ALDH 1, or E1, is of cytosolic origin, and another major isozyme, designated as ALDH2 or E2, is of mitochondrial origin. The two isozymes are different from each other with respect to their kinetic properties, sensitivity to disulfiram inactivation, and protein structure [1-5]. Remarkable racial differences be- tween Caucasians and Orientals have been found in these isozymes. Approxi- mately 50% of Orientals have a variant form of ALDH2 associated with dimin- ished activity, while virtually all Caucasians have the wild-type active ALDH2 Received July 10, 1985; revised September 23, 1985. This work was supported by grant AA05763 from the National Institutes of Health. ' Department of Biochemical Genetics, Beckman Research Institute of the City of Hope, Duarte, CA 91010. -
AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA503371 AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] Product data: Product Type: Primary Antibodies Clone Name: OTI3A9 Applications: FC, WB Recommended Dilution: WB 1:2000, FLOW 1:100 Reactivity: Human, Mouse, Rat Host: Mouse Isotype: IgG2b Clonality: Monoclonal Immunogen: Full length human recombinant protein of human AK4(NP_037542) produced in HEK293T cell. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 25.1 kDa Gene Name: adenylate kinase 4 Database Link: NP_037542 Entrez Gene 11639 MouseEntrez Gene 29223 RatEntrez Gene 205 Human P27144 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 3 AK3L1 (AK4) Mouse Monoclonal Antibody [Clone ID: OTI3A9] – TA503371 Background: This gene encodes a member of the adenylate kinase family of enzymes. The encoded protein is localized to the mitochondrial matrix. Adenylate kinases regulate the adenine and guanine nucleotide compositions within a cell by catalyzing the reversible transfer of phosphate group among these nucleotides. Five isozymes of adenylate kinase have been identified in vertebrates. -
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. -
ARTICLE Doi:10.1038/Nature10523
ARTICLE doi:10.1038/nature10523 Spatio-temporal transcriptome of the human brain Hyo Jung Kang1*, Yuka Imamura Kawasawa1*, Feng Cheng1*, Ying Zhu1*, Xuming Xu1*, Mingfeng Li1*, Andre´ M. M. Sousa1,2, Mihovil Pletikos1,3, Kyle A. Meyer1, Goran Sedmak1,3, Tobias Guennel4, Yurae Shin1, Matthew B. Johnson1,Zˇeljka Krsnik1, Simone Mayer1,5, Sofia Fertuzinhos1, Sheila Umlauf6, Steven N. Lisgo7, Alexander Vortmeyer8, Daniel R. Weinberger9, Shrikant Mane6, Thomas M. Hyde9,10, Anita Huttner8, Mark Reimers4, Joel E. Kleinman9 & Nenad Sˇestan1 Brain development and function depend on the precise regulation of gene expression. However, our understanding of the complexity and dynamics of the transcriptome of the human brain is incomplete. Here we report the generation and analysis of exon-level transcriptome and associated genotyping data, representing males and females of different ethnicities, from multiple brain regions and neocortical areas of developing and adult post-mortem human brains. We found that 86 per cent of the genes analysed were expressed, and that 90 per cent of these were differentially regulated at the whole-transcript or exon level across brain regions and/or time. The majority of these spatio-temporal differences were detected before birth, with subsequent increases in the similarity among regional transcriptomes. The transcriptome is organized into distinct co-expression networks, and shows sex-biased gene expression and exon usage. We also profiled trajectories of genes associated with neurobiological categories and diseases, and identified associations between single nucleotide polymorphisms and gene expression. This study provides a comprehensive data set on the human brain transcriptome and insights into the transcriptional foundations of human neurodevelopment. -
The Characterization of Human Adenylate Kinases 7 and 8
The characterization of human adenylate kinases 7 and 8 demonstrates differences in kinetic parameters and structural organization among the family of adenylate kinase isoenzymes Christakis Panayiotou, Nicola Solaroli, Yunjian Xu, Magnus Johansson, Anna Karlsson To cite this version: Christakis Panayiotou, Nicola Solaroli, Yunjian Xu, Magnus Johansson, Anna Karlsson. The char- acterization of human adenylate kinases 7 and 8 demonstrates differences in kinetic parameters and structural organization among the family of adenylate kinase isoenzymes. Biochemical Journal, Port- land Press, 2011, 433 (3), pp.527-534. 10.1042/BJ20101443. hal-00558097 HAL Id: hal-00558097 https://hal.archives-ouvertes.fr/hal-00558097 Submitted on 21 Jan 2011 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. Biochemical Journal Immediate Publication. Published on 16 Nov 2010 as manuscript BJ20101443 The characterization of human adenylate kinases 7 and 8 demonstrates differences in kinetic parameters and structural organization among the family of adenylate kinase isoenzymes -
Phylogenetic Analysis, Subcellular Localization, and Expression
BMC Plant Biology BioMed Central Research article Open Access Phylogenetic analysis, subcellular localization, and expression patterns of RPD3/HDA1 family histone deacetylases in plants Malona V Alinsug, Chun-Wei Yu and Keqiang Wu* Address: Institute of Plant Biology, College of Life Science, National Taiwan University, Taipei, Taiwan Email: Malona V Alinsug - [email protected]; Chun-Wei Yu - [email protected]; Keqiang Wu* - [email protected] * Corresponding author Published: 28 March 2009 Received: 26 November 2008 Accepted: 28 March 2009 BMC Plant Biology 2009, 9:37 doi:10.1186/1471-2229-9-37 This article is available from: http://www.biomedcentral.com/1471-2229/9/37 © 2009 Alinsug 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. Abstract Background: Although histone deacetylases from model organisms have been previously identified, there is no clear basis for the classification of histone deacetylases under the RPD3/ HDA1 superfamily, particularly on plants. Thus, this study aims to reconstruct a phylogenetic tree to determine evolutionary relationships between RPD3/HDA1 histone deacetylases from six different plants representing dicots with Arabidopsis thaliana, Populus trichocarpa, and Pinus taeda, monocots with Oryza sativa and Zea mays, and the lower plants with Physcomitrella patens. Results: Sixty two histone deacetylases of RPD3/HDA1 family from the six plant species were phylogenetically analyzed to determine corresponding orthologues. Three clusters were formed separating Class I, Class II, and Class IV.