Differential Interactome Proposes Subtype-Specific Biomarkers And
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Isyte: Integrated Systems Tool for Eye Gene Discovery
Lens iSyTE: Integrated Systems Tool for Eye Gene Discovery Salil A. Lachke,1,2,3,4 Joshua W. K. Ho,1,4,5 Gregory V. Kryukov,1,4,6 Daniel J. O’Connell,1 Anton Aboukhalil,1,7 Martha L. Bulyk,1,8,9 Peter J. Park,1,5,10 and Richard L. Maas1 PURPOSE. To facilitate the identification of genes associated ther investigation. Extension of this approach to other ocular with cataract and other ocular defects, the authors developed tissue components will facilitate eye disease gene discovery. and validated a computational tool termed iSyTE (integrated (Invest Ophthalmol Vis Sci. 2012;53:1617–1627) DOI: Systems Tool for Eye gene discovery; http://bioinformatics. 10.1167/iovs.11-8839 udel.edu/Research/iSyTE). iSyTE uses a mouse embryonic lens gene expression data set as a bioinformatics filter to select candidate genes from human or mouse genomic regions impli- ven with the advent of high-throughput sequencing, the cated in disease and to prioritize them for further mutational Ediscovery of genes associated with congenital birth defects and functional analyses. such as eye defects remains a challenge. We sought to develop METHODS. Microarray gene expression profiles were obtained a straightforward experimental approach that could facilitate for microdissected embryonic mouse lens at three key devel- the identification of candidate genes for developmental disor- opmental time points in the transition from the embryonic day ders, and, as proof-of-principle, we chose defects involving the (E)10.5 stage of lens placode invagination to E12.5 lens primary ocular lens. Opacification of the lens results in cataract, a leading cause of blindness that affects 77 million persons and fiber cell differentiation. -
DFFA Monoclonal Antibody (M05), Degradation of the Chromosomal DNA Into Nucleosomal Clone 3A11 Units
DFFA monoclonal antibody (M05), degradation of the chromosomal DNA into nucleosomal clone 3A11 units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. Catalog Number: H00001676-M05 DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated Regulatory Status: For research use only (RUO) when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active Product Description: Mouse monoclonal antibody component of DFF. DFFB has been found to trigger both raised against a partial recombinant DFFA. DNA fragmentation and chromatin condensation during apoptosis. Two alternatively spliced transcript variants Clone Name: 3A11 encoding distinct isoforms have been found for this gene. [provided by RefSeq] Immunogen: DFFA (NP_004392.1, 231 a.a. ~ 331 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: TSSDVALASHILTALREKQAPELSLSSQDLELVTKEDPK ALAVALNWDIKKTETVQEACERELALRLQQTQSLHSLR SISASKASPPGDLQNPKRARQDPT Host: Mouse Reactivity: Human Applications: ELISA, PLA-Ce, S-ELISA, WB-Re, WB-Tr (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Isotype: IgG2a Kappa Storage Buffer: In 1x PBS, pH 7.4 Storage Instruction: Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 1676 Gene Symbol: DFFA Gene Alias: DFF-45, DFF1, ICAD Gene Summary: Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and Page 1/1 Powered by TCPDF (www.tcpdf.org). -
FBXW8 (NM 153348) Human Recombinant Protein 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 TP761689 FBXW8 (NM_153348) Human Recombinant Protein Product data: Product Type: Recombinant Proteins Description: Purified recombinant protein of Human F-box and WD repeat domain containing 8 (FBXW8), transcript variant 1, full length, with N-terminal HIS tag, expressed in E. coli, 50ug Species: Human Expression Host: E. coli Tag: N-His Predicted MW: 67.2 kDa Concentration: >50 ug/mL as determined by microplate BCA method Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining Buffer: 50mM Tris, pH8.0,8M Urea. Storage: Store at -80°C. Stability: Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles. RefSeq: NP_699179 Locus ID: 26259 UniProt ID: Q8N3Y1 RefSeq Size: 4871 Cytogenetics: 12q24.22 RefSeq ORF: 1794 Synonyms: FBW6; FBW8; FBX29; FBXO29; FBXW6 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 / 2 FBXW8 (NM_153348) Human Recombinant Protein – TP761689 Summary: This gene encodes a member of the F-box protein family, members of which are characterized by an approximately 40 amino acid motif, the F-box. The F-box proteins constitute one of the four subunits of ubiquitin protein ligase complex called SCFs (SKP1- cullin-F-box), which function in phosphorylation-dependent ubiquitination. -
Environmental Influences on Endothelial Gene Expression
ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community. -
University of Groningen the Human HSP70/HSP40 Chaperone Family
University of Groningen The human HSP70/HSP40 chaperone family Hageman, Jurre IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2008 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Hageman, J. (2008). The human HSP70/HSP40 chaperone family: a study on its capacity to combat proteotoxic stress. s.n. Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license. More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne- amendment. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. Download date: 30-09-2021 CHAPTER 1 Introduction - Structural and functional diversities between members of the human HSPH, HSPA and DNAJ chaperone families Jurre Hageman and Harm H. -
List of Genes Associated with Sudden Cardiac Death (Scdgseta) Gene
List of genes associated with sudden cardiac death (SCDgseta) mRNA expression in normal human heart Entrez_I Gene symbol Gene name Uniprot ID Uniprot name fromb D GTEx BioGPS SAGE c d e ATP-binding cassette subfamily B ABCB1 P08183 MDR1_HUMAN 5243 √ √ member 1 ATP-binding cassette subfamily C ABCC9 O60706 ABCC9_HUMAN 10060 √ √ member 9 ACE Angiotensin I–converting enzyme P12821 ACE_HUMAN 1636 √ √ ACE2 Angiotensin I–converting enzyme 2 Q9BYF1 ACE2_HUMAN 59272 √ √ Acetylcholinesterase (Cartwright ACHE P22303 ACES_HUMAN 43 √ √ blood group) ACTC1 Actin, alpha, cardiac muscle 1 P68032 ACTC_HUMAN 70 √ √ ACTN2 Actinin alpha 2 P35609 ACTN2_HUMAN 88 √ √ √ ACTN4 Actinin alpha 4 O43707 ACTN4_HUMAN 81 √ √ √ ADRA2B Adrenoceptor alpha 2B P18089 ADA2B_HUMAN 151 √ √ AGT Angiotensinogen P01019 ANGT_HUMAN 183 √ √ √ AGTR1 Angiotensin II receptor type 1 P30556 AGTR1_HUMAN 185 √ √ AGTR2 Angiotensin II receptor type 2 P50052 AGTR2_HUMAN 186 √ √ AKAP9 A-kinase anchoring protein 9 Q99996 AKAP9_HUMAN 10142 √ √ √ ANK2/ANKB/ANKYRI Ankyrin 2 Q01484 ANK2_HUMAN 287 √ √ √ N B ANKRD1 Ankyrin repeat domain 1 Q15327 ANKR1_HUMAN 27063 √ √ √ ANKRD9 Ankyrin repeat domain 9 Q96BM1 ANKR9_HUMAN 122416 √ √ ARHGAP24 Rho GTPase–activating protein 24 Q8N264 RHG24_HUMAN 83478 √ √ ATPase Na+/K+–transporting ATP1B1 P05026 AT1B1_HUMAN 481 √ √ √ subunit beta 1 ATPase sarcoplasmic/endoplasmic ATP2A2 P16615 AT2A2_HUMAN 488 √ √ √ reticulum Ca2+ transporting 2 AZIN1 Antizyme inhibitor 1 O14977 AZIN1_HUMAN 51582 √ √ √ UDP-GlcNAc: betaGal B3GNT7 beta-1,3-N-acetylglucosaminyltransfe Q8NFL0 -
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. -
Involvement of Corepressor Complex Subunit GPS2 in Transcriptional Pathways Governing Human Bile Acid Biosynthesis
Involvement of corepressor complex subunit GPS2 in transcriptional pathways governing human bile acid biosynthesis Sabyasachi Sanyal*†, Ann Båvner‡, Anna Haroniti§, Lisa-Mari Nilsson¶, Thomas Lunda˚ senʈ, Stefan Rehnmark‡, Michael Robin Witt‡, Curt Einarsson¶, Iannis Talianidis§, Jan-Åke Gustafsson*, and Eckardt Treuter*† *Department of Biosciences and Nutrition, Karolinska Institutet, ‡Karo Bio AB, ¶Department of Gastroenterology and Hepatology, and ʈDepartment of Endocrinology, Metabolism, and Diabetes, Karolinska University Hospital, S-14157 Huddinge, Sweden; and §Biomedical Sciences Research Center, Alexander Fleming, 16672 Vari, Athens, Greece Edited by David W. Russell, University of Texas Southwestern Medical Center, Dallas, TX, and approved August 16, 2007 (received for review July 18, 2007) Coordinated regulation of bile acid biosynthesis, the predominant histone methyltransferase (G9a) (ref. 15 and references therein). pathway for hepatic cholesterol catabolism, is mediated by few Here we identify GPS2 (G protein pathway suppressor 2), a key nuclear receptors including the orphan receptors liver receptor subunit of the NR corepressor (N-CoR) complex (16–18), as a homolog 1 (LRH-1), hepatocyte nuclear factor 4␣ (HNF4␣), small SHP cofactor that, by means of additional interactions with heterodimer partner (SHP), and the bile acid receptor FXR (farne- LRH-1, HNF4␣, and FXR, participates in the differential reg- soid X receptor). Activation of FXR initiates a feedback regulatory ulation of CYP7A1 and CYP8B1 expression in human liver cell loop via induction of SHP, which suppresses LRH-1- and HNF4␣- lines and primary human hepatocytes. Additionally, we provide dependent expression of cholesterol 7␣ hydroxylase (CYP7A1) and insights into the species- and gene-specific regulations of these sterol 12␣ hydroxylase (CYP8B1), the two major pathway enzymes. -
Mutation and Expression Analysis in Medulloblastoma Yields Prognostic
Bien-Willner and Mitra Acta Neuropathologica Communications 2014, 2:74 http://www.actaneurocomms.org/content/2/1/74 RESEARCH Open Access Mutation and expression analysis in medulloblastoma yields prognostic variants and a putative mechanism of disease for i17q tumors Gabriel A Bien-Willner1,2* and Robi D Mitra2 Abstract Current consensus identifies four molecular subtypes of medulloblastoma (MB): WNT, sonic hedgehog (SHH), and groups “3/C” and “4/D”. Group 4 is not well characterized, but harbors the most frequently observed chromosomal abnormality in MB, i17q, whose presence may confer a worse outcome. Recent publications have identified mutations in chromatin remodeling genes that may be overrepresented in this group, suggesting a biological role for these genes in i17q. This work seeks to explore the pathology that underlies i17q in MB. Specifically, we examine the prognostic significance of the previously-identified gene mutations in an independent set of MBs as well as to examine biological relevance of these genes and related pathways by gene expression profiling. The previously-implicated p53 signaling pathway is also examined as a putative driver of i17q tumor oncogenesis. The data show gene mutations associated with i17q tumors in previous studies (KMD6A, ZMYM3, MLL3 and GPS2) were correlated with significantly worse outcomes despite not being specific to i17q in this set. Expression of these genes did not appear to underlie the biology of the molecular variants. TP53 expression was significantly reduced in i17q/ group 4 tumors; this could not be accounted for by dosage effects alone. Expression of regulators and mediators of p53 signaling were significantly altered in i17q tumors. -
Proteome Analysis of the HIV-1 Gag Interactome
Virology 460-461 (2014) 194–206 Contents lists available at ScienceDirect Virology journal homepage: www.elsevier.com/locate/yviro Proteome analysis of the HIV-1 Gag interactome Christine E. Engeland a, Nigel P. Brown b, Kathleen Börner a,b, Michael Schümann c, Eberhard Krause c, Lars Kaderali d, Gerd A. Müller e, Hans-Georg Kräusslich a,n a Department of Infectious Diseases, Virology, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany b Bioquant, Im Neuenheimer Feld 267, 69120 Heidelberg, Germany c Leibniz-Institut für Molekulare Pharmakologie, Robert-Rössle-Straße 10, D-13125 Berlin, Germany d Institute for Medical Informatics and Biometry (IMB), Medical Faculty Carl Gustav Carus, Dresden University of Technology, Fetscherstraße 74, D-01307 Dresden, Germany e Molecular Oncology, Medical School, University of Leipzig, Semmelweisstraße 14, D-04103 Leipzig, Germany article info abstract Article history: Human immunodeficiency virus Gag drives assembly of virions in infected cells and interacts with host Received 20 January 2014 factors which facilitate or restrict viral replication. Although several Gag-binding proteins have been Returned to author for revisions characterized, understanding of virus–host interactions remains incomplete. In a series of six affinity 6 February 2014 purification screens, we have identified protein candidates for interaction with HIV-1 Gag. Proteins Accepted 19 April 2014 previously found in virions or identified in siRNA screens for host factors influencing HIV-1 replication Available online 10 June 2014 were recovered. Helicases, translation factors, cytoskeletal and motor proteins, factors involved in RNA Keywords: degradation and RNA interference were enriched in the interaction data. Cellular networks of HIV Gag cytoskeleton, SR proteins and tRNA synthetases were identified. -
1 Supporting Information for a Microrna Network Regulates
Supporting Information for A microRNA Network Regulates Expression and Biosynthesis of CFTR and CFTR-ΔF508 Shyam Ramachandrana,b, Philip H. Karpc, Peng Jiangc, Lynda S. Ostedgaardc, Amy E. Walza, John T. Fishere, Shaf Keshavjeeh, Kim A. Lennoxi, Ashley M. Jacobii, Scott D. Rosei, Mark A. Behlkei, Michael J. Welshb,c,d,g, Yi Xingb,c,f, Paul B. McCray Jr.a,b,c Author Affiliations: Department of Pediatricsa, Interdisciplinary Program in Geneticsb, Departments of Internal Medicinec, Molecular Physiology and Biophysicsd, Anatomy and Cell Biologye, Biomedical Engineeringf, Howard Hughes Medical Instituteg, Carver College of Medicine, University of Iowa, Iowa City, IA-52242 Division of Thoracic Surgeryh, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Canada-M5G 2C4 Integrated DNA Technologiesi, Coralville, IA-52241 To whom correspondence should be addressed: Email: [email protected] (M.J.W.); yi- [email protected] (Y.X.); Email: [email protected] (P.B.M.) This PDF file includes: Materials and Methods References Fig. S1. miR-138 regulates SIN3A in a dose-dependent and site-specific manner. Fig. S2. miR-138 regulates endogenous SIN3A protein expression. Fig. S3. miR-138 regulates endogenous CFTR protein expression in Calu-3 cells. Fig. S4. miR-138 regulates endogenous CFTR protein expression in primary human airway epithelia. Fig. S5. miR-138 regulates CFTR expression in HeLa cells. Fig. S6. miR-138 regulates CFTR expression in HEK293T cells. Fig. S7. HeLa cells exhibit CFTR channel activity. Fig. S8. miR-138 improves CFTR processing. Fig. S9. miR-138 improves CFTR-ΔF508 processing. Fig. S10. SIN3A inhibition yields partial rescue of Cl- transport in CF epithelia. -
Characterising the Role of Valosin Containing Protein (VCP) in Autophagy and Cell Differentiation
Characterising the role of Valosin Containing Protein (VCP) in autophagy and cell differentiation. Autophagy vs. aberrant osteoclastogenesis in the IBMPFD mouse model Doctor of Philosophy Thesis, October 2015 Milka B. Budnik-Zawilska Project Supervisors: Dr Giles Watts, Prof Ian Clark Norwich Medical School, Health Policy and Practice University of East Anglia This copy of the thesis has been supplied on condition that anyone who consults it is understood to recognise that its copyright rests with the author and that use of any information derived there from must be in accordance with current UK Copyright Law. In addition, any quotation or extract must include full attribution. 1 Contents LIST OF TABLES ............................................................................................................................ 5 LIST OF FIGURES .......................................................................................................................... 6 ABSTRACT .................................................................................................................................... 9 ABBREVATIONS ......................................................................................................................... 10 ACKNOWLEDGMENTS ............................................................................................................... 15 CHAPTER 1: INTRODUCTION .................................................................................................... 17 1.1 Mutations in the VCP gene cause a