WIPI-Mediated Autophagy and Longevity
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Analysis of Trans Esnps Infers Regulatory Network Architecture
Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2014 © 2014 Anat Kreimer All rights reserved ABSTRACT Analysis of trans eSNPs infers regulatory network architecture Anat Kreimer eSNPs are genetic variants associated with transcript expression levels. The characteristics of such variants highlight their importance and present a unique opportunity for studying gene regulation. eSNPs affect most genes and their cell type specificity can shed light on different processes that are activated in each cell. They can identify functional variants by connecting SNPs that are implicated in disease to a molecular mechanism. Examining eSNPs that are associated with distal genes can provide insights regarding the inference of regulatory networks but also presents challenges due to the high statistical burden of multiple testing. Such association studies allow: simultaneous investigation of many gene expression phenotypes without assuming any prior knowledge and identification of unknown regulators of gene expression while uncovering directionality. This thesis will focus on such distal eSNPs to map regulatory interactions between different loci and expose the architecture of the regulatory network defined by such interactions. We develop novel computational approaches and apply them to genetics-genomics data in human. We go beyond pairwise interactions to define network motifs, including regulatory modules and bi-fan structures, showing them to be prevalent in real data and exposing distinct attributes of such arrangements. We project eSNP associations onto a protein-protein interaction network to expose topological properties of eSNPs and their targets and highlight different modes of distal regulation. -
Genetic and Genomic Analysis of Hyperlipidemia, Obesity and Diabetes Using (C57BL/6J × TALLYHO/Jngj) F2 Mice
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Nutrition Publications and Other Works Nutrition 12-19-2010 Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P. Stewart Marshall University Hyoung Y. Kim University of Tennessee - Knoxville, [email protected] Arnold M. Saxton University of Tennessee - Knoxville, [email protected] Jung H. Kim Marshall University Follow this and additional works at: https://trace.tennessee.edu/utk_nutrpubs Part of the Animal Sciences Commons, and the Nutrition Commons Recommended Citation BMC Genomics 2010, 11:713 doi:10.1186/1471-2164-11-713 This Article is brought to you for free and open access by the Nutrition at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Nutrition Publications and Other Works by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. Stewart et al. BMC Genomics 2010, 11:713 http://www.biomedcentral.com/1471-2164/11/713 RESEARCH ARTICLE Open Access Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P Stewart1, Hyoung Yon Kim2, Arnold M Saxton3, Jung Han Kim1* Abstract Background: Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/ JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia. -
WIPI-1 (38-W): Sc-100901
SANTA CRUZ BIOTECHNOLOGY, INC. WIPI-1 (38-W): sc-100901 BACKGROUND APPLICATIONS WIPI-1 (WD repeat domain, phosphoinositide interacting-1), also known as WIPI-1 (38-W) is recommended for detection of WIPI-1 of mouse, rat and WIPI1, ATG18 or WIPI49, is a 446 amino acid protein that localizes to cyto- human origin by Western Blotting (starting dilution 1:200, dilution range plasmic vesicles, endosomes, clathrin-coated vesicles and the trans-Golgi 1:100-1:1000), immunoprecipitation [1-2 µg per 100-500 µg of total protein network. Ubiquitously expressed with highest expression in heart, testis, (1 ml of cell lysate)] and solid phase ELISA (starting dilution 1:30, dilution placenta, pancreas and skeletal muscle, WIPI-1 is thought to play a role in range 1:30-1:3000). autophagy and may regulate protein trafficking in certain recycling pathways. Suitable for use as control antibody for WIPI-1 siRNA (h): sc-72210, WIPI-1 In addition, WIPI-1 interacts with androgen and estrogen receptors (ARs and siRNA (m): sc-72211, WIPI-1 shRNA Plasmid (h): sc-72210-SH, WIPI-1 shRNA ERs, respectively) and, through this interaction, may modify receptor function. Plasmid (m): sc-72211-SH, WIPI-1 shRNA (h) Lentiviral Particles: sc-72210-V WIPI-1 contains three WD repeats and has a 7-bladed propeller structure and WIPI-1 shRNA (m) Lentiviral Particles: sc-72211-V. with a conserved motif that facilitates its interaction with other proteins. WIPI-1 is expressed as two isoforms, designated a and b, and its expression Molecular Weight of WIPI-1: 49 kDa. -
Exploring Autophagy with Gene Ontology
Autophagy ISSN: 1554-8627 (Print) 1554-8635 (Online) Journal homepage: https://www.tandfonline.com/loi/kaup20 Exploring autophagy with Gene Ontology Paul Denny, Marc Feuermann, David P. Hill, Ruth C. Lovering, Helene Plun- Favreau & Paola Roncaglia To cite this article: Paul Denny, Marc Feuermann, David P. Hill, Ruth C. Lovering, Helene Plun- Favreau & Paola Roncaglia (2018) Exploring autophagy with Gene Ontology, Autophagy, 14:3, 419-436, DOI: 10.1080/15548627.2017.1415189 To link to this article: https://doi.org/10.1080/15548627.2017.1415189 © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. View supplementary material Published online: 17 Feb 2018. Submit your article to this journal Article views: 1097 View Crossmark data Full Terms & Conditions of access and use can be found at https://www.tandfonline.com/action/journalInformation?journalCode=kaup20 AUTOPHAGY, 2018 VOL. 14, NO. 3, 419–436 https://doi.org/10.1080/15548627.2017.1415189 RESEARCH PAPER - BASIC SCIENCE Exploring autophagy with Gene Ontology Paul Denny a,†,§, Marc Feuermann b,§, David P. Hill c,f,§, Ruth C. Lovering a,§, Helene Plun-Favreau d and Paola Roncaglia e,f,§ aFunctional Gene Annotation, Institute of Cardiovascular Science, University College London, London, UK; bSIB Swiss Institute of Bioinformatics, Geneva, Switzerland; cThe Jackson Laboratory, Bar Harbor, ME, USA; dDepartment of Molecular Neuroscience, UCL Institute of Neurology, London, UK; eEuropean Bioinformatics Institute (EMBL-EBI), European Molecular Biology Laboratory, Wellcome Genome Campus, Hinxton, Cambridge, UK; fThe Gene Ontology Consortium ABSTRACT ARTICLE HISTORY Autophagy is a fundamental cellular process that is well conserved among eukaryotes. It is one of the Received 18 May 2017 strategies that cells use to catabolize substances in a controlled way. -
Genome-Wide Association Study of Cardiac Structure and Systolic Function in African Americans the Candidate Gene Association Resource (Care) Study Ervin R
Genome-Wide Association Study of Cardiac Structure and Systolic Function in African Americans The Candidate Gene Association Resource (CARe) Study Ervin R. Fox, University of Mississippi Solomon K. Musani, University of Mississippi Maja Barbalic, University of Texas Health Science Center Honghuang Lin, Boston University Bing Yu, University of Mississippi Kofo O. Ogunyankin, Northwestern University Nicholas L. Smith, University of Washington Abdullah Kutlar, Georgia Health Sciences University Nicole L. Glazer, Boston University Wendy S. Post, Johns Hopkins University Only first 10 authors above; see publication for full author list. Journal Title: Circulation: Cardiovascular Genetics Volume: Volume 6, Number 1 Publisher: American Heart Association | 2013-02-01, Pages 37-46 Type of Work: Article | Post-print: After Peer Review Publisher DOI: 10.1161/CIRCGENETICS.111.962365 Permanent URL: https://pid.emory.edu/ark:/25593/v8g7t Final published version: http://dx.doi.org/10.1161/CIRCGENETICS.111.962365 Copyright information: © 2013 American Heart Association, Inc. Accessed September 30, 2021 9:00 PM EDT NIH Public Access Author Manuscript Circ Cardiovasc Genet. Author manuscript; available in PMC 2014 February 01. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Circ Cardiovasc Genet. 2013 February 1; 6(1): 37–46. doi:10.1161/CIRCGENETICS.111.962365. Genome-Wide Association Study of Cardiac Structure and Systolic Function in African Americans: The Candidate Gene Association Resource (CARe) Study Ervin R. Fox, MD1,*, Solomon K. Musani, PhD1,*, Maja Barbalic, PhD2,*, Honghuang Lin, PhD3, Bing Yu, MS1, Kofo O. Ogunyankin, MD4, Nicholas L. Smith, PhD5, Abdullah Kutlar, MD6, Nicole L. Glazer, MD3, Wendy S. -
Datasheet: MCA5780GA Product Details
Datasheet: MCA5780GA Description: MOUSE ANTI WIPI2 Specificity: WIPI2 Format: Purified Product Type: Monoclonal Antibody Clone: 2A2 Isotype: IgG1 Quantity: 0.1 mg Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio-rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Flow Cytometry Immunohistology - Frozen Immunohistology - Paraffin ELISA Immunoprecipitation Western Blotting Immunofluorescence Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using the appropriate negative/positive controls. Target Species Human Species Cross Reacts with: Mouse Reactivity N.B. Antibody reactivity and working conditions may vary between species. Product Form Purified IgG - liquid Buffer Solution Phosphate buffered saline Preservative 0.09% Sodium Azide (NaN ) Stabilisers 3 Carrier Free Yes Approx. Protein IgG concentration 1.0 mg/ml Concentrations Immunogen Synthetic peptide corresponding to the C-terminus of WIPI2b (CSALRLDEDSEHPPMILRTD) Page 1 of 3 External Database Links UniProt: Q9Y4P8 Related reagents Q80W47 Related reagents Entrez Gene: 26100 WIPI2 Related reagents 74781 Wipi2 Related reagents Specificity Mouse anti Human WIPI2 antibody, clone 2A2 recognies WD repeat domain phosphoinositide- interacting protein 2 (WIPI-2), also known as WIPI49-like protein 2. WIPI2 is a 454 amino acid ~54 kDa autophagosomal marker containing three WD repeats. -
Primepcr™Assay Validation Report
PrimePCR™Assay Validation Report Gene Information Gene Name WD repeat domain, phosphoinositide interacting 1 Gene Symbol WIPI1 Organism Human Gene Summary WD40 repeat proteins are key components of many essential biologic functions. They regulate the assembly of multiprotein complexes by presenting a beta-propeller platform for simultaneous and reversible protein-protein interactions. Members of the WIPI subfamily of WD40 repeat proteins such as WIPI1 have a 7-bladed propeller structure and contain a conserved motif for interaction with phospholipids (Proikas-Cezanne et al. 2004 Gene Aliases ATG18, ATG18A, FLJ10055, WIPI49 RefSeq Accession No. NC_000017.10, NT_010783.15 UniGene ID Hs.463964 Ensembl Gene ID ENSG00000070540 Entrez Gene ID 55062 Assay Information Unique Assay ID qHsaCIP0030544 Assay Type Probe - Validation information is for the primer pair using SYBR® Green detection Detected Coding Transcript(s) ENST00000262139, ENST00000546360 Amplicon Context Sequence TTCTCATCATGACTGCTTCGTTTTGCCCTTCTGATTTCCACGGCACAAGATTATAG GAGGAAACTCATTCTCATCATCAAGACACACTGGTCCCGTCGCAAACTCATGTTC AGGAATAA Amplicon Length (bp) 89 Chromosome Location 17:66417908-66422280 Assay Design Intron-spanning Purification Desalted Validation Results Efficiency (%) 99 R2 0.9995 cDNA Cq 21.43 cDNA Tm (Celsius) 80.5 Page 1/5 PrimePCR™Assay Validation Report gDNA Cq 35.07 Specificity (%) 100 Information to assist with data interpretation is provided at the end of this report. Page 2/5 PrimePCR™Assay Validation Report WIPI1, Human Amplification Plot Amplification of cDNA -
Targeting Melanoma-Initiating Cells by Caffeine: in Silico and in Vitro Approaches
molecules Article Targeting Melanoma-Initiating Cells by Caffeine: In Silico and In Vitro Approaches Claudio Tabolacci 1,* , Martina Cordella 1, Stefania Rossi 1 , Marialaura Bonaccio 2 , Adriana Eramo 1, Carlo Mischiati 3 , Simone Beninati 4 , Licia Iacoviello 2,5 , Antonio Facchiano 6,† and Francesco Facchiano 1,† 1 Department of Oncology and Molecular Medicine, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy; [email protected] (M.C.); [email protected] (S.R.); [email protected] (A.E.); [email protected] (F.F.) 2 Department of Epidemiology and Prevention, IRCCS Neuromed, 86077 Pozzilli, Italy; [email protected] (M.B.); [email protected] (L.I.) 3 Department of Neuroscience and Rehabilitation, School of Medicine, University of Ferrara, 44121 Ferrara, Italy; [email protected] 4 Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy; [email protected] 5 Department of Medicine and Surgery, Research Center in Epidemiology and Preventive Medicine (EPIMED), University of Insubria, 21100 Varese-Como, Italy 6 Laboratory of Molecular Oncology, IDI-IRCCS, 00167 Rome, Italy; [email protected] * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: The beneficial effects of coffee on human diseases are well documented, but the molecular mechanisms of its bioactive compounds on cancer are not completely elucidated. This is likely due to the large heterogeneity of coffee preparations and different coffee-based beverages, but also to Citation: Tabolacci, C.; Cordella, M.; the choice of experimental models where proliferation, differentiation and immune responses are Rossi, S.; Bonaccio, M.; Eramo, A.; differently affected. -
NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer
Florida International University FIU Digital Commons FIU Electronic Theses and Dissertations University Graduate School 11-7-2018 Decipher Mechanisms by which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer Jairo Ramos [email protected] Follow this and additional works at: https://digitalcommons.fiu.edu/etd Part of the Clinical Epidemiology Commons Recommended Citation Ramos, Jairo, "Decipher Mechanisms by which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer" (2018). FIU Electronic Theses and Dissertations. 3872. https://digitalcommons.fiu.edu/etd/3872 This work is brought to you for free and open access by the University Graduate School at FIU Digital Commons. It has been accepted for inclusion in FIU Electronic Theses and Dissertations by an authorized administrator of FIU Digital Commons. For more information, please contact [email protected]. FLORIDA INTERNATIONAL UNIVERSITY Miami, Florida DECIPHER MECHANISMS BY WHICH NUCLEAR RESPIRATORY FACTOR ONE (NRF1) COORDINATES CHANGES IN THE TRANSCRIPTIONAL AND CHROMATIN LANDSCAPE AFFECTING DEVELOPMENT AND PROGRESSION OF INVASIVE BREAST CANCER A dissertation submitted in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY in PUBLIC HEALTH by Jairo Ramos 2018 To: Dean Tomás R. Guilarte Robert Stempel College of Public Health and Social Work This dissertation, Written by Jairo Ramos, and entitled Decipher Mechanisms by Which Nuclear Respiratory Factor One (NRF1) Coordinates Changes in the Transcriptional and Chromatin Landscape Affecting Development and Progression of Invasive Breast Cancer, having been approved in respect to style and intellectual content, is referred to you for judgment. -
WIPI2 Antibody A
Revision 1 C 0 2 - t WIPI2 Antibody a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 7 6 Web: [email protected] 5 www.cellsignal.com 8 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source: UniProt ID: Entrez-Gene Id: WB H M R Endogenous 49 Rabbit Q9Y4P8 26100 Product Usage Information positive autophagosomes during autophagy; this translocation may be used as an autophagy marker (12). Application Dilution 1. Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21. 2. Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18. Western Blotting 1:1000 3. Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88. 4. Corvera, S. (2001) Traffic 2, 859-66. Storage 5. Yan, Y. and Backer, J.M. (2007) Biochem Soc Trans 35, 239-41. 6. Krick, R. et al. (2006) FEBS Lett 580, 4632-8. Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% 7. Strømhaug, P.E. et al. (2004) Mol Biol Cell 15, 3553-66. glycerol. Store at –20°C. Do not aliquot the antibody. 8. Obara, K. et al. (2008) J Biol Chem 283, 23972-80. 9. Jeffries, T.R. et al. (2004) Mol Biol Cell 15, 2652-63. Specificity / Sensitivity 10. Proikas-Cezanne, T. et al. (2007) FEBS Lett 581, 3396-404. 11. Polson, H.E. et al. -
The Emerging Roles of Mtorc1 in Macromanaging Autophagy
cancers Review The Emerging Roles of mTORC1 in Macromanaging Autophagy Akpedje S. Dossou and Alakananda Basu * Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-817-735-2487 Received: 25 August 2019; Accepted: 23 September 2019; Published: 24 September 2019 Abstract: Autophagy is a process of self-degradation that enables the cell to survive when faced with starvation or stressful conditions. The mechanistic target of rapamycin (mTOR), also known as the mammalian target of rapamycin, plays a critical role in maintaining a balance between cellular anabolism and catabolism. mTOR complex 1 (mTORC1) was unveiled as a master regulator of autophagy since inhibition of mTORC1 was required to initiate the autophagy process. Evidence has emerged in recent years to indicate that mTORC1 also directly regulates the subsequent steps of the autophagy process, including the nucleation, autophagosome elongation, autophagosome maturation and termination. By phosphorylating select protein targets of the autophagy core machinery and/or their regulators, mTORC1 can alter their functions, increase their proteasomal degradation or modulate their acetylation status, which is a key switch of the autophagy process. Moreover, it phosphorylates and alters the subcellular localization of transcription factors to suppress the expression of genes needed for autophagosome formation and lysosome biogenesis. The purpose of this review article is to critically analyze current literatures to provide an integrated view of how mTORC1 regulates various steps of the autophagy process. Keywords: macroautophagy; autophagy regulation; mTORC1 substrates; AMPK; ULK1; autophagy initiation; nucleation; elongation; autophagosome maturation; transcriptional regulation 1. -
Whole-Exome Sequencing Points to Considerable Genetic Heterogeneity of Cerebral Palsy
Molecular Psychiatry (2015) 20, 176–182 © 2015 Macmillan Publishers Limited All rights reserved 1359-4184/15 www.nature.com/mp IMMEDIATE COMMUNICATION Whole-exome sequencing points to considerable genetic heterogeneity of cerebral palsy G McMichael1, MN Bainbridge2, E Haan3,4, M Corbett1,4, A Gardner1,4, S Thompson4,5, BWM van Bon3,6, CL van Eyk1, J Broadbent1, C Reynolds1,MEO’Callaghan1, LS Nguyen4, DL Adelson7, R Russo8, S Jhangiani2, H Doddapaneni2, DM Muzny2, RA Gibbs2, J Gecz1,4,9,10 and AH MacLennan1,9,10 Cerebral palsy (CP) is a common, clinically heterogeneous group of disorders affecting movement and posture. Its prevalence has changed little in 50 years and the causes remain largely unknown. The genetic contribution to CP causation has been predicted to be ~ 2%. We performed whole-exome sequencing of 183 cases with CP including both parents (98 cases) or one parent (67 cases) and 18 singleton cases (no parental DNA). We identified and validated 61 de novo protein-altering variants in 43 out of 98 (44%) case-parent trios. Initial prioritization of variants for causality was by mutation type, whether they were known or predicted to be deleterious and whether they occurred in known disease genes whose clinical spectrum overlaps CP. Further, prioritization used two multidimensional frameworks—the Residual Variation Intolerance Score and the Combined Annotation-dependent Depletion score. Ten de novo mutations in three previously identified disease genes (TUBA1A (n =2),SCN8A (n =1)andKDM5C (n = 1)) and in six novel candidate CP genes (AGAP1, JHDM1D, MAST1, NAA35, RFX2 and WIPI2) were predicted to be potentially pathogenic for CP.