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Increased Expression of the Tail-Anchored Membrane Protein SLMAP in Adipose Tissue from Type 2 Tally Ho Diabetic Mice
Hindawi Publishing Corporation Experimental Diabetes Research Volume 2011, Article ID 421982, 10 pages doi:10.1155/2011/421982 Research Article Increased Expression of the Tail-Anchored Membrane Protein SLMAP in Adipose Tissue from Type 2 Tally Ho Diabetic Mice Xiaoliang Chen1 and Hong Ding2 1 Second People Hospital of Hangzhou, No. 1 Wenzhou Road, Hangzhou 310015, China 2 Department of Pharmacology, Weill Cornell Medical College in Qatar, P.O. Box 24144, Doha, Qatar Correspondence should be addressed to Hong Ding, [email protected] Received 6 April 2011; Accepted 5 May 2011 Academic Editor: N. Cameron Copyright © 2011 X. Chen and H. Ding. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The tail-anchored membrane protein, sarcolemmal membrane associated protein (SLMAP) is encoded to a single gene that maps to the chromosome 3p14 region and has also been reported in certain diabetic populations. Our previous studies with db/db mice shown that a deregulation of SLMAP expression plays an important role in type 2 diabetes. Male Tally Ho mice were bred to present with either normoglycemia (NG) or hyperglycemia (HG). Abdominal adipose tissue from male Tally Ho mice of the HG group was found to have a significantly lower expression of the membrane associated glucose transporter-4 (GLUT-4) and higher expression of SLMAP compared to tissue from NG mice. There were 3 isoforms expressed in the abdominal adipose tissue, but only 45 kDa isoform of SLMAP was associated with the GLUT-4 revealed by immunoprecipitation data. -
Estrogen Receptor Α Polymorphism in a Species with Alternative Behavioral Phenotypes
Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes Brent M. Hortona, William H. Hudsonb, Eric A. Ortlundb, Sandra Shirka, James W. Thomasc, Emily R. Youngd, Wendy M. Zinzow-Kramera, and Donna L. Maneya,1 aDepartment of Psychology, Emory University, Atlanta, GA 30322; bDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322; cNIH Intramural Sequencing Center, National Human Genome Research Institute, National Institutes of Health, Rockville, MD 20852; and dDepartment of Biology, Georgia Institute of Technology, Atlanta, GA 30332 Edited by Ellen D. Ketterson, Indiana University, Bloomington, IN, and accepted by the Editorial Board December 5, 2013 (received for review September 12, 2013) The evolution of behavior relies on changes at the level of the (7, 8). Morph differences in behavior cannot be entirely explained genome; yet the ability to attribute a behavioral change to by these hormones, however, because the differences persist even a specific, naturally occurring genetic change is rare in vertebrates. when plasma levels are experimentally equalized (9). Individual In the white-throated sparrow (Zonotrichia albicollis), a chromo- variation in steroid-dependent behavior may be better explained somal polymorphism (ZAL2/2m) is known to segregate with a be- by neural sensitivity to the hormones, for example by variation in havioral phenotype. Individuals with the ZAL2m haplotype engage the distribution and abundance of steroid receptors (10, 11). in more territorial aggression and less parental behavior than indi- The gene encoding estrogen receptor α (ERα), estrogen re- m viduals without it. These behaviors are thought to be mediated by ceptor 1 (ESR1), has been captured by the ZAL2 rearrange- sensitivity to sex steroids, and the chromosomal rearrangement ment (3) and has therefore likely differentiated between the underlying the polymorphism has captured a prime candidate haplotypes. -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
WO 2012/174282 A2 20 December 2012 (20.12.2012) 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 2012/174282 A2 20 December 2012 (20.12.2012) P O P C T (51) International Patent Classification: David [US/US]; 13539 N . 95th Way, Scottsdale, AZ C12Q 1/68 (2006.01) 85260 (US). (21) International Application Number: (74) Agent: AKHAVAN, Ramin; Caris Science, Inc., 6655 N . PCT/US20 12/0425 19 Macarthur Blvd., Irving, TX 75039 (US). (22) International Filing Date: (81) Designated States (unless otherwise indicated, for every 14 June 2012 (14.06.2012) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, English (25) Filing Language: CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, Publication Language: English DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (30) Priority Data: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, 61/497,895 16 June 201 1 (16.06.201 1) US MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, 61/499,138 20 June 201 1 (20.06.201 1) US OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, 61/501,680 27 June 201 1 (27.06.201 1) u s SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, 61/506,019 8 July 201 1(08.07.201 1) u s TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. -
Genetic Networks Controlling Retinal Injury Felix R
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2005 Genetic networks controlling retinal injury Felix R. Vazquez-Chona University of Tennessee Health Science Center Amna N. Khan University of Tennessee Health Science Center Chun K. Chan University of Tennessee Health Science Center Anthony N. Moore University of Texas Health Science Center at Houston Pramod K. Dash University of Texas Health Science Center at Houston See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Vazquez-Chona, Felix R.; Khan, Amna N.; Chan, Chun K.; Moore, Anthony N.; Dash, Pramod K.; Hernandez, M. Rosario; Lu, Lu; Chesler, Elissa J.; Manly, Kenneth F.; Williams, Robert W.; and Geisert, Eldon E. Jr., ,"Genetic networks controlling retinal injury." Molecular Vision.11,. 958-970. (2005). https://digitalcommons.wustl.edu/open_access_pubs/1807 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 Felix R. Vazquez-Chona, Amna N. Khan, Chun K. Chan, Anthony N. Moore, Pramod K. Dash, M. Rosario Hernandez, Lu Lu, Elissa J. Chesler, Kenneth F. Manly, Robert W. Williams, and Eldon E. Geisert Jr. This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/1807 Molecular Vision 2005; 11:958-70 <http://www.molvis.org/molvis/v11/a115/> ©2005 Molecular Vision Received 3 March 2005 | Accepted 10 October 2005 | Published 4 November 2005 Genetic networks controlling retinal injury Felix R. -
ID AKI Vs Control Fold Change P Value Symbol Entrez Gene Name *In
ID AKI vs control P value Symbol Entrez Gene Name *In case of multiple probesets per gene, one with the highest fold change was selected. Fold Change 208083_s_at 7.88 0.000932 ITGB6 integrin, beta 6 202376_at 6.12 0.000518 SERPINA3 serpin peptidase inhibitor, clade A (alpha-1 antiproteinase, antitrypsin), member 3 1553575_at 5.62 0.0033 MT-ND6 NADH dehydrogenase, subunit 6 (complex I) 212768_s_at 5.50 0.000896 OLFM4 olfactomedin 4 206157_at 5.26 0.00177 PTX3 pentraxin 3, long 212531_at 4.26 0.00405 LCN2 lipocalin 2 215646_s_at 4.13 0.00408 VCAN versican 202018_s_at 4.12 0.0318 LTF lactotransferrin 203021_at 4.05 0.0129 SLPI secretory leukocyte peptidase inhibitor 222486_s_at 4.03 0.000329 ADAMTS1 ADAM metallopeptidase with thrombospondin type 1 motif, 1 1552439_s_at 3.82 0.000714 MEGF11 multiple EGF-like-domains 11 210602_s_at 3.74 0.000408 CDH6 cadherin 6, type 2, K-cadherin (fetal kidney) 229947_at 3.62 0.00843 PI15 peptidase inhibitor 15 204006_s_at 3.39 0.00241 FCGR3A Fc fragment of IgG, low affinity IIIa, receptor (CD16a) 202238_s_at 3.29 0.00492 NNMT nicotinamide N-methyltransferase 202917_s_at 3.20 0.00369 S100A8 S100 calcium binding protein A8 215223_s_at 3.17 0.000516 SOD2 superoxide dismutase 2, mitochondrial 204627_s_at 3.04 0.00619 ITGB3 integrin, beta 3 (platelet glycoprotein IIIa, antigen CD61) 223217_s_at 2.99 0.00397 NFKBIZ nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, zeta 231067_s_at 2.97 0.00681 AKAP12 A kinase (PRKA) anchor protein 12 224917_at 2.94 0.00256 VMP1/ mir-21likely ortholog -
Role of SLMAP Genetic Variants in Susceptibility Of
Upadhyay et al. Journal of Translational Medicine (2015) 13:61 DOI 10.1186/s12967-015-0411-6 RESEARCH Open Access Role of SLMAP genetic variants in susceptibility of diabetes and diabetic retinopathy in Qatari population Rohit Upadhyay1, Amal Robay2, Khalid Fakhro2, Charbel Abi Khadil2, Mahmoud Zirie3, Amin Jayyousi3, Maha El-Shafei4, Szilard Kiss5, Donald J D′Amico5, Jacqueline Salit6, Michelle R Staudt6, Sarah L O′Beirne6, Xiaoliang Chen7, Balwant Tuana8, Ronald G Crystal6 and Hong Ding1* Abstract Background: Overexpression of SLMAP gene has been associated with diabetes and endothelial dysfunction of macro- and micro-blood vessels. In this study our primary objective is to explore the role of SLMAP gene polymorphisms in the susceptibility of type 2 diabetes (T2DM) with or without diabetic retinopathy (DR) in the Qatari population. Methods: A total of 342 Qatari subjects (non-diabetic controls and T2DM patients with or without DR) were genotyped for SLMAP gene polymorphisms (rs17058639 C > T; rs1043045 C > T and rs1057719 A > G) using Taqman SNP genotyping assay. Results: SLMAP rs17058639 C > T polymorphism was associated with the presence of DR among Qataris with T2DM. One-way ANOVA and multiple logistic regression analysis showed SLMAP SNP rs17058639 C > T as an independent risk factor for DR development. SLMAP rs17058639 C > T polymorphism also had a predictive role for the severity of DR. Haplotype Crs17058639Trs1043045Ars1057719 was associated with the increased risk for DR among Qataris with T2DM. Conclusions: The data suggests the potential role of SLMAP SNPs as a risk factor for the susceptibility of DR among T2DM patients in the Qatari population. -
Gene Expression Profiles of Ductal Versus Acinar Adenocarcinoma of the Prostate
Modern Pathology (2009) 22, 1273–1279 & 2009 USCAP, Inc. All rights reserved 0893-3952/09 $32.00 1273 Gene expression profiles of ductal versus acinar adenocarcinoma of the prostate Souzan Sanati1, Mark A Watson2, Andrea L Salavaggione2 and Peter A Humphrey1 1Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, St Louis, MO, USA and 2Department of Pathology and Immunology, Division of Laboratory and Genomic Medicine, Washington University School of Medicine, St Louis, MO, USA Ductal adenocarcinoma is an uncommon variant of prostatic adenocarcinoma with a generally more aggressive clinical course than usual acinar adenocarcinoma. However, the molecular distinction between ductal and acinar adenocarcinomas is not well characterized. The aim of this investigation was to evaluate the relatedness of ductal versus acinar prostatic adenocarcinoma by comparative gene expression profiling. Archived, de- identified, snap frozen tumor tissue from 5 ductal adenocarcinomas, 3 mixed ductal–acinar adenocarcinomas, and 11 acinar adenocarcinomas cases were analyzed. All cases of acinar and ductal adenocarcinomas were matched by Gleason grade. RNA from whole tissue sections of the 5 ductal and 11 acinar adenocarcinomas cases were subjected to gene expression profiling on Affymetrix U133Plus2 microarrays. Independently, laser- capture microdissection was also performed on the three mixed ductal–acinar cases and five pure acinar cases to isolate homogeneous populations of ductal and acinar carcinoma cells from the same tumor. Seven of these laser-capture microdissected samples (three ductal and four acinar cell populations) were similarly analyzed on U133Plus2 arrays. Analysis of data from whole sections of ductal and acinar carcinomas identified only 25 gene transcripts whose expression was significantly and at least two-fold different between ductal and acinar adenocarcinomas. -
Lineage-Defined Leiomyosarcoma Subtypes Emerge Years Before Diagnosis and Determine Patient Survival
ARTICLE https://doi.org/10.1038/s41467-021-24677-6 OPEN Lineage-defined leiomyosarcoma subtypes emerge years before diagnosis and determine patient survival Nathaniel D. Anderson 1,2, Yael Babichev3,17, Fabio Fuligni4,17, Federico Comitani 1, Mehdi Layeghifard 1, Rosemarie E. Venier 3, Stefan C. Dentro5, Anant Maheshwari1, Sheena Guram3, Claire Wunker3,6, J. Drew Thompson1, Kyoko E. Yuki1, Huayun Hou 1, Matthew Zatzman1,2, Nicholas Light1,6, Marcus Q. Bernardini7,8, Jay S. Wunder 3,9,10, Irene L. Andrulis 2,3,11, Peter Ferguson7,9,10, Albiruni R. Abdul Razak7, Carol J. Swallow3,6,9,12, James J. Dowling1,11, Rima S. Al-Awar13,14, Richard Marcellus13, 1234567890():,; Marjan Rouzbahman2,7, Moritz Gerstung 5, Daniel Durocher 3,11, Ludmil B. Alexandrov 15, ✉ ✉ Brendan C. Dickson 2,3,16, Rebecca A. Gladdy 3,6,9,12 & Adam Shlien 1,2,4 Leiomyosarcomas (LMS) are genetically heterogeneous tumors differentiating along smooth muscle lines. Currently, LMS treatment is not informed by molecular subtyping and is associated with highly variable survival. While disease site continues to dictate clinical management, the contribution of genetic factors to LMS subtype, origins, and timing are unknown. Here we analyze 70 genomes and 130 transcriptomes of LMS, including multiple tumor regions and paired metastases. Molecular profiling highlight the very early origins of LMS. We uncover three specific subtypes of LMS that likely develop from distinct lineages of smooth muscle cells. Of these, dedifferentiated LMS with high immune infiltration and tumors primarily of gynecological origin harbor genomic dystrophin deletions and/or loss of dystrophin expression, acquire the highest burden of genomic mutation, and are associated with worse survival. -
Exploiting Native Forces to Capture Chromosome Conformation in Mammalian Cell Nuclei
Edinburgh Research Explorer Exploiting native forces to capture chromosome conformation in mammalian cell nuclei Citation for published version: Brant, L, Georgomanolis, T, Nikolic, M, Brackley, CA, Kolovos, P, van Ijcken, W, Grosveld, FG, Marenduzzo, D & Papantonis, A 2016, 'Exploiting native forces to capture chromosome conformation in mammalian cell nuclei', Molecular Systems Biology, vol. 12, no. 12, pp. 891. https://doi.org/10.15252/msb.20167311 Digital Object Identifier (DOI): 10.15252/msb.20167311 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Molecular Systems Biology General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Published online: December 9, 2016 Report Exploiting native forces to capture chromosome conformation in mammalian cell nuclei Lilija Brant1, Theodore Georgomanolis1,†, Milos Nikolic1,†, Chris A Brackley2, Petros Kolovos3, Wilfred van Ijcken4 , Frank G Grosveld3, Davide Marenduzzo2 & Argyris Papantonis1,* Abstract et al, 2013; Pombo & Dillon, 2015; Denker & de Laat, 2016) and allowed us to address diverse biological questions (e.g., Tolhuis et al, Mammalian interphase chromosomes fold into a multitude of 2002; Papantonis et al, 2012; Zhang et al, 2012; Naumova et al, loops to fit the confines of cell nuclei, and looping is tightly 2013; Rao et al, 2014). -
STRIPAK, a Highly Conserved Signaling Complex, Controls Multiple
Biol. Chem. 2019; 400(8): 1005–1022 Review Ulrich Kück*, Daria Radchenko and Ines Teichert STRIPAK, a highly conserved signaling complex, controls multiple eukaryotic cellular and developmental processes and is linked with human diseases https://doi.org/10.1515/hsz-2019-0173 networks are now known to underlie the transmission and Received February 27, 2019; accepted March 28, 2019; previously modulation of such signals. These networks, controlled published online May 1, 2019 by diverse regulators at different cellular levels, are highly conserved across eukaryotic organisms. Abstract: The striatin-interacting phosphatases and Among the signaling components that have received kinases (STRIPAK) complex is evolutionary highly con- increased attention in the last decade is the STRIPAK served and has been structurally and functionally complex, which was initially identified in mammals by described in diverse lower and higher eukaryotes. In recent mass spectrometry (MS) analysis (Goudreault et al., 2009). years, this complex has been biochemically characterized Here we will provide a summary of the key studies leading better and further analyses in different model systems have to the discovery of striatin, the major regulatory phos- shown that it is also involved in numerous cellular and phatase subunit of the STRIPAK complex. Further, the developmental processes in eukaryotic organisms. Fur- components and architecture as well as the assembly and ther recent results have shown that the STRIPAK complex structural insights of the STRIPAK complex will be com- functions as a macromolecular assembly communicating prehensively reviewed. Another focus will be the control through physical interaction with other conserved signal- of developmental processes as a result of bi-directional ing protein complexes to constitute larger dynamic protein interaction of STRIPAK with other components involved networks. -
UC San Diego Electronic Theses and Dissertations
UC San Diego UC San Diego Electronic Theses and Dissertations Title Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent Permalink https://escholarship.org/uc/item/7m04f0b0 Author Buchholz, Kyle Stephen Publication Date 2016 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Bioengineering by Kyle Stephen Buchholz Committee in Charge: Professor Jeffrey Omens, Chair Professor Andrew McCulloch, Co-Chair Professor Ju Chen Professor Karen Christman Professor Robert Ross Professor Alexander Zambon 2016 Copyright Kyle Stephen Buchholz, 2016 All rights reserved Signature Page The Dissertation of Kyle Stephen Buchholz is approved and it is acceptable in quality and form for publication on microfilm and electronically: Co-Chair Chair University of California, San Diego 2016 iii Dedication To my beautiful wife, Rhia. iv Table of Contents Signature Page ................................................................................................................... iii Dedication .......................................................................................................................... iv Table of Contents ................................................................................................................ v List of Figures ...................................................................................................................