DOCSLIB.ORG

The Association of Toll-Like Receptor Polymorphisms With

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Association of Toll-Like Receptor Polymorphisms With THE ASSOCIATION OF TOLL-LIKE RECEPTOR POLYMORPHISMS WITH HUMAN IMMUNODEFICIENCY VIRUS INFECTION IN NORTH AMERICANS by BARNE WILLIE Submitted in partial fulfillment of the requirement for the degree of Master of Science Dissertation Advisor: Dr. Peter A Zimmerman (PhD) Biology Case Western Reserve University May 2014 Case Western Reserve University School of Graduate Studies We hereby approve the thesis/dissertation of BARNE WILLIE ………………………………………………………………………………………………………………… candidate for the Master in Science degree*. (signed) Roy Ritzmann (PhD) …………………………………………………………………………………………………………………… (Chair of the committee) Peter A Zimmerman (PhD) …………………………………………………………………………………………………………………… Daniel Tisch (PhD) …………………………………………………………………………………………………………………… Christopher Cullis (PhD) …………………………………………………………………………………………………………………… (date) 21st March 2014 ………………………………………………… * We also certify that the written approval has been obtained for any proprietary material contained therein. II Dedication I would take this precious time that I have to dedicate this work to my Bikpela Papa - Naiyo Niniko and Bikpela Ankol - Phillip Felix Buri. I know you twos will be proud to see me through this time of my life journey. But now, I could only wish you twos were here to witness this. Miss you twos so much, and what more can I say...? I shall see you twos one day. III Table of Content List of Tables ............................................................................................................... VII List of Figures ............................................................................................................. VIII Acknowledgement ....................................................................................................... IX List of Abbreviations ..................................................................................................... X Thesis Abstract ............................................................................................................ XII 1.0 Introduction ............................................................................................................ 1 1.1. General Immunology ........................................................................................... 1 1.3. Innate Immunity .................................................................................................. 3 1.4. Toll-Like Receptors .............................................................................................. 6 1.5. TLR1-9 properties ................................................................................................ 8 1.5.1. TLR1 (cluster of differentiation 281-CD281) ................................................ 8 1.5.2. TLR2 (cluster of differentiation 282-CD282) ................................................ 9 1.5.3. TLR3 (cluster of differentiation 283-CD283) ................................................ 9 1.5.4. TLR4 (cluster of differentiation 284-CD284) .............................................. 10 1.5.5. TLR5 (cluster of differentiation 285-CD285) .............................................. 10 1.5.6. TLR6 (cluster of differentiation 286-CD286) .............................................. 11 1.5.7. TLR7 (cluster of differentiation 287-CD287) .............................................. 11 1.5.8. TLR8 (cluster of differentiation 288-CD288) .............................................. 12 1.5.9. TLR9 (cluster of differentiation 289-CD289) .............................................. 12 1.5.10. TLR10 (cluster of differentiation 290-CD290) .......................................... 13 1.6. Human TLR Groupings ....................................................................................... 13 IV 1.7. Chemistry of ligand binding .............................................................................. 14 1.8. PAMPs Recognition by TLRs .............................................................................. 15 1.9. TLR signaling pathways ..................................................................................... 17 1.10. SNPs, gene expression and functionality ........................................................ 19 1.11. SNP analysis-Genome Wide Association Studies ............................................ 21 1.12. TLR genes SNPs and disease association ......................................................... 22 1.13. Thesis Objectives ............................................................................................. 27 2.0 Methods ................................................................................................................ 28 2.1. Selection of TLR gene SNPs ............................................................................... 28 2.2. Sample preparation for genotyping .................................................................. 29 2.3. Genotyping assay .............................................................................................. 30 2.3.1. Golden Gate Vera Code Bead Express Platform ......................................... 30 2.3.2. Establishing the Bead Express Genotyping Assay ...................................... 31 2.4. Sample ............................................................................................................... 32 2.5. Genotype data processing ................................................................................ 33 2.6. Statistical association analysis .......................................................................... 35 3.0 Result .................................................................................................................... 37 3.1. Batch Effect (Plate - Plate) ................................................................................ 37 3.2. Hardy Weinberg Equilibrium Test (HWE) .......................................................... 37 3.3. Allele frequencies .............................................................................................. 37 3.4. Statistical analysis - Logistic regression ............................................................. 39 3.4.1. Unadjusted ................................................................................................. 39 3.4.2. Adjusted: Stratified by race with HIV status as covariant .......................... 40 V 3.4.3. Haplotype analysis ...................................................................................... 41 3.5. Linkage Disequilibrium analysis ........................................................................ 42 4.0 Discussion .............................................................................................................. 45 4.1. Logistic regression, Linkage Disequilibrium and Haplotype analysis ................ 47 4.2. Biological importance of statistical significant SNPs in this study .................... 51 4.2.1. TLR1 rs5743618 .......................................................................................... 51 4.2.2. TLR1 rs5743551 .......................................................................................... 52 4.2.3. TLR4 rs10759932 ........................................................................................ 53 4.2.4. TLR6 rs5743810 .......................................................................................... 53 4.2.5. TLR6 rs1039559 .......................................................................................... 54 4.2.6 Biological summary ...................................................................................... 54 5.0 Conclusion ............................................................................................................. 56 Reference .................................................................................................................... 58 VI List of Tables Table 1: Differences between Innate and Adaptive Immunity ...................................... 2 Table 2: Innate immunity germ line encoded receptors-the pattern recognition receptors, PAMPs and function. .................................................................................... 5 Table 3: TLR and associated PAMPs ............................................................................. 15 Table 4: TLRs and associated adaptor recruitment ..................................................... 18 Table 5: Summary of studies that have been done and what was found with infection/disease.......................................................................................................... 24 Table 6: Individual demography in the study .............................................................. 33 Table 7: Fishers Exact t-test plate to plate variation results ....................................... 37 Table 8: Observed allele frequency in HIV status and within each population........... 38 Table 9: Logistic regression statistical analysis results showing only significant alleles at p < 0.05 .................................................................................................................... 39 Table 10: Additive and Dominant genetic model test statistical analysis results showing significant alleles at p < 0.05 in AfA population ............................................ 40 Table 11: Additive and Dominant genetic model test statistical analysis results showing significant alleles at p < 0.05 in CA population ............................................. 41 Table 12: Haplotype analysis results showing only significant alleles at p < 0.05 in CA population in CA group
Load more

Recommended publications
  • Bioinformatic Analysis of Structure and Function of LIM Domains of Human Zyxin Family Proteins
    International Journal of Molecular Sciences Article Bioinformatic Analysis of Structure and Function of LIM Domains of Human Zyxin Family Proteins M. Quadir Siddiqui 1,† , Maulik D. Badmalia 1,† and Trushar R. Patel 1,2,3,* 1 Alberta RNA Research and Training Institute, Department of Chemistry and Biochemistry, University of Lethbridge, 4401 University Drive, Lethbridge, AB T1K 3M4, Canada; [email protected] (M.Q.S.); [email protected] (M.D.B.) 2 Department of Microbiology, Immunology and Infectious Disease, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive, Calgary, AB T2N 4N1, Canada 3 Li Ka Shing Institute of Virology, University of Alberta, Edmonton, AB T6G 2E1, Canada * Correspondence: [email protected] † These authors contributed equally to the work. Abstract: Members of the human Zyxin family are LIM domain-containing proteins that perform critical cellular functions and are indispensable for cellular integrity. Despite their importance, not much is known about their structure, functions, interactions and dynamics. To provide insights into these, we used a set of in-silico tools and databases and analyzed their amino acid sequence, phylogeny, post-translational modifications, structure-dynamics, molecular interactions, and func- tions. Our analysis revealed that zyxin members are ohnologs. Presence of a conserved nuclear export signal composed of LxxLxL/LxxxLxL consensus sequence, as well as a possible nuclear localization signal, suggesting that Zyxin family members may have nuclear and cytoplasmic roles. The molecular modeling and structural analysis indicated that Zyxin family LIM domains share Citation: Siddiqui, M.Q.; Badmalia, similarities with transcriptional regulators and have positively charged electrostatic patches, which M.D.; Patel, T.R.
    [Show full text]
  • LPP (8B3A11) Mouse Mab A
    Revision 1 C 0 2 - t LPP (8B3A11) Mouse mAb a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 9 8 Web: [email protected] 3 www.cellsignal.com 3 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source/Isotype: UniProt ID: Entrez-Gene Id: WB, IP, IHC-P, IF-IC H M Hm Mk Endogenous 75 Mouse IgG1 Q93052 4026 Product Usage Information Application Dilution Western Blotting 1:1000 Immunoprecipitation 1:50 Immunohistochemistry (Paraffin) 1:100 Immunofluorescence (Immunocytochemistry) 1:100 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody. Specificity / Sensitivity LPP (8B3A11) Mouse mAb detects endogenous levels of total LPP protein. Species Reactivity: Human, Mouse, Hamster, Monkey Source / Purification Monoclonal antibody is produced by immunizing animals with a HIS-tagged recombinant fragment of human LPP. Background LIM-containing lipoma-preferred partner (LPP) belongs to the zyxin family, members of which include LIMD1, ajuba, trip6 and zyxin. Three LIM domains at the carboxy-terminus characterize this family of proteins. Zyxin family members associate with the actin cytoskeleton and are components of both the cell-cell junction adhesive complex and the integrin-mediated adhesive complex (1). They shuttle in and out of the nucleus where they may function in transcriptional activation (1). LPP binding partners at cell-cell contacts include the actin regulator α-actinin (2) and the human tumor suppressor scrib which regulates cell migration and polarity (3).
    [Show full text]
  • Cep-2020-00633.Pdf
    Clin Exp Pediatr Vol. 64, No. 5, 208–222, 2021 Review article CEP https://doi.org/10.3345/cep.2020.00633 Understanding the genetics of systemic lupus erythematosus using Bayesian statistics and gene network analysis Seoung Wan Nam, MD, PhD1,*, Kwang Seob Lee, MD2,*, Jae Won Yang, MD, PhD3,*, Younhee Ko, PhD4, Michael Eisenhut, MD, FRCP, FRCPCH, DTM&H5, Keum Hwa Lee, MD, MS6,7,8, Jae Il Shin, MD, PhD6,7,8, Andreas Kronbichler, MD, PhD9 1Department of Rheumatology, Wonju Severance Christian Hospital, Yonsei University Wonju College of Medicine, Wonju, Korea; 2Severance Hospital, Yonsei University College of Medicine, Seoul, Korea; 3Department of Nephrology, Yonsei University Wonju College of Medicine, Wonju, Korea; 4Division of Biomedical Engineering, Hankuk University of Foreign Studies, Yongin, Korea; 5Department of Pediatrics, Luton & Dunstable University Hospital NHS Foundation Trust, Luton, UK; 6Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea; 7Division of Pediatric Nephrology, Severance Children’s Hospital, Seoul, Korea; 8Institute of Kidney Disease Research, Yonsei University College of Medicine, Seoul, Korea; 9Department of Internal Medicine IV (Nephrology and Hypertension), Medical University Innsbruck, Innsbruck, Austria 1,3) The publication of genetic epidemiology meta-analyses has analyses have redundant duplicate topics and many errors. increased rapidly, but it has been suggested that many of the Although there has been an impressive increase in meta-analyses statistically significant results are false positive. In addition, from China, particularly those on genetic associa tions, most most such meta-analyses have been redundant, duplicate, and claimed candidate gene associations are likely false-positives, erroneous, leading to research waste. In addition, since most suggesting an urgent global need to incorporate genome-wide claimed candidate gene associations were false-positives, cor- data and state-of-the art statistical inferences to avoid a flood of rectly interpreting the published results is important.
    [Show full text]
  • DNA Sequence of the Serratia Marcescens Lipoprotein Gene
    Proc. NatI. Acad. Sci. USA Vol. 77, No. 3, pp. 1369-1373, March 1980 Biochemistry DNA sequence of the Serratia marcescens lipoprotein gene (promoter/A-T base pairs/secretion/signal peptide/loop model/gene evolution) KENZO NAKAMURA AND MASAYORI INOUYE Department of Biochemistry, State University of New York, Stony Brook, New York 11794 Communicated by Charles Yanofsky, December 12, 1979 ABSTRACT The Serratia marcescens gene for the outer gene of S. marcescens with that of E. coli revealed several in- membrane lipoprotein (lpp) was cloned in A phage vector teresting and unique features concerning the mechanism of Charon 14. The recombinant phage was very unstable, and the expression of this gene, the secretion of the lipoprotein across Ipp gene with a 300-base-pair deletion at the transcription ter- mination site was further cloned in pBR322. The DNA sequence the cytoplasmic membrane, and the evolution of the gene. of 834 base pairs encompassing the Ipp gene was determined and compared with that of the Escherichia coli ipp gene. The MATERIALS AND METHODS sequence comparisons exhibit several unique features. (i) The Materials. [y-32P]ATP (m9000 Ci/mmol; 1 Ci = 3.7 X 101O promoter region is highly conserved (84% homology) and has becquerels), prepared by the method of Johnson and Walseth an extremely high A+T content (78%) as in E. coli (80%). (ii) (8) from carrier-free The 5' nontranslated region of the lipoprotein mRNA is also [32P]orthophosphate (New England Nu- highly conserved (95% homology). (iii) In the DNA sequence clear) and ADP (Sigma), was used for 5'-end-labeling of DNA corresponding to the signal peptide of this secretory protein, fragments.
    [Show full text]
  • The Chromosome 3P21.3-Encoded Gene, LIMD1, Is a Critical Tumor Suppressor Involved in Human Lung Cancer Development
    The chromosome 3p21.3-encoded gene, LIMD1, is a critical tumor suppressor involved in human lung cancer development Tyson V. Sharpa, Ahmad Al-Attarb,1, Daniel E. Foxlera,1, Li Dingc, Thomas Q. de A. Vallima, Yining Zhanga, Hala S. Nijmeha, Thomas M. Webba, Andrew G. Nicholsond, Qunyuan Zhange, Aldi Krajae, Ian Spendloveb, John Osbornec, Elaine Mardisc,e, and Gregory D. Longmoref,2 aSchool of Biomedical Sciences, Queen’s Medical Centre, University of Nottingham Medical School, Nottingham NG7 2UH, United Kingdom; bAcademic and Clinical Departments of Oncology, University of Nottingham, Nottingham NG5 1PB, United Kingdom; dDepartment of Histopathology, Royal Brompton Hospital, London SW3 6NP, United Kingdom; cDepartment of Genetics, Genome Sequencing Center, and eDivision of Statistical Genomics, Washington University School of Medicine, St. Louis, MO 63108; and fDepartments of Medicine and Cell Biology, Washington University, St Louis, MO 63110 Edited by George Klein, Karolinska Institutet, Stockholm, Sweden, and approved October 7, 2008 (received for review May 23, 2008) Loss of heterozygosity (LOH) and homozygous deletions at chro- toma protein (pRB), inhibits E2F-mediated transcription, and mosome 3p21.3 are common in both small and nonsmall cell lung suppresses expression of the majority of genes with E2F1- cancers, indicating the likely presence of tumor suppressor genes responsive elements (9). Moreover, forced expression of LIMD1 (TSGs). Although genetic and epigenetic changes within this region in A549 lung tumor cell line blocks tumor growth in vitro and in have been identified, the functional significance of these changes vivo (9). Here, we show that expression of the 3p21.3 gene, has not been explored.
    [Show full text]
  • Fine Mapping of the Celiac Disease-Associated LPP Locus Reveals a Potential Functional Variant
    Human Molecular Genetics, 2014, Vol. 23, No. 9 2481–2489 doi:10.1093/hmg/ddt619 Advance Access published on December 11, 2013 Fine mapping of the celiac disease-associated LPP locus reveals a potential functional variant Rodrigo Almeida1,2,{, Isis Rican˜ o-Ponce1,{, Vinod Kumar1, Patrick Deelen1, Agata Szperl1, Gosia Trynka1,{, Javier Gutierrez-Achury1, Alexandros Kanterakis1, Harm-Jan Westra1, Lude Franke1, Morris A. Swertz1, Mathieu Platteel1, Jose Ramon Bilbao3, Donatella Barisani4, Luigi Greco5, Luisa Mearin6, Victorien M. Wolters7, Chris Mulder8, Maria Cristina Mazzilli9, Ajit Sood10, Bozena Cukrowska11, Concepcio´ nNu´ n˜ ez12, Riccardo Pratesi2, Sebo Withoff1 Downloaded from https://academic.oup.com/hmg/article/23/9/2481/631913 by guest on 25 September 2021 and Cisca Wijmenga1,∗ 1Department of Genetics, University of Groningen, University Medical Center Groningen, PO Box 30001, Groningen 9700 RB, The Netherlands, 2Graduate Program in Health Sciences, University of Brasilia School of Health Sciences, Brasilia, Brazil, 3Immunogenetics Research Laboratory, Hospital Universitario de Cruces, Barakaldo, Bizkaia 48903, Spain, 4Department of Experimental Medicine, Faculty of Medicine, University of Milano-Bicocca, Monza, Italy, 5European Laboratory for Food Induced Disease, University of Naples Federico II, Naples, Italy, 6Department of Pediatric Gastroenterology, Leiden University Medical Centre, Leiden, The Netherlands, 7Department of Pediatric Gastroenterology, University Medical Centre Utrecht, Utrecht, The Netherlands, 8Department
    [Show full text]
  • A Causal Gene Network with Genetic Variations Incorporating Biological Knowledge and Latent Variables
    A CAUSAL GENE NETWORK WITH GENETIC VARIATIONS INCORPORATING BIOLOGICAL KNOWLEDGE AND LATENT VARIABLES By Jee Young Moon A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Statistics) at the UNIVERSITY OF WISCONSIN–MADISON 2013 Date of final oral examination: 12/21/2012 The dissertation is approved by the following members of the Final Oral Committee: Brian S. Yandell. Professor, Statistics, Horticulture Alan D. Attie. Professor, Biochemistry Karl W. Broman. Professor, Biostatistics and Medical Informatics Christina Kendziorski. Associate Professor, Biostatistics and Medical Informatics Sushmita Roy. Assistant Professor, Biostatistics and Medical Informatics, Computer Science, Systems Biology in Wisconsin Institute of Discovery (WID) i To my parents and brother, ii ACKNOWLEDGMENTS I greatly appreciate my adviser, Prof. Brian S. Yandell, who has always encouraged, inspired and supported me. I am grateful to him for introducing me to the exciting research areas of statis- tical genetics and causal gene network analysis. He also allowed me to explore various statistical and biological problems on my own and guided me to see the problems in a bigger picture. Most importantly, he waited patiently as I progressed at my own pace. I would also like to thank Dr. Elias Chaibub Neto and Prof. Xinwei Deng who my adviser arranged for me to work together. These three improved my rigorous writing and thinking a lot when we prepared the second chapter of this dissertation for publication. It was such a nice opportunity for me to join the group of Prof. Alan D. Attie, Dr. Mark P. Keller, Prof. Karl W. Broman and Prof.
    [Show full text]
  • Skeletal Muscle Transcriptome in Healthy Aging
    ARTICLE https://doi.org/10.1038/s41467-021-22168-2 OPEN Skeletal muscle transcriptome in healthy aging Robert A. Tumasian III 1, Abhinav Harish1, Gautam Kundu1, Jen-Hao Yang1, Ceereena Ubaida-Mohien1, Marta Gonzalez-Freire1, Mary Kaileh1, Linda M. Zukley1, Chee W. Chia1, Alexey Lyashkov1, William H. Wood III1, ✉ Yulan Piao1, Christopher Coletta1, Jun Ding1, Myriam Gorospe1, Ranjan Sen1, Supriyo De1 & Luigi Ferrucci 1 Age-associated changes in gene expression in skeletal muscle of healthy individuals reflect accumulation of damage and compensatory adaptations to preserve tissue integrity. To characterize these changes, RNA was extracted and sequenced from muscle biopsies col- 1234567890():,; lected from 53 healthy individuals (22–83 years old) of the GESTALT study of the National Institute on Aging–NIH. Expression levels of 57,205 protein-coding and non-coding RNAs were studied as a function of aging by linear and negative binomial regression models. From both models, 1134 RNAs changed significantly with age. The most differentially abundant mRNAs encoded proteins implicated in several age-related processes, including cellular senescence, insulin signaling, and myogenesis. Specific mRNA isoforms that changed sig- nificantly with age in skeletal muscle were enriched for proteins involved in oxidative phosphorylation and adipogenesis. Our study establishes a detailed framework of the global transcriptome and mRNA isoforms that govern muscle damage and homeostasis with age. ✉ 1 National Institute on Aging–Intramural Research Program, National
    [Show full text]
  • Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
    Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein
    [Show full text]
  • Fusion, Disruption, and Expression of HMGA2 in Bone and Soft Tissue
    Fusion, Disruption, and Expression of HMGA2 in Bone and Soft Tissue Chondromas Anna Dahlén, Fredrik Mertens, M.D., Anders Rydholm, M.D., Otte Brosjö, M.D., Johan Wejde, M.D., Nils Mandahl, Ph.D., Ioannis Panagopoulos, Ph.D. Department of Clinical Genetics (AD, FM, NM, IP) and Department of Orthopedics (AR), University Hospital, Lund; and Department of Orthopedics (OB) and Department of Pathology (JW), Karolinska Hospital, Stockholm, Sweden found in 8 of 13 chondrosarcomas, 4 of which dis- Soft tissue and skeletal chondromas are rare enti- played 12q rearrangements. Possibly, cryptic rear- ties, and only 21 cases with abnormal karyotypes rangements were present among the many complex have been reported. A survey of these, and 10 new marker chromosomes in the remaining 4 cases. cases reported herein, showed that the 12q13–15 segment is nonrandomly involved in structural re- KEY WORDS: Chondroma, Chondrosarcoma, FISH, arrangements in chondromas. The HMGA2 HMGA2, HMGA2-LPP, RT-PCR. (HMGI-C) locus in 12q15 is frequently rearranged in Mod Pathol 2003;16(11):1132–1140 other benign mesenchymal tumors, and this study aimed at characterizing the expression of HMGA2 in Benign cartilage tumors (enchondromas and peri- chondromatous tumors. The material consisted of 8 osteal chondromas) represent some 10–25% of all soft tissue and 6 skeletal chondromas, as well as of primary bone tumors. Enchondromas typically oc- 14 skeletal chondrosarcomas. All cases had been cur in the small tubular bones of the hands and cytogenetically analyzed. Expression of HMGA2 feet, whereas the rare periosteal chondromas pre- could be assessed by RT-PCR in 8 chondromas and dominantly appear on the surface of the long tubu- 13 chondrosarcomas.
    [Show full text]
  • Monoclonal Antibody to LPP - Ascites
    OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] AM06208SU-N Monoclonal Antibody to LPP - Ascites Alternate names: LIM domain-containing preferred translocation partner in lipoma, LPP, Lipoma- preferred partner Quantity: 0.1 ml Background: LIM domain containing preferred translocation partner in lipoma. The Zyxin family of proteins contains five members, Ajuba, LIMD1, LPP,TRIP6 and Zyxin. LPP (LIM- containing lipoma-preferred partner), a LIM domain-containing scaffolding protein contains three LIM domains at its carboxyterminus, which are preceded by a proline- rich pre-LIM region containing a number of protein interaction domains. LPP, an 80 kDa protein, localizes to sites of cell adhesion, such as focal adhesions and cell-cell contacts,and shuttles to the nucleus where it has transcriptional activation capacity.The human LPP gene maps to chromosomal location 3q28, and preferentiallytranslocates to the HMGIC gene in a subclass of human benign mesenchymal tumors known as lipomas. Uniprot ID: Q93052 NCBI: NP_001161143.1 GeneID: 4026 Host / Isotype: Mouse / IgG1 Clone: 8B3A11 Immunogen: Purified recombinant fragment of Human LPP expressed in E. Coli. Format: State: Ascitic fluid Preservatives: 0.03% Sodium Azide Applications: ELISA: 1/10000. Western Blotting: 1/500-1/2000. Immunofluorescence: 1/200-1/1000. Immunohistochemistry on Paraffin Sections: 1/200-1/1000. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
    [Show full text]
  • RNA Expression Analysis Using a 30 Base Pair Resolution Escherichia Coli Genome Array
    © 2000 Nature America Inc. • http://biotech.nature.com RESEARCH ARTICLES RNA expression analysis using a 30 base pair resolution Escherichia coli genome array Douglas W. Selinger1, Kevin J. Cheung2, Rui Mei3, Erik M. Johansson3, Craig S. Richmond5, Frederick R. Blattner5, David J. Lockhart3,4, and George M. Church1* 1Department of Genetics, Harvard Medical School, 200 Longwood Avenue Boston, MA 02115. 2Harvard College, Cambridge, MA 02138. 3Affymetrix Inc., 3380 Central Expressway, Santa Clara, CA. 4Genomics Institute of the Novartis Research Foundation, 3115 Merryfield Row, San Diego, CA 92121. 5Laboratory of Genetics, University of Wisconsin, Madison, WI 53706. *Corresponding author ([email protected]). Received 3 May 2000; accepted 30 August 2000 We have developed a high-resolution "genome array" for the study of gene expression and regulation in Escherichia coli. This array contains on average one 25-mer oligonucleotide probe per 30 base pairs over .com the entire genome, with one every 6 bases for the intergenic regions and every 60 bases for the 4,290 open reading frames (ORFs). Twofold concentration differences can be detected at levels as low as 0.2 messen- ger RNA (mRNA) copies per cell, and differences can be seen over a dynamic range of three orders of mag- h.nature nitude. In rich medium we detected transcripts for 97% and 87% of the ORFs in stationary and log phases, respectively. We found that 1,529 transcripts were differentially expressed under these conditions. As expected, genes involved in translation were expressed at higher levels in log phase, whereas many genes known to be involved in the starvation response were expressed at higher levels in stationary phase.
    [Show full text]