Identification of Genes and Signaling Pathways Associated with Squamous Cell Carcinoma by Bioinformatics Analysis
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ONCOGENOMICS Through the Use of Chemotherapeutic Agents
Oncogene (2002) 21, 7749 – 7763 ª 2002 Nature Publishing Group All rights reserved 0950 – 9232/02 $25.00 www.nature.com/onc Expression profiling of primary non-small cell lung cancer for target identification Jim Heighway*,1, Teresa Knapp1, Lenetta Boyce1, Shelley Brennand1, John K Field1, Daniel C Betticher2, Daniel Ratschiller2, Mathias Gugger2, Michael Donovan3, Amy Lasek3 and Paula Rickert*,3 1Target Identification Group, Roy Castle International Centre for Lung Cancer Research, University of Liverpool, 200 London Road, Liverpool L3 9TA, UK; 2Institute of Medical Oncology, University of Bern, 3010 Bern, Switzerland; 3Incyte Genomics Inc., 3160 Porter Drive, Palo Alto, California, CA 94304, USA Using a panel of cDNA microarrays comprising 47 650 Introduction transcript elements, we have carried out a dual-channel analysis of gene expression in 39 resected primary The lack of generally effective therapies for lung cancer human non-small cell lung tumours versus normal lung leads to the high mortality rate associated with this tissue. Whilst *11 000 elements were scored as common disease. Recorded 5-year survival figures vary, differentially expressed at least twofold in at least one to some extent perhaps reflecting differences in sample, 96 transcripts were scored as over-represented ascertainment methods, but across Europe are approxi- fourfold or more in at least seven out of 39 tumours mately 10% (Bray et al., 2002). Whilst surgery is an and 30 sequences 16-fold in at least two out of 39 effective strategy for the treatment of localized lesions, tumours, including 24 transcripts in common. Tran- most patients present with overtly or covertly dissemi- scripts (178) were found under-represented fourfold in nated disease. -
Altered Integrin Alpha 6 Expression As a Rescue for Muscle Fiber Detachment in Zebrafish (Danio Rerio)
The University of Maine DigitalCommons@UMaine Honors College Spring 2014 Altered Integrin Alpha 6 Expression As A Rescue For Muscle Fiber Detachment In Zebrafish (Danio Rerio) Rose E. McGlauflin Follow this and additional works at: https://digitalcommons.library.umaine.edu/honors Part of the Animal Diseases Commons, and the Musculoskeletal Diseases Commons Recommended Citation McGlauflin, Rose E., Alter" ed Integrin Alpha 6 Expression As A Rescue For Muscle Fiber Detachment In Zebrafish (Danio Rerio)" (2014). Honors College. 140. https://digitalcommons.library.umaine.edu/honors/140 This Honors Thesis is brought to you for free and open access by DigitalCommons@UMaine. It has been accepted for inclusion in Honors College by an authorized administrator of DigitalCommons@UMaine. For more information, please contact [email protected]. ALTERED INTEGRIN ALPHA 6 EXPRESSION AS A RESCUE FOR MUSCLE FIBER DETACHMENT IN ZEBRAFISH (DANIO RERIO) by Rose E. McGlauflin A Thesis Submitted in Partial Fulfillment of the Requirements for a Degree with Honors (Biology) The Honors College University of Maine May 2014 Advisory Committee: Clarissa A. Henry, Ph.D., Associate Professor of Biological Sciences, Advisor Mary S. Tyler, Ph.D., Professor of Zoology Mary Astumian, Henry Lab Manager Michelle Smith, Ph.D., Assistant Professor of Biological Sciences Mark Haggerty, Ph.D., Honors Preceptor for Civic Engagement Abstract Cells adhere to their extracellular matrix by way of integrins, transmembrane molecules that attach the cytoskeleton to the extracellular basement membrane (one kind of extracellular matrix). In some muscular dystrophies, specific integrins are disrupted and muscle fibers detach from the myotendenous junction and degenerate. This integrin disruption causes a constant cycle of regeneration and degeneration, which greatly harms the tissue over time. -
Ige-Mediated Mast Cell Activation Promotes Inflammation And
RESEARCH COMMUNICATION IgE-mediated mast cell activation promotes inflammation and cartilage destruction in osteoarthritis Qian Wang1,2†, Christin M Lepus1,2†, Harini Raghu1,2†, Laurent L Reber3‡, Mindy M Tsai3, Heidi H Wong1,2, Ericka von Kaeppler1,2, Nithya Lingampalli1,2, Michelle S Bloom1,2, Nick Hu1,2, Eileen E Elliott1,2, Francesca Oliviero4, Leonardo Punzi4, Nicholas J Giori1,5, Stuart B Goodman5, Constance R Chu1,5, Jeremy Sokolove1,2, Yoshihiro Fukuoka6, Lawrence B Schwartz6, Stephen J Galli3,7, William H Robinson1,2* 1GRECC, VA Palo Alto Health Care System, Palo Alto, United States; 2Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, United States; 3Department of Pathology, Stanford University School of Medicine, Stanford, United States; 4Rheumatology Unit, Department of Medicine, University of Padova, Padova, Italy; 5Department of Orthopedic Surgery, Stanford University School of Medicine, Stanford, United States; 6Department of Internal Medicine, Virginia Commonwealth University School of Medicine, Richmond, United States; 7Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, United States *For correspondence: [email protected] Abstract Osteoarthritis is characterized by articular cartilage breakdown, and emerging †These authors contributed evidence suggests that dysregulated innate immunity is likely involved. Here, we performed equally to this work proteomic, transcriptomic, and electron microscopic analyses to demonstrate that mast cells are Present address: ‡Center for aberrantly activated in human and murine osteoarthritic joint tissues. Using genetic models of mast Physiopathology of Toulouse- cell deficiency, we demonstrate that lack of mast cells attenuates osteoarthritis in mice. Using Purpan (CPTP), UMR 1043, genetic and pharmacologic approaches, we show that the IgE/FceRI/Syk signaling axis is critical for University of Toulouse, INSERM, the development of osteoarthritis. -
Identification of the Binding Partners for Hspb2 and Cryab Reveals
Brigham Young University BYU ScholarsArchive Theses and Dissertations 2013-12-12 Identification of the Binding arP tners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non- Redundant Roles for Small Heat Shock Proteins Kelsey Murphey Langston Brigham Young University - Provo Follow this and additional works at: https://scholarsarchive.byu.edu/etd Part of the Microbiology Commons BYU ScholarsArchive Citation Langston, Kelsey Murphey, "Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins" (2013). Theses and Dissertations. 3822. https://scholarsarchive.byu.edu/etd/3822 This Thesis is brought to you for free and open access by BYU ScholarsArchive. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of BYU ScholarsArchive. For more information, please contact [email protected], [email protected]. Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactions and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston A thesis submitted to the faculty of Brigham Young University in partial fulfillment of the requirements for the degree of Master of Science Julianne H. Grose, Chair William R. McCleary Brian Poole Department of Microbiology and Molecular Biology Brigham Young University December 2013 Copyright © 2013 Kelsey Langston All Rights Reserved ABSTRACT Identification of the Binding Partners for HspB2 and CryAB Reveals Myofibril and Mitochondrial Protein Interactors and Non-Redundant Roles for Small Heat Shock Proteins Kelsey Langston Department of Microbiology and Molecular Biology, BYU Master of Science Small Heat Shock Proteins (sHSP) are molecular chaperones that play protective roles in cell survival and have been shown to possess chaperone activity. -
Human FGFBP1 ELISA Kit (ARG82056)
Product datasheet [email protected] ARG82056 Package: 96 wells Human FGFBP1 ELISA Kit Store at: 4°C Summary Product Description Human FGFBP1 ELISA Kit is an Enzyme Immunoassay kit for the quantification of Human FGFBP1 in serum, plasma and cell culture supernatants. Tested Reactivity Hu Tested Application ELISA Target Name FGFBP1 Conjugation HRP Conjugation Note Substrate: TMB and read at 450 nm. Sensitivity 11.7 pg/ml Sample Type Serum, plasma and cell culture supernatants. Standard Range 23.4 - 1500 pg/ml Sample Volume 100 µl Alternate Names Fibroblast growth factor-binding protein 1; 17 kDa heparin-binding growth factor-binding protein; FGF- BP; FGF-binding protein 1; HBp17; FGFBP; 17 kDa HBGF-binding protein; FGFBP-1; HBP17; FGF-BP1 Application Instructions Assay Time 4.5 hours Properties Form 96 well Storage instruction Store the kit at 2-8°C. Keep microplate wells sealed in a dry bag with desiccants. Do not expose test reagents to heat, sun or strong light during storage and usage. Please refer to the product user manual for detail temperatures of the components. Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol FGFBP1 Gene Full Name fibroblast growth factor binding protein 1 Background This gene encodes a secreted fibroblast growth factor carrier protein. The encoded protein plays a critical role in cell proliferation, differentiation and migration by binding to fibroblast growth factors and potentiating their biological effects on target cells. The encoded protein may also play a role in tumor growth as an angiogenic switch molecule, and expression of this gene has been associated with several types of cancer including pancreatic and colorectal adenocarcinoma. -
Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-Like Mouse Models: Tracking the Role of the Hairless Gene
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 5-2006 Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene Yutao Liu University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Liu, Yutao, "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino- like Mouse Models: Tracking the Role of the Hairless Gene. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1824 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yutao Liu entitled "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, with a major in Life Sciences. Brynn H. Voy, Major Professor We have read this dissertation and recommend its acceptance: Naima Moustaid-Moussa, Yisong Wang, Rogert Hettich Accepted for the Council: Carolyn R. -
Biological Function of Mast Cell Chymase
Biological Function of Mast Cell Chymase In vitro and in vivo studies: a thorny pathway Elena Chugunova Department of Molecular Biosciences Uppsala Doctoral thesis Swedish University of Agricultural Sciences Uppsala 2004 Acta Universitatis Agriculturae Sueciae Veterinaria 181 ISSN 1401-6257 ISBN 91-576-6680-6 © 2004 Elena Chugunova, Uppsala Tryck: SLU Service/Repro, Uppsala 2004 Abstract Chugunova, E., 2004. Biological function of mast cell chymase mMCP-4. In vitro and in vivo studies: a thorny pathway. Doctor's dissertation. ISSN 1401-6257, ISBN 91-576-6680-6 Mast cells (MCs) are key effector cells in various types of inflammatory conditions. The MC secretory granules contain inflammatory mediators such as histamine, heparin proteoglycan (PG), cytokines and various heparin-binding proteases, including tryptases, chymases and carboxypeptidase A. Previously, a mouse strain with a defect in its heparin biosynthesis was produced by targeting the gene for NDST-2 (N-deacetylase/N-sulfotransferase-2). These mice showed reduced levels of MC inflammatory mediators such as histamine and various heparin- binding proteases, including chymases, tryptases, and carboxypeptidase A. By using this mouse strain, we found that chymase in complex with heparin PG degraded fibronectin, suggesting a role for chymase in the regulation of connective tissue composition. Further, we found that chymase/heparin PG complexes degraded and thereby inactivated both thrombin and plasmin, suggesting an additional role for chymase in regulation of extravascular coagulation and fibrinolysis. However, although our findings implicated chymase in these processes, it was not possible to exclude the contribution to the observed activities by other MC components that are influenced by the knockout of NDST-2. -
A Cell Line P53 Mutation Type UM
A Cell line p53 mutation Type UM-SCC 1 wt UM-SCC5 Exon 5, 157 GTC --> TTC Missense mutation by transversion (Valine --> Phenylalanine UM-SCC6 wt UM-SCC9 wt UM-SCC11A wt UM-SCC11B Exon 7, 242 TGC --> TCC Missense mutation by transversion (Cysteine --> Serine) UM-SCC22A Exon 6, 220 TAT --> TGT Missense mutation by transition (Tyrosine --> Cysteine) UM-SCC22B Exon 6, 220 TAT --> TGT Missense mutation by transition (Tyrosine --> Cysteine) UM-SCC38 Exon 5, 132 AAG --> AAT Missense mutation by transversion (Lysine --> Asparagine) UM-SCC46 Exon 8, 278 CCT --> CGT Missense mutation by transversion (Proline --> Alanine) B 1 Supplementary Methods Cell Lines and Cell Culture A panel of ten established HNSCC cell lines from the University of Michigan series (UM-SCC) was obtained from Dr. T. E. Carey at the University of Michigan, Ann Arbor, MI. The UM-SCC cell lines were derived from eight patients with SCC of the upper aerodigestive tract (supplemental Table 1). Patient age at tumor diagnosis ranged from 37 to 72 years. The cell lines selected were obtained from patients with stage I-IV tumors, distributed among oral, pharyngeal and laryngeal sites. All the patients had aggressive disease, with early recurrence and death within two years of therapy. Cell lines established from single isolates of a patient specimen are designated by a numeric designation, and where isolates from two time points or anatomical sites were obtained, the designation includes an alphabetical suffix (i.e., "A" or "B"). The cell lines were maintained in Eagle's minimal essential media supplemented with 10% fetal bovine serum and penicillin/streptomycin. -
Divergence of the Genes on Human Chromosome 21 Between Human and Other Hominoids and Variation of Substitution Rates Among Transcription Units
Divergence of the genes on human chromosome 21 between human and other hominoids and variation of substitution rates among transcription units Jinxiu Shi*†‡, Huifeng Xi*‡§, Ying Wang*, Chenghui Zhang*, Zhengwen Jiang§¶, Kuixing Zhang*, Yayun Shen*, Lin Jin*, Kaiyue Zhang*, Wentao Yuan*, Ying Wang*, Jie Lin*, Qi Hua*, Fengqing Wang*, Shuhua Xu*, Suangxi Ren*, Shijie Xu*†, Guoping Zhao*, Zhu Chen*†§, Li Jin*§¶ʈ, and Wei Huang*†ʈ *Chinese National Human Genome Center at Shanghai, 250 Bi Bo Road, Shanghai 201203, People’s Republic of China; †Health Science Center, Shanghai Second Medical University and Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 225 Chongqing Nan Road, Shanghai 200025, People’s Republic of China; §Morgan-Tan International Center for Life Science and Center for Anthropological Sciences, School of Biological Sciences, Fudan University, 220 Han Dan Road, Shanghai 200433, People’s Republic of China; and ¶Center for Genome Information, Department of Environmental Health, University of Cincinnati College of Medicine, P.O. Box 670056, Cincinnati, OH 45267-0056 Communicated by Jiazhen Tan, Fudan University, Shanghai, People’s Republic of China, May 5, 2003 (received for review December 16, 2002) The study of genomic divergence between humans and primates of human beings and a pool of 20 chimpanzee samples, which may provide insight into the origins of human beings and the allows a direct comparison of the genomes of these two species. genetic basis of unique human traits and diseases. Chromosome 21 As outgroups, partial sequences of those genes were also deter- is the smallest chromosome in the human genome, and some of its mined for a gorilla, an orangutan, and a macaque. -
2335 Roles of Molecules Involved in Epithelial/Mesenchymal Transition
[Frontiers in Bioscience 13, 2335-2355, January 1, 2008] Roles of molecules involved in epithelial/mesenchymal transition during angiogenesis Giulio Ghersi Dipartimento di Biologia Cellulare e dello Sviluppo, Universita di Palermo, Italy TABLE OF CONTENTS 1. Abstract 2. Introduction 3. Extracellular matrix 3.1. ECM and integrins 3.2. Basal lamina components 4. Cadherins. 4.1. Cadherins in angiogenesis 5. Integrins. 5.1. Integrins in angiogenesis 6. Focal adhesion molecules 7. Proteolytic enzymes 7.1. Proteolytic enzymes inhibitors 7.2. Proteolytic enzymes in angiogenesis 8. Perspective 9. Acknowledgements 10. References 1.ABSTRACT 2. INTRODUCTION Formation of vessels requires “epithelial- Growth of new blood vessels (angiogenesis) mesenchymal” transition of endothelial cells, with several plays a key role in several physiological processes, such modifications at the level of endothelial cell plasma as vascular remodeling during embryogenesis and membranes. These processes are associated with wound healing tissue repair in the adult; as well as redistribution of cell-cell and cell-substrate adhesion pathological processes, including rheumatoid arthritis, molecules, cross talk between external ECM and internal diabetic retinopathy, psoriasis, hemangiomas, and cytoskeleton through focal adhesion molecules and the cancer (1). Vessel formation entails the “epithelial- expression of several proteolytic enzymes, including matrix mesenchymal” transition of endothelial cells (ECs) “in metalloproteases and serine proteases. These enzymes with vivo”; a similar phenotypic exchange can be induced “in their degradative action on ECM components, generate vitro” by growing ECs to low cell density, or in “wound molecules acting as activators and/or inhibitors of healing” experiments or perturbing cell adhesion and angiogenesis. The purpose of this review is to provide an associated molecule functions. -
Salivary Exrna Biomarkers to Detect Gingivitis and Monitor Disease Regression
Received: 3 December 2017 | Revised: 14 April 2018 | Accepted: 13 May 2018 DOI: 10.1111/jcpe.12930 OTHER Salivary exRNA biomarkers to detect gingivitis and monitor disease regression Karolina E. Kaczor-Urbanowicz1,2* | Harsh M. Trivedi3* | Patricia O. Lima1,4 | Paulo M. Camargo5 | William V. Giannobile6 | Tristan R. Grogan7 | Frederico O. Gleber-Netto8 | Yair Whiteman9 | Feng Li1 | Hyo Jung Lee10 | Karan Dharia11 | Katri Aro1 | Carmen Martin Carerras-Presas12 | Saarah Amuthan11 | Manjiri Vartak11 | David Akin1 | Hiba Al-adbullah11 | Kanika Bembey11 | Perry R. Klokkevold5 | David Elashoff7 | Virginia M. Barnes13 | Rose Richter13 | William DeVizio13 | James G. Masters3 | David T. W. Wong1 1UCLA School of Dentistry, Center for Oral/Head & Neck Oncology Research, University of California at Los Angeles, Los Angeles, California 2Section of Orthodontics, UCLA School of Dentistry, University of California at Los Angeles, Los Angeles, California 3Early Research Oral Care, Colgate Palmolive Co., Piscataway, New Jersey 4Department of Physiological Sciences, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil 5Section of Periodontics, UCLA School of Dentistry, University of California at Los Angeles, Los Angeles, California 6Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, Michigan 7Department of Biostatistics, University of California at Los Angeles, Los Angeles, California 8Medical Genomics Laboratory, Centro Internacional de Pesquisa e Ensino (CIPE), AC Camargo Cancer -
Analysis of Mouse Keratin 6A Regulatory Sequences in Transgenic Mice Reveals Constitutive, Tissue-Speci®C Expression by a Keratin 6A Minigene
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Analysis of Mouse Keratin 6a Regulatory Sequences in Transgenic Mice Reveals Constitutive, Tissue-Speci®c Expression by a Keratin 6a Minigene Donna Mahony, Seetha Karunaratne, Graham Cam,* and Joseph A. Rothnagel Department of Biochemistry and the Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland, and *Division of Animal Production, CSIRO, Blacktown, New South Wales, Australia The analysis of keratin 6 expression is complicated atin 6 expressing tissues, including the hair follicle, by the presence of multiple isoforms that are tongue, footpad, and nail bed, showing that both expressed constitutively in a number of internal stra- transgenes retained keratinocyte-speci®c expression. ti®ed epithelia, in palmoplantar epidermis, and in Quantitative analysis of b-galactosidase activity veri- the companion cell layer of the hair follicle. In addi- ®ed that both the 1.3 and 0.12 kb keratin 6a promo- tion, keratin 6 expression is inducible in interfollicu- ter constructs produced similar levels of the reporter. lar epidermis and the outer root sheath of the Notably, bothconstructs were constitutively follicle, in response to wounding stimuli, phorbol expressed in the outer root sheath and interfollicular esters, or retinoic acid. In order to establishthecriti- epidermis in the absence of any activating stimulus, cal regions involved in the regulation of keratin 6a suggesting that they lack the regulatory elements (the dominant isoform in mice), we generated trans- that normally silence transcription in these cells. This genic mice withtwo different-sized mouse keratin 6a study has revealed that a keratin 6a minigene con- constructs containing either 1.3 kb or 0.12 kb of 5¢ tains critical cis elements that mediate tissue-speci®c ¯anking sequence linked to the lacZ reporter gene.