Supplementary Table 1
Total Page:16
File Type:pdf, Size:1020Kb

Load more
Recommended publications
-
Contribution of MSMB Promoter Region Gene Polymorphism to Early-Onset Prostate Cancer Risk in Mexican Males
www.oncotarget.com Oncotarget, 2019, Vol. 10, (No. 7), pp: 738-748 Research Paper Contribution of MSMB promoter region gene polymorphism to early-onset prostate cancer risk in Mexican males Silvia Juliana Trujillo-Cáceres1, Luisa Torres-Sánchez1, Ana I. Burguete-García2, Yaneth Citlalli Orbe Orihuela2, Ruth Argelia Vázquez-Salas3, Esmeralda Álvarez- Topete4 and Rocío Gómez4 1Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública (INSP), Cuernavaca, Morelos, Mexico 2Centro de Investigación en Enfermedades Infecciosas, INSP, Cuernavaca, Morelos, Mexico 3Conacyt-Centro de Investigación en Salud Poblacional, INSP, Cuernavaca, Morelos, Mexico 4Departamento de Toxicología, Cinvestav-IPN, Mexico City, Mexico Correspondence to: Luisa Torres-Sánchez, email: [email protected] Keywords: genetic polymorphisms; MSMB; prostate cancer; rs10993994; sexually transmitted diseases Received: July 13, 2018 Accepted: December 16, 2018 Published: January 22, 2019 Copyright: Trujillo-Cáceres et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Sexually transmitted infections and its contribution to prostate cancer (PC) development have been relevant in different populations. MSMB gene polymorphism (rs10993994) has exhibited an association both with PC as well as the susceptibility to sexually transmitted infections. Hitherto, these conditions have been not studied in Mexico yet, neither if sexually transmitted infections could modify the MSMB and PC association. Herein, socio-demographic features, sexually transmitted infections records, the reproductive backgrounds, and the genetic characterisation were analysed in 322 incident PC cases and 628 population healthy controls from Mexico City. -
The Landscape of Genomic Imprinting Across Diverse Adult Human Tissues
Downloaded from genome.cshlp.org on October 3, 2021 - Published by Cold Spring Harbor Laboratory Press Research The landscape of genomic imprinting across diverse adult human tissues Yael Baran,1 Meena Subramaniam,2 Anne Biton,2 Taru Tukiainen,3,4 Emily K. Tsang,5,6 Manuel A. Rivas,7 Matti Pirinen,8 Maria Gutierrez-Arcelus,9 Kevin S. Smith,5,10 Kim R. Kukurba,5,10 Rui Zhang,10 Celeste Eng,2 Dara G. Torgerson,2 Cydney Urbanek,11 the GTEx Consortium, Jin Billy Li,10 Jose R. Rodriguez-Santana,12 Esteban G. Burchard,2,13 Max A. Seibold,11,14,15 Daniel G. MacArthur,3,4,16 Stephen B. Montgomery,5,10 Noah A. Zaitlen,2,19 and Tuuli Lappalainen17,18,19 1The Blavatnik School of Computer Science, Tel-Aviv University, Tel Aviv 69978, Israel; 2Department of Medicine, University of California San Francisco, San Francisco, California 94158, USA; 3Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; 4Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA; 5Department of Pathology, Stanford University, Stanford, California 94305, USA; 6Biomedical Informatics Program, Stanford University, Stanford, California 94305, USA; 7Wellcome Trust Center for Human Genetics, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7BN, United Kingdom; 8Institute for Molecular Medicine Finland, University of Helsinki, 00014 Helsinki, Finland; 9Department of Genetic Medicine and Development, University of Geneva, 1211 Geneva, Switzerland; -
Associated Palmoplantar Keratoderma
DR ABIGAIL ZIEMAN (Orcid ID : 0000-0001-8236-207X) Article type : Review Article Pathophysiology of pachyonychia congenita-associated palmoplantar keratoderma: New insight into skin epithelial homeostasis and avenues for treatment Authors: A. G. Zieman1 and P. A. Coulombe1,2 # Affiliations: 1Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109, USA; 2Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI 48109, USA #Corresponding author: Pierre A. Coulombe, PhD, 3071 Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA. Tel: 734-615-7509. Email: [email protected]. Funding Sources: These studies were supported by grant AR044232 issued to P.A.C. from the National Institute of Arthritis, Musculoskeletal and Skin Disease (NIAMS). A.G.Z. received support from grant T32 CA009110 from the National Cancer Institute. Author Manuscript This is the author manuscript accepted for publication and has undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/BJD.18033 This article is protected by copyright. All rights reserved Conflict of interest disclosures: None declared. Bulleted statements: What’s already known about this topic? Pachyonychia congenita is a rare genodermatosis caused by mutations in KRT6A, KRT6B, KRT6C, KRT16, KRT17, which are normally expressed in skin appendages and induced following injury. Individuals with PC present with multiple clinical symptoms that usually include thickened and dystrophic nails, palmoplantar keratoderma (PPK), glandular cysts, and oral leukokeratosis. -
Tumor Suppressive Microrna-375 Regulates Lactate Dehydrogenase B in Maxillary Sinus Squamous Cell Carcinoma
INTERNATIONAL JOURNAL OF ONCOLOGY 40: 185-193, 2012 Tumor suppressive microRNA-375 regulates lactate dehydrogenase B in maxillary sinus squamous cell carcinoma TAKASHI KINoshita1,2, NIjIRo Nohata1,2, HIRoFUMI YoSHINo3, ToYoYUKI HANAzAwA2, NAoKo KIKKAwA2, LISA FUjIMURA4, TAKeSHI CHIYoMARU3, KAzUMoRI KAwAKAMI3, HIDeKI eNoKIDA3, Masayuki NAKAGAwA3, Yoshitaka oKAMoTo2 and NAoHIKo SeKI1 Departments of 1Functional Genomics, 2otorhinolaryngology/Head and Neck Surgery, Chiba University Graduate School of Medicine, 1-8-1 Inohana Chuo-ku, Chiba 260-8670; 3Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520; 4Biomedical Research Center, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, japan Received july 6, 2011; Accepted August 23, 2011 DoI: 10.3892/ijo.2011.1196 Abstract. The expression of microRNA-375 (miR-375) is head and neck tumors, with an annual incidence of 0.5-1.0 per significantly reduced in cancer tissues of maxillary sinus squa- 100,000 people (1,2). Since the clinical symptoms of patients mous cell carcinoma (MSSCC). The aim of this study was to with MSSCC are very insidious, tumors are often diagnosed at investigate the functional significance ofmiR-375 and a possible advanced stages. Despite advances in multimodality therapy regulatory role in the MSSCC networks. Restoration of miR-375 including surgery, radiotherapy and chemotherapy, the 5-year significantly inhibited cancer cell proliferation and invasion survival rate for MSSCC has remained ~50%. Although regional in IMC-3 cells, suggesting that miR-375 functions as a tumor lymph node metastasis and distant metastasis are uncommon suppressor in MSSCC. Genome-wide gene expression data and (20%), the high rate of locoregional recurrence (60%) contributes luciferase reporter assays indicated that lactate dehydro genase B to poor survival (3). -
Plasma Kallikrein Activation and Inhibition During Typhoid Fever
Plasma Kallikrein Activation and Inhibition during Typhoid Fever Robert W. Colman, … , Cheryl F. Scott, Robert H. Gilman J Clin Invest. 1978;61(2):287-296. https://doi.org/10.1172/JCI108938. Research Article As an ancillary part of a typhoid fever vaccine study, 10 healthy adult male volunteers (nonimmunized controls) were serially bled 6 days before to 30 days after ingesting 105Salmonella typhi organisms. Five persons developed typhoid fever 6-10 days after challenge, while five remained well. During the febrile illness, significant changes (P < 0.05) in the following hematological parameters were measured: a rise in α1-antitrypsin antigen concentration and high molecular weight kininogen clotting activity; a progressive decrease of platelet count (to 60% of the predisease state), functional prekallikrein (55%) and kallikrein inhibitor (47%) with a nadir reached on day 5 of the fever and a subsequent overshoot during convalescence. Despite the drop in functional prekallikrein and kallikrein inhibitor, there was no change in factor XII clotting activity or antigenic concentrations of prekallikrein and the kallikrein inhibitors, C1 esterase inhibitor (C1-̄ INH) and α2-macroglobulin. Plasma from febrile patients subjected to immunoelectrophoresis and crossed immunoelectrophoresis contained a new complex displaying antigenic characteristics of both prekallikrein and C1-̄ INH; the α2-macroglobulin, antithrombin III, and α1-antitrypsin immunoprecipitates were unchanged. Plasma drawn from infected-well subjects showed no significant change in these components of the kinin generating system. The finding of a reduction in functional prekallikrein and kallikrein inhibitor (C1-̄ INH) and the formation of a kallikrein C1-̄ INH complex is consistent with prekallikrein activation in typhoid fever. -
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. -
Supplementary Table 3 Complete List of RNA-Sequencing Analysis of Gene Expression Changed by ≥ Tenfold Between Xenograft and Cells Cultured in 10%O2
Supplementary Table 3 Complete list of RNA-Sequencing analysis of gene expression changed by ≥ tenfold between xenograft and cells cultured in 10%O2 Expr Log2 Ratio Symbol Entrez Gene Name (culture/xenograft) -7.182 PGM5 phosphoglucomutase 5 -6.883 GPBAR1 G protein-coupled bile acid receptor 1 -6.683 CPVL carboxypeptidase, vitellogenic like -6.398 MTMR9LP myotubularin related protein 9-like, pseudogene -6.131 SCN7A sodium voltage-gated channel alpha subunit 7 -6.115 POPDC2 popeye domain containing 2 -6.014 LGI1 leucine rich glioma inactivated 1 -5.86 SCN1A sodium voltage-gated channel alpha subunit 1 -5.713 C6 complement C6 -5.365 ANGPTL1 angiopoietin like 1 -5.327 TNN tenascin N -5.228 DHRS2 dehydrogenase/reductase 2 leucine rich repeat and fibronectin type III domain -5.115 LRFN2 containing 2 -5.076 FOXO6 forkhead box O6 -5.035 ETNPPL ethanolamine-phosphate phospho-lyase -4.993 MYO15A myosin XVA -4.972 IGF1 insulin like growth factor 1 -4.956 DLG2 discs large MAGUK scaffold protein 2 -4.86 SCML4 sex comb on midleg like 4 (Drosophila) Src homology 2 domain containing transforming -4.816 SHD protein D -4.764 PLP1 proteolipid protein 1 -4.764 TSPAN32 tetraspanin 32 -4.713 N4BP3 NEDD4 binding protein 3 -4.705 MYOC myocilin -4.646 CLEC3B C-type lectin domain family 3 member B -4.646 C7 complement C7 -4.62 TGM2 transglutaminase 2 -4.562 COL9A1 collagen type IX alpha 1 chain -4.55 SOSTDC1 sclerostin domain containing 1 -4.55 OGN osteoglycin -4.505 DAPL1 death associated protein like 1 -4.491 C10orf105 chromosome 10 open reading frame 105 -4.491 -
DF6720-MSMB Antibody
Affinity Biosciences website:www.affbiotech.com order:[email protected] MSMB Antibody Cat.#: DF6720 Concn.: 1mg/ml Mol.Wt.: 13kDa Size: 50ul,100ul,200ul Source: Rabbit Clonality: Polyclonal Application: WB 1:500-1:2000, IHC 1:50-1:200, ELISA(peptide) 1:20000-1:40000 *The optimal dilutions should be determined by the end user. Reactivity: Human,Mouse Purification: The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific). Specificity: MSMB Antibody detects endogenous levels of total MSMB. Immunogen: A synthesized peptide derived from human MSMB, corresponding to a region within the internal amino acids. Uniprot: P08118 Description: The protein encoded by this gene is a member of the immunoglobulin binding factor family. It is synthesized by the epithelial cells of the prostate gland and secreted into the seminal plasma. This protein has inhibin-like activity. It may have a role as an autocrine paracrine factor in uterine, breast and other female reproductive tissues. The expression of the encoded protein is found to be decreased in prostate cancer. Two alternatively spliced transcript variants encoding different isoforms are described for this gene. The use of alternate polyadenylation sites has been found for this gene. Storage Condition and Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM Buffer: NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt. Western blot analysis of HepG2 cell lysates, using MSMB Antibody. The lane on the left was treated with the antigen- specific peptide. 1 / 2 Affinity Biosciences website:www.affbiotech.com order:[email protected] DF6720 at 1/100 staining Mouse liver tissue by IHC-P. -
Expressed Sequence Tag Analysis of the Response of Apple
Physiologia Plantarum 133: 298–317. 2008 Copyright ª Physiologia Plantarum 2008, ISSN 0031-9317 Expressed sequence tag analysis of the response of apple (Malus x domestica ‘Royal Gala’) to low temperature and water deficit Michael Wisniewskia,*, Carole Bassetta,*, John Norellia, Dumitru Macarisina, Timothy Artlipa, Ksenija Gasicb and Schuyler Korbanb aUnited States Department of Agriculture – Agricultural Research Service (USDA-ARS), Appalachian Fruit Research Station, 2217 Wiltshire Road, Kearneysville, WV 25430, USA bDepartment of Natural Resources and Environmental Sciences, University of Illinois, 310 ERML, 1201 W. Gregory Drive, Urbana, IL 61801, USA Correspondence Leaf, bark, xylem and root tissues were used to make nine cDNA libraries from *Corresponding author, non-stressed (control) ‘Royal Gala’ apple trees, and from ‘Royal Gala’ trees e-mail: [email protected]; exposed to either low temperature (5°C for 24 h) or water deficit (45% of [email protected] saturated pot mass for 2 weeks). Over 22 600 clones from the nine libraries # Received 26 September 2007; revised 3 were subjected to 5 single-pass sequencing, clustered and annotated using January 2008 BLASTX. The number of clusters in the libraries ranged from 170 to 1430. Regarding annotation of the sequences, BLASTX analysis indicated that within doi: 10.1111/j.1399-3054.2008.01063.x the libraries 65–72% of the clones had a high similarity to known function genes, 6–15% had no functional assignment and 15–26% were completely novel. The expressed sequence tags were combined into three classes (control, low-temperature and water deficit) and the annotated genes in each class were placed into 1 of 10 different functional categories. -
Transcriptional Regulation Differs in Affected Facioscapulohumeral Muscular Dystrophy Patients Compared to Asymptomatic Related Carriers
University of Massachusetts Medical School eScholarship@UMMS Wellstone Center for FSHD Publications Wellstone Center for FSHD 2009-04-14 Transcriptional regulation differs in affected facioscapulohumeral muscular dystrophy patients compared to asymptomatic related carriers Patricia Arashiro University of Sao Paulo Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/wellstone_pubs Part of the Cell Biology Commons, Developmental Biology Commons, Molecular Biology Commons, Molecular Genetics Commons, Musculoskeletal Diseases Commons, and the Nervous System Diseases Commons Repository Citation Arashiro P, Eisenberg I, Kho AT, Cerqueira AM, Canovas M, Silva HC, Pavanello RC, Verjovski-Almeida S, Kunkel LM, Zatz M. (2009). Transcriptional regulation differs in affected facioscapulohumeral muscular dystrophy patients compared to asymptomatic related carriers. Wellstone Center for FSHD Publications. https://doi.org/10.1073/pnas.0901573106. Retrieved from https://escholarship.umassmed.edu/ wellstone_pubs/18 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Wellstone Center for FSHD Publications by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. Transcriptional regulation differs in affected facioscapulohumeral muscular dystrophy patients compared to asymptomatic related carriers Patricia Arashiroa, Iris Eisenbergb, Alvin T. Khoc, Antonia M. P. Cerqueiraa, Marta -
Keratin 9 Point Mutation in the Pedigree of Epidermolytic Hereditary Palmoplantar Keratoderma Perturbs Keratin Intermediate Filament Network Formation
FEBS 17004 FEBS Letters 386 (1996) 149-155 Keratin 9 point mutation in the pedigree of epidermolytic hereditary palmoplantar keratoderma perturbs keratin intermediate filament network formation Setsu Kobayashi, Toshihiro Tanaka*, Norihisa Matsuyoshi, Sadao Imamura Department of Dermatology, Graduate School of Medicine, Kyoto University, Kyoto, 606 Japan Received 12 January 1996; revised version received 4 April 1996 Abstract Keratins form an intracellular keratin filament net- point mutations in the K9 gene in EHPPK [4-8] but none work in keratinocytes. Point mutations in the epidermal keratins showed a function assay with these mutations. Here, we pro- could lead to the disruption of keratin filament formation, vide the first demonstration that the point mutation found in developing skin diseases such as epidermolytic hereditary a pedigree of EHPPK has a dominant-negative effect on the palmoplantar keratoderma (EHPPK). We found a G to A assembly of keratin intermediate filaments in the cells. transition in keratin 9 (K9) cDNA, resulting in the substitution of glutamine for arginine at 162, in all patients of a pedigree of 2. Materials and methods EHPPK. Transfection into MDCK cells and DJM-1 cells revealed that the plasmid CMX vector containing normal keratin 2.1. PCR and DNA sequence 9 cDNA showed normal keratin network formation, whereas the Genomic DNA was extracted and purified from blood or biopsy vector with a G to A point mutated keratin 9 cDNA showed specimens from the patients. The primers were designed at nucleotide disrupted keratin filaments with droplet formation in the cells. 263 282 and 664-683 based on the K9 cDNA sequence [9]. -
Identification of Novel Nasopharyngeal Carcinoma
Imaging, Diagnosis, Prognosis Identification of Novel Nasopharyngeal Carcinoma Biomarkers by Laser Capture Microdissection and Proteomic Analysis Ai-Lan Cheng,1, 3 Wei-Guo Huang,1, 3 Zhu-Chu Chen,1, 2 Fang Peng,1Peng-Fei Zhang,1Mao-Yu Li,1 Feng Li,1, 2 Jian-Ling Li,1Cui Li,1Hong Yi,1Bin Yi,1and Zhi-Qiang Xiao1 Abstract Purpose: To identify novel nasopharyngeal carcinoma (NPC) biomarkers by laser capture microdissection and a proteomic approach. Experimental Design: Proteins from pooled microdissected NPC and normal nasopharyngeal epithelial tissues (NNET) were separated by two-dimensional gel electrophoresis, and differential proteins were identified by mass spectrometry. Expression of three differential proteins (stathmin, 14 -3 -3j, and annexin I) in the above two tissues as well as four NPC cell lines was determined by Western blotting. Immunohistochemistry was also done to detect the expression ofthree differential proteins in 98 cases of primary NPC, 30 cases of NNET, and 20 cases of cervical lymph node metastases, and the correlation oftheir expression levels with clinicopathologic features and clinical outcomes were evaluated. Results: Thirty-six differential proteins between the NPC and NNET were identified. The expression levels ofstathmin, 14-3-3 j, and annexin I in the two types oftissues were confirmed and related to differentiation degree and/or metastatic potential of the NPC cell lines. Significant stathmin up-regulation and down-regulation of14-3-3 j and annexin I were observed in NPC versus NNET, and significant down-regulation of 14-3-3j and annexin I was also observed in lymph node metastasis versus primary NPC. In addition, stathmin up-regulation and down- regulation of14-3-3 j and annexin I were significantly correlated with poor histologic differentiation, advanced clinical stage, and recurrence, whereas down-regulation of 14-3-3j and annexin I was also significantly correlated with lymph node and distant metastasis.