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A Genome-Wide Association Study of a Coronary Artery Disease Risk Variant
Journal of Human Genetics (2013) 58, 120–126 & 2013 The Japan Society of Human Genetics All rights reserved 1434-5161/13 www.nature.com/jhg ORIGINAL ARTICLE A genome-wide association study of a coronary artery diseaseriskvariant Ji-Young Lee1,16, Bok-Soo Lee2,16, Dong-Jik Shin3,16, Kyung Woo Park4,16, Young-Ah Shin1, Kwang Joong Kim1, Lyong Heo1, Ji Young Lee1, Yun Kyoung Kim1, Young Jin Kim1, Chang Bum Hong1, Sang-Hak Lee3, Dankyu Yoon5, Hyo Jung Ku2, Il-Young Oh4, Bong-Jo Kim1, Juyoung Lee1, Seon-Joo Park1, Jimin Kim1, Hye-kyung Kawk1, Jong-Eun Lee6, Hye-kyung Park1, Jae-Eun Lee1, Hye-young Nam1, Hyun-young Park7, Chol Shin8, Mitsuhiro Yokota9, Hiroyuki Asano10, Masahiro Nakatochi11, Tatsuaki Matsubara12, Hidetoshi Kitajima13, Ken Yamamoto13, Hyung-Lae Kim14, Bok-Ghee Han1, Myeong-Chan Cho15, Yangsoo Jang3,17, Hyo-Soo Kim4,17, Jeong Euy Park2,17 and Jong-Young Lee1,17 Although over 30 common genetic susceptibility loci have been identified to be independently associated with coronary artery disease (CAD) risk through genome-wide association studies (GWAS), genetic risk variants reported to date explain only a small fraction of heritability. To identify novel susceptibility variants for CAD and confirm those previously identified in European population, GWAS and a replication study were performed in the Koreans and Japanese. In the discovery stage, we genotyped 2123 cases and 3591 controls with 521 786 SNPs using the Affymetrix SNP Array 6.0 chips in Korean. In the replication, direct genotyping was performed using 3052 cases and 4976 controls from the KItaNagoya Genome study of Japan with 14 selected SNPs. -
Eradication of ENO1-Deleted Glioblastoma Through Collateral Lethality
bioRxiv preprint doi: https://doi.org/10.1101/331538; this version posted May 25, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Eradication of ENO1-deleted Glioblastoma through Collateral Lethality Yu-Hsi Lin1, Nikunj Satani1,2, Naima Hammoudi1, Jeffrey J. Ackroyd1, Sunada Khadka1, Victoria C. Yan1, Dimitra K. Georgiou1, Yuting Sun3, Rafal Zielinski4, Theresa Tran1, Susana Castro Pando1, Xiaobo Wang1, David Maxwell5, Zhenghong Peng6, Federica Pisaneschi1, Pijus Mandal7, Paul G. Leonard8, Quanyu Xu,9 Qi Wu9, Yongying Jiang9, Barbara Czako10, Zhijun Kang10, John M. Asara11, Waldemar Priebe4, William Bornmann12, Joseph R. Marszalek3, Ronald A. DePinho13 and Florian L. Muller#1 1) Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX 77054 2) Institute of Stroke and Cerebrovascular Disease, The University of Texas Health Science Center at Houston, TX 77030 3) Center for Co-Clinical Trials, The University of Texas MD Anderson Cancer Center, Houston, TX 77054 4) Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77054 5) Institutional Analytics & Informatics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030 6) Cardtronics, Inc., Houston, TX 77042 7) Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX 77054 bioRxiv preprint doi: https://doi.org/10.1101/331538; this version posted May 25, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. -
The Tumor Suppressor Notch Inhibits Head and Neck Squamous Cell
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 12-2015 THE TUMOR SUPPRESSOR NOTCH INHIBITS HEAD AND NECK SQUAMOUS CELL CARCINOMA (HNSCC) TUMOR GROWTH AND PROGRESSION BY MODULATING PROTO-ONCOGENES AXL AND CTNNAL1 (α-CATULIN) Shhyam Moorthy Shhyam Moorthy Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biochemistry, Biophysics, and Structural Biology Commons, Cancer Biology Commons, Cell Biology Commons, and the Medicine and Health Sciences Commons Recommended Citation Moorthy, Shhyam and Moorthy, Shhyam, "THE TUMOR SUPPRESSOR NOTCH INHIBITS HEAD AND NECK SQUAMOUS CELL CARCINOMA (HNSCC) TUMOR GROWTH AND PROGRESSION BY MODULATING PROTO-ONCOGENES AXL AND CTNNAL1 (α-CATULIN)" (2015). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 638. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/638 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. THE TUMOR SUPPRESSOR NOTCH INHIBITS HEAD AND NECK SQUAMOUS CELL CARCINOMA (HNSCC) TUMOR GROWTH AND PROGRESSION BY MODULATING PROTO-ONCOGENES AXL AND CTNNAL1 (α-CATULIN) by Shhyam Moorthy, B.S. -
Identification of Potential Key Genes and Pathway Linked with Sporadic Creutzfeldt-Jakob Disease Based on Integrated Bioinformatics Analyses
medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification of potential key genes and pathway linked with sporadic Creutzfeldt-Jakob disease based on integrated bioinformatics analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract Sporadic Creutzfeldt-Jakob disease (sCJD) is neurodegenerative disease also called prion disease linked with poor prognosis. The aim of the current study was to illuminate the underlying molecular mechanisms of sCJD. The mRNA microarray dataset GSE124571 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened. -
Apoptotic Genes As Potential Markers of Metastatic Phenotype in Human Osteosarcoma Cell Lines
17-31 10/12/07 14:53 Page 17 INTERNATIONAL JOURNAL OF ONCOLOGY 32: 17-31, 2008 17 Apoptotic genes as potential markers of metastatic phenotype in human osteosarcoma cell lines CINZIA ZUCCHINI1, ANNA ROCCHI2, MARIA CRISTINA MANARA2, PAOLA DE SANCTIS1, CRISTINA CAPANNI3, MICHELE BIANCHINI1, PAOLO CARINCI1, KATIA SCOTLANDI2 and LUISA VALVASSORI1 1Dipartimento di Istologia, Embriologia e Biologia Applicata, Università di Bologna, Via Belmeloro 8, 40126 Bologna; 2Laboratorio di Ricerca Oncologica, Istituti Ortopedici Rizzoli; 3IGM-CNR, Unit of Bologna, c/o Istituti Ortopedici Rizzoli, Via di Barbiano 1/10, 40136 Bologna, Italy Received May 29, 2007; Accepted July 19, 2007 Abstract. Metastasis is the most frequent cause of death among malignant primitive bone tumor, usually developing in children patients with osteosarcoma. We have previously demonstrated and adolescents, with a high tendency to metastasize (2). in independent experiments that the forced expression of Metastases in osteosarcoma patients spread through peripheral L/B/K ALP and CD99 in U-2 OS osteosarcoma cell lines blood very early and colonize primarily the lung, and later markedly reduces the metastatic ability of these cancer cells. other skeleton districts (3). Since disseminated hidden micro- This behavior makes these cell lines a useful model to assess metastases are present in 80-90% of OS patients at the time the intersection of multiple and independent gene expression of diagnosis, the identification of markers of invasiveness signatures concerning the biological problem of dissemination. and metastasis forms a target of paramount importance in With the aim to characterize a common transcriptional profile planning the treatment of osteosarcoma lesions and enhancing reflecting the essential features of metastatic behavior, we the prognosis. -
Rabbit Mab A
Revision 1 C 0 2 - t Enolase-2 (D20H2) Rabbit mAb a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 1 7 Web: [email protected] 1 www.cellsignal.com 8 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source/Isotype: UniProt ID: Entrez-Gene Id: WB, IP H M R Mk Endogenous 47 Rabbit IgG P09104 2026 Product Usage Information Application Dilution Western Blotting 1:1000 Immunoprecipitation 1:50 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 Enolase-2 (D20H2) Rabbit mAb recognizes endogenous levels of total enolase-2 protein. May cross-react with exogenous levels of enolase-1. Species Reactivity: Human, Mouse, Rat, Monkey Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human enolase-2 protein. Background Enolase is a glycolytic enzyme that is involved in the conversion of 2-phosphoglycerate to phosphoenolpyruvate (1). Mammalian enolase has three subunits: α, β, and γ, that can form homo and heterodimers. Homodimers of γ enolase are neuronal-specific (2). Research studies have shown elevated levels of neuro-specific enolase-2 in neuroblastoma (2) and small-cell lung cancer (3,4). 1. Van Obberghen, E. et al. (1988) J Neurosci Res 19, 450-6. 2. -
Neuron Specific Enolase (NSE) ELISA Kit
Package Insert Neuron Specific Enolase (NSE) ELISA Kit Catalog Number: NSE31-K01 (1 x 96 wells) For Research Use Only. Not for use in diagnostic procedures. v. 1.0 Eagle Biosciences, Inc. 20A Northwest Blvd., Suite 112, Nashua, NH 03063 Phone: 617-419-2019 Fax: 617-419-1110 www.EagleBio.com INTENDED USE The Eagle Biosciences Human Neuron Specific Enolase (NSE) ELISA Assay Kit (enzyme-linked immunoassay kit) is intended for the quantitative determination of human neuron specific enolase (NSE) levels in serum. The Eagle Biosciences Human Neuron Specific (NSE) ELISA Assay Kit is for research use only and not to be used in diagnostic procedures. INTRODUCTION The glycolytic enzyme enolase (2-phospho-D-glycerate hydrolyase) exists as several dimeric isoenzymes (αα, αβ, ββ and γγ) composed of three distinct subunits: α, β, and γ. Three isoenzymes are found in human brain: αα, αβ, and γγ. The heterologous αγ-isoenzyme and the homologous γγ -enolase isoenzymes are known as neuron-specific enolase (NSE) as these isoenzymes initially were detected in neurons and neuroendocrine cells. By using monoclonal antibodies specific to the γ-subunit of the enzyme allow the test to detect both the αγ and the γγ forms. The NSE levels are quite low in normal healthy people and in people with benign disease. Lung cancer is one of the most common cancer forms with incidences about 50-100 per 100,000 population. Approximately 20% of the lung cancer is small cell lung cancer. NSE has been shown to be a valuable tumor marker of neuroendocrine origin, particularly in small cell lung cancer and in neuroblastoma. -
In-Depth Proteomic Analysis of Tissue Interstitial Fluid for Hepatocellular Carcinoma Serum Biomarker Discovery
FULL PAPER British Journal of Cancer (2017) 117, 1676–1684 | doi: 10.1038/bjc.2017.344 Keywords: biomarker; tissue interstitial fluid; hepatocellular carcinoma; proteomics; prognosis In-depth proteomic analysis of tissue interstitial fluid for hepatocellular carcinoma serum biomarker discovery Jian Zhang1, Ning Hao1, Wei Liu2, Min Lu3, Longqin Sun1, Ning Chen1, Miantao Wu4, Xiaohang Zhao5, Baocai Xing2,7, Wei Sun*,1,7 and Fuchu He*,1,6,7 1State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences Beijing, Beijing Institute of Radiation Medicine, Beijing 102206, China; 2Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Hepato-Pancreato-Biliary Surgery I, Peking University Cancer Hospital and Institute, Beijing 100036, China; 3Department of Pathology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; 4State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China; 5State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China and 6Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China Background: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. New serum biomarkers for HCC screening are needed, especially for alpha-fetoprotein (AFP) negative patients. As a proximal fluid between body fluids and intracellular fluid, tissue interstitial fluid (TIF) is a suitable source for serum biomarker discovery. Methods: Sixteen paired TIF samples from HCC tumour and adjacent non-tumour tissues were analysed by isobaric tags for relative and absolute quantitation (iTRAQ) method. -
Genome-Wide Association Studies of Retinal Vessel Tortuosity Identify 173
medRxiv preprint doi: https://doi.org/10.1101/2020.06.25.20139725; this version posted March 24, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license . Genome-Wide Association Studies of retinal vessel tortuosity identify 173 novel loci, capturing genes and pathways associated with disease and vascular tissue pathomechanics Mattia Tomasoni1,2, Michael Johannes Beyeler1,2, Ninon Mounier2,3, Eleonora Porcu2,3,4, Sofia Ortin Vela1,2, Alexander Luke Button1,2, Tanguy Corre1,2,3, Hana Abouzeid5,6, Murielle Bochud3, Daniel Krefl1,2, Sven Bergmann1,2,7 1 Dept. of Computational Biology, University of Lausanne, Lausanne, Switzerland 2 Swiss Institute of Bioinformatics, Lausanne, Switzerland 3 Center for Primary Care and Public Health (Unisanté), University of Lausanne, Lausanne, Switzerland 4 Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland 5 Division of Ophthalmology, Geneva University Hospitals, Switzerland 6 Clinical Eye Research Center Memorial Adolphe de Rothschild, Geneva, Switzerland 7 Dept. of Integrative Biomedical Sciences, University of Cape Town, Cape Town, South Africa Corresponding authors: [email protected] [email protected] Abstract Fundus images of the eye allow for non-invasive inspection of the microvasculature system of the retina, which is informative of systemic cardiovascular health. We set up a fully automated image processing pipeline enabling the massively parallelised annotation of such images in terms of vessel type (i.e., artery or vein) and quantitative morphological properties, such as tortuosity (“bendiness”). -
(NSE) ELISA Kit Cat. #. EK-0050
ELISA kits available from GSI (see details at the web site) #EK-0010 Human Leptin Instruction Manual No. M-EK-0050 # EK-0700 Human Sex Hormone Binding Glob (SHBG) # EK-0900 Human IGF-Binding Protein 1 (IGFBP1) # EK-1000 Human C-Reactive Protein (CRP) # EK-1190 Human Serum Albumin # EK-1200 Human Albumin (Urinary) Human Neuron Specific Enolase (NSE) # EK-1750 Human IgG (total) # EK-1760 Human IgM # EK-1800 Human IgE # EK-1810 Human Ferritin # EK-1210 Human Transferrin (Tf) # EK-0020 Beta-2 microglobulin ELISA Kit Cat. #. EK-0050 # EK-1600 Human Growth Hormone (GH) # EK-0060 Human Pancreatic Colorectal cancer (CA-242) # EK-1820 Human Ovarian Cancer (CA125) # EK-1830 Human CA153 For Quantitative Determination of # EK-1840 Human Pancreatic & GI Cancer (CA199) # EK-1310 Human Pancreatic Lipase Neuron specific enolase In Human Serum # EK-1400 Human Prostatic Acid Phosphatase (PAP) # EK-1500 Human Prostate Specific Antigen (PSA) # EK-1510 free PSA (fPSA) # EK-0500 Human Alpha Fetoprotein (AFP) # EK-0050 Human Neuron Specific Enolase (NSE) For In Vitro Research Use Only # EK-0030 Human Insulin # EK-0040 Human C-peptide # EK-0100 Human Luteinizing Hormone (LH) # EK-0200 Human Follicle Stimulating Hormone (FSH) # EK-0300 Human Prolactin (PRL) # EK-0400 Human Chorionic Gonadotropin (HCG) # EK-0410 HCG-free beta # EK-0600 Human Thyroid Stimulating Hormone (TSH) # EK-1100 Human Total Thyroxine (T4) # EK-1110 Human Free T4 (fT4) # EK-1650 Human free triiodothyronine (fT3) # EK-1700 Human T3 (total) # EK-1850 Human Cortisol # EK-1860 Human Progesterone # EK-1865 Human Pregnolone # EK-1875 Human Aldosterone # EK-1880 Human Testosterone # EK-1885 Human free Testosterone # EK-1910 Human Androstenedione # EK-1920 Human Estradiol # EK-1925 Human Estrone # EK-1940 Dihydrotestosterone (DHT) # EK-1950 Human DHEA-sulphate (DHEA-S) # EK-3400 Human serum Neopterin] # EK-3000 Human Rheumatoid Factors IgM (RF) # EK-3100 Human anti-dsDNA # EK-3200 Anti-Nuclear Antibodies (ANA) Page 7 EK-0050 (ub61222A) Human Neuron Specific Enolase (NSE) ELISA KIT PERFORMANCE CHARACTERISTICS Cat. -
Datasheet (Pdf)
alpha-Enolase/Enolase 1 Data Sheet Catalog Number: MO22153 Host: Mouse Product Type: Monoclonal IgG1 Species Rat Affinity Purified Antibody Reactivity: Immunogen Sequence: N-terminal 12 amino acids of bovine Format: Liquid, 100 ul aliquot enolase 1 Concentration: 1 mg/ml HGNC name for this protein is ENO1 Applications: Immunofluorescence/Immunocytochemistry: 1:2,000-5,00 Immunohistochemistry: 1:2,000-5,000 Western Blot: 1:5,000-10,000 Dilutions listed as a recommendation. Optimal dilution should be determined by investigator. Storage: Antibody can also be aliquoted and stored frozen at -20° C to -70° C in a manual defrost freezer for six months without detectable loss of activity. The antibody can be stored at 2° - 8° C for 1 month without detectable loss of activity. Avoid repeated freeze-thaw cycles. Application Notes Description/Data: Enolase 1 or α is also known as non-neuronal enolase (NNE) and is expressed in most kinds of tissue, but is absent from neurons. Abnormal expression of NNE is associated with tumor progression in some breast and head and neck cancer (1, 2). Enolase 2 or γ is also known as neuron specific enolase (NSE), (We offer Neuron Specific Enolase (NSE)). A switch from NNE to NSE occurs in the development of neurons (3). Enolase 3 or β is expressed primarily in muscle cells. Monoclonal antibody MO22153 was raised against the N-terminal 12 amino acids of bovine enolase 1 which was synthesized on a 8-amine lysine core using the multiple antigen presentation method. The antibody was tested for binding to expressed bovine enolase 1, 2 and 3 and shown to be specific for only enolase 1. -
Alisertib Induces Cell Cycle Arrest, Apoptosis, Autophagy and Suppresses EMT in HT29 and Caco-2 Cells
Article Alisertib Induces Cell Cycle Arrest, Apoptosis, Autophagy and Suppresses EMT in HT29 and Caco-2 Cells Bao-Jun Ren 1,2, Zhi-Wei Zhou 2, Da-Jian Zhu 1, Yong-Le Ju 1, Jin-Hao Wu 1, Man-Zhao Ouyang 1, Xiao-Wu Chen 1,* and Shu-Feng Zhou 2,* Received: 2 November 2015; Accepted: 9 December 2015; Published: 29 December 2015 Academic Editor: William Chi-shing Cho 1 Department of Gastrointestinal Surgery, Shunde First People’s Hospital Affiliated to Southern Medical University, Guangdong 528300, China; [email protected] (B.-J.R.); [email protected] (D.-J.Z.); [email protected] (Y.-L.J.); [email protected] (J.-H.W.); [email protected] (M.-Z.O.) 2 Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, 12901 Bruce B. Downs Blvd., MDC 30, Tampa, FL 33612, USA; [email protected] * Correspondence: [email protected] (X.-W.C.); [email protected] (S.-F.Z.); Tel.: +86-757-2231-8555 (X.-W.C.); +1-813-974-6276 (S.-F.Z.); Fax: +86-757-2222-3899 (X.-W.C.); +1-813-905-9885 (S.-F.Z.) Abstract: Colorectal cancer (CRC) is one of the most common malignancies worldwide with substantial mortality and morbidity. Alisertib (ALS) is a selective Aurora kinase A (AURKA) inhibitor with unclear effect and molecular interactome on CRC. This study aimed to evaluate the molecular interactome and anticancer effect of ALS and explore the underlying mechanisms in HT29 and Caco-2 cells. ALS markedly arrested cells in G2/M phase in both cell lines, accompanied by remarkable alterations in the expression level of key cell cycle regulators.