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Variation in FCN1 Affects Biosynthesis of Ficolin-1 and Is Associated With
Genes and Immunity (2012) 13, 515–522 & 2012 Macmillan Publishers Limited All rights reserved 1466-4879/12 www.nature.com/gene ORIGINAL ARTICLE Variation in FCN1 affects biosynthesis of ficolin-1 and is associated with outcome of systemic inflammation L Munthe-Fog1, T Hummelshoj1, C Honore´ 1, ME Moller1, MO Skjoedt1, I Palsgaard1, N Borregaard2, HO Madsen1 and P Garred1 Ficolin-1 is a recognition molecule of the lectin complement pathway. The ficolin-1 gene FCN1 is polymorphic, but the functional and clinical consequences are unknown.The concentration of ficolin-1 in plasma and FCN1 polymorphisms in positions À 1981 (rs2989727), À 791 (rs28909068), À 542 (rs10120023), À 271 (rs28909976), À 144 (rs10117466) and þ 7918 (rs1071583) were determined in 100 healthy individuals. FCN1 expression by isolated monocytes and granulocytes and ficolin-1 levels in monocyte culture supernatants were assessed in 21 FCN1-genotyped individuals. FCN1 polymorphisms were determined in a cohort of 251 patients with systemic inflammation. High ficolin-1 plasma levels were significantly associated with the minor alleles in position À 542 and À 144. These alleles were also significantly associated with high FCN1 mRNA expression. The level of ficolin-1 in culture supernatants was significantly higher in individuals homozygous for the minor alleles at positions À 542 and À 144. Homozygosity for these alleles was significantly associated with fatal outcome in patients with systemic inflammation. None of the other investigated polymorphisms were associated with FCN1 and ficolin-1 expression, concentration or disease outcome. Functional polymorphic sites in the promoter region of FCN1 regulate both the expression and synthesis of ficolin-1 and are associated with outcome in severe inflammation. -
Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2010 Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis Ryan Fassnacht Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Physiology Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/2246 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. Ryan C. Fassnacht 2010 All Rights Reserved Molecular Mechanisms Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University. by Ryan Christopher Fassnacht, B.S. Hampden Sydney University, 2005 M.S. Virginia Commonwealth University, 2010 Director: Valeria Mas, Ph.D., Associate Professor of Surgery and Pathology Division of Transplant Department of Surgery Virginia Commonwealth University Richmond, Virginia July 9, 2010 Acknowledgement The Author wishes to thank his family and close friends for their support. He would also like to thank the members of the molecular transplant team for their help and advice. This project would not have been possible with out the help of Dr. Valeria Mas and her endearing -
Chromosomal Aberrations in Head and Neck Squamous Cell Carcinomas in Norwegian and Sudanese Populations by Array Comparative Genomic Hybridization
825-843 12/9/08 15:31 Page 825 ONCOLOGY REPORTS 20: 825-843, 2008 825 Chromosomal aberrations in head and neck squamous cell carcinomas in Norwegian and Sudanese populations by array comparative genomic hybridization ERIC ROMAN1,2, LEONARDO A. MEZA-ZEPEDA3, STINE H. KRESSE3, OLA MYKLEBOST3,4, ENDRE N. VASSTRAND2 and SALAH O. IBRAHIM1,2 1Department of Biomedicine, Faculty of Medicine and Dentistry, University of Bergen, Jonas Lies vei 91; 2Department of Oral Sciences - Periodontology, Faculty of Medicine and Dentistry, University of Bergen, Årstadveien 17, 5009 Bergen; 3Department of Tumor Biology, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center, Montebello, 0310 Oslo; 4Department of Molecular Biosciences, University of Oslo, Blindernveien 31, 0371 Oslo, Norway Received January 30, 2008; Accepted April 29, 2008 DOI: 10.3892/or_00000080 Abstract. We used microarray-based comparative genomic logical parameters showed little correlation, suggesting an hybridization to explore genome-wide profiles of chromosomal occurrence of gains/losses regardless of ethnic differences and aberrations in 26 samples of head and neck cancers compared clinicopathological status between the patients from the two to their pair-wise normal controls. The samples were obtained countries. Our findings indicate the existence of common from Sudanese (n=11) and Norwegian (n=15) patients. The gene-specific amplifications/deletions in these tumors, findings were correlated with clinicopathological variables. regardless of the source of the samples or attributed We identified the amplification of 41 common chromosomal carcinogenic risk factors. regions (harboring 149 candidate genes) and the deletion of 22 (28 candidate genes). Predominant chromosomal alterations Introduction that were observed included high-level amplification at 1q21 (harboring the S100A gene family) and 11q22 (including Head and neck squamous cell carcinoma (HNSCC), including several MMP family members). -
SPP1 and AGER As Potential Prognostic Biomarkers for Lung Adenocarcinoma
7028 ONCOLOGY LETTERS 15: 7028-7036, 2018 SPP1 and AGER as potential prognostic biomarkers for lung adenocarcinoma WEIGUO ZHANG, JUNLI FAN, QIANG CHEN, CAIPENG LEI, BIN QIAO and QIN LIU Henan Key Laboratory of Cancer Epigenetics, Department of Oncology Surgery, Cancer Institute and College of Clinical Medicine, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China Received August 11, 2017; Accepted January 5, 2018 DOI: 10.3892/ol.2018.8235 Abstract. Overdue treatment and prognostic evaluation lead Introduction to low survival rates in patients with lung adenocarcinoma (LUAD). To date, effective biomarkers for prognosis are still Lung adenocarcinoma (LUAD) is one of the three major required. The aim of the present study was to screen differen- histopathological subtypes along with squamous cell carci- tially expressed genes (DEGs) as biomarkers for prognostic noma (SqCLC) and large cell carcinoma (1). Currently, LUAD evaluation of LUAD. DEGs in tumor and normal samples has become the most common lung cancer with increasing were identified and analyzed for Kyoto Encyclopedia of Genes morbidity. This uptrend of incidence may be due to increasing and Genomes/Gene Ontology functional enrichments. The smoking rate and air pollution (2). Furthermore, LUAD is common genes that are up and downregulated were selected diagnosed at late stages (stage III and IV), when the cancer for prognostic analysis using RNAseq data in The Cancer has spread to nearby tissues and metastasis has occurred (3). Genome Atlas. Differential expression analysis was performed As well as overdue diagnosis that leads to delayed treatment, with 164 samples in GSE10072 and GSE7670 datasets. -
An Amplified Fatty Acid-Binding Protein Gene Cluster In
cancers Review An Amplified Fatty Acid-Binding Protein Gene Cluster in Prostate Cancer: Emerging Roles in Lipid Metabolism and Metastasis Rong-Zong Liu and Roseline Godbout * Department of Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB T6G 1Z2, Canada; [email protected] * Correspondence: [email protected]; Tel.: +1-780-432-8901 Received: 6 November 2020; Accepted: 16 December 2020; Published: 18 December 2020 Simple Summary: Prostate cancer is the second most common cancer in men. In many cases, prostate cancer grows very slowly and remains confined to the prostate. These localized cancers can usually be cured. However, prostate cancer can also metastasize to other organs of the body, which often results in death of the patient. We found that a cluster of genes involved in accumulation and utilization of fats exists in multiple copies and is expressed at much higher levels in metastatic prostate cancer compared to localized disease. These genes, called fatty acid-binding protein (or FABP) genes, individually and collectively, promote properties associated with prostate cancer metastasis. We propose that levels of these FABP genes may serve as an indicator of prostate cancer aggressiveness, and that inhibiting the action of FABP genes may provide a new approach to prevent and/or treat metastatic prostate cancer. Abstract: Treatment for early stage and localized prostate cancer (PCa) is highly effective. Patient survival, however, drops dramatically upon metastasis due to drug resistance and cancer recurrence. The molecular mechanisms underlying PCa metastasis are complex and remain unclear. It is therefore crucial to decipher the key genetic alterations and relevant molecular pathways driving PCa metastatic progression so that predictive biomarkers and precise therapeutic targets can be developed. -
Interoperability in Toxicology: Connecting Chemical, Biological, and Complex Disease Data
INTEROPERABILITY IN TOXICOLOGY: CONNECTING CHEMICAL, BIOLOGICAL, AND COMPLEX DISEASE DATA Sean Mackey Watford A dissertation submitted to the faculty at the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Gillings School of Global Public Health (Environmental Sciences and Engineering). Chapel Hill 2019 Approved by: Rebecca Fry Matt Martin Avram Gold David Reif Ivan Rusyn © 2019 Sean Mackey Watford ALL RIGHTS RESERVED ii ABSTRACT Sean Mackey Watford: Interoperability in Toxicology: Connecting Chemical, Biological, and Complex Disease Data (Under the direction of Rebecca Fry) The current regulatory framework in toXicology is expanding beyond traditional animal toXicity testing to include new approach methodologies (NAMs) like computational models built using rapidly generated dose-response information like US Environmental Protection Agency’s ToXicity Forecaster (ToXCast) and the interagency collaborative ToX21 initiative. These programs have provided new opportunities for research but also introduced challenges in application of this information to current regulatory needs. One such challenge is linking in vitro chemical bioactivity to adverse outcomes like cancer or other complex diseases. To utilize NAMs in prediction of compleX disease, information from traditional and new sources must be interoperable for easy integration. The work presented here describes the development of a bioinformatic tool, a database of traditional toXicity information with improved interoperability, and efforts to use these new tools together to inform prediction of cancer and complex disease. First, a bioinformatic tool was developed to provide a ranked list of Medical Subject Heading (MeSH) to gene associations based on literature support, enabling connection of compleX diseases to genes potentially involved. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
DDX5 Promotes Oncogene C3 and FABP1 Expressions and Drives Intestinal Inflammation and Tumorigenesis
Published Online: 18 August, 2020 | Supp Info: http://doi.org/10.26508/lsa.202000772 Downloaded from life-science-alliance.org on 19 August, 2020 Research Article DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis Nazia Abbasi1,*, Tianyun Long1,*, Yuxin Li1, Brian A Yee1,BenjaminSCho1, Juan E Hernandez1 ,EvelynMa1, Parth R Patel1, Debashis Sahoo4, Ibrahim M Sayed2, Nissi Varki2,SoumitaDas2, Pradipta Ghosh1,3,GeneWYeo1, Wendy Jia Men Huang1 Tumorigenesis in different segments of the intestinal tract in- α in response to stimulation from pro-inflammatory cytokines, volves tissue-specific oncogenic drivers. In the colon, comple- such as TNFα,IFNγ,andIL1β (11, 12, 13, 14, 15, 16, 17). Fabp1 ment component 3 (C3) activation is a major contributor to transcription is controlled by GATA-binding protein 4 (GATA4), inflammation and malignancies. By contrast, tumorigenesis in C/EBP, peroxisome proliferator-activated receptor α, pancreatic the small intestine involves fatty acid–binding protein 1 (FABP1). and duodenal homeobox 1 (PDX1), and hypoxia-inducible factor However, little is known of the upstream mechanisms driving (HIF1α)(18, 19, 20, 21, 22). However, little is known about how C3 and their expressions in different segments of the intestinal tract. FABP1 expressions are regulated posttranscriptionally in intestinal Here, we report that the RNA-binding protein DDX5 binds to the epithelial cells (IECs). mRNA transcripts of C3 and Fabp1 to augment their expressions Posttranscriptional regulation of gene products can be or- posttranscriptionally. Knocking out DDX5 in epithelial cells chestrated, in part, by RNA-binding proteins (23 ). One member protected mice from intestinal tumorigenesis and dextran so- of the DEAD-box containing RNA-binding protein family, DDX5, is dium sulfate (DSS)–induced colitis. -
Análise Integrativa De Perfis Transcricionais De Pacientes Com
UNIVERSIDADE DE SÃO PAULO FACULDADE DE MEDICINA DE RIBEIRÃO PRETO PROGRAMA DE PÓS-GRADUAÇÃO EM GENÉTICA ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Ribeirão Preto – 2012 ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Tese apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo para obtenção do título de Doutor em Ciências. Área de Concentração: Genética Orientador: Prof. Dr. Eduardo Antonio Donadi Co-orientador: Prof. Dr. Geraldo A. S. Passos Ribeirão Preto – 2012 AUTORIZO A REPRODUÇÃO E DIVULGAÇÃO TOTAL OU PARCIAL DESTE TRABALHO, POR QUALQUER MEIO CONVENCIONAL OU ELETRÔNICO, PARA FINS DE ESTUDO E PESQUISA, DESDE QUE CITADA A FONTE. FICHA CATALOGRÁFICA Evangelista, Adriane Feijó Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. Ribeirão Preto, 2012 192p. Tese de Doutorado apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Área de Concentração: Genética. Orientador: Donadi, Eduardo Antonio Co-orientador: Passos, Geraldo A. 1. Expressão gênica – microarrays 2. Análise bioinformática por module maps 3. Diabetes mellitus tipo 1 4. Diabetes mellitus tipo 2 5. Diabetes mellitus gestacional FOLHA DE APROVAÇÃO ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. -
Human Lectins, Their Carbohydrate Affinities and Where to Find Them
biomolecules Review Human Lectins, Their Carbohydrate Affinities and Where to Review HumanFind Them Lectins, Their Carbohydrate Affinities and Where to FindCláudia ThemD. Raposo 1,*, André B. Canelas 2 and M. Teresa Barros 1 1, 2 1 Cláudia D. Raposo * , Andr1 é LAQVB. Canelas‐Requimte,and Department M. Teresa of Chemistry, Barros NOVA School of Science and Technology, Universidade NOVA de Lisboa, 2829‐516 Caparica, Portugal; [email protected] 12 GlanbiaLAQV-Requimte,‐AgriChemWhey, Department Lisheen of Chemistry, Mine, Killoran, NOVA Moyne, School E41 of ScienceR622 Co. and Tipperary, Technology, Ireland; canelas‐ [email protected] NOVA de Lisboa, 2829-516 Caparica, Portugal; [email protected] 2* Correspondence:Glanbia-AgriChemWhey, [email protected]; Lisheen Mine, Tel.: Killoran, +351‐212948550 Moyne, E41 R622 Tipperary, Ireland; [email protected] * Correspondence: [email protected]; Tel.: +351-212948550 Abstract: Lectins are a class of proteins responsible for several biological roles such as cell‐cell in‐ Abstract:teractions,Lectins signaling are pathways, a class of and proteins several responsible innate immune for several responses biological against roles pathogens. such as Since cell-cell lec‐ interactions,tins are able signalingto bind to pathways, carbohydrates, and several they can innate be a immuneviable target responses for targeted against drug pathogens. delivery Since sys‐ lectinstems. In are fact, able several to bind lectins to carbohydrates, were approved they by canFood be and a viable Drug targetAdministration for targeted for drugthat purpose. delivery systems.Information In fact, about several specific lectins carbohydrate were approved recognition by Food by andlectin Drug receptors Administration was gathered for that herein, purpose. plus Informationthe specific organs about specific where those carbohydrate lectins can recognition be found by within lectin the receptors human was body. -
The Association Between FABP7 Serum Levels with Survival And
Karvellas et al. Ann. Intensive Care (2017) 7:99 DOI 10.1186/s13613-017-0323-0 RESEARCH Open Access The association between FABP7 serum levels with survival and neurological complications in acetaminophen‑induced acute liver failure: a nested case–control study Constantine J. Karvellas1* , Jaime L. Speiser2, Mélanie Tremblay3, William M. Lee4, Christopher F. Rose3 and For the US Acute Liver Failure Study Group Abstract Background: Acetaminophen (APAP)-induced acute liver failure (ALF) is associated with signifcant mortality due to intracranial hypertension (ICH), a result of cerebral edema (CE) and astrocyte swelling. Brain-type fatty acid-binding protein (FABP7) is a small (15 kDa) cytoplasmic protein abundantly expressed in astrocytes. The aim of this study was to determine whether serum FABP7 levels early (day 1) or late (days 3–5) level were associated with 21-day mortality and/or the presence of ICH/CE in APAP-ALF patients. Methods: Serum samples from 198 APAP-ALF patients (nested case–control study with 99 survivors and 99 non-sur- vivors) were analyzed by ELISA methods and assessed with clinical data from the US Acute Liver Failure Study Group (ALFSG) Registry (1998–2014). Results: APAP-ALF survivors had signifcantly lower serum FABP7 levels on admission (147.9 vs. 316.5 ng/ml, p 0.0002) and late (87.3 vs. 286.2 ng/ml, p < 0.0001) compared with non-survivors. However, a signifcant association between= 21-day mortality and increased serum FABP7 early [log FABP7 odds ratio (OR) 1.16, p 0.32] and late (log FABP7 ~ OR 1.34, p 0.21) was not detected after adjusting for signifcant covariates (MELD, vasopressor= use). -
Bioinformatics Analysis of Differentially Expressed Genes in Rotator Cuff Tear
Ren et al. Journal of Orthopaedic Surgery and Research (2018) 13:284 https://doi.org/10.1186/s13018-018-0989-5 RESEARCHARTICLE Open Access Bioinformatics analysis of differentially expressed genes in rotator cuff tear patients using microarray data Yi-Ming Ren†, Yuan-Hui Duan†, Yun-Bo Sun†, Tao Yang and Meng-Qiang Tian* Abstract Background: Rotator cuff tear (RCT) is a common shoulder disorder in the elderly. Muscle atrophy, denervation and fatty infiltration exert secondary injuries on torn rotator cuff muscles. It has been reported that satellite cells (SCs) play roles in pathogenic process and regenerative capacity of human RCT via regulating of target genes. This study aims to complement the differentially expressed genes (DEGs) of SCs that regulated between the torn supraspinatus (SSP) samples and intact subscapularis (SSC) samples, identify their functions and molecular pathways. Methods: The gene expression profile GSE93661 was downloaded and bioinformatics analysis was made. Results: Five hundred fifty one DEGs totally were identified. Among them, 272 DEGs were overexpressed, and the remaining 279 DEGs were underexpressed. Gene ontology (GO) and pathway enrichment analysis of target genes were performed. We furthermore identified some relevant core genes using gene–gene interaction network analysis such as GNG13, GCG, NOTCH1, BCL2, NMUR2, PMCH, FFAR1, AVPR2, GNA14, and KALRN, that may contribute to the understanding of the molecular mechanisms of secondary injuries in RCT. We also discovered that GNG13/calcium signaling pathway is highly correlated with the denervation atrophy pathological process of RCT. Conclusion: These genes and pathways provide a new perspective for revealing the underlying pathological mechanisms and therapy strategy of RCT.