Molecular Characterization of Tob1 in Muscle Development in Pigs
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BTG2: a Rising Star of Tumor Suppressors (Review)
INTERNATIONAL JOURNAL OF ONCOLOGY 46: 459-464, 2015 BTG2: A rising star of tumor suppressors (Review) BIjING MAO1, ZHIMIN ZHANG1,2 and GE WANG1 1Cancer Center, Institute of Surgical Research, Daping Hospital, Third Military Medical University, Chongqing 400042; 2Department of Oncology, Wuhan General Hospital of Guangzhou Command, People's Liberation Army, Wuhan, Hubei 430070, P.R. China Received September 22, 2014; Accepted November 3, 2014 DOI: 10.3892/ijo.2014.2765 Abstract. B-cell translocation gene 2 (BTG2), the first 1. Discovery of BTG2 in TOB/BTG gene family gene identified in the BTG/TOB gene family, is involved in many biological activities in cancer cells acting as a tumor The TOB/BTG genes belong to the anti-proliferative gene suppressor. The BTG2 expression is downregulated in many family that includes six different genes in vertebrates: TOB1, human cancers. It is an instantaneous early response gene and TOB2, BTG1 BTG2/TIS21/PC3, BTG3 and BTG4 (Fig. 1). plays important roles in cell differentiation, proliferation, DNA The conserved domain of BTG N-terminal contains two damage repair, and apoptosis in cancer cells. Moreover, BTG2 regions, named box A and box B, which show a high level of is regulated by many factors involving different signal path- homology to the other domains (1-5). Box A has a major effect ways. However, the regulatory mechanism of BTG2 is largely on cell proliferation, while box B plays a role in combination unknown. Recently, the relationship between microRNAs and with many target molecules. Compared with other family BTG2 has attracted much attention. MicroRNA-21 (miR-21) members, BTG1 and BTG2 have an additional region named has been found to regulate BTG2 gene during carcinogenesis. -
Original Article Long Noncoding RNA TOB1-AS1, an Epigenetically Silenced Gene, Functioned As a Novel Tumor Suppressor by Sponging Mir-27B in Cervical Cancer
Am J Cancer Res 2018;8(8):1483-1498 www.ajcr.us /ISSN:2156-6976/ajcr0079106 Original Article Long noncoding RNA TOB1-AS1, an epigenetically silenced gene, functioned as a novel tumor suppressor by sponging miR-27b in cervical cancer Jihang Yao1, Zhenghong Li1, Ziwei Yang2, Hui Xue1, Hua Chang1, Xue Zhang1, Tianren Li1, Kejun Guo1 Departments of 1Gynecology, 2Clinical Laboratory, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China Received April 21, 2018; Accepted July 9, 2018; Epub August 1, 2018; Published August 15, 2018 Abstract: Cervical cancer is one of the most common cancers in females, accounting for a majority of cancer- related deaths in worldwide. Long non-coding RNAs (lncRNAs) have been identified as critical regulators in many tumor-related biological processes. Thus, investigation into the function and mechanism of lncRNAs in the develop- ment of cervical cancer is very necessary. In this study, we found that the expression of TOB1-AS1 was significantly decreased in cervical cancer tissues compared with the adjacent normal tissues. The methylation status of TOB1- AS1-related CpG island was analyzed using methylation specific PCR and bisulfite sequencing analysis, revealing that the aberrant hypermethylation of TOB1-AS1-related CpG island was frequently observed in primary tumors and cervical cancer cells. The expression of TOB1-AS1 in cervical cancer cells could be reversed by demethylation agent treatment. Functionally, overexpression of TOB1-AS1 significantly inhibited cell proliferation, cell cycle progression, invasion and induced apoptosis, while knockdown of TOB1-AS1 exhibited the opposite effect. Furthermore, it was determined that TOB1-AS1 was able to bind and degrade the expression of miR-27b. -
A Deficiency in the Region Homologous to Human 17Q21.33
Copyright Ó 2006 by the Genetics Society of America DOI: 10.1534/genetics.105.054833 A Deficiency in the Region Homologous to Human 17q21.33–q23.2 Causes Heart Defects in Mice Y. Eugene Yu,*,†,1,2 Masae Morishima,‡ Annie Pao,* Ding-Yan Wang,§ Xiao-Yan Wen,§ Antonio Baldini*,‡,** and Allan Bradley††,1 *Department of Molecular and Human Genetics, ‡Department of Pediatrics (Cardiology), **Center for Cardiovascular Development, Baylor College of Medicine, Houston, Texas 77030, †Department of Cancer Genetics and Genetics Program, Roswell Park Cancer Institute, Buffalo, New York 14263, §Division of Cellular and Molecular Biology, Toronto General Research Institute, University of Toronto, Toronto, Ontario M5G 2C1, Canada and ††Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom Manuscript received December 17, 2005 Accepted for publication February 14, 2006 ABSTRACT Several constitutional chromosomal rearrangements occur on human chromosome 17. Patients who carry constitutional deletions of 17q21.3–q24 exhibit distinct phenotypic features. Within the deletion interval, there is a genomic segment that is bounded by the myeloperoxidase and homeobox B1 genes. This genomic segment is syntenically conserved on mouse chromosome 11 and is bounded by the mouse homologs of the same genes (Mpo and HoxB1). To attain functional information about this syntenic segment in mice, we have generated a 6.9-Mb deletion [Df(11)18], the reciprocal duplication [Dp(11)18] between Mpo and Chad (the chondroadherin gene), and a 1.8-Mb deletion between Chad and HoxB1. Phenotypic analyses of the mutant mouse lines showed that the Dp(11)18/Dp(11)18 genotype was responsible for embryonic or adolescent lethality, whereas the Df(11)18/1 genotype was responsible for heart defects. -
Novelty Indicator for Enhanced Prioritization of Predicted Gene Ontology Annotations
IEEE/ACM TRANSACTIONS ON COMPUTATIONAL BIOLOGY AND BIOINFORMATICS, VOL. X, NO. X, MONTHXXX 20XX 1 Novelty Indicator for Enhanced Prioritization of Predicted Gene Ontology Annotations Davide Chicco, Fernando Palluzzi, and Marco Masseroli Abstract—Biomolecular controlled annotations have become pivotal in computational biology, because they allow scientists to analyze large amounts of biological data to better understand their test results, and to infer new knowledge. Yet, biomolecular annotation databases are incomplete by definition, like our knowledge of biology, and may contain errors and inconsistent information. In this context, machine-learning algorithms able to predict and prioritize new biomolecular annotations are both effective and efficient, especially if compared with the time-consuming trials of biological validation. To limit the possibility that these techniques predict obvious and trivial high-level features, and to help prioritizing their results, we introduce here a new element that can improve the accuracy and relevance of the results of an annotation prediction and prioritization pipeline. We propose a novelty indicator able to state the level of ”newness” (or ”originality”) of the annotations predicted for a specific gene to Gene Ontology terms, and to help prioritizing the most novel and interesting annotations predicted. We performed a thorough biological functional analysis of the prioritized annotations predicted with high accuracy by using this indicator and our previously proposed prediction algorithms. The relevance -
Transcriptome Analysis of Different Multidrug-Resistant Gastric Carcinoma Cells
in vivo 19: 583-590 (2005) Transcriptome Analysis of Different Multidrug-resistant Gastric Carcinoma Cells STEFFEN HEIM1 and HERMANN LAGE2 1Europroteome AG, Berlin-Hennigsdorf; 2Institute of Pathology, Charité Campus Mitte, Schumannstr. 20/21, D-10117 Berlin, Germany Abstract. Multidrug resistance (MDR) of human cancers is advanced cancer. These therapeutic protocols produce an the major cause of failure of chemotherapy. To better overall response rate of about 20% at best using a single- understand the molecular events associated with the agent, and up to 50% using combination chemotherapy. development of different types of MDR, two different multidrug- Thus, a large number of malignancies are incurable. resistant gastric carcinoma cell lines, the MDR1/P-glycoprotein- Generally, gastrointestinal cancers, including gastric expressing cell line EPG85-257RDB and the MDR1/P- carcinoma, are naturally resistant to many anticancer drugs. glycoprotein-negative cell variant EPG85-257RNOV, as well as Additionally, these tumors are able to develop acquired the corresponding drug-sensitive parental cell line EPG85-257P, drug resistance phenotypes, which include the multidrug were used for analyses of the mRNA expression profiles by resistance (MDR) phenomenon. cDNA array hybridization. Of more than 12,000 genes spotted The MDR phenotype is characterized by simultaneous on the arrays, 156 genes were detected as being significantly resistance of tumor cells to various antineoplastic agents regulated in the cell line EPG85-257RDB in comparison to the which are structurally and functionally unrelated. Besides non-resistant cell variant, and 61 genes were found to be the classical MDR phenotype, mediated by the enhanced differentially expressed in the cell line EPG85-257RNOV. -
Structural and Functional Studies of Mrna Stability Regulators
Research Collection Doctoral Thesis Structural and Functional Studies of mRNA Stability Regulators Author(s): Ripin, Nina Publication Date: 2018-11 Permanent Link: https://doi.org/10.3929/ethz-b-000303696 Rights / License: In Copyright - Non-Commercial Use Permitted This page was generated automatically upon download from the ETH Zurich Research Collection. For more information please consult the Terms of use. ETH Library DISS. ETH NO. 25327 Structural and functional studies of mRNA stability regulators A thesis submitted to attain the degree of DOCTOR OF SCIENCES of ETH ZÜRICH (Dr. sc. ETH Zürich) presented by NINA RIPIN Diplom-Biochemikerin, Goethe University, Frankfurt, Germany Born on 06.08.1986 citizen of Germany accepted on the recommendation of Prof. Dr. Frédéric Allain Prof. Dr. Stefanie Jonas Prof. Dr. Michael Sattler Prof. Dr. Witold Filipowicz 2018 “Success consists of going from failure to failure without loss of enthusiasm.” Winston Churchill Summary Posttranscriptional gene regulation (PTGR) is the process by which every step of the life cycle of an mRNA following transcription – maturation, transport, translation, subcellular localization and decay - is tightly regulated. This is accomplished by a complex network of multiple RNA binding proteins (RNPs) binding to several specific mRNA elements. Such cis-acting elements are or can be found within the 5’ cap, the 5’ untranslated region (UTR), the open reading frame (ORF), the 3’UTR and the poly(A) tail at the 3’ end of the mRNA. Adenylate-uridylate-rich elements (AU-rich elements; AREs) are heavily investigated regulatory cis- acting elements within 3’untranslated regions (3’UTRs). These are found in short-lived mRNAs and function as a signal for rapid degradation. -
Meta-Analysis of Genomewide Association Studies Reveals Genetic Variants for Hip Bone Geometry
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author J Bone Miner Manuscript Author Res. Author Manuscript Author manuscript; available in PMC 2019 July 23. Published in final edited form as: J Bone Miner Res. 2019 July ; 34(7): 1284–1296. doi:10.1002/jbmr.3698. Meta-Analysis of Genomewide Association Studies Reveals Genetic Variants for Hip Bone Geometry A full list of authors and affiliations appears at the end of the article. Abstract Hip geometry is an important predictor of fracture. We performed a meta-analysis of GWAS studies in adults to identify genetic variants that are associated with proximal femur geometry phenotypes. We analyzed four phenotypes: (i) femoral neck length; (ii) neck-shaft angle; (iii) femoral neck width, and (iv) femoral neck section modulus, estimated from DXA scans using algorithms of hip structure analysis. In the Discovery stage, 10 cohort studies were included in the fixed-effect meta-analysis, with up to 18,719 men and women ages 16 to 93 years. Association analyses were performed with ~2.5 million polymorphisms under an additive model adjusted for age, body mass index, and height. Replication analyses of meta-GWAS significant loci (at adjusted genomewide significance [GWS], threshold p ≤ 2.6 × 10−8) were performed in seven additional cohorts in silico. We looked up SNPs associated in our analysis, for association with height, bone mineral density (BMD), and fracture. In meta-analysis (combined Discovery and Replication stages), GWS associations were found at 5p15 (IRX1 and ADAMTS16); 5q35 near FGFR4; at 12p11 (in CCDC91); 11q13 (near LRP5 and PPP6R3 (rs7102273)). Several hip geometry signals overlapped with BMD, including LRP5 (chr. -
A Deficiency in the Region Homologous to Human 17Q21.33- Q23.2 Causes Heart Defects in Mice
Genetics: Published Articles Ahead of Print, published on February 19, 2006 as 10.1534/genetics.105.054833 A deficiency in the region homologous to human 17q21.33- q23.2 causes heart defects in mice Y. Eugene Yu*,§, Masae Morishima†, Annie Pao*, Ding-Yan Wang**, Xiao- Yan Wen**, Antonio Baldini*,†,‡, and Allan Bradley††,1 *Department of Molecular and Human Genetics, †Department of Pediatrics (Cardiology), ‡Center for Cardiovascular Development, Baylor College of Medicine, Houston, Texas 77030; §Department of Cancer Genetics and Genetics Program, Roswell Park Cancer Institute, Buffalo, New York 14263; **Division of Cellular and Molecular Biology, Toronto General Research Institute, University of Toronto, Toronto, Ontario, M5G 2C1, Canada; and ††Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK 1Corresponding author: [email protected] FAX: +44 1223 494714 Phone: +44 1223 494881 1 Running head: Chromosomal deletion and phenotype Key words: Chromosome, defects, deletion, heart, mouse Corresponding author: Allan Bradley, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK. FAX: +44 1223 494714; Phone: +44 1223 494881; Email: [email protected] 2 ABSTRACT Several constitutional chromosomal rearrangements occur on human chromosome 17. Patients who carry constitutional deletions of 17q21.3-q24 exhibit distinct phenotypic features. Within the deletion interval, there is a genomic segment which is bounded by the myeloperoxidase and homeobox B1 genes. This genomic segment is syntenically conserved on mouse chromosome 11 and is bounded by the mouse homologs of the same genes (Mpo and HoxB1). To attain functional information about this syntenic segment in mice, we have generated a 6.9-Mb deletion [Df(11)18], the reciprocal duplication [Dp(11)18] between Mpo and Chad (the chondroadherin gene), and a 1.8-Mb deletion between Chad and HoxB1. -
The Role of the TOB1 Gene in Growth Suppression of Hepatocellular Carcinoma
ONCOLOGY LETTERS 4: 981-987, 2012 The role of the TOB1 gene in growth suppression of hepatocellular carcinoma SHEYU LIN1,4*, QINGFENG ZHU2*, YANG XU2, HUI LIU3, JUNYU ZHANG1, JIAWEI XU1, HONGLIAN WANG1, QING SANG1, QINGHE XING1 and JIA FAN2 1Institutes of Biomedical Sciences and Children's Hospital, Fudan University, Shanghai 200032; 2Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032; 3Henan Cancer Hospital, Zhengzhou University, Zhengzhou 450003; 4School of Life Sciences, Nantong University, Nantong 226019, P.R. China Received April 11, 2012; Accepted July 25, 2012 DOI: 10.3892/ol.2012.864 Abstract. The TOB1 gene, mapped on 17q21, is a member Introduction of the BTG/Tob family. In breast cancer it has been identi- fied as a candidate tumor suppressor gene. However, whether The BTG/Tob family comprises at least six distinct members TOB1 is a bona fide tumor suppressor and downregulated in in vertebrates, namely BTG1, BTG2/TIS21/PC3, BTG3/ANA, hepatocellular carcinoma (HCC) remains unclear. In addi- PC3B, TOB2 and TOB. The family may be divided into two tion, whether its expression is regulated through methylation subgroups, the BTG family and the TOB family (1‑3). Both requires investigation. In the present study, we therefore families have been reported to suppress cell proliferation when analyzed the expression of TOB1 in HCC and its methyla- expressed exogenously in cultured cells (4‑7). They commonly tion levels in human HCC and breast cancer. No significant share a conserved amino‑terminal region known as the BTG difference in the expression levels of TOB1 was observed homology domain which is responsible for their antiprolifera- between tumor tissues and adjacent normal tissues in HCC. -
Quantitative Trait Loci Mapping of Macrophage Atherogenic Phenotypes
QUANTITATIVE TRAIT LOCI MAPPING OF MACROPHAGE ATHEROGENIC PHENOTYPES BRIAN RITCHEY Bachelor of Science Biochemistry John Carroll University May 2009 submitted in partial fulfillment of requirements for the degree DOCTOR OF PHILOSOPHY IN CLINICAL AND BIOANALYTICAL CHEMISTRY at the CLEVELAND STATE UNIVERSITY December 2017 We hereby approve this thesis/dissertation for Brian Ritchey Candidate for the Doctor of Philosophy in Clinical-Bioanalytical Chemistry degree for the Department of Chemistry and the CLEVELAND STATE UNIVERSITY College of Graduate Studies by ______________________________ Date: _________ Dissertation Chairperson, Johnathan D. Smith, PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, David J. Anderson, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Baochuan Guo, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Stanley L. Hazen, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Renliang Zhang, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Aimin Zhou, PhD Department of Chemistry, Cleveland State University Date of Defense: October 23, 2017 DEDICATION I dedicate this work to my entire family. In particular, my brother Greg Ritchey, and most especially my father Dr. Michael Ritchey, without whose support none of this work would be possible. I am forever grateful to you for your devotion to me and our family. You are an eternal inspiration that will fuel me for the remainder of my life. I am extraordinarily lucky to have grown up in the family I did, which I will never forget. -
Program in Human Neutrophils Fails To
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 is online at: average * The Journal of Immunology Anaplasma phagocytophilum , 20 of which you can access for free at: 2005; 174:6364-6372; ; from submission to initial decision 4 weeks from acceptance to publication J Immunol doi: 10.4049/jimmunol.174.10.6364 http://www.jimmunol.org/content/174/10/6364 Insights into Pathogen Immune Evasion Mechanisms: Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils Dori L. Borjesson, Scott D. Kobayashi, Adeline R. Whitney, Jovanka M. Voyich, Cynthia M. Argue and Frank R. DeLeo cites 28 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2005/05/03/174.10.6364.DC1 This article http://www.jimmunol.org/content/174/10/6364.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* • Why • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Insights into Pathogen Immune Evasion Mechanisms: Anaplasma phagocytophilum Fails to Induce an Apoptosis Differentiation Program in Human Neutrophils1 Dori L. -
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Supplementary Material Investigating the role of microRNA and Transcription Factor co-regulatory networks in Multiple Sclerosis pathogenesis Nicoletta Nuzziello1, Laura Vilardo2, Paride Pelucchi2, Arianna Consiglio1, Sabino Liuni1, Maria Trojano3 and Maria Liguori1* 1National Research Council, Institute of Biomedical Technologies, Bari Unit, Bari, Italy 2National Research Council, Institute of Biomedical Technologies, Segrate Unit, Milan, Italy 3Department of Basic Sciences, Neurosciences and Sense Organs, University of Bari, Bari, Italy Supplementary Figure S1 Frequencies of GO terms and canonical pathways. (a) Histogram illustrates the GO terms associated to assembled sub-networks. (b) Histogram illustrates the canonical pathways associated to assembled sub-network. a b Legends for Supplementary Tables Supplementary Table S1 List of feedback (FBL) and feed-forward (FFL) loops in miRNA-TF co-regulatory network. Supplementary Table S2 List of significantly (adj p-value < 0.05) GO-term involved in MS. The first column (from the left) listed the GO-term (biological processes) involved in MS. For each functional class, the main attributes (gene count, p-value, adjusted p-value of the enriched terms for multiple testing using the Benjamini correction) have been detailed. In the last column (on the right), we summarized the target genes involved in each enriched GO-term. Supplementary Table S3 List of significantly (adj p-value < 0.05) enriched pathway involved in MS. The first column (from the left) listed the enriched pathway involved in MS. For each pathway, the main attributes (gene count, p-value, adjusted p-value of the enriched terms for multiple testing using the Benjamini correction) have been detailed. In the last column (on the right), we summarized the target genes involved in each enriched pathway.