Nutrigenetics

Total Page:16

File Type:pdf, Size:1020Kb

Nutrigenetics nutrients Nutrigenetics Edited by Dolores Corella Printed Edition of the Special Issue Published in Nutrients www.mdpi.com/journal/nutrients Nutrigenetics Nutrigenetics Special Issue Editor Dolores Corella MDPI • Basel • Beijing • Wuhan • Barcelona • Belgrade Special Issue Editor Dolores Corella University of Valencia Spain Editorial Office MDPI St. Alban-Anlage 66 Basel, Switzerland This is a reprint of articles from the Special Issue published online in the open access journal Nutrients (ISSN 2072-6643) from 2016 to 2017 (available at: http://www.mdpi.com/journal/nutrients/special issues/nutrigenetics) For citation purposes, cite each article independently as indicated on the article page online and as indicated below: LastName, A.A.; LastName, B.B.; LastName, C.C. Article Title. Journal Name Year, Article Number, Page Range. ISBN 978-3-03842-995-1 (Pbk) ISBN 978-3-03842-996-8 (PDF) Articles in this volume are Open Access and distributed under the Creative Commons Attribution (CC BY) license, which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. The book taken as a whole is c 2018 MDPI, Basel, Switzerland, distributed under the terms and conditions of the Creative Commons license CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/). Contents About the Special Issue Editor ...................................... vii Preface to ”Nutrigenetics” ......................................... ix Dolores Corella, Oscar Coltell, Jose V. Sorl´ı, Ram´on Estruch, Laura Quiles, Miguel Angel´ Mart´ınez-Gonz´alez, Jordi Salas-Salvad´o, Olga Casta ˜ner, Fernando Ar´os, Manuel Ortega-Calvo, Llu´ıs Serra-Majem, Enrique G´omez-Gracia, Olga Portol´es, Miquel Fiol, Javier D´ıez Espino, Josep Basora, Montserrat Fit´o, Emilio Ros and Jos´eM. Ordov´as Polymorphism of the Transcription Factor 7-Like 2 Gene (TCF7L2) Interacts with Obesity on Type-2 Diabetes in the PREDIMED Study Emphasizing the Heterogeneity of Genetic Variants in Type-2 Diabetes Risk Prediction: Time for Obesity-Specific Genetic Risk Scores Reprinted from: Nutrients 2016, 8, 793, doi: 10.3390/nu8120793 ................... 1 Nikul K. Soni, Alastair B. Ross, Nathalie Scheers, Otto I. Savolainen, Intawat Nookaew, Britt G. Gabrielsson and Ann-Sofie Sandberg Splenic Immune Response Is Down-Regulated in C57BL/6J Mice Fed Eicosapentaenoic Acid and Docosahexaenoic Acid Enriched High Fat Diet Reprinted from: Nutrients 2017, 9, 50, doi: 10.3390/nu9010050 .................... 19 Abraham Wall-Medrano, Laura A. de la Rosa, Alma A. V´azquez-Flores, Gilberto Mercado-Mercado, Rogelio Gonz´alez-Arellanes,Jos´eA.L´opez-D´ıaz, Aar´onF. Gonz´alez-C´ordova, Gustavo A. Gonz´alez-Aguilar, Belinda Vallejo-Cordoba and Francisco J. Molina-Corral Lipidomic and Antioxidant Response to Grape Seed, Corn and Coconut Oils in Healthy Wistar Rats Reprinted from: Nutrients 2017, 9, 82, doi: 10.3390/nu9010082 .................... 36 Kaitlin J. Day, Melissa M. Adamski, Aimee L. Dordevic and Chiara Murgia Genetic Variations as Modifying Factors to Dietary Zinc Requirements—A Systematic Review Reprinted from: Nutrients 2017, 9, 148, doi: 10.3390/nu9020148 ................... 53 Kaitlin Roke, Kathryn Walton, Shannon L. Klingel, Amber Harnett, Sanjeena Subedi, Jess Haines and David M. Mutch Evaluating Changes in Omega-3 Fatty Acid Intake after Receiving Personal FADS1 Genetic Information: A Randomized Nutrigenetic Intervention Reprinted from: Nutrients 2017, 9, 240, doi: 10.3390/nu9030240 ................... 69 Patrick Borel and Charles Desmarchelier Genetic Variations Associated with Vitamin A Status and Vitamin A Bioavailability Reprinted from: Nutrients 2017, 9, 246, doi: 10.3390/nu9030246 ................... 83 Juan J. Salinero, Beatriz Lara, Diana Ruiz-Vicente, Francisco Areces, Carlos Puente-Torres, C´esar Gallo-Salazar, Teodoro Pascual and Juan Del Coso CYP1A2 Genotype Variations Do Not Modify the Benefits and Drawbacks of Caffeine during Exercise: A Pilot Study Reprinted from: Nutrients 2017, 9, 269, doi: 10.3390/nu9030269 ...................100 v You-Lin Tain, Yu-Ju Lin, Jiunn-Ming Sheen, Hong-Ren Yu, Mao-Meng Tiao, Chih-Cheng Chen, Ching-Chou Tsai, Li-Tung Huang and Chien-Ning Hsu High Fat Diets Sex-Specifically Affect the Renal Transcriptome and Program Obesity, Kidney Injury, and Hypertension in the Offspring Reprinted from: Nutrients 2017, 9, 357, doi: 10.3390/nu9040357 ...................112 Chiara Murgia and Melissa M. Adamski Translation of Nutritional Genomics into Nutrition Practice: The Next Step Reprinted from: Nutrients 2017, 9, 366, doi: 10.3390/nu9040366 ...................131 Min Yang, Min Xiong, Huan Chen, Lanlan Geng, Peiyu Chen, Jing Xie, Shui Qing Ye, Ding-You Li and Sitang Gong Novel Genetic Variants Associated with Child Refractory Esophageal Stricture with Food Allergy by Exome Sequencing Reprinted from: Nutrients 2017, 9, 390, doi: 10.3390/nu9040390 ...................135 Josiane Steluti, Aline M. Carvalho, Antonio A. F. Carioca, Andreia Miranda, Gilka J. F. Gatt´as, Regina M. Fisberg and Dirce M. Marchioni Genetic Variants Involved in One-Carbon Metabolism: Polymorphism Frequencies and Differences in Homocysteine Concentrations in the Folic Acid Fortification Era Reprinted from: Nutrients 2017, 9, 539, doi: 10.3390/nu9060539 ...................142 Brinda K. Rana, Shirley W. Flatt, Dennis D. Health, Bilge Pakiz, Elizabeth L. Quintana, Loki Natarajan and Cheryl L. Rock The IL6 Gene Promoter SNP and Plasma IL-6 in Response to Diet Intervention Reprinted from: Nutrients 2017, 9, 552, doi: 10.3390/nu9060552 ...................154 Fr´ed´eric Gu´enard, Annie Bouchard-Mercier, Iwona Rudkowska, Simone Lemieux, Patrick Couture and Marie-Claude Vohl Genome-Wide Association Study of Dietary Pattern Scores Reprinted from: Nutrients 2017, 9, 649, doi: 10.3390/nu9070649 ...................159 Xingxing Song, Zongyao Li, Xinqiang Ji and Dongfeng Zhang Calcium Intake and the Risk of Ovarian Cancer: A Meta-Analysis Reprinted from: Nutrients 2017, 9, 679, doi: 10.3390/nu9070679 ...................176 Kevin B. Comerford and Gonca Pasin Gene–Dairy Food Interactions and Health Outcomes: A Review of Nutrigenetic Studies Reprinted from: Nutrients 2017, 9, 710, doi: 10.3390/nu9070710 ...................191 Janaina L. S. Donadio, Marcelo M. Rogero, Simon Cockell, John Hesketh and Silvia M. F. Cozzolino Influence of Genetic Variations in Selenoprotein Genes on the Pattern of Gene Expression after Supplementation with Brazil Nuts Reprinted from: Nutrients 2017, 9, 739, doi: 10.3390/nu9070739 ...................208 vi About the Special Issue Editor Dolores Corella, is Full Professor of Preventive Medicine and Public Health at the University of Valencia, Valencia, Spain. She has a background in Nutrition, Omics and Epidemiology. Since 1998, she has been the Director of the Genetic and Molecular Epidemiology Rresearch Unit. She focuses on the study of genetic determinants of disease and has developed research methodology for analyzing gene—environment interactions. Within In the a gene—environment interaction study, gene—diet interactions have constituted an important research line giving rise to the development of Nutritional Genomics, Nutrigenetics and Nutrigenomics. She has also been a principal investigator (PI) in the CIBER of Physiopathology of Obesity and Nutrition, a center of excellence for networking research in Spain. She has directed more than 23 PhD dissertations and has been the PI for more than 30 research projects. Currently, she is focused on omics (genomics, epigenomics, transcriptomics, metabolomics, proteomics, phenomics, etc.) integration into the field of diet, obesity, and cardiovascular-related diseases. vii viii Preface to ”Nutrigenetics” In the new era of Precision Nutrition, it is crucial to provide scientific evidence of gene–diet interactions that can result in a practical application. Although enormous progress has been made in the development of omic technologies (genomics, epigenomics, transcriptomis, metabolomics, etc.), the integration of these technologies in the nutrition field is still scarce. Therefore, more studies are needed in Nutritional Genomics to provide the evidence required for Precision Nutrition. Moreover, Nutritional Genomics is a multidisciplinary field and both studies in humans and in animal models are required. In human studies, mainly epidemiological findings related to the associations between genetic variants and disease phenotypes have been published. Large cohorts have been analyzed and genome-wide association studies (GWAs) published. However, the dietary modulation of the reported genetic associations in the GWAs studies is largely unknown. Thus, both observational and experimental gene-diet interaction studies analyzing dietary modulations in determining the genetic risk of disease are needed. In this book, relevant epidemiological studies in the nutrigenetic field are included. These chapters analyze a wide range of study designs and clinical phenotypes, as well as dietary exposures and include, among others, a general overview of the translation of nutritional genomics into nutrition practice; a review of the nutrigenetic studies on gene–dairy food interactions and health outcomes; an analysis of the role of genetic variations associated with vitamin A status and bioavailability; the study of genetic variants involved in one-carbon metabolism and their effects; a meta-analysis
Recommended publications
  • THE ROLE of HOMEODOMAIN TRANSCRIPTION FACTOR IRX5 in CARDIAC CONTRACTILITY and HYPERTROPHIC RESPONSE by © COPYRIGHT by KYOUNG H
    THE ROLE OF HOMEODOMAIN TRANSCRIPTION FACTOR IRX5 IN CARDIAC CONTRACTILITY AND HYPERTROPHIC RESPONSE By KYOUNG HAN KIM A THESIS SUBMITTED IN CONFORMITY WITH THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY GRADUATE DEPARTMENT OF PHYSIOLOGY UNIVERSITY OF TORONTO © COPYRIGHT BY KYOUNG HAN KIM (2011) THE ROLE OF HOMEODOMAIN TRANSCRIPTION FACTOR IRX5 IN CARDIAC CONTRACTILITY AND HYPERTROPHIC RESPONSE KYOUNG HAN KIM DOCTOR OF PHILOSOPHY GRADUATE DEPARTMENT OF PHYSIOLOGY UNIVERSITY OF TORONTO 2011 ABSTRACT Irx5 is a homeodomain transcription factor that negatively regulates cardiac fast transient + outward K currents (Ito,f) via the KV4.2 gene and is thereby a major determinant of the transmural repolarization gradient. While Ito,f is invariably reduced in heart disease and changes in Ito,f can modulate both cardiac contractility and hypertrophy, less is known about a functional role of Irx5, and its relationship with Ito,f, in the normal and diseased heart. Here I show that Irx5 plays crucial roles in the regulation of cardiac contractility and proper adaptive hypertrophy. Specifically, Irx5-deficient (Irx5-/-) hearts had reduced cardiac contractility and lacked the normal regional difference in excitation-contraction with decreased action potential duration, Ca2+ transients and myocyte shortening in sub-endocardial, but not sub-epicardial, myocytes. In addition, Irx5-/- mice showed less cardiac hypertrophy, but increased interstitial fibrosis and greater contractility impairment following pressure overload. A defect in hypertrophic responses in Irx5-/- myocardium was confirmed in cultured neonatal mouse ventricular myocytes, exposed to norepinephrine while being restored with Irx5 replacement. Interestingly, studies using mice ii -/- virtually lacking Ito,f (i.e. KV4.2-deficient) showed that reduced contractility in Irx5 mice was completely restored by loss of KV4.2, whereas hypertrophic responses to pressure-overload in hearts remained impaired when both Irx5 and Ito,f were absent.
    [Show full text]
  • Gene Expression Polarization
    Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression This information is current as of September 27, 2021. Fernando O. Martinez, Siamon Gordon, Massimo Locati and Alberto Mantovani J Immunol 2006; 177:7303-7311; ; doi: 10.4049/jimmunol.177.10.7303 http://www.jimmunol.org/content/177/10/7303 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2006/11/03/177.10.7303.DC1 Material http://www.jimmunol.org/ References This article cites 61 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/177/10/7303.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 27, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression1 Fernando O.
    [Show full text]
  • Novel Observations from Next-Generation RNA Sequencing of Highly Purified Human Adult and Fetal Islet Cell Subsets
    3172 Diabetes Volume 64, September 2015 David M. Blodgett,1 Anetta Nowosielska,2 Shaked Afik,3 Susanne Pechhold,1 Anthony J. Cura,1 Norman J. Kennedy,4 Soyoung Kim,2 Alper Kucukural,5 Roger J. Davis,6 Sally C. Kent,1 Dale L. Greiner,2 Manuel G. Garber,3 David M. Harlan,1 and Philip diIorio2† Novel Observations From Next-Generation RNA Sequencing of Highly Purified Human Adult and Fetal Islet Cell Subsets Diabetes 2015;64:3172–3181 | DOI: 10.2337/db15-0039 Understanding distinct gene expression patterns of blindness, kidney failure, amputation, lost work, and pre- normal adult and developing fetal human pancreatic a- mature mortality (2,3). While diabetes is easily diagnosed and b-cells is crucial for developing stem cell therapies, by simple blood glucose measurements, it ultimately islet regeneration strategies, and therapies designed to results from a loss of functional b-cell mass. We need increase b-cell function in patients with diabetes (type 1 to better understand the molecular mediators driving or 2). Toward that end, we have developed methods to that loss and limited b-cell regeneration capacity (4,5). highly purify a-, b-, and d-cells from human fetal and This knowledge gap exists because it has not previously adult pancreata by intracellular staining for the cell- been possible to study homogeneous, highly enriched en- specific hormone content, sorting the subpopulations docrine cell populations from human islets. Recent stud- by flow cytometry, and, using next-generation RNA se- ies have reported expression profiles on whole islets (6) quencing, we report the detailed transcriptomes of fetal and individual cell types using techniques like laser cap- and adult a- and b-cells.
    [Show full text]
  • Prospective Isolation of NKX2-1–Expressing Human Lung Progenitors Derived from Pluripotent Stem Cells
    The Journal of Clinical Investigation RESEARCH ARTICLE Prospective isolation of NKX2-1–expressing human lung progenitors derived from pluripotent stem cells Finn Hawkins,1,2 Philipp Kramer,3 Anjali Jacob,1,2 Ian Driver,4 Dylan C. Thomas,1 Katherine B. McCauley,1,2 Nicholas Skvir,1 Ana M. Crane,3 Anita A. Kurmann,1,5 Anthony N. Hollenberg,5 Sinead Nguyen,1 Brandon G. Wong,6 Ahmad S. Khalil,6,7 Sarah X.L. Huang,3,8 Susan Guttentag,9 Jason R. Rock,4 John M. Shannon,10 Brian R. Davis,3 and Darrell N. Kotton1,2 2 1Center for Regenerative Medicine, and The Pulmonary Center and Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA. 3Center for Stem Cell and Regenerative Medicine, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center, Houston, Texas, USA. 4Department of Anatomy, UCSF, San Francisco, California, USA. 5Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA. 6Department of Biomedical Engineering and Biological Design Center, Boston University, Boston, Massachusetts, USA. 7Wyss Institute for Biologically Inspired Engineering, Harvard University, Boston, Massachusetts, USA. 8Columbia Center for Translational Immunology & Columbia Center for Human Development, Columbia University Medical Center, New York, New York, USA. 9Department of Pediatrics, Monroe Carell Jr. Children’s Hospital, Vanderbilt University, Nashville, Tennessee, USA. 10Division of Pulmonary Biology, Cincinnati Children’s Hospital, Cincinnati, Ohio, USA. It has been postulated that during human fetal development, all cells of the lung epithelium derive from embryonic, endodermal, NK2 homeobox 1–expressing (NKX2-1+) precursor cells.
    [Show full text]
  • Overlap of Vitamin a and Vitamin D Target Genes with CAKUT- Related Processes [Version 1; Peer Review: 1 Approved with Reservations]
    F1000Research 2021, 10:395 Last updated: 21 JUL 2021 BRIEF REPORT Overlap of vitamin A and vitamin D target genes with CAKUT- related processes [version 1; peer review: 1 approved with reservations] Ozan Ozisik1, Friederike Ehrhart 2,3, Chris T Evelo 2, Alberto Mantovani4, Anaı̈s Baudot 1,5 1Aix Marseille University, Inserm, MMG, Marseille, 13385, France 2Department of Bioinformatics - BiGCaT, Maastricht University, Maastricht, 6200 MD, The Netherlands 3Department of Bioinformatics, NUTRIM/MHeNs, Maastricht University, Maastricht, 6200 MD, The Netherlands 4Istituto Superiore di Sanità, Rome, 00161, Italy 5Barcelona Supercomputing Center (BSC), Barcelona, 08034, Spain v1 First published: 18 May 2021, 10:395 Open Peer Review https://doi.org/10.12688/f1000research.51018.1 Latest published: 18 May 2021, 10:395 https://doi.org/10.12688/f1000research.51018.1 Reviewer Status Invited Reviewers Abstract Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) are a 1 group of abnormalities affecting the kidneys and their outflow tracts, which include the ureters, the bladder, and the urethra. CAKUT version 1 patients display a large clinical variability as well as a complex 18 May 2021 report aetiology, as only 5% to 20% of the cases have a monogenic origin. It is thereby suspected that interactions of both genetic and 1. Elena Menegola, Università degli Studi di environmental factors contribute to the disease. Vitamins are among the environmental factors that are considered for CAKUT aetiology. In Milano, Milan, Italy this study, we collected vitamin A and vitamin D target genes and Any reports and responses or comments on the computed their overlap with CAKUT-related gene sets.
    [Show full text]
  • Downloaded from GEO
    bioRxiv preprint doi: https://doi.org/10.1101/2020.08.17.252007; this version posted November 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Oxylipin metabolism is controlled by mitochondrial b-oxidation during bacterial inflammation. Mariya Misheva1, Konstantinos Kotzamanis1*, Luke C Davies1*, Victoria J Tyrrell1, Patricia R S Rodrigues1, Gloria A Benavides2, Christine Hinz1, Robert C Murphy3, Paul Kennedy4, Philip R Taylor1,5, Marcela Rosas1, Simon A Jones1, Sumukh Deshpande1, Robert Andrews1, Magdalena A Czubala1, Mark Gurney1, Maceler Aldrovandi1, Sven W Meckelmann1, Peter Ghazal1, Victor Darley-Usmar2, Daniel White1, and Valerie B O’Donnell1 1Systems Immunity Research Institute and Division of Infection and Immunity, and School of Medicine, Cardiff University, UK, 2Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA, 3Department of Pharmacology, University of Colorado Denver, Aurora, CO 80045, USA, 4Cayman Chemical 1180 E Ellsworth Rd, Ann Arbor, MI 48108, United States, 5UK Dementia Research Institute at Cardiff, Cardiff University, UK Address correspondence: Valerie O’Donnell, [email protected] or Daniel White, [email protected], Systems Immunity Research Institute, Cardiff University *Both authors contributed equally to the study 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.17.252007; this version posted November 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [Show full text]
  • Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
    Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897
    [Show full text]
  • Amplitude Modulation of Androgen Signaling by C-MYC
    Downloaded from genesdev.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Amplitude modulation of androgen signaling by c-MYC Min Ni,1,2 Yiwen Chen,3,4 Teng Fei,1,2 Dan Li,1,2 Elgene Lim,1,2 X. Shirley Liu,3,4,5 and Myles Brown1,2,5 1Division of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; 2Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA; 3Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA; 4Harvard School of Public Health, Boston, Massachusetts 02215, USA Androgen-stimulated growth of the molecular apocrine breast cancer subtype is mediated by an androgen receptor (AR)-regulated transcriptional program. However, the molecular details of this AR-centered regulatory network and the roles of other transcription factors that cooperate with AR in the network remain elusive. Here we report a positive feed-forward loop that enhances breast cancer growth involving AR, AR coregulators, and downstream target genes. In the absence of an androgen signal, TCF7L2 interacts with FOXA1 at AR-binding sites and represses the basal expression of AR target genes, including MYC. Direct AR regulation of MYC cooperates with AR-mediated activation of HER2/HER3 signaling. HER2/HER3 signaling increases the transcriptional activity of MYC through phosphorylation of MAD1, leading to increased levels of MYC/MAX heterodimers. MYC in turn reinforces the transcriptional activation of androgen-responsive genes. These results reveal a novel regulatory network in molecular apocrine breast cancers regulated by androgen and AR in which MYC plays a central role as both a key target and a cooperating transcription factor to drive oncogenic growth.
    [Show full text]
  • An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Netwo
    Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis Sriram Devanathan Washington University School of Medicine in St. Louis Timothy Whitehead Washington University School of Medicine in St. Louis George G. Schweitzer Washington University School of Medicine in St. Louis Nicole Fettig Washington University School of Medicine in St. Louis Attila Kovacs Washington University School of Medicine in St. Louis See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Devanathan, Sriram; Whitehead, Timothy; Schweitzer, George G.; Fettig, Nicole; Kovacs, Attila; Korach, Kenneth S.; Finck, Brian N.; and Shoghi, Kooresh I., ,"An animal model with a cardiomyocyte-specific deletion of estrogen receptor alpha: Functional, metabolic, and differential network analysis." PLoS One.9,7. e101900. (2014). https://digitalcommons.wustl.edu/open_access_pubs/3326 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Sriram Devanathan, Timothy Whitehead, George G. Schweitzer, Nicole Fettig, Attila Kovacs, Kenneth S. Korach, Brian N. Finck, and Kooresh I. Shoghi This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/3326 An Animal Model with a Cardiomyocyte-Specific Deletion of Estrogen Receptor Alpha: Functional, Metabolic, and Differential Network Analysis Sriram Devanathan1, Timothy Whitehead1, George G. Schweitzer2, Nicole Fettig1, Attila Kovacs3, Kenneth S.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Supplemental Materials ZNF281 Enhances Cardiac Reprogramming
    Supplemental Materials ZNF281 enhances cardiac reprogramming by modulating cardiac and inflammatory gene expression Huanyu Zhou, Maria Gabriela Morales, Hisayuki Hashimoto, Matthew E. Dickson, Kunhua Song, Wenduo Ye, Min S. Kim, Hanspeter Niederstrasser, Zhaoning Wang, Beibei Chen, Bruce A. Posner, Rhonda Bassel-Duby and Eric N. Olson Supplemental Table 1; related to Figure 1. Supplemental Table 2; related to Figure 1. Supplemental Table 3; related to the “quantitative mRNA measurement” in Materials and Methods section. Supplemental Table 4; related to the “ChIP-seq, gene ontology and pathway analysis” and “RNA-seq” and gene ontology analysis” in Materials and Methods section. Supplemental Figure S1; related to Figure 1. Supplemental Figure S2; related to Figure 2. Supplemental Figure S3; related to Figure 3. Supplemental Figure S4; related to Figure 4. Supplemental Figure S5; related to Figure 6. Supplemental Table S1. Genes included in human retroviral ORF cDNA library. Gene Gene Gene Gene Gene Gene Gene Gene Symbol Symbol Symbol Symbol Symbol Symbol Symbol Symbol AATF BMP8A CEBPE CTNNB1 ESR2 GDF3 HOXA5 IL17D ADIPOQ BRPF1 CEBPG CUX1 ESRRA GDF6 HOXA6 IL17F ADNP BRPF3 CERS1 CX3CL1 ETS1 GIN1 HOXA7 IL18 AEBP1 BUD31 CERS2 CXCL10 ETS2 GLIS3 HOXB1 IL19 AFF4 C17ORF77 CERS4 CXCL11 ETV3 GMEB1 HOXB13 IL1A AHR C1QTNF4 CFL2 CXCL12 ETV7 GPBP1 HOXB5 IL1B AIMP1 C21ORF66 CHIA CXCL13 FAM3B GPER HOXB6 IL1F3 ALS2CR8 CBFA2T2 CIR1 CXCL14 FAM3D GPI HOXB7 IL1F5 ALX1 CBFA2T3 CITED1 CXCL16 FASLG GREM1 HOXB9 IL1F6 ARGFX CBFB CITED2 CXCL3 FBLN1 GREM2 HOXC4 IL1F7
    [Show full text]
  • Genome-Wide DNA Methylation Analysis of KRAS Mutant Cell Lines Ben Yi Tew1,5, Joel K
    www.nature.com/scientificreports OPEN Genome-wide DNA methylation analysis of KRAS mutant cell lines Ben Yi Tew1,5, Joel K. Durand2,5, Kirsten L. Bryant2, Tikvah K. Hayes2, Sen Peng3, Nhan L. Tran4, Gerald C. Gooden1, David N. Buckley1, Channing J. Der2, Albert S. Baldwin2 ✉ & Bodour Salhia1 ✉ Oncogenic RAS mutations are associated with DNA methylation changes that alter gene expression to drive cancer. Recent studies suggest that DNA methylation changes may be stochastic in nature, while other groups propose distinct signaling pathways responsible for aberrant methylation. Better understanding of DNA methylation events associated with oncogenic KRAS expression could enhance therapeutic approaches. Here we analyzed the basal CpG methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly similar methylation patterns. KRAS knockdown resulted in unique methylation changes with limited overlap between each cell line. In KRAS-mutant Pa16C pancreatic cancer cells, while KRAS knockdown resulted in over 8,000 diferentially methylated (DM) CpGs, treatment with the ERK1/2-selective inhibitor SCH772984 showed less than 40 DM CpGs, suggesting that ERK is not a broadly active driver of KRAS-associated DNA methylation. KRAS G12V overexpression in an isogenic lung model reveals >50,600 DM CpGs compared to non-transformed controls. In lung and pancreatic cells, gene ontology analyses of DM promoters show an enrichment for genes involved in diferentiation and development. Taken all together, KRAS-mediated DNA methylation are stochastic and independent of canonical downstream efector signaling. These epigenetically altered genes associated with KRAS expression could represent potential therapeutic targets in KRAS-driven cancer. Activating KRAS mutations can be found in nearly 25 percent of all cancers1.
    [Show full text]