Enhancer-Derived Noncoding RNA in the Regulation of Gnrh1 Gene Expression
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Rule Mining on Microrna Expression Profiles For
Faculty of Engineering and Information Technology University of Technology, Sydney Rule Mining on MicroRNA Expression Profiles for Human Disease Understanding A thesis submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy by Renhua Song July 2016 CERTIFICATE OF AUTHORSHIP/ORIGINALITY I certify that the work in this thesis has not previously been submitted for a degree nor has it been submitted as part of requirements for a degree except as fully acknowledged within the text. I also certify that the thesis has been written by me. Any help that I have received in my research work and the preparation of the thesis itself has been acknowledged. In addition, I certify that all information sources and literature used are indicated in the thesis. Signature of Candidate i Acknowledgments First, and foremost, I would like to express my gratitude to my chief supervisor, Assoc. Prof. Jinyan Li, and to my co-supervisors Assoc. Prof. Paul Kennedy and Assoc. Prof. Daniel Catchpoole. I am extremely grateful for all the advice and guidance so unselfishly given to me over the last three and half years by these three distinguished academics. This research would not have been possible without their high order supervision, support, assistance and leadership. The wonderful support and assistance provided by many people during this research is very much appreciated by me and my family. I am very grateful for the help that I received from all of these people but there are some special individuals that I must thank by name. A very sincere thank you is definitely owed to my loving husband Jing Liu, not only for his tremendous support during the last three and half years, but also his unfailing and often sorely tested patience. -
Exploring Prostate Cancer Genome Reveals Simultaneous Losses of PTEN, FAS and PAPSS2 in Patients with PSA Recurrence After Radical Prostatectomy
Int. J. Mol. Sci. 2015, 16, 3856-3869; doi:10.3390/ijms16023856 OPEN ACCESS International Journal of Molecular Sciences ISSN 1422-0067 www.mdpi.com/journal/ijms Article Exploring Prostate Cancer Genome Reveals Simultaneous Losses of PTEN, FAS and PAPSS2 in Patients with PSA Recurrence after Radical Prostatectomy Chinyere Ibeawuchi 1, Hartmut Schmidt 2, Reinhard Voss 3, Ulf Titze 4, Mahmoud Abbas 5, Joerg Neumann 6, Elke Eltze 7, Agnes Marije Hoogland 8, Guido Jenster 9, Burkhard Brandt 10 and Axel Semjonow 1,* 1 Prostate Center, Department of Urology, University Hospital Muenster, Albert-Schweitzer-Campus 1, Gebaeude 1A, Muenster D-48149, Germany; E-Mail: [email protected] 2 Center for Laboratory Medicine, University Hospital Muenster, Albert-Schweitzer-Campus 1, Gebaeude 1A, Muenster D-48149, Germany; E-Mail: [email protected] 3 Interdisciplinary Center for Clinical Research, University of Muenster, Albert-Schweitzer-Campus 1, Gebaeude D3, Domagkstrasse 3, Muenster D-48149, Germany; E-Mail: [email protected] 4 Pathology, Lippe Hospital Detmold, Röntgenstrasse 18, Detmold D-32756, Germany; E-Mail: [email protected] 5 Institute of Pathology, Mathias-Spital-Rheine, Frankenburg Street 31, Rheine D-48431, Germany; E-Mail: [email protected] 6 Institute of Pathology, Klinikum Osnabrueck, Am Finkenhuegel 1, Osnabrueck D-49076, Germany; E-Mail: [email protected] 7 Institute of Pathology, Saarbrücken-Rastpfuhl, Rheinstrasse 2, Saarbrücken D-66113, Germany; E-Mail: [email protected] 8 Department -
Modulating Hallmarks of Cholangiocarcinoma
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Fall 12-14-2018 Modulating Hallmarks of Cholangiocarcinoma Cody Wehrkamp University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Molecular Biology Commons Recommended Citation Wehrkamp, Cody, "Modulating Hallmarks of Cholangiocarcinoma" (2018). Theses & Dissertations. 337. https://digitalcommons.unmc.edu/etd/337 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. MODULATING HALLMARKS OF CHOLANGIOCARCINOMA by Cody J. Wehrkamp A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor Justin L. Mott University of Nebraska Medical Center Omaha, Nebraska November 2018 Supervisory Committee: Kaustubh Datta, Ph.D. Melissa Teoh‐Fitzgerald, Ph.D. Richard G. MacDonald, Ph.D. Acknowledgements This endeavor has led to scientific as well as personal growth for me. I am indebted to many for their knowledge, influence, and support along the way. To my mentor, Dr. Justin L. Mott, you have been an incomparable teacher and invaluable guide. You upheld for me the concept that science is intrepid, even when the experience is trying. Through my training, and now here at the end, I can say that it has been an honor to be your protégé. When you have shaped your future graduates to be and do great, I will be privileged to say that I was your first one. -
Molecular Effects of Isoflavone Supplementation Human Intervention Studies and Quantitative Models for Risk Assessment
Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis committee Promotors Prof. Dr Pieter van ‘t Veer Professor of Nutritional Epidemiology Wageningen University Prof. Dr Evert G. Schouten Emeritus Professor of Epidemiology and Prevention Wageningen University Co-promotors Dr Anouk Geelen Assistant professor, Division of Human Nutrition Wageningen University Dr Lydia A. Afman Assistant professor, Division of Human Nutrition Wageningen University Other members Prof. Dr Jaap Keijer, Wageningen University Dr Hubert P.J.M. Noteborn, Netherlands Food en Consumer Product Safety Authority Prof. Dr Yvonne T. van der Schouw, UMC Utrecht Dr Wendy L. Hall, King’s College London This research was conducted under the auspices of the Graduate School VLAG (Advanced studies in Food Technology, Agrobiotechnology, Nutrition and Health Sciences). Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis submitted in fulfilment of the requirements for the degree of doctor at Wageningen University by the authority of the Rector Magnificus Prof. Dr M.J. Kropff, in the presence of the Thesis Committee appointed by the Academic Board to be defended in public on Friday 20 June 2014 at 13.30 p.m. in the Aula. Vera van der Velpen Molecular effects of isoflavone supplementation: Human intervention studies and quantitative models for risk assessment 154 pages PhD thesis, Wageningen University, Wageningen, NL (2014) With references, with summaries in Dutch and English ISBN: 978-94-6173-952-0 ABSTRact Background: Risk assessment can potentially be improved by closely linked experiments in the disciplines of epidemiology and toxicology. -
Variation in Protein Coding Genes Identifies Information
bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. 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-NC-ND 4.0 International license. Animal complexity and information flow 1 1 2 3 4 5 Variation in protein coding genes identifies information flow as a contributor to 6 animal complexity 7 8 Jack Dean, Daniela Lopes Cardoso and Colin Sharpe* 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Institute of Biological and Biomedical Sciences 25 School of Biological Science 26 University of Portsmouth, 27 Portsmouth, UK 28 PO16 7YH 29 30 * Author for correspondence 31 [email protected] 32 33 Orcid numbers: 34 DLC: 0000-0003-2683-1745 35 CS: 0000-0002-5022-0840 36 37 38 39 40 41 42 43 44 45 46 47 48 49 Abstract bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. 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-NC-ND 4.0 International license. Animal complexity and information flow 2 1 Across the metazoans there is a trend towards greater organismal complexity. How 2 complexity is generated, however, is uncertain. Since C.elegans and humans have 3 approximately the same number of genes, the explanation will depend on how genes are 4 used, rather than their absolute number. -
The KCTD Family of Proteins: Structure, Function, Disease Relevance Zhepeng Liu1†, Yaqian Xiang2† and Guihong Sun1*
Liu et al. Cell & Bioscience 2013, 3:45 http://www.cellandbioscience.com/content/3/1/45 Cell & Bioscience REVIEW Open Access The KCTD family of proteins: structure, function, disease relevance Zhepeng Liu1†, Yaqian Xiang2† and Guihong Sun1* Abstract The family of potassium channel tetramerizationdomain (KCTD) proteins consists of 26 members with mostly unknown functions. The name of the protein family is due to the sequence similarity between the conserved N-terminal region of KCTD proteins and the tetramerization domain in some voltage-gated potassium channels. Dozens of publications suggest that KCTD proteins have roles in various biological processes and diseases. In this review, we summarize the character of Bric-a-brack,Tram-track, Broad complex(BTB) of KCTD proteins, their roles in the ubiquitination pathway, and the roles of KCTD mutants in diseases. Furthermore, we review potential downstream signaling pathways and discuss future studies that should be performed. Keywords: KCTD, BTB domain, Adaptor Introduction BTB domain and homology between KCTD family members The human potassium (K+) channel tetramerization The human genome includes approximately 400 BTB domain (KCTD)family of proteins consists of 26 mem- domain-containing proteins. The BTB domain is a highly bers that share sequence similarity with the cytoplasmic conserved motif of about 100 amino acids and can be + domain of voltage-gated K channels(Kv channels) [1-3]. found at the N-terminusof C2H2-type zinc-finger tran- The KCTD proteins have relatively conserved N-terminal scription factors and in some actin-binding proteins [11]. domains and variable C-termini. Comparative analyses of BTB domain-containing proteins include transcription the conserved N-terminal sequence suggest the presence factors, oncogenic proteins, ion channel proteins, and of a common Bric-a-brack,Tram-track, Broad complex KCTD proteins [2,12-14]. -
Genomic and Functional Profiling of Duplicated Chromosome
Human Molecular Genetics, 2006, Vol. 15, No. 6 853–869 doi:10.1093/hmg/ddl004 Advance Access published on January 30, 2006 Genomic and functional profiling of duplicated chromosome 15 cell lines reveal regulatory alterations in UBE3A-associated ubiquitin–proteasome pathway processes Colin A. Baron1, Clifford G. Tepper2, Stephenie Y. Liu1, Ryan R. Davis1, Nicholas J. Wang3, N. Carolyn Schanen4 and Jeffrey P. Gregg1,* 1Department of Pathology and 2Department of Biochemistry and Molecular Medicine, University of California, Davis School of Medicine, Sacramento, CA 95817, USA, 3Department of Human Genetics, University of 4 California–Los Angeles, Los Angeles, CA, USA and Center for Pediatric Research, Nemours Biomedical Research, Downloaded from Alfred I. duPont Hospital for Children, Wilmington, DE, USA Received November 21, 2005; Revised and Accepted January 25, 2006 Autism is a complex neurodevelopmental disorder having both genetic and epigenetic etiological elements. hmg.oxfordjournals.org Isodicentric chromosome 15 (Idic15), characterized by duplications of the multi-disorder critical region of 15q11–q14, is a relatively common cytogenetic event. When the duplication involves maternally derived con- tent, this abnormality is strongly correlated with autism disorder. However, the mechanistic links between Idic15 and autism are ill-defined. To gain insight into the potential role of these duplications, we performed a comprehensive, genomics-based characterization of an in vitro model system consisting of lymphoblast cell lines derived from individuals with both autism and Idic15. Array-based comparative genomic hybridiz- ation using commercial single nucleotide polymorphism arrays was conducted and found to be capable of by guest on December 17, 2010 sub-classifying Idic15 samples by virtue of the lengths of the duplicated chromosomal region. -
Genomic and Transcriptomic Investigations Into the Feed Efficiency Phenotype of Beef Cattle
Provided by the author(s) and NUI Galway in accordance with publisher policies. Please cite the published version when available. Title Genomic and transcriptomic investigations into the feed efficiency phenotype of beef cattle Author(s) Higgins, Marc Publication Date 2019-03-06 Publisher NUI Galway Item record http://hdl.handle.net/10379/15008 Downloaded 2021-09-25T18:07:39Z Some rights reserved. For more information, please see the item record link above. Genomic and Transcriptomic Investigations into the Feed Efficiency Phenotype of Beef Cattle Marc Higgins, B.Sc., M.Sc. A thesis submitted for the Degree of Doctor of Philosophy to the Discipline of Biochemistry, School of Natural Sciences, National University of Ireland, Galway. Supervisor: Dr. Derek Morris Discipline of Biochemistry, School of Natural Sciences, National University of Ireland, Galway. Supervisor: Dr. Sinéad Waters Teagasc, Animal and Bioscience Research Department, Animal & Grassland Research and Innovation Centre, Teagasc, Grange. Submitted November 2018 Table of Contents Declaration ................................................................................................................ vii Funding .................................................................................................................... viii Acknowledgements .................................................................................................... ix Abstract ...................................................................................................................... -
Gene Expression Profiles Reveal Alternative Targets of Therapeutic Intervention for the Treatment of Drug-Resistant Non-Small Cell Lung Cancers
University of Kentucky UKnowledge Theses and Dissertations--Pharmacy College of Pharmacy 2017 GENE EXPRESSION PROFILES REVEAL ALTERNATIVE TARGETS OF THERAPEUTIC INTERVENTION FOR THE TREATMENT OF DRUG-RESISTANT NON-SMALL CELL LUNG CANCERS Madeline J. Krentz Gober University of Kentucky, [email protected] Author ORCID Identifier: https://orcid.org/0000-0001-7761-6741 Digital Object Identifier: https://doi.org/10.13023/ETD.2017.309 Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Krentz Gober, Madeline J., "GENE EXPRESSION PROFILES REVEAL ALTERNATIVE TARGETS OF THERAPEUTIC INTERVENTION FOR THE TREATMENT OF DRUG-RESISTANT NON-SMALL CELL LUNG CANCERS" (2017). Theses and Dissertations--Pharmacy. 78. https://uknowledge.uky.edu/pharmacy_etds/78 This Doctoral Dissertation is brought to you for free and open access by the College of Pharmacy at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Pharmacy by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. -
Analyses of Long-Term Fine Particulate Air Pollution Exposure, Genetic Variants, and Blood DNA Methylation Age in the Elderly
On Aging: Analyses of Long-Term Fine Particulate Air Pollution Exposure, Genetic Variants, and Blood DNA Methylation Age in the Elderly The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:40050003 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA On Aging: Analyses of Long-term Fine Particulate Air Pollution Exposure, Genetic Variants, and Blood DNA Methylation Age in the Elderly A dissertation presented by Jamaji Chilaka Nwanaji-Enwerem to The Committee on Higher Degrees in Biological Sciences in Public Health in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Biological Sciences in Public Health Harvard University Cambridge, Massachusetts November, 2017 © 2017 Jamaji Chilaka Nwanaji-Enwerem All rights reserved. Dissertation Advisors: Andrea A. Baccarelli, MD, PhD Jamaji Chilaka Nwanaji-Enwerem & Marc G. Weisskopf, PhD, ScD On Aging: Analyses of Long-term Fine Particulate Air Pollution Exposure, Genetic Variants, and Blood DNA Methylation Age in the Elderly Abstract Human aging is often accompanied by the development of chronic disease. Research has identified molecular processes that are shared by aging-related diseases, and it is widely believed that pre- clinical changes in these aging-related molecular processes (i.e. measures of “biological age”) may be more informative of morbidity and mortality risks than simple chronological age. -
Downloaded, Each with Over 20 Samples for AD-Specific Pathways, Biological Processes, and Driver Each Specific Brain Region in Each Condition
Xiang et al. BMC Medical Genomics 2018, 11(Suppl 6):115 https://doi.org/10.1186/s12920-018-0431-1 RESEARCH Open Access Condition-specific gene co-expression network mining identifies key pathways and regulators in the brain tissue of Alzheimer’s disease patients Shunian Xiang1,2, Zhi Huang4, Wang Tianfu1, Zhi Han3, Christina Y. Yu3,5, Dong Ni1*, Kun Huang3* and Jie Zhang2* From 29th International Conference on Genome Informatics Yunnan, China. 3-5 December 2018 Abstract Background: Gene co-expression network (GCN) mining is a systematic approach to efficiently identify novel disease pathways, predict novel gene functions and search for potential disease biomarkers. However, few studies have systematically identified GCNs in multiple brain transcriptomic data of Alzheimer’s disease (AD) patients and looked for their specific functions. Methods: In this study, we first mined GCN modules from AD and normal brain samples in multiple datasets respectively; then identified gene modules that are specific to AD or normal samples; lastly, condition-specific modules with similar functional enrichments were merged and enriched differentially expressed upstream transcription factors were further examined for the AD/normal-specific modules. Results: We obtained 30 AD-specific modules which showed gain of correlation in AD samples and 31 normal- specific modules with loss of correlation in AD samples compared to normal ones, using the network mining tool lmQCM. Functional and pathway enrichment analysis not only confirmed known gene functional categories related to AD, but also identified novel regulatory factors and pathways. Remarkably, pathway analysis suggested that a variety of viral, bacteria, and parasitic infection pathways are activated in AD samples. -
Variation in Protein Coding Genes Identifies Information Flow
bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. 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-NC-ND 4.0 International license. Animal complexity and information flow 1 1 2 3 4 5 Variation in protein coding genes identifies information flow as a contributor to 6 animal complexity 7 8 Jack Dean, Daniela Lopes Cardoso and Colin Sharpe* 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Institute of Biological and Biomedical Sciences 25 School of Biological Science 26 University of Portsmouth, 27 Portsmouth, UK 28 PO16 7YH 29 30 * Author for correspondence 31 [email protected] 32 33 Orcid numbers: 34 DLC: 0000-0003-2683-1745 35 CS: 0000-0002-5022-0840 36 37 38 39 40 41 42 43 44 45 46 47 48 49 Abstract bioRxiv preprint doi: https://doi.org/10.1101/679456; this version posted June 21, 2019. 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-NC-ND 4.0 International license. Animal complexity and information flow 2 1 Across the metazoans there is a trend towards greater organismal complexity. How 2 complexity is generated, however, is uncertain. Since C.elegans and humans have 3 approximately the same number of genes, the explanation will depend on how genes are 4 used, rather than their absolute number.