Mouse Stab1 Conditional Knockout Project (CRISPR/Cas9)
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Environmental Influences on Endothelial Gene Expression
ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community. -
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, -
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. -
Transcriptional Recapitulation and Subversion Of
Open Access Research2007KaiseretVolume al. 8, Issue 7, Article R131 Transcriptional recapitulation and subversion of embryonic colon comment development by mouse colon tumor models and human colon cancer Sergio Kaiser¤*, Young-Kyu Park¤†, Jeffrey L Franklin†, Richard B Halberg‡, Ming Yu§, Walter J Jessen*, Johannes Freudenberg*, Xiaodi Chen‡, Kevin Haigis¶, Anil G Jegga*, Sue Kong*, Bhuvaneswari Sakthivel*, Huan Xu*, Timothy Reichling¥, Mohammad Azhar#, Gregory P Boivin**, reviews Reade B Roberts§, Anika C Bissahoyo§, Fausto Gonzales††, Greg C Bloom††, Steven Eschrich††, Scott L Carter‡‡, Jeremy E Aronow*, John Kleimeyer*, Michael Kleimeyer*, Vivek Ramaswamy*, Stephen H Settle†, Braden Boone†, Shawn Levy†, Jonathan M Graff§§, Thomas Doetschman#, Joanna Groden¥, William F Dove‡, David W Threadgill§, Timothy J Yeatman††, reports Robert J Coffey Jr† and Bruce J Aronow* Addresses: *Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. †Departments of Medicine, and Cell and Developmental Biology, Vanderbilt University and Department of Veterans Affairs Medical Center, Nashville, TN 37232, USA. ‡McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, WI 53706, USA. §Department of Genetics and Lineberger Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA. ¶Molecular Pathology Unit and Center for Cancer Research, Massachusetts deposited research General Hospital, Charlestown, MA 02129, USA. ¥Division of Human Cancer Genetics, The Ohio State University College of Medicine, Columbus, Ohio 43210-2207, USA. #Institute for Collaborative BioResearch, University of Arizona, Tucson, AZ 85721-0036, USA. **University of Cincinnati, Department of Pathology and Laboratory Medicine, Cincinnati, OH 45267, USA. ††H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA. ‡‡Children's Hospital Informatics Program at the Harvard-MIT Division of Health Sciences and Technology (CHIP@HST), Harvard Medical School, Boston, Massachusetts 02115, USA. -
Gene Expression in Blood Reflects Smoking Exposure Among Cancer
www.nature.com/scientificreports OPEN Gene expression in blood refects smoking exposure among cancer‑free women in the Norwegian Women and Cancer (NOWAC) postgenome cohort Nikita Baiju1*, Torkjel M. Sandanger1, Pål Sætrom2,3,4,5 & Therese H. Nøst1,5 Active smoking has been linked to modulated gene expression in blood. However, there is a need for a more thorough understanding of how quantitative measures of smoking exposure relate to diferentially expressed genes (DEGs) in whole‑blood among ever smokers. This study analysed microarray‑based gene expression profles from whole‑blood samples according to smoking status and quantitative measures of smoking exposure among cancer‑free women (n = 1708) in the Norwegian Women and Cancer postgenome cohort. When compared with never smokers and former smokers, current smokers had 911 and 1082 DEGs, respectively and their biological functions could indicate systemic impacts of smoking. LRRN3 was associated with smoking status with the lowest FDR‑adjusted p‑value. When never smokers and all former smokers were compared, no DEGs were observed, but LRRN3 was diferentially expressed when never smokers were compared with former smokers who quit smoking ≤ 10 years ago. Further, LRRN3 was positively associated with smoking intensity, pack‑years, and comprehensive smoking index score among current smokers; and negatively associated with time since cessation among former smokers. Consequently, LRRN3 expression in whole‑blood is a molecular signal of smoking exposure that could supplant self‑reported smoking data in further research targeting blood‑based markers related to the health efects of smoking. Tobacco smoking is one of the major threats to public health, and it is currently responsible for more than 8 million deaths worldwide each year 1. -
Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands That Promote Axonal Growth
Research Article: New Research Development Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands that Promote Axonal Growth Jeremy S. Toma,1 Konstantina Karamboulas,1,ª Matthew J. Carr,1,2,ª Adelaida Kolaj,1,3 Scott A. Yuzwa,1 Neemat Mahmud,1,3 Mekayla A. Storer,1 David R. Kaplan,1,2,4 and Freda D. Miller1,2,3,4 https://doi.org/10.1523/ENEURO.0066-20.2020 1Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada, 2Institute of Medical Sciences University of Toronto, Toronto, Ontario M5G 1A8, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario M5G 1A8, Canada, and 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada Abstract Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are es- sential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, in- cluding known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesen- chymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons. -
Primepcr™Assay Validation Report
PrimePCR™Assay Validation Report Gene Information Gene Name stabilin 1 Gene Symbol STAB1 Organism Human Gene Summary This gene encodes a large transmembrane receptor protein which may function in angiogenesis lymphocyte homing cell adhesion or receptor scavenging. The protein contains 7 fasciclin 16 epidermal growth factor (EGF)-like and 2 laminin-type EGF-like domains as well as a C-type lectin-like hyaluronan-binding Link module. The protein is primarily expressed on sinusoidal endothelial cells of liver spleen and lymph node. The receptor has been shown to endocytose ligands such as low density lipoprotein Gram-positive and Gram-negative bacteria and advanced glycosylation end products. Supporting its possible role as a scavenger receptor the protein rapidly cycles between the plasma membrane and early endosomes. Gene Aliases CLEVER-1, FEEL-1, FELE-1, FEX1, KIAA0246, STAB-1 RefSeq Accession No. NC_000003.11, NT_022517.18 UniGene ID Hs.301989 Ensembl Gene ID ENSG00000010327 Entrez Gene ID 23166 Assay Information Unique Assay ID qHsaCEP0025089 Assay Type Probe - Validation information is for the primer pair using SYBR® Green detection Detected Coding Transcript(s) ENST00000321725 Amplicon Context Sequence TGCCCACCCTGTGGTTTTCCCTGTGGCGGACTGTGGCAATGGTCGGGTGGGCA TAGTCAGCCTGGGTGCCCGCAAGAACCTCTCAGAACGCTGGGATGCCTACTGCT TCCGTGTGCAAGAT Amplicon Length (bp) 90 Chromosome Location 3:52556838-52557042 Assay Design Exonic Purification Desalted Validation Results Efficiency (%) 100 R2 0.9992 cDNA Cq 26.69 Page 1/5 PrimePCR™Assay Validation Report cDNA -
Chromosome Transfer Induced Aneuploidy Results in Complex Dysregulation of the Cellular Transcriptome in Immortalized and Cancer Cells
[CANCER RESEARCH 64, 6941–6949, October 1, 2004] Chromosome Transfer Induced Aneuploidy Results in Complex Dysregulation of the Cellular Transcriptome in Immortalized and Cancer Cells Madhvi B. Upender,1 Jens K. Habermann,1,4 Lisa M. McShane,3 Edward L. Korn,3 J. Carl Barrett,2 Michael J. Difilippantonio,1 and Thomas Ried1 1Genetics Branch and 2Laboratory for Biosystems and Cancer, Center for Cancer Research and 3Biometric Research Branch, National Cancer Institute/NIH, Bethesda, Maryland; and 4Department of Oncology and Pathology, Cancer Center Karolinska, Karolinska Institute, Stockholm, Sweden ABSTRACT tumor cells (4, 18–20). Additionally, in cell culture model systems in which cells are exposed to different carcinogens, chromosomal ane- Chromosomal aneuploidies are observed in essentially all sporadic uploidy is the earliest detectable genomic aberration (21, 22). carcinomas. These aneuploidies result in tumor-specific patterns of The conservation of these tumor and tumor-stage–specific patterns genomic imbalances that are acquired early during tumorigenesis, con- tinuously selected for and faithfully maintained in cancer cells. Although of chromosomal aneuploidies suggests that they play a fundamental the paradigm of translocation induced oncogene activation in hematologic biological role in tumorigenesis. It remains, however, unresolved how malignancies is firmly established, it is not known how genomic imbal- such genomic imbalances affect global gene expression patterns. One ances affect chromosome-specific gene expression patterns in particular could postulate that expression levels of all transcriptionally active and how chromosomal aneuploidy dysregulates the genetic equilibrium of genes on trisomic chromosomes would increase in accordance with cells in general. To model specific chromosomal aneuploidies in cancer the chromosome copy number. -
Transcriptional Profile of Human Anti-Inflamatory Macrophages Under Homeostatic, Activating and Pathological Conditions
UNIVERSIDAD COMPLUTENSE DE MADRID FACULTAD DE CIENCIAS QUÍMICAS Departamento de Bioquímica y Biología Molecular I TESIS DOCTORAL Transcriptional profile of human anti-inflamatory macrophages under homeostatic, activating and pathological conditions Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas MEMORIA PARA OPTAR AL GRADO DE DOCTOR PRESENTADA POR Víctor Delgado Cuevas Directores María Marta Escribese Alonso Ángel Luís Corbí López Madrid, 2017 © Víctor Delgado Cuevas, 2016 Universidad Complutense de Madrid Facultad de Ciencias Químicas Dpto. de Bioquímica y Biología Molecular I TRANSCRIPTIONAL PROFILE OF HUMAN ANTI-INFLAMMATORY MACROPHAGES UNDER HOMEOSTATIC, ACTIVATING AND PATHOLOGICAL CONDITIONS Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas. Víctor Delgado Cuevas Tesis Doctoral Madrid 2016 Universidad Complutense de Madrid Facultad de Ciencias Químicas Dpto. de Bioquímica y Biología Molecular I TRANSCRIPTIONAL PROFILE OF HUMAN ANTI-INFLAMMATORY MACROPHAGES UNDER HOMEOSTATIC, ACTIVATING AND PATHOLOGICAL CONDITIONS Perfil transcripcional de macrófagos antiinflamatorios humanos en condiciones de homeostasis, activación y patológicas. Este trabajo ha sido realizado por Víctor Delgado Cuevas para optar al grado de Doctor en el Centro de Investigaciones Biológicas de Madrid (CSIC), bajo la dirección de la Dra. María Marta Escribese Alonso y el Dr. Ángel Luís Corbí López Fdo. Dra. María Marta Escribese -
New Genetic Loci Link Adipose and Insulin Biology to Body Fat Distribution
Europe PMC Funders Group Author Manuscript Nature. Author manuscript; available in PMC 2015 August 12. Published in final edited form as: Nature. 2015 February 12; 518(7538): 187–196. doi:10.1038/nature14132. Europe PMC Funders Author Manuscripts New genetic loci link adipose and insulin biology to body fat distribution A full list of authors and affiliations appears at the end of the article. # These authors contributed equally to this work. Abstract Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, we conducted genome-wide association meta-analyses of waist and hip circumference-related traits in up to 224,459 individuals. We identified 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (WHRadjBMI) and an additional 19 loci newly associated with related waist and hip circumference measures (P<5×10−8). Twenty of the 49 WHRadjBMI loci showed significant sexual dimorphism, 19 of which displayed a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation, and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms. Europe PMC Funders Author Manuscripts Depot-specific accumulation of fat, particularly in the central abdomen, confers an elevated risk of metabolic and cardiovascular diseases and mortality1. An easily accessible measure of body fat distribution is waist-to-hip ratio (WHR), a comparison of waist and hip circumferences. -
A Consensus Definitive Classification of Scavenger Receptors and Their Roles in Health and Disease
A Consensus Definitive Classification of Scavenger Receptors and Their Roles in Health and Disease The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. Citation PrabhuDas, Mercy R. et al. “A Consensus Definitive Classification of Scavenger Receptors and Their Roles in Health and Disease.” The Journal of Immunology 198, 10 (May 2017): 3775–3789 © 2017 by The American Association of Immunologists, Inc As Published http://dx.doi.org/10.4049/JIMMUNOL.1700373 Publisher American Association of Immunologists Version Author's final manuscript Citable link http://hdl.handle.net/1721.1/116696 Terms of Use Creative Commons Attribution-Noncommercial-Share Alike Detailed Terms http://creativecommons.org/licenses/by-nc-sa/4.0/ HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author J Immunol Manuscript Author . Author manuscript; Manuscript Author available in PMC 2017 November 15. Published in final edited form as: J Immunol. 2017 May 15; 198(10): 3775–3789. doi:10.4049/jimmunol.1700373. A Consensus Definitive Classification of Scavenger Receptors and Their Roles in Health and Disease Mercy R. PrabhuDas*, Cynthia L. Baldwin†,‡, Paul L. Bollyky§, Dawn M. E. Bowdish¶, Kurt Drickamerǁ, Maria Febbraio#, Joachim Herz**,††,‡‡,§§,¶¶, Lester Kobzikǁǁ, Monty Krieger##, John Loike***, Benita McVicker†††, Terry K. Means‡‡‡, Soren K. Moestrup§§§, Steven R. Post¶¶¶, Tatsuya Sawamuraǁǁǁ, Samuel Silverstein###, Robert C. Speth****, Janice C. Telfer†, Geoffrey M. Thiele††††, Xiang-Yang -
Single-Cell Transcriptome Analysis Reveals Mesenchymal Stem Cells In
bioRxiv preprint doi: https://doi.org/10.1101/2021.09.02.458742; this version posted September 3, 2021. 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. 1 Single-cell transcriptome analysis reveals mesenchymal stem cells 2 in cavernous hemangioma 3 Fulong Ji1$, Yong Liu2$, Jinsong Shi3$, Chunxiang Liu1, Siqi Fu1 4 Heng Wang1, Bingbing Ren1, Dong Mi4, Shan Gao2*, Daqing Sun1* 5 1 Department of Paediatric Surgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China. 6 China. 7 2 College of Life Sciences, Nankai University, Tianjin, Tianjin 300071, P.R. China; 8 3 National Clinical Research Center of Kidney Disease, Jinling Hospital, Nanjing University School of 9 Medicine, Nanjing, Jiangsu 210016, P.R. China; 10 4 School of Mathematical Sciences, Nankai University, Tianjin, Tianjin 300071, P.R. China; 11 12 13 $ These authors contributed equally to this paper. 14 * Corresponding authors. 15 SG：[email protected] 16 DS：[email protected] 17 bioRxiv preprint doi: https://doi.org/10.1101/2021.09.02.458742; this version posted September 3, 2021. 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. 18 Abstract 19 A cavernous hemangioma, well-known as vascular malformation, is present at birth, grows 20 proportionately with the child, and does not undergo regression.