Endothelial Perspective on Tumor Development
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Versican V2 Assembles the Extracellular Matrix Surrounding the Nodes of Ranvier in the CNS
The Journal of Neuroscience, June 17, 2009 • 29(24):7731–7742 • 7731 Cellular/Molecular Versican V2 Assembles the Extracellular Matrix Surrounding the Nodes of Ranvier in the CNS María T. Dours-Zimmermann,1 Konrad Maurer,2 Uwe Rauch,3 Wilhelm Stoffel,4 Reinhard Fa¨ssler,5 and Dieter R. Zimmermann1 Institutes of 1Surgical Pathology and 2Anesthesiology, University Hospital Zurich, CH-8091 Zurich, Switzerland, 3Vascular Wall Biology, Department of Experimental Medical Science, University of Lund, S-221 00 Lund, Sweden, 4Center for Biochemistry, Medical Faculty, University of Cologne, D-50931 Cologne, Germany, and 5Department of Molecular Medicine, Max Planck Institute of Biochemistry, D-82152 Martinsried, Germany The CNS-restricted versican splice-variant V2 is a large chondroitin sulfate proteoglycan incorporated in the extracellular matrix sur- rounding myelinated fibers and particularly accumulating at nodes of Ranvier. In vitro, it is a potent inhibitor of axonal growth and therefore considered to participate in the reduction of structural plasticity connected to myelination. To study the role of versican V2 during postnatal development, we designed a novel isoform-specific gene inactivation approach circumventing early embryonic lethality of the complete knock-out and preventing compensation by the remaining versican splice variants. These mice are viable and fertile; however, they display major molecular alterations at the nodes of Ranvier. While the clustering of nodal sodium channels and paranodal structures appear in versican V2-deficient mice unaffected, the formation of the extracellular matrix surrounding the nodes is largely impaired. The conjoint loss of tenascin-R and phosphacan from the perinodal matrix provide strong evidence that versican V2, possibly controlled by a nodal receptor, organizes the extracellular matrix assembly in vivo. -
Kids First Pediatric Research Program (Kids First) Poster Session at ASHG Accelerating Pediatric Genomics Research Through Collaboration October 15Th, 2019
The Gabriella Miller Kids First Pediatric Research Program (Kids First) Poster Session at ASHG Accelerating Pediatric Genomics Research through Collaboration October 15th, 2019 Background The Gabriella Miller Kids First Pediatric Research Program (Kids First) is a trans- NIH Common Fund program initiated in response to the 2014 Gabriella Miller Kids First Research Act. The program’s vision is to alleviate suffering from childhood cancer and structural birth defects by fostering collaborative research to uncover the etiology of these diseases and support data sharing within the pediatric research community. This is implemented through developing the Gabriella Miller Kids First Data Resource (Kids First Data Resource) and populating this resource with whole genome sequence datasets and associated clinical and phenotypic information. Both childhood cancers and structural birth defects are critical and costly conditions associated with substantial morbidity and mortality. Elucidating the underlying genetic etiology of these diseases has the potential to profoundly improve preventative measures, diagnostics, and therapeutic interventions. Purpose During this evening poster session, attendees will gain a broad understanding of the utility of the genomic data generated by Kids First, learn about the progress of Kids First X01 cohort projects, and observe demonstrations of the tools and functionalities of the recently launched Kids First Data Resource Portal. The session is an opportunity for the scientific community and public to engage with Kids First investigators, collaborators, and a growing community of researchers, patient foundations, and families. Several other NIH and external data efforts will present posters and be available to discuss collaboration opportunities as we work together to accelerate pediatric research. -
A Single-Cell Transcriptomic Landscape of Primate Arterial Aging
ARTICLE https://doi.org/10.1038/s41467-020-15997-0 OPEN A single-cell transcriptomic landscape of primate arterial aging Weiqi Zhang 1,2,3,4,5,13, Shu Zhang6,7,13, Pengze Yan3,8,13, Jie Ren7,9,13, Moshi Song3,5,8, Jingyi Li2,3,8, Jinghui Lei4, Huize Pan2,3, Si Wang3,5,8, Xibo Ma3,10, Shuai Ma2,3,8, Hongyu Li2,3, Fei Sun2,3, Haifeng Wan3,5,11, ✉ ✉ ✉ Wei Li 3,5,11, Piu Chan4, Qi Zhou3,5,11, Guang-Hui Liu 2,3,4,5,8 , Fuchou Tang 6,7,9,12 & Jing Qu 3,5,11 Our understanding of how aging affects the cellular and molecular components of the vas- 1234567890():,; culature and contributes to cardiovascular diseases is still limited. Here we report a single-cell transcriptomic survey of aortas and coronary arteries in young and old cynomolgus monkeys. Our data define the molecular signatures of specialized arteries and identify eight markers discriminating aortic and coronary vasculatures. Gene network analyses characterize tran- scriptional landmarks that regulate vascular senility and position FOXO3A, a longevity- associated transcription factor, as a master regulator gene that is downregulated in six subtypes of monkey vascular cells during aging. Targeted inactivation of FOXO3A in human vascular endothelial cells recapitulates the major phenotypic defects observed in aged monkey arteries, verifying FOXO3A loss as a key driver for arterial endothelial aging. Our study provides a critical resource for understanding the principles underlying primate arterial aging and contributes important clues to future treatment of age-associated vascular disorders. 1 CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China. -
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, -
Anti-P4HA2 (Aa 289-338) Polyclonal Antibody (DPABH-10980) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Anti-P4HA2 (aa 289-338) polyclonal antibody (DPABH-10980) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description Catalyzes the post-translational formation of 4-hydroxyproline in -Xaa-Pro-Gly- sequences in collagens and other proteins. Immunogen Synthetic peptide corresponding to a region within C terminal amino acids 289-338 (VYESLCRGEG VKLTPRRQKR LFCRYHHGNR APQLLIAPFK EEDEWDSPHI) of Human P4HA2, isoform 2 (NP_001017973). Isotype IgG Source/Host Rabbit Species Reactivity Human Purification Immunogen affinity purified Conjugate Unconjugated Applications IHC - Wholemount, WB Format Liquid Size 50 μg Buffer Constituents: 97% PBS, 2% Sucrose Preservative None Storage Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid repeated freeze / thaw cycles. GENE INFORMATION Gene Name P4HA2 prolyl 4-hydroxylase, alpha polypeptide II [ Homo sapiens ] Official Symbol P4HA2 Synonyms P4HA2; prolyl 4-hydroxylase, alpha polypeptide II; procollagen proline, 2 oxoglutarate 4 dioxygenase (proline 4 hydroxylase), alpha polypeptide II; prolyl 4-hydroxylase subunit alpha-2; 4 PH alpha 2; C P4Halpha(II); collagen prolyl 4 hydroxylase alpha(II); 4-PH alpha 2; 4-PH alpha-2; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved C-P4Halpha(II); collagen prolyl 4-hydroxylase alpha(II); procollagen-proline,2-oxoglutarate-4- dioxygenase subunit alpha-2; procollagen-proline, 2-oxoglutarate -
Distinct Genetic Alterations in Colorectal Cancer
Distinct Genetic Alterations in Colorectal Cancer Hassan Ashktorab1*, Alejandro A. Scha¨ffer2, Mohammad Daremipouran3, Duane T. Smoot3, Edward Lee3, Hassan Brim3 1 Department of Medicine and Cancer Center, Howard University, College of Medicine, Washington, DC, United States of America, 2 National Center for Biotechnology Information, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, Maryland, United States of America, 3 Department of Pathology, Howard University, College of Medicine, Washington, DC, United States of America Abstract Background: Colon cancer (CRC) development often includes chromosomal instability (CIN) leading to amplifications and deletions of large DNA segments. Epidemiological, clinical, and cytogenetic studies showed that there are considerable differences between CRC tumors from African Americans (AAs) and Caucasian patients. In this study, we determined genomic copy number aberrations in sporadic CRC tumors from AAs, in order to investigate possible explanations for the observed disparities. Methodology/Principal Findings: We applied genome-wide array comparative genome hybridization (aCGH) using a 105k chip to identify copy number aberrations in samples from 15 AAs. In addition, we did a population comparative analysis with aCGH data in Caucasians as well as with a widely publicized list of colon cancer genes (CAN genes). There was an average of 20 aberrations per patient with more amplifications than deletions. Analysis of DNA copy number of frequently altered chromosomes revealed that deletions occurred primarily in chromosomes 4, 8 and 18. Chromosomal duplications occurred in more than 50% of cases on chromosomes 7, 8, 13, 20 and X. The CIN profile showed some differences when compared to Caucasian alterations. Conclusions/Significance: Chromosome X amplification in male patients and chromosomes 4, 8 and 18 deletions were prominent aberrations in AAs. -
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing -
Perineuronal Nets and Metal Cation Concentrations in The
biomolecules Review Perineuronal Nets and Metal Cation Concentrations in the Microenvironments of Fast-Spiking, Parvalbumin-Expressing GABAergic Interneurons: Relevance to Neurodevelopment and Neurodevelopmental Disorders Jessica A. Burket 1, Jason D. Webb 1 and Stephen I. Deutsch 2,* 1 Department of Molecular Biology & Chemistry, Christopher Newport University, Newport News, VA 23606, USA; [email protected] (J.A.B.); [email protected] (J.D.W.) 2 Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, 825 Fairfax Avenue, Suite 710, Norfolk, VA 23507, USA * Correspondence: [email protected]; Tel.: +1-757-446-5888 Abstract: Because of their abilities to catalyze generation of toxic free radical species, free concen- trations of the redox reactive metals iron and copper are highly regulated. Importantly, desired neurobiological effects of these redox reactive metal cations occur within very narrow ranges of their local concentrations. For example, synaptic release of free copper acts locally to modulate NMDA receptor-mediated neurotransmission. Moreover, within the developing brain, iron is criti- cal to hippocampal maturation and the differentiation of parvalbumin-expressing neurons, whose soma and dendrites are surrounded by perineuronal nets (PNNs). The PNNs are a specialized Citation: Burket, J.A.; Webb, J.D.; component of brain extracellular matrix, whose polyanionic character supports the fast-spiking elec- Deutsch, S.I. Perineuronal Nets and trophysiological properties of these parvalbumin-expressing GABAergic interneurons. In addition Metal Cation Concentrations in the to binding cations and creation of the Donnan equilibrium that support the fast-spiking properties Microenvironments of Fast-Spiking, of this subset of interneurons, the complex architecture of PNNs also binds metal cations, which Parvalbumin-Expressing GABAergic may serve a protective function against oxidative damage, especially of these fast-spiking neurons. -
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in -
Rna-Sequencing Applications: Gene Expression Quantification and Methylator Phenotype Identification
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 8-2013 RNA-SEQUENCING APPLICATIONS: GENE EXPRESSION QUANTIFICATION AND METHYLATOR PHENOTYPE IDENTIFICATION Guoshuai Cai Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Bioinformatics Commons, Computational Biology Commons, and the Medicine and Health Sciences Commons Recommended Citation Cai, Guoshuai, "RNA-SEQUENCING APPLICATIONS: GENE EXPRESSION QUANTIFICATION AND METHYLATOR PHENOTYPE IDENTIFICATION" (2013). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 386. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/386 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. RNA-SEQUENCING APPLICATIONS: GENE EXPRESSION QUANTIFICATION AND METHYLATOR PHENOTYPE IDENTIFICATION -
The Function of the Hyalectan Class of Proteoglycans and Their Binding Partners During Vertebrate Development
In: Advances in Medicine and Biology. Volume 52 ISBN: 978-1-62081-314-0 Editor: Leon V. Berhardt © 2012 Nova Science Publishers, Inc. No part of this digital document may be reproduced, stored in a retrieval system or transmitted commercially in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services. Chapter II The Function of the Hyalectan Class of Proteoglycans and Their Binding Partners during Vertebrate Development Frédéric Brunet,1 ,* Christopher Kintakas,2 Adam D. Smith2 and Daniel R. McCulloch2,† 1Institut de Génomique Fonctionnelle de Lyon, UMR5242 CNRS/INRA/Université Claude Bernard Lyon I/ENS, Ecole Normale Supérieure de Lyon, Lyon, France, 2Molecular and Medical Research (MMR) Strategic Research Centre, Molecular Medicine Research Facility, School of Medicine, Faculty of Health, Deakin University, Australia Abstract The hyalectan family of extracellular matrix (ECM) chondroitin sulphate proteoglycans comprises aggrecan, brevican, neurocan and versican. Although they share common structural domains including a G1 domain that is invariably linked to hyaluronan, their tissue distribution and biological roles in vertebrates are diverse. During vertebrate embryonic development, complex interactions between cells and their surrounding ECM precede profound cellular behaviour and morphogenetic events. Studies in several vertebrate species have identified specific roles for the hyalectans in numerous embryonic processes from early through late embryogenesis that are necessary for shaping the body plan and subsequent morphogenesis. -
A Genome-Wide Association Study Identifies Risk Alleles in Plasminogen and P4HA2 Associated with Giant Cell Arteritis
This is a repository copy of A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis. White Rose Research Online URL for this paper: https://eprints.whiterose.ac.uk/108046/ Version: Accepted Version Article: Carmona, DF, Vaglio, A, Mackie, SL orcid.org/0000-0003-2483-5873 et al. (53 more authors) (2017) A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis. American Journal of Human Genetics, 100 (1). pp. 64-74. ISSN 0002-9297 https://doi.org/10.1016/j.ajhg.2016.11.013 �© 2017, American Society of Human Genetics. This is an author produced version of a paper published in American Journal of Human Genetics. Uploaded in accordance with the publisher's self-archiving policy. Reuse Items deposited in White Rose Research Online are protected by copyright, with all rights reserved unless indicated otherwise. They may be downloaded and/or printed for private study, or other acts as permitted by national copyright laws. The publisher or other rights holders may allow further reproduction and re-use of the full text version. This is indicated by the licence information on the White Rose Research Online record for the item. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ A genome-wide association study identifies risk alleles in plasminogen and P4HA2 associated with giant cell arteritis F.