RAPGEF5/Repac Polyclonal Antibody, Cy5 Conjugated Catalog No

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Product Name: RAPGEF5/Repac Polyclonal Antibody, Cy5 Conjugated Catalog No. : TAP01-88418R-Cy5 Intended Use: For Research Use Only. Not for used in diagnostic procedures. Size 100ul Concentration 1ug/ul Gene ID ISO Type Rabbit IgG Clone N/A Immunogen Range Conjugation Cy5 Subcellular Locations Applications IF(IHC-P) Cross Reactive Species Human, Mouse, Rat Source KLH conjugated synthetic peptide derived from human RAPGEF5 Applications with IF(IHC-P)(1:50-200) Dilutions Purification Purified by Protein A. Background Members of the RAS subfamily of GTPases function in signal transduction as GTP/GDP-regulated switches that cycle between inactive GDP- and active GTP-bound states. Guanine nucleotide exchange factors (GEFs), such as Repac, serve as RAS activators by promoting acquisition of GTP to maintain the active GTP-bound state and are the key link between cell surface receptors and RAS activation. Repac, also known as Rap guanine nucleotide exchange factor 5 (RAPGEF5), is a 580 amino acid protein that is expressed in brain and testis, with weaker expression in heart, placenta, lung, pancreas and small intestine. Existing as two alternatively spliced isoforms, the Repac gene is conserved in cow, mouse and rat. The gene that encodes Repac maps to human chromosome 7p15.3, with high expression of this region linking to positive response to erlotinib therapy for those with non-small-cell lung cancer. Synonyms GFR; Guanine nucleotide exchange factor for Rap1; KIAA0277; M Ras regulated Rap GEF; M-Ras-regulated Rap GEF; MR GEF; MR-GEF; MRGEF; Rap guanine nucleotide exchange factor 5; Rapgef5; Related to Epac; Repac; RPGF5_HUMAN. Storage Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months. If unexpected results are observed which cannot be explained by variations in laboratory procedures and a problem with the reagent is suspected, contact Technical Support at [email protected] or your distributor service. .

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S41467-020-18249-3.Pdf
ARTICLE https://doi.org/10.1038/s41467-020-18249-3 OPEN Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes with neurodegenerative disease associations in the aged brain Lei Zhao1,2,17, Zhongqi Li 1,2,17, Joaquim S. L. Vong2,3,17, Xinyi Chen1,2, Hei-Ming Lai1,2,4,5,6, Leo Y. C. Yan1,2, Junzhe Huang1,2, Samuel K. H. Sy1,2,7, Xiaoyu Tian 8, Yu Huang 8, Ho Yin Edwin Chan5,9, Hon-Cheong So6,8, ✉ ✉ Wai-Lung Ng 10, Yamei Tang11, Wei-Jye Lin12,13, Vincent C. T. Mok1,5,6,14,15 &HoKo 1,2,4,5,6,8,14,16 1234567890():,; The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovas- cular dysfunction in neurodegenerative diseases remain elusive. Here, we report zonation- dependent transcriptomic changes in aged mouse brain endothelial cells (ECs), which pro- minently implicate altered immune/cytokine signaling in ECs of all vascular segments, and functional changes impacting the blood–brain barrier (BBB) and glucose/energy metabolism especially in capillary ECs (capECs). An overrepresentation of Alzheimer disease (AD) GWAS genes is evident among the human orthologs of the differentially expressed genes of aged capECs, while comparative analysis revealed a subset of concordantly downregulated, functionally important genes in human AD brains. Treatment with exenatide, a glucagon-like peptide-1 receptor agonist, strongly reverses aged mouse brain EC transcriptomic changes and BBB leakage, with associated attenuation of microglial priming. We thus revealed tran- scriptomic alterations underlying brain EC ageing that are complex yet pharmacologically reversible.
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Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement.
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bioRxiv preprint doi: https://doi.org/10.1101/152892; this version posted June 20, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Title: RAPGEF5 regulates nuclear translocation of β-catenin Authors: John N. Griffin1,2, Florencia del Viso1, Anna R. Duncan1, Andrew Robson1, Saurabh Kulkarni1, Karen J. Liu2 and Mustafa K. Khokha1* Affiliations: 1 Pediatric Genomics Discovery Program, Departments of Pediatrics and Genetics Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510, USA 2 Department of Craniofacial Development and Stem Cell Biology, King’s College London, London SE1 9RT, United Kingdom * Correspondence to: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/152892; this version posted June 20, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. SUMMARY: Canonical Wnt signaling coordinates many critical aspects of embryonic development, while dysregulated Wnt signaling contributes to common diseases, including congenital malformations and cancer. The nuclear localization of β-catenin is the defining step in pathway activation. However, despite intensive investigation, the mechanisms regulating β-catenin nuclear transport remain undefined. In a patient with congenital heart disease and heterotaxy, a disorder of left-right patterning, we previously identified the guanine nucleotide exchange factor, RAPGEF5. Here, we demonstrate that RAPGEF5 regulates left-right patterning via Wnt signaling. In particular, RAPGEF5, regulates the nuclear translocation of β-catenin independently of both β-catenin cytoplasmic stabilization and the importin β1/Ran mediated transport system.
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Genetics of Plgf Plasma Levels Highlights a Role of Its Receptors And
www.nature.com/scientificreports OPEN Genetics of PlGF plasma levels highlights a role of its receptors and supports the link between angiogenesis and immunity Daniela Ruggiero1,2*, Teresa Nutile1, Stefania Nappo3, Alfonsina Tirozzi2, Celine Bellenguez4, Anne‑Louise Leutenegger5,6 & Marina Ciullo1,2* Placental growth factor (PlGF) is a member of the vascular endothelial growth factor family and is involved in bone marrow‑derived cell activation, endothelial stimulation and pathological angiogenesis. High levels of PlGF have been observed in several pathological conditions especially in cancer, cardiovascular, autoimmune and infammatory diseases. Little is known about the genetics of circulating PlGF levels. Indeed, although the heritability of circulating PlGF levels is around 40%, no studies have assessed the relation between PlGF plasma levels and genetic variants at a genome‑wide level. In the current study, PlGF plasma levels were measured in a population‑based sample of 2085 adult individuals from three isolated populations of South Italy. A GWAS was performed in a discovery cohort (N = 1600), followed by a de novo replication (N = 468) from the same populations. The meta‑ analysis of the discovery and replication samples revealed one signal signifcantly associated with PlGF circulating levels. This signal was mapped to the PlGF co‑receptor coding gene NRP1, indicating its important role in modulating the PlGF plasma levels. Two additional signals, at the PlGF receptor coding gene FLT1 and RAPGEF5 gene, were identifed at a suggestive level. Pathway and TWAS analyses highlighted genes known to be involved in angiogenesis and immune response, supporting the link between these processes and PlGF regulation. Overall, these data improve our understanding of the genetic variation underlying circulating PlGF levels.
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bioRxiv preprint doi: https://doi.org/10.1101/2021.04.17.440269; this version posted April 19, 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-NC-ND 4.0 International license. 1 Adipose gene expression profiles reveal novel insights into the 2 adaptation of northern Eurasian semi-domestic reindeer 3 (Rangifer tarandus) 4 Short title: Reindeer adipose transcriptome 5 6 Melak Weldenegodguad1, 2, Kisun Pokharel1¶, Laura Niiranen3¶, Päivi Soppela4, 7 Innokentyi Ammosov5, Mervi Honkatukia6, Heli Lindeberg1, Jaana Peippo1, 6, Tiina 8 Reilas1, Nuccio Mazzullo4, Kari A. Mäkelä3, Tommi Nyman7, Arja Tervahauta2, 9 Karl-Heinz Herzig8, 9, 10, Florian Stammler4, Juha Kantanen1* 10 11 1 Natural Resources Institute Finland (Luke), Jokioinen, Finland 12 2 Department of Environmental and Biological Sciences, University of Eastern 13 Finland, Kuopio, Finland 14 3 Research Unit of Biomedicine, Faculty of Medicine, University of Oulu, Oulu, 15 Finland 16 4 Arctic Centre, University of Lapland, Rovaniemi, Finland 17 5 Board of Agricultural Office of Eveno-Bytantaj Region, Batagay-Alyta, The Sakha 18 Republic (Yakutia), Russia 19 6 NordGen—Nordic Genetic Resource Center, Ås, Norway 20 7 Department of Ecosystems in the Barents Region, Norwegian Institute of 21 Bioeconomy Research, Svanvik, Norway 22 8 Research Unit of Biomedicine, Medical Research Center, Faculty of Medicine, 23 University of Oulu bioRxiv preprint doi: https://doi.org/10.1101/2021.04.17.440269; this version posted April 19, 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.
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bioRxiv preprint doi: https://doi.org/10.1101/2021.03.09.434569; this version posted March 10, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus Basavaraj Vastrad1, Chanabasayya Vastrad*2, Anandkumar Tengli3 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karnataka, India. 3. Department of Pharmaceutical Chemistry, JSS College of Pharmacy, Mysuru and JSS Academy of Higher Education & Research, Mysuru, Karnataka, 570015, India * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2021.03.09.434569; this version posted March 10, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Abstract Gestational diabetes mellitus (GDM) is one of the metabolic diseases during pregnancy. The identification of the central molecular mechanisms liable for the disease pathogenesis might lead to the advancement of new therapeutic options. The current investigation aimed to identify central differentially expressed genes (DEGs) in GDM. The transcription profiling by array data (E-MTAB-6418) was obtained from the ArrayExpress database. The DEGs between GDM samples and non GDM samples were analyzed with limma package. Gene ontology (GO) and REACTOME enrichment analysis were performed using ToppGene. Then we constructed the protein-protein interaction (PPI) network of DEGs by the Search Tool for the Retrieval of Interacting Genes database (STRING) and module analysis was performed.
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bioRxiv preprint doi: https://doi.org/10.1101/148049; this version posted October 10, 2017. 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. 1 Single-cell RNA-seq of mouse dopaminergic neurons informs candidate gene selection for 2 sporadic Parkinson's disease 3 4 Paul W. Hook1, Sarah A. McClymont1, Gabrielle H. Cannon1, William D. Law1, A. Jennifer 5 Morton2, Loyal A. Goff1,3*, Andrew S. McCallion1,4,5* 6 7 1McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of 8 Medicine, Baltimore, Maryland, United States of America 9 2Department of Physiology Development and Neuroscience, University of Cambridge, 10 Cambridge, United Kingdom 11 3Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, 12 Maryland, United States of America 13 4Department of Comparative and Molecular Pathobiology, Johns Hopkins University School of 14 Medicine, Baltimore, Maryland, United States of America 15 5Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, 16 United States of America 17 *, To whom correspondence should be addressed: [email protected] and [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/148049; this version posted October 10, 2017. 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.
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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.
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