Anti-SEMA6A (Aa 36-65) Polyclonal Antibody (DPABH-11186) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

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Anti-SEMA6A (aa 36-65) polyclonal antibody (DPABH-11186) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description Cell surface receptor for PLXNA2 that plays an important role in cell-cell signaling. Required for normal granule cell migration in the developing cerebellum. Promotes reorganization of the actin cytoskeleton and plays an important role in axon guidance in the developing central nervous system. Can act as repulsive axon guidance cue. Has repulsive action towards migrating granular neurons. May play a role in channeling sympathetic axons into the sympathetic chains and controlling the temporal sequence of sympathetic target innervation. Immunogen Synthetic peptide within Human Sema6A aa 36-65 (N terminal) conjugated to Keyhole Limpet Haemocyanin (KLH). The exact sequence is proprietary.Database link: Q9H2E6 Isotype IgG Source/Host Rabbit Species Reactivity Human Purification Immunogen affinity purified Conjugate Unconjugated Applications WB Format Liquid Size 400 μl Buffer Constituent: 99% PBS Preservative 0.09% Sodium Azide Storage Shipped at 4°C. Store at 4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. GENE INFORMATION Gene Name SEMA6A sema domain, transmembrane domain (TM), and cytoplasmic domain, (semaphorin) 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 6A [ Homo sapiens ] Official Symbol Sema6A Synonyms SEMA6A; sema domain, transmembrane domain (TM), and cytoplasmic domain, (semaphorin) 6A; SEMAQ; semaphorin-6A; HT018; KIAA1368; SEMA; sema VIa; SEMA6A1; SEMA6A-1; semaphorin VIA; semaphorin 6A-1; semaphorin-6A-1; VIA; Entrez Gene ID 57556 Protein Refseq NP_065847 UniProt ID Q9H2E6 Chromosome Location 5q23 Pathway Axon guidance; Developmental Biology; Other semaphorin interactions; Semaphorin interactions; Function protein binding; receptor activity; semaphorin receptor binding; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

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University of Kentucky UKnowledge Theses and Dissertations--Molecular and Cellular Biochemistry Molecular and Cellular Biochemistry 2019 COMPUTATIONAL TOOLS FOR THE DYNAMIC CATEGORIZATION AND AUGMENTED UTILIZATION OF THE GENE ONTOLOGY Eugene Waverly Hinderer III University of Kentucky, [email protected] Author ORCID Identifier: https://orcid.org/0000-0001-8045-7083 Digital Object Identifier: https://doi.org/10.13023/etd.2019.362 Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Hinderer, Eugene Waverly III, "COMPUTATIONAL TOOLS FOR THE DYNAMIC CATEGORIZATION AND AUGMENTED UTILIZATION OF THE GENE ONTOLOGY" (2019). Theses and Dissertations--Molecular and Cellular Biochemistry. 43. https://uknowledge.uky.edu/biochem_etds/43 This Doctoral Dissertation is brought to you for free and open access by the Molecular and Cellular Biochemistry at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Molecular and Cellular Biochemistry 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.
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Supplementary Tables S1-S3
Supplementary Table S1: Real time RT-PCR primers COX-2 Forward 5’- CCACTTCAAGGGAGTCTGGA -3’ Reverse 5’- AAGGGCCCTGGTGTAGTAGG -3’ Wnt5a Forward 5’- TGAATAACCCTGTTCAGATGTCA -3’ Reverse 5’- TGTACTGCATGTGGTCCTGA -3’ Spp1 Forward 5'- GACCCATCTCAGAAGCAGAA -3' Reverse 5'- TTCGTCAGATTCATCCGAGT -3' CUGBP2 Forward 5’- ATGCAACAGCTCAACACTGC -3’ Reverse 5’- CAGCGTTGCCAGATTCTGTA -3’ Supplementary Table S2: Genes synergistically regulated by oncogenic Ras and TGF-β AU-rich probe_id Gene Name Gene Symbol element Fold change RasV12 + TGF-β RasV12 TGF-β 1368519_at serine (or cysteine) peptidase inhibitor, clade E, member 1 Serpine1 ARE 42.22 5.53 75.28 1373000_at sushi-repeat-containing protein, X-linked 2 (predicted) Srpx2 19.24 25.59 73.63 1383486_at Transcribed locus --- ARE 5.93 27.94 52.85 1367581_a_at secreted phosphoprotein 1 Spp1 2.46 19.28 49.76 1368359_a_at VGF nerve growth factor inducible Vgf 3.11 4.61 48.10 1392618_at Transcribed locus --- ARE 3.48 24.30 45.76 1398302_at prolactin-like protein F Prlpf ARE 1.39 3.29 45.23 1392264_s_at serine (or cysteine) peptidase inhibitor, clade E, member 1 Serpine1 ARE 24.92 3.67 40.09 1391022_at laminin, beta 3 Lamb3 2.13 3.31 38.15 1384605_at Transcribed locus --- 2.94 14.57 37.91 1367973_at chemokine (C-C motif) ligand 2 Ccl2 ARE 5.47 17.28 37.90 1369249_at progressive ankylosis homolog (mouse) Ank ARE 3.12 8.33 33.58 1398479_at ryanodine receptor 3 Ryr3 ARE 1.42 9.28 29.65 1371194_at tumor necrosis factor alpha induced protein 6 Tnfaip6 ARE 2.95 7.90 29.24 1386344_at Progressive ankylosis homolog (mouse)
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Developmental Enhancers Revealed by Extensive DNA Methylome Maps of Zebrafish Early Embryos
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1 in Vivo Epigenetic Editing of Sema6a Promoter Reverses Impaired
bioRxiv preprint doi: https://doi.org/10.1101/491779; this version posted December 10, 2018. 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. In vivo epigenetic editing of sema6a promoter reverses impaired transcallosal connectivity caused by C11orf46/ARL14EP neurodevelopmental risk gene Cyril J. Peter1,*, Atsushi Saito2,*, Yuto Hasegawa2, Yuya Tanaka2, Gabriel Perez2, Emily Alway2, Sergio Espeso-gil1, Tariq Fayyad1, Chana Ratner1, Aslihan Dincer1, Achla Gupta1,8, Lakshmi Devi1,8, John G. Pappas3, François M. Lalonde4, John A. Butman5, Joan C. Han6,7, Schahram Akbarian1,#, and Atsushi Kamiya2,# 1Friedman Brain Institute and Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA 2Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA 3Department of Pediatrics, New York University School of Medicine, New York, NY 4Human Genetics Branch, National Institute of Mental Health, Bethesda, MD 20892, USA. 5Diagnostic Radiology Department, The Clinical Center of the National Institutes of Health, Bethesda, MD 20892, USA 6Unit on Metabolism and Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD 20892, USA 7Departments of Pediatrics and Physiology, University of Tennessee Health Science Center, and Children's Foundation Research Institute, Le Bonheur Children's Hospital, Memphis, TN, 38103, USA 8Department of Pharmacology and System Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA *These authors contributed equally to this work. #Correspondence: [email protected] (A.K.), [email protected] (S.A.).
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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.
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Downloaded from the European Nucleotide Archive (ENA; 126
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Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
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Identifying Factors That Conctribute to Phenotypic Heterogeneity in Melanoma Progression
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2012 Identifying factors that conctribute to Phenotypic heterogeneity in melanoma progression Widmer, Daniel Simon Posted at the Zurich Open Repository and Archive, University of Zurich ZORA URL: https://doi.org/10.5167/uzh-73667 Dissertation Originally published at: Widmer, Daniel Simon. Identifying factors that conctribute to Phenotypic heterogeneity in melanoma progression. 2012, University of Zurich, Faculty of Medicine. Eidgenössische Technische Hochschule Zürich Swiss Federal Institute of Technology Zurich Identifying factors that conctribute to Phenotypic heterogeneity in melanoma progression Daniel Simon Widmer 2012 Diss ETH No. 20537 DISS. ETH NO. 20537 IDENTIFYING FACTORS THAT CONTRIBUTE TO PHENOTYPIC HETEROGENEITY IN MELANOMA PROGRESSION A dissertation submitted to ETH ZURICH for the degree of Doctor of Sciences presented by Daniel Simon Widmer Master of Science UZH University of Zurich born on February 26th 1982 citizen of Gränichen AG accepted on the recommendation of Professor Sabine Werner, examinor Professor Reinhard Dummer, co-examinor Professor Michael Detmar, co-examinor 2012 Contents 1. ZUSAMMENFASSUNG...................................................................................................... 7 2. SUMMARY ................................................................................................................... 11 3. INTRODUCTION ...........................................................................................................
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Supplemental Material
SUPPLEMENTAL MATERIAL Online OnlY Supplemental material miRNA expression profiling of cerebrospinal fluid in patients with cerebral aneurysmal subarachnoid hemorrhage S. S. Stylli et al. http://thejns.org/doi/abs/10.3171/2016.1.JNS151454 DisClaimer The Journal of Neurosurgery acknowledges that the following section is published verbatim as submitted by the authors and did not go through either the Journal’s peer-review or editing process. ©AANS, 2016 J Neurosurg Supplementary Table 1 nSolver Differential Expression Analysis Comparison Groups Comparison 1 No SAH SAH / No vasospasm (combined) CSF0012, CSF0018, CSF0030, CSF0034 CSF0020, CSF0023, CSF0024, CSF0025, CSF0038, CSF0039, CSF0040, CSF0041, CSF0042 Comparison 2 No SAH SAH / No vasospasm (Sample Day 1) CSF0012, CSF0018, CSF0030, CSF0034 CSF0020, CSF0023, CSF0024, CSF0027, CSF0041, CSF0038 Comparison 3 No SAH SAH / Vasospasm (combined) CSF0012, CSF0018, CSF0030, CSF0034 CSF0 022, CSF0027, CSF0032, CSF0033, CSF0036, CSF0044, CSF0045, CSF0048, CSF0052, CSF0053 Comparison 4 No SAH SAH / Vasospasm (Sample Day 1) CSF0012, CSF0018, CSF0030, CSF0034 CSF0027, CSF0032, CSF0036, CSF0044, CSF0052 Comparison 5 No SAH SAH / Vasospasm (post Sample Day 1) CSF0012, CSF0018, CSF0030, CSF0034 CSF0022, CSF0033, CSF0045, CSF0048, CSF0053 Comparison 6 SAH / No vasospasm (combined) SAH / Vasospasm (combined) CSF0020, CSF0023, CSF0024, CSF0025, CSF0022, CSF0027, CSF0032, CSF0033, CSF0036, CSF0038, CSF0039, CSF0040, CSF0041, CSF0044, CSF0045, CSF0048, CSF0052, CSF0053 CSF0042 Comparison 7 SAH / No vasospasm
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(IJDSIR) Page 62
ISSN: 2581-5989 PubMed - National Library of Medicine - ID: 101738774 International Journal of Dental Science and Innovative Research (IJDSIR) IJDSIR : Dental Publication Service Available Online at: www.ijdsir.com Volume – 2, Issue – 5, September – October - 2019, Page No. : 62 - 69 Transmembrane Semaphorin 6A controls timing of entrance of the Sensory Innervation into mice mandibular first molar tooth germ Salma Ali, PhD, Department of Diagnostic Dental Sciences and Oral Biology, College of Dentistry, King Khalid University, Abha, Kingdom of Saudi Arabia. Corresponding Author: Salma Ali, PhD, Department of Diagnostic Dental Sciences and Oral Biology, College of Dentistry, King Khalid University, Abha, Kingdom of Saudi Arabia. Type of Publication: Original Research Paper Conflicts of Interest: Nil Abstract ethylcarbazole (AEC) chromogen, were the main Background: Semaphorins are 9membrane-spanning and materials used in the study. Microscopical methods soluble proteins that have many important neuronal enabled revealing the results. and non neuronal functions during development as well Results: Serial sections of PostNatal day 0, 1, 3, 5 and 7 as in adult physiology. They regulate axon growth and were examined under bright field microscope and revealed guidance, angiogenesis, cell movement, and have that sensory nerve fibers were prematurely present inside functions in several organ systems. Semaphorin6A the dental pulp of sema6a knockout mice between PN0 (sema6a) is a membrane-spanning protein, which acts as a and PN1. In wild type kind of mice sensory nerve fibers repellant for sympathetic as well as sensory dorsal root were absent at PN3 and numerous at PN5 and that was in axons. It has been reported that embryonic and postnatal accordance to previous studies which showed that they murine dental mesenchyme expresses Sema6a mRNAs.
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Novel MITF Targets Identified Using a Two-Step DNA Microarray Strategy
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Genome-Wide Analysis of Epigenetics and Alternative Promoters in Cancer Cells
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