Mouse Sema4b Knockout Project (CRISPR/Cas9)

Total Page:16

File Type:pdf, Size:1020Kb

Mouse Sema4b Knockout Project (CRISPR/Cas9) https://www.alphaknockout.com Mouse Sema4b Knockout Project (CRISPR/Cas9) Objective: To create a Sema4b knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Sema4b gene (NCBI Reference Sequence: NM_013659 ; Ensembl: ENSMUSG00000030539 ) is located on Mouse chromosome 7. 15 exons are identified, with the ATG start codon in exon 2 and the TGA stop codon in exon 15 (Transcript: ENSMUST00000032754). Exon 3~13 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Mice homozygous for a gene trap allele exhibit normal cerebellar morphology. Mice homozygous for a knock-out allele exhibit enhanced memory response by way of increased IgE and IgG1 serum levels. Exon 3 starts from about 4.82% of the coding region. Exon 3~13 covers 62.01% of the coding region. The size of effective KO region: ~8159 bp. The KO region does not have any other known gene. Page 1 of 9 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 3 4 5 6 7 8 9 10 1112 13 15 Legends Exon of mouse Sema4b Knockout region Page 2 of 9 https://www.alphaknockout.com Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section upstream of Exon 3 is aligned with itself to determine if there are tandem repeats. No significant tandem repeat is found in the dot plot matrix. So this region is suitable for PCR screening or sequencing analysis. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section downstream of Exon 13 is aligned with itself to determine if there are tandem repeats. Tandem repeats are found in the dot plot matrix. The gRNA site is selected outside of these tandem repeats. Page 3 of 9 https://www.alphaknockout.com Overview of the GC Content Distribution (up) Window size: 300 bp Sequence 12 Summary: Full Length(2000bp) | A(23.2% 464) | C(25.85% 517) | T(29.95% 599) | G(21.0% 420) Note: The 2000 bp section upstream of Exon 3 is analyzed to determine the GC content. No significant high GC-content region is found. So this region is suitable for PCR screening or sequencing analysis. Overview of the GC Content Distribution (down) Window size: 300 bp Sequence 12 Summary: Full Length(2000bp) | A(29.65% 593) | C(21.4% 428) | T(26.75% 535) | G(22.2% 444) Note: The 2000 bp section downstream of Exon 13 is analyzed to determine the GC content. No significant high GC-content region is found. So this region is suitable for PCR screening or sequencing analysis. Page 4 of 9 https://www.alphaknockout.com BLAT Search Results (up) QUERY SCORE START END QSIZE IDENTITY CHROM STRAND START END SPAN -------------------------------------------------------------------------------------------------------------- browser details YourSeq 2000 1 2000 2000 100.0% chr7 + 80210797 80212796 2000 browser details YourSeq 178 1407 1768 2000 93.6% chr3 - 94743830 94744253 424 browser details YourSeq 177 1578 1771 2000 96.4% chr12 - 111277752 111278121 370 browser details YourSeq 173 1581 1781 2000 95.3% chr11 - 97266771 97266971 201 browser details YourSeq 169 1384 1763 2000 84.9% chr11 - 107499220 107499461 242 browser details YourSeq 169 1582 1781 2000 91.6% chr2 + 34466910 34467104 195 browser details YourSeq 167 1580 1766 2000 96.2% chr7 - 130110141 130110328 188 browser details YourSeq 167 1577 1766 2000 92.5% chr14 - 66932731 66932916 186 browser details YourSeq 167 1594 1844 2000 89.5% chr4 + 108336674 108336876 203 browser details YourSeq 166 1578 1773 2000 92.9% chr5 - 117278107 117278304 198 browser details YourSeq 166 1578 1781 2000 91.1% chr2 - 121831076 121831275 200 browser details YourSeq 166 1576 1768 2000 93.7% chr6 + 137324372 137324568 197 browser details YourSeq 165 1578 1771 2000 94.7% chr7 - 29177573 29178154 582 browser details YourSeq 165 1576 1766 2000 92.0% chr19 - 57074827 57075014 188 browser details YourSeq 165 1580 1766 2000 94.2% chr17 - 37135601 37135787 187 browser details YourSeq 165 1578 1766 2000 93.0% chr10 - 76109287 76109473 187 browser details YourSeq 165 1578 1766 2000 93.7% chr10 + 75190898 75191086 189 browser details YourSeq 164 1578 1770 2000 92.0% chr11 - 119511240 119511429 190 browser details YourSeq 163 1578 1766 2000 94.1% chr8 - 105576768 105576959 192 browser details YourSeq 163 1577 1767 2000 96.1% chr4 - 153938366 153938556 191 Note: The 2000 bp section upstream of Exon 3 is BLAT searched against the genome. No significant similarity is found. BLAT Search Results (down) QUERY SCORE START END QSIZE IDENTITY CHROM STRAND START END SPAN ----------------------------------------------------------------------------------------------- browser details YourSeq 2000 1 2000 2000 100.0% chr7 + 80220956 80222955 2000 browser details YourSeq 157 1336 1867 2000 90.4% chr1 - 164024147 164024702 556 browser details YourSeq 105 1516 1824 2000 94.2% chr15 - 85739340 85739904 565 browser details YourSeq 89 1754 1879 2000 91.1% chr11 + 73259085 73262165 3081 browser details YourSeq 85 1734 1867 2000 89.8% chr1 - 191642574 191642716 143 browser details YourSeq 85 1337 1812 2000 86.6% chr8 + 90807417 90807972 556 browser details YourSeq 82 1336 1836 2000 74.8% chr12 - 83845196 83845633 438 browser details YourSeq 80 1358 1826 2000 75.9% chr11 + 89191685 89191939 255 browser details YourSeq 78 1733 1854 2000 88.7% chr11 + 97031716 97031833 118 browser details YourSeq 76 1749 1862 2000 90.6% chr15 + 12275549 12275667 119 browser details YourSeq 75 1747 1862 2000 95.2% chr19 - 22084844 22084964 121 browser details YourSeq 75 1745 1883 2000 81.7% chr12 + 41057748 41057891 144 browser details YourSeq 75 1514 1836 2000 73.8% chr11 + 79797574 79797790 217 browser details YourSeq 74 1747 1854 2000 87.8% chr2 + 29478300 29478410 111 browser details YourSeq 74 1750 1862 2000 91.2% chr1 + 87702049 87702166 118 browser details YourSeq 73 1750 1862 2000 91.1% chr11 + 84173878 84173993 116 browser details YourSeq 71 1735 1836 2000 85.4% chr2 - 117096302 117096398 97 browser details YourSeq 71 1733 1867 2000 89.1% chr4 + 123980916 123981207 292 browser details YourSeq 70 1750 1854 2000 87.3% chr11 - 118320642 118320764 123 browser details YourSeq 69 1739 1854 2000 89.7% chr1 + 151459809 151460293 485 Note: The 2000 bp section downstream of Exon 13 is BLAT searched against the genome. No significant similarity is found. Page 5 of 9 https://www.alphaknockout.com Gene and protein information: Sema4b sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4B [ Mus musculus (house mouse) ] Gene ID: 20352, updated on 24-Oct-2019 Gene summary Official Symbol Sema4b provided by MGI Official Full Name sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) Primary source 4B provided by MGI See related MGI:MGI:107559 Gene type Ensembl:ENSMUSG00000030539 RefSeq status protein coding Organism VALIDATED Lineage Mus musculus Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Also known as Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus Expression SemC; Semac; mKIAA1745 Orthologs Broad expression in spleen adult (RPKM 31.2), duodenum adult (RPKM 28.9) and 27 other tissues See more human all Genomic context Location: 7; 7 D2 See Sema4b in Genome Data Viewer Exon count: 16 Annotation release Status Assembly Chr Location 108 current GRCm38.p6 (GCF_000001635.26) 7 NC_000073.6 (80186841..80226646) Build 37.2 previous assembly MGSCv37 (GCF_000001635.18) 7 NC_000073.5 (87331727..87371410) Chromosome 7 - NC_000073.6 Page 6 of 9 https://www.alphaknockout.com Transcript information: This gene has 4 transcripts Gene: Sema4b ENSMUSG00000030539 Description sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4B [Source:MGI Symbol;Acc:MGI:107559] Gene Synonyms SemC, Semac Location Chromosome 7: 80,186,841-80,226,527 forward strand. GRCm38:CM001000.2 About this gene This gene has 4 transcripts (splice variants), 254 orthologues, 19 paralogues, is a member of 1 Ensembl protein family and is associated with 3 phenotypes. Transcripts Name Transcript ID bp Protein Translation ID Biotype CCDS UniProt Flags Sema4b-201 ENSMUST00000032754.8 3949 823aa ENSMUSP00000032754.7 Protein coding CCDS21391 Q62179 TSL:1 GENCODE basic APPRIS P1 Sema4b-204 ENSMUST00000205822.1 3760 823aa ENSMUSP00000145622.1 Protein coding CCDS21391 Q62179 TSL:1 GENCODE basic APPRIS P1 Sema4b-202 ENSMUST00000107383.7 2775 No protein - Retained intron - - TSL:1 Sema4b-203 ENSMUST00000123023.2 1202 No protein - Retained intron - - TSL:1 Page 7 of 9 https://www.alphaknockout.com 59.69 kb Forward strand 80.18Mb 80.19Mb 80.20Mb 80.21Mb 80.22Mb 80.23Mb Genes (Comprehensive set... Sema4b-201 >protein coding Gdpgp1-201 >protein coding Sema4b-202 >retained intron Sema4b-204 >protein coding Sema4b-203 >retained intron Gm45206-201 >TEC Contigs AC109232.17 > Genes < Cib1-210nonsense mediated decay (Comprehensive set... < Cib1-201protein coding < Cib1-202protein coding < Cib1-207protein coding < Cib1-203protein coding < Cib1-208retained intron < Cib1-206protein coding < Cib1-204retained intron < Cib1-205retained intron < Cib1-209retained intron Regulatory Build 80.18Mb 80.19Mb 80.20Mb 80.21Mb 80.22Mb 80.23Mb Reverse strand 59.69 kb Regulation Legend CTCF Enhancer Open Chromatin Promoter Promoter Flank Transcription Factor Binding Site Gene Legend Protein Coding Ensembl protein coding merged Ensembl/Havana Non-Protein Coding processed transcript Page 8 of 9 https://www.alphaknockout.com Transcript: ENSMUST00000032754 39.69 kb Forward strand Sema4b-201 >protein coding ENSMUSP00000032... Transmembrane heli... Low complexity (Seg) Cleavage site (Sign... Superfamily Sema domain superfamily SSF103575 SMART Sema domain PSI domain Pfam Sema domain Plexin repeat PROSITE profiles Sema domain PANTHER Semaphorin PTHR11036:SF14 Gene3D WD40/YVTN repeat-like-containing domain superfamily 3.30.1680.10 CDD cd05872 All sequence SNPs/i..
Recommended publications
  • 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.
    [Show full text]
  • Peichel Et Al Revised
    The master sex-determination locus in threespine sticklebacks is on a nascent Y chromosome Catherine L. Peichel,1,2* Joseph A. Ross,2,3 Clinton K. Matson,2 Mark Dickson,4 Jane Grimwood,4 Jeremy Schmutz,4 Richard M. Myers,4 Seiichi Mori,5 Dolph Schluter,6 and David M. Kingsley1 1Department of Developmental Biology and HHMI, Stanford University School of Medicine, Palo Alto, California 94305, USA. 2Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. 3Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA. 4Stanford Human Genome Center, Department of Genetics, Stanford University School of Medicine, Palo Alto, California 94304, USA. 5Biological Laboratory, Gifu Keizai University, Ogaki, Gifu 503-8550, Japan. 6Department of Zoology, University of British Columbia, Vancouver V6T 1Z4, Canada. *Correspondence: [email protected] Running head: Sex chromosome evolution in sticklebacks 1 Summary Background: Many different environmental and genetic sex-determination mechanisms are found in nature. Closely related species can use different master sex-determination switches, suggesting that these developmental pathways can evolve very rapidly. Previous cytological studies suggest that recently diverged species of stickleback fish have different sex chromosome complements. Here we investigate the genetic and chromosomal mechanisms that underlie sex determination in the threespine stickleback (Gasterosteus aculeatus). Results: Genome-wide linkage mapping identifies
    [Show full text]
  • UC San Diego Electronic Theses and Dissertations
    UC San Diego UC San Diego Electronic Theses and Dissertations Title Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent Permalink https://escholarship.org/uc/item/7m04f0b0 Author Buchholz, Kyle Stephen Publication Date 2016 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent A dissertation submitted in partial satisfaction of the requirements for the degree Doctor of Philosophy in Bioengineering by Kyle Stephen Buchholz Committee in Charge: Professor Jeffrey Omens, Chair Professor Andrew McCulloch, Co-Chair Professor Ju Chen Professor Karen Christman Professor Robert Ross Professor Alexander Zambon 2016 Copyright Kyle Stephen Buchholz, 2016 All rights reserved Signature Page The Dissertation of Kyle Stephen Buchholz is approved and it is acceptable in quality and form for publication on microfilm and electronically: Co-Chair Chair University of California, San Diego 2016 iii Dedication To my beautiful wife, Rhia. iv Table of Contents Signature Page ................................................................................................................... iii Dedication .......................................................................................................................... iv Table of Contents ................................................................................................................ v List of Figures ...................................................................................................................
    [Show full text]
  • 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.
    [Show full text]
  • Genome-Wide Meta-Analysis Implicates Mediators of Hair Follicle Development and Morphogenesis in Risk for Severe Acne
    ARTICLE DOI: 10.1038/s41467-018-07459-5 OPEN Genome-wide meta-analysis implicates mediators of hair follicle development and morphogenesis in risk for severe acne Christos Petridis1, Alexander A. Navarini1,2, Nick Dand 1, Jake Saklatvala1, David Baudry3, Michael Duckworth3, Michael H. Allen3, Charles J. Curtis4,5, Sang Hyuck Lee4,5, A. David Burden6, Alison Layton7, Veronique Bataille8, Andrew E. Pink3, The Acne Genetic Study Group#, Isabelle Carlavan9, Johannes J. Voegel9, Timothy D. Spector8, Richard C. Trembath 1, John A. McGrath 3, Catherine H. Smith3, Jonathan N. Barker3 & Michael A. Simpson1 1234567890():,; Acne vulgaris is a highly heritable common, chronic inflammatory disease of the skin for which five genetic risk loci have so far been identified. Here, we perform a genome-wide association study of 3823 cases and 16,144 controls followed by meta-analysis with summary statistics from a previous study, with a total sample size of 26,722. We identify 20 inde- pendent association signals at 15 risk loci, 12 of which have not been previously implicated in the disease. Likely causal variants disrupt the coding region of WNT10A and a P63 tran- scription factor binding site in SEMA4B. Risk alleles at the 1q25 locus are associated with increased expression of LAMC2, in which biallelic loss-of-function mutations cause the blistering skin disease epidermolysis bullosa. These findings indicate that variation affecting the structure and maintenance of the skin, in particular the pilosebaceous unit, is a critical aspect of the genetic predisposition to severe acne. 1 Department of Medical and Molecular Genetics, School of Basic & Medical Biosciences, King’s College London, London SE1 9RT, UK.
    [Show full text]
  • Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
    Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
    [Show full text]
  • Whole Exome Sequencing Identifies APCDD1 and HDAC5 Genes As Potentially Cancer Predisposing in Familial Colorectal Cancer
    International Journal of Molecular Sciences Article Whole Exome Sequencing Identifies APCDD1 and HDAC5 Genes as Potentially Cancer Predisposing in Familial Colorectal Cancer Diamanto Skopelitou 1,2,3,4, Beiping Miao 1,2,3, Aayushi Srivastava 1,2,3,4, Abhishek Kumar 1,5,6, Magdalena Ku´swik 7, Dagmara Dymerska 7, Nagarajan Paramasivam 8, Matthias Schlesner 9 , Jan Lubinski 7, Kari Hemminki 1,10,11, Asta Försti 1,2,3 and Obul Reddy Bandapalli 1,2,3,4,* 1 Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; [email protected] (D.S.); [email protected] (B.M.); [email protected] (A.S.); [email protected] (A.K.); [email protected] (K.H.); [email protected] (A.F.) 2 Hopp Children’s Cancer Center (KiTZ), 69120 Heidelberg, Germany 3 Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), 69120 Heidelberg, Germany 4 Medical Faculty, Heidelberg University, 69120 Heidelberg, Germany 5 Institute of Bioinformatics, International Technology Park, Bangalore 560066, India 6 Manipal Academy of Higher Education (MAHE), Manipal 576104, India 7 Department of Genetics and Pathology, Pomeranian Medical University, 71252 Szczecin, Poland; [email protected] (M.K.); [email protected] (D.D.); [email protected] (J.L.) 8 Computational Oncology, Molecular Diagnostics Program, National Center for Tumor Diseases (NCT), 69120 Heidelberg, Germany; [email protected] 9 Bioinformatics and Omics Data Analytics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany; Citation: Skopelitou, D.; Miao, B.; [email protected] 10 Srivastava, A.; Kumar, A.; Ku´swik, Cancer Epidemiology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany 11 Biomedical Center, Faculty of Medicine in Pilsen, Charles University in Prague, 30605 Pilsen, Czech Republic M.; Dymerska, D.; Paramasivam, N.; * Correspondence: [email protected]; Tel.: +49-6221-421809 Schlesner, M.; Lubinski, J.; Hemminki, K.; et al.
    [Show full text]
  • Transcriptional Regulation by DAX-1 in Pluripotent and Differentiated Cells Alexandra C
    The University of San Francisco USF Scholarship: a digital repository @ Gleeson Library | Geschke Center Master's Theses Theses, Dissertations, Capstones and Projects Fall 5-22-2015 Transcriptional Regulation by DAX-1 in Pluripotent and Differentiated Cells Alexandra C. Maramba University of San Francisco, [email protected] Follow this and additional works at: https://repository.usfca.edu/thes Part of the Bioinformatics Commons, Biology Commons, and the Laboratory and Basic Science Research Commons Recommended Citation Maramba, Alexandra C., "Transcriptional Regulation by DAX-1 in Pluripotent and Differentiated Cells" (2015). Master's Theses. 153. https://repository.usfca.edu/thes/153 This Thesis is brought to you for free and open access by the Theses, Dissertations, Capstones and Projects at USF Scholarship: a digital repository @ Gleeson Library | Geschke Center. It has been accepted for inclusion in Master's Theses by an authorized administrator of USF Scholarship: a digital repository @ Gleeson Library | Geschke Center. For more information, please contact [email protected]. Abstract DAX-1, an orphan nuclear hormone receptor, acts mainly as a repressor through transcriptional protein complexes. Its unique structure and specific expression raises questions as to what its precise interactions are and how it mediates its repressive function. While it is known to play a role in sexual development and adrenal insufficiency, expression in certain types of cancer suggests additional functions and interactions. Knock in of DAX-1 into a low-DAX-1 expressing cancer cell line has been previously observed to increase apoptosis, while, inversely, down in a high-DAX-1 expressing cancer cell line shows a decrease in apoptosis.
    [Show full text]
  • Immune Cells in Spleen and Mucosa + CD127 Neg Production of IL-17
    Downloaded from http://www.jimmunol.org/ by guest on September 26, 2021 neg is online at: average * The Journal of Immunology published online 21 June 2010 Immune Cells in Spleen and Mucosa from submission to initial decision + 4 weeks from acceptance to publication TLR5 Signaling Stimulates the Innate Production of IL-17 and IL-22 by CD3 CD127 Laurye Van Maele, Christophe Carnoy, Delphine Cayet, Pascal Songhet, Laure Dumoutier, Isabel Ferrero, Laure Janot, François Erard, Julie Bertout, Hélène Leger, Florent Sebbane, Arndt Benecke, Jean-Christophe Renauld, Wolf-Dietrich Hardt, Bernhard Ryffel and Jean-Claude Sirard http://www.jimmunol.org/content/early/2010/06/21/jimmun ol.1000115 J Immunol Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2010/06/21/jimmunol.100011 5.DC1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 26, 2021. Published June 21, 2010, doi:10.4049/jimmunol.1000115
    [Show full text]
  • Multi-Omics Study of Chronic Obstructive Pulmonary Disease and Related Disorders
    S E R IV T E C D U R R O T S I S D B O D E C I T A N L O E R R H C D N F A O E Y S D A U E T S S I D S C I Y R M A O N - I O T M L L U U M P MULTI-OMICS STUDY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND RELATED DISORDERS I va n a P r o k I ć I va n a P r o k I ć Multi-omics Study of Chronic Obstructive Pulmonary Disease and Related Disorders Ivana Prokić Acknowledgements The work described in this thesis was conducted at the Genetic Epidemiology Unit, Department of Epidemiology, Erasmus Medical Center, Rotterdam, The Netherlands. The work presented in this thesis was supported by grant number 4.1.13.007 of Lung Foundation Netherlands (Longfonds), Biobanking and Biomolecular Resources arship. Research Infrastracture (BBMRI)-NL (184.021.007), Corbell, and by ERAWEB schol- The Erasmus Rucphen Family study as a part of EUROSPAN (European Special Populations Research Network) was supported by European Commission FP6 STRP grant number 018947 (LSHG-CT-2006-01947) and also received funding from the European Community’s Seventh Framework Programme (FP7/2007-2013)/ grant agreement HEALTH-F4-2007-201413 by the European Commission under the programme “Quality of Life and Management of the Living Resources” of 5th by Erasmus Medical Center and Erasmus University, Rotterdam, Netherlands Orga Framework Programme (no. QLG2-CT-2002-01254). The Rotterdam Study is funded - nization for the Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission (DG XII), and ists, researchers, institutions and funders of all other studies from this thesis are the Municipality of Rotterdam.
    [Show full text]
  • 1 Supplementary Material Figure S1. Volcano Plot of Differentially
    Supplementary material Figure S1. Volcano Plot of differentially expressed genes between preterm infants fed own mother’s milk (OMM) or pasteurized donated human milk (DHM). Table S1. The 10 most representative biological processes filtered for enrichment p- value in preterm infants. Biological Processes p-value Quantity of DEG* Transcription, DNA-templated 3.62x10-24 189 Regulation of transcription, DNA-templated 5.34x10-22 188 Transport 3.75x10-17 140 Cell cycle 1.03x10-13 65 Gene expression 3.38x10-10 60 Multicellular organismal development 6.97x10-10 86 1 Protein transport 1.73x10-09 56 Cell division 2.75x10-09 39 Blood coagulation 3.38x10-09 46 DNA repair 8.34x10-09 39 Table S2. Differential genes in transcriptomic analysis of exfoliated epithelial intestinal cells between preterm infants fed own mother’s milk (OMM) and pasteurized donated human milk (DHM). Gene name Gene Symbol p-value Fold-Change (OMM vs. DHM) (OMM vs. DHM) Lactalbumin, alpha LALBA 0.0024 2.92 Casein kappa CSN3 0.0024 2.59 Casein beta CSN2 0.0093 2.13 Cytochrome c oxidase subunit I COX1 0.0263 2.07 Casein alpha s1 CSN1S1 0.0084 1.71 Espin ESPN 0.0008 1.58 MTND2 ND2 0.0138 1.57 Small ubiquitin-like modifier 3 SUMO3 0.0037 1.54 Eukaryotic translation elongation EEF1A1 0.0365 1.53 factor 1 alpha 1 Ribosomal protein L10 RPL10 0.0195 1.52 Keratin associated protein 2-4 KRTAP2-4 0.0019 1.46 Serine peptidase inhibitor, Kunitz SPINT1 0.0007 1.44 type 1 Zinc finger family member 788 ZNF788 0.0000 1.43 Mitochondrial ribosomal protein MRPL38 0.0020 1.41 L38 Diacylglycerol
    [Show full text]
  • Downloaded from Onment of Regions Bound by PU.1 Or Spi-B, Significant Published GEO Datasets
    Solomon et al. BMC Genomics (2015) 16:76 DOI 10.1186/s12864-015-1303-0 RESEARCH ARTICLE Open Access Genome-wide comparison of PU.1 and Spi-B binding sites in a mouse B lymphoma cell line Lauren A Solomon1, Stephen KH Li1, Jan Piskorz1,LiSXu1 and Rodney P DeKoter1,2,3* Abstract Background: Spi-B and PU.1 are highly related members of the E26-transformation-specific (ETS) family of transcription factors that have similar, but not identical, roles in B cell development. PU.1 and Spi-B are both expressed in B cells, and have been demonstrated to redundantly activate transcription of genes required for B cell differentiation and function. It was hypothesized that Spi-B and PU.1 occupy a similar set of regions within the genome of a B lymphoma cell line. Results: To compare binding regions of Spi-B and PU.1, murine WEHI-279 lymphoma cells were infected with retroviral vectors encoding 3XFLAG-tagged PU.1 or Spi-B. Anti-FLAG chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) was performed. Analysis for high-stringency enriched genomic regions demonstrated that PU.1 occupied 4528 regions and Spi-B occupied 3360 regions. The majority of regions occupied by Spi-B were also occupied by PU.1. Regions bound by Spi-B and PU.1 were frequently located immediately upstream of genes associated with immune response and activation of B cells. Motif-finding revealed that both transcription factors were predominantly located at the ETS core domain (GGAA), however, other unique motifs were identified when examining regions associated with only one of the two factors.
    [Show full text]