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ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A ZBTB7A E2F6EGR1 EGR1 E2F6 E2F6EGR1 E2F6 EGR1 E2F6 EGR1 EGR1 E2F6 E2F6 EGR1 E2F6 EGR1 E2F6EGR1 EGR1 E2F6 E2F6EGR1 EGR1 E2F6 E2F6EGR1 E2F6 EGR1 E2F6EGR1 EGR1 E2F6 E2F6 EGR1 E2F6 EGR1 E2F6EGR1 EGR1 E2F6 ZBTB7Ainput ZBTB7Ainput ZBTB7Ainput inputZBTB7A input ZBTB7A ZBTB7Ainput ZBTB7Ainput inputZBTB7A inputZBTB7A ZBTB7Ainput MAX MAX MAX MAX MAX MAX MAX MAX MAX MAX MAXETS1 ETS1MAX MAX ETS1 MAX ETS1 MAXETS1 ETS1MAX ETS1MAX ETS1MAX ETS1MAX ETS1MAX GATA2SIN3AFOSL1input input GATA2FOSL1SIN3A GATA2FOSL1SIN3A input input GATA2SIN3AFOSL1 SIN3A GATA2FOSL1 input FOSL1GATA2SIN3Ainput GATA2SIN3AFOSL1input inputSIN3AFOSL1GATA2 inputFOSL1GATA2SIN3A input FOSL1GATA2SIN3A SIN3ATHAP1MAXELF1MAX SP1 SP1SIN3ATHAP1ELF1 MAXMAX SP1MAXMAXTHAP1SIN3AELF1 MAXMAX SIN3ASP1THAP1 ELF1 ELF1 MAXMAXSIN3A THAP1SP1 SIN3ASP1MAXMAXTHAP1ELF1 ELF1SIN3AMAXSP1THAP1 THAP1MAXSIN3ASP1 ELF1 ELF1THAP1 SP1MAXMAXSIN3A ELF1THAP1SP1SIN3AMAX YY1YY1GATA2MEF2AMYCTEAD4PMLMYC YY1YY1PMLTEAD4GATA2MEF2AMYCMYC GATA2MYCPMLTEAD4MEF2AYY1YY1 MYCTEAD4GATA2MEF2APML YY1YY1 MYCMYCPMLYY1YY1MEF2AGATA2TEAD4 PMLGATA2MEF2ATEAD4MYCYY1YY1 PMLGATA2MYCMEF2AMYCTEAD4 YY1YY1 YY1YY1 PMLMYCTEAD4MYCMEF2AGATA2 PMLTEAD4MEF2AGATA2MYCYY1YY1 PMLMEF2AGATA2TEAD4YY1YY1 MYCMYC LV1 ZBTB33TAL1ATF3JUNDFOSL1SPI1MXI1NRF1JUN SP1 SPI1SP1ZBTB33FOSL1JUNDTAL1ATF3NRF1JUNMXI1 SP1ZBTB33TAL1NRF1FOSL1ATF3MXI1JUNJUNDSPI1 NRF1MXI1ZBTB33TAL1FOSL1ATF3JUNDJUNSP1SPI1 NRF1 SPI1MXI1 JUNZBTB33FOSL1ATF3JUNDTAL1SP1 NRF1ZBTB33TAL1JUNJUNDFOSL1ATF3SP1MXI1 SPI1 SPI1TAL1ZBTB33FOSL1MXI1SP1JUNDATF3JUN NRF1 TAL1ZBTB33FOSL1MXI1JUNDSP1ATF3JUNNRF1 SPI1 NRF1 SPI1JUNATF3JUNDFOSL1TAL1ZBTB33SP1MXI1 ATF3JUNDSPI1JUNFOSL1ZBTB33SP1TAL1 MXI1NRF1 TAL1PMLMEF2ATEAD4BHLHE40ETS1BHLHE40JUNDSPI1ELF1ATF3 SP2 SP2ELF1SPI1PMLTEAD4TAL1JUNDMEF2AETS1BHLHE40BHLHE40ATF3 SP2BHLHE40TAL1PMLTEAD4MEF2AJUNDATF3SPI1ETS1ELF1 BHLHE40BHLHE40TEAD4TAL1ATF3JUNDPMLMEF2ASPI1ETS1SP2ELF1 ELF1 ATF3SPI1BHLHE40PMLETS1MEF2AJUNDTEAD4TAL1SP2 TAL1ATF3ETS1JUNDPMLTEAD4MEF2ABHLHE40BHLHE40SP2SPI1ELF1 ELF1PMLSP2TAL1SPI1MEF2ATEAD4ETS1BHLHE40JUNDATF3 ATF3ETS1BHLHE40PMLTAL1TEAD4MEF2ASP2JUNDSPI1ELF1 ELF1ATF3PMLSPI1BHLHE40TAL1JUNDTEAD4BHLHE40MEF2AETS1SP2 BHLHE40ATF3BHLHE40JUNDELF1SPI1MEF2APMLTEAD4TAL1SP2ETS1 36% of variance ZBTB33BCLAF1YY1MYCTHAP1MXI1SRFMAFK YY1 ZBTB33MAFKSRFBCLAF1THAP1MXI1MYC ZBTB33MYCBCLAF1MXI1MAFKTHAP1SRFYY1 MYCMXI1MAFKZBTB33BCLAF1SRFTHAP1YY1 MYCMXI1YY1THAP1SRFMAFKBCLAF1ZBTB33 ZBTB33BCLAF1MAFKMYCSRFMXI1YY1THAP1 BCLAF1MYCZBTB33MAFKSRFMXI1THAP1 YY1 YY1 THAP1 MAFKMYCBCLAF1ZBTB33SRFMXI1 THAP1MAFKBCLAF1SRFZBTB33MYCMXI1YY1 THAP1BCLAF1SRFYY1ZBTB33MAFK MYCMXI1 YY1BCLAF1NRF1SRFMAFKMAXMAX SP2 YY1SP2MAFKBCLAF1NRF1SRF MAX SP2MAXMAXNRF1YY1BCLAF1MAFKSRF MAXMAX NRF1MAFKBCLAF1SRFYY1 SP2 NRF1 MAXMAX SRFYY1MAFKBCLAF1SP2 NRF1BCLAF1SRFMAFKMAXSP2MAXYY1 BCLAF1SP2 MAFKMAXMAXSRF YY1 NRF1YY1 MAXMAXMAFKBCLAF1SP2SRFNRF1 NRF1 MAFKBCLAF1SRFMAXMAXSP2YY1 SRFMAFKBCLAF1YY1SP2MAXMAX NRF1 MYC RFX5SIX5 RFX5SIX5 MYC RFX5MYC SIX5 MYCRFX5SIX5 MYC RFX5SIX5 SIX5RFX5MYC MYCSIX5RFX5 SIX5MYCRFX5 SIX5RFX5MYC RFX5 SIX5MYC inputRFX5ZNF143inputZNF143 NFYA NFYB inputNFYANFYB RFX5ZNF143inputZNF143 NFYB NFYA RFX5input input ZNF143ZNF143 input RFX5inputNFYBNFYAZNF143ZNF143 NFYBRFX5inputNFYAZNF143ZNF143input ZNF143ZNF143 RFX5inputNFYBNFYAinput NFYBZNF143NFYAinputRFX5input NFYBZNF143NFYARFX5inputinput inputRFX5NFYBZNF143inputNFYAZNF143 input RFX5inputNFYANFYBZNF143ZNF143 MAFFCEBPBJUNinputUSF1 FOS NFYB NFYBCEBPBMAFFFOSinputJUN USF1NFYBFOS USF1inputCEBPBJUNMAFF USF1CEBPBMAFFinputJUNNFYBFOS USF1 inputFOSNFYBJUNCEBPBMAFF JUNMAFFinputCEBPBFOSUSF1NFYB NFYBUSF1MAFFinputFOSCEBPBJUN USF1NFYBFOSinputMAFFCEBPBJUN CEBPBinputJUNNFYBMAFFFOSUSF1 USF1 CEBPBJUNFOSMAFFinputNFYB GABPA NFYAFOS NFYAGABPAGABPAFOS NFYAFOS GABPAGABPA FOSNFYA GABPAGABPAGABPAGABPA FOSNFYA FOSNFYA GABPAGABPAGABPAGABPA NFYAFOS NFYAFOS GABPA GABPAGABPANFYAFOS GABPAGABPAFOS NFYA inputinputCEBPBNFE2 CEBPBinputinput NFE2 NFE2inputinputCEBPB NFE2CEBPBinputinput NFE2 CEBPB inputinput NFE2CEBPBinputinput inputinput NFE2CEBPB NFE2inputinputCEBPB CEBPBinputinputNFE2 NFE2CEBPB input input USF2SIX5 FOS FOS SIX5 USF2 FOS USF2 SIX5 USF2 FOS SIX5 USF2 FOSSIX5 SIX5 FOSUSF2 USF2FOSSIX5 USF2SIX5 FOS SIX5USF2FOS USF2 FOS SIX5 SIX5MAFFinputNFE2SIX5USF1 MAFF input SIX5 NFE2 USF1 USF1NFE2inputMAFF SIX5SIX5MAFFUSF1NFE2input SIX5SIX5 USF1 NFE2inputSIX5MAFF SIX5SIX5 MAFFUSF1inputNFE2 USF1inputSIX5MAFFSIX5NFE2 USF1SIX5SIX5NFE2 inputMAFF NFE2inputSIX5SIX5 MAFFUSF1 USF1 NFE2 MAFFinputSIX5SIX5 USF2 USF2 USF2 USF2 USF2 USF2 USF2 USF2 USF2 USF2 input input input input input input input input input input NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYBNFYB NFYAFOS NFYAFOS NFYAFOS FOSNFYA FOSNFYA FOSNFYA NFYAFOS NFYAFOS NFYAFOS FOS NFYA FOSFOSNFYA NFYAFOSFOS FOSFOSNFYA FOSNFYAFOS FOSFOSNFYA FOSNFYAFOS NFYAFOSFOS FOSNFYAFOS NFYAFOSFOS FOSFOS NFYA SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 LV2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP2 SP1 8% of variance SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 SP1 USF1USF1ZNF143 ZNF143 USF1USF1 USF1USF1 ZNF143 USF1USF1 ZNF143 USF1USF1 ZNF143 ZNF143 USF1 ZNF143USF1USF1 USF1USF1ZNF143 ZNF143USF1 USF1USF1 ZNF143 USF2NFE2NFE2ZNF143 ZNF143NFE2NFE2USF2 NFE2NFE2USF2 ZNF143USF2 NFE2NFE2 ZNF143 USF2NFE2NFE2 ZNF143 ZNF143 NFE2NFE2USF2 USF2ZNF143NFE2NFE2 USF2NFE2NFE2ZNF143 NFE2NFE2USF2ZNF143 NFE2USF2 ZNF143 MAFFinputUSF2SIX5SIX5inputSIX5RFX5 MAFF inputinput RFX5SIX5SIX5 USF2 RFX5USF2inputinputMAFFSIX5 SIX5SIX5MAFFUSF2inputinput RFX5SIX5SIX5SIX5 USF2 RFX5inputSIX5MAFFSIX5SIX5input SIX5SIX5RFX5MAFFinputinputUSF2 USF2inputinputMAFFSIX5RFX5 USF2SIX5SIX5SIX5inputinputRFX5MAFF inputSIX5SIX5SIX5RFX5USF2inputMAFF input USF2 RFX5MAFFinputSIX5SIX5SIX5 SIX5CEBPBinputRFX5ATF3 input inputCEBPBRFX5inputSIX5 ATF3 RFX5inputCEBPBATF3input SIX5 inputCEBPBATF3inputRFX5 SIX5 ATF3 inputRFX5SIX5CEBPBinput SIX5ATF3RFX5inputCEBPBinput RFX5SIX5inputinputATF3CEBPB SIX5ATF3RFX5inputinputCEBPB CEBPBinputATF3SIX5RFX5input input ATF3CEBPBRFX5input SIX5 CEBPBJUNinputMAXBHLHE40MAFKBHLHE40ELF1JUN CEBPBELF1MAFKJUNinputJUN BHLHE40BHLHE40MAX BHLHE40MAXMAXinputCEBPBJUNJUNMAFK ELF1 MAXMAXBHLHE40BHLHE40CEBPBMAFKJUNinputJUN ELF1 ELF1 MAXMAXBHLHE40JUNinputMAFKJUNCEBPB JUNJUNMAFKinputBHLHE40BHLHE40CEBPBMAXMAX ELF1 ELF1BHLHE40MAFKinputMAXMAXJUNCEBPBJUN BHLHE40MAXMAXinputMAFKCEBPBJUNJUNELF1 ELF1CEBPBinputJUNJUNMAFKBHLHE40BHLHE40MAXMAX BHLHE40BHLHE40CEBPBJUNJUNELF1MAFKMAXinputMAX input GABPAGABPANRF1SRFTHAP1MXI1MAFKJUNDFOSL1SPI1JUNDMXI1NRF1SPI1THAP1 input inputGABPASPI1GABPASPI1MAFKJUNDFOSL1JUNDNRF1NRF1SRFTHAP1MXI1THAP1MXI1input inputNRF1FOSL1THAP1MXI1JUNDMXI1JUNDMAFKTHAP1SPI1SRFinputSPI1 GABPAGABPA input NRF1MXI1NRF1MXI1MAFKFOSL1JUNDJUNDSPI1SPI1inputSRFTHAP1 GABPAGABPAGABPANRF1GABPANRF1 SPI1MXI1MXI1SPI1SRFinputTHAP1inputMAFKTHAP1FOSL1JUNDJUND NRF1NRF1JUNDJUNDSRFFOSL1MAFKinputMXI1MXI1inputTHAP1SPI1THAP1SPI1 GABPAGABPAGABPAGABPA SPI1SPI1MAFKinputFOSL1MXI1inputMXI1JUNDSRFTHAP1 NRF1NRF1 THAP1THAP1inputinputMAFKFOSL1MXI1MXI1JUNDSRFNRF1NRF1SPI1SPI1GABPANRF1NRF1 THAP1THAP1GABPAinputSPI1GABPASPI1MAFKinputJUNDFOSL1SRFMXI1MXI1 JUNDGABPAGABPAJUNDSPI1SRFFOSL1SPI1THAP1THAP1MAFKinputinputMXI1NRF1NRF1 MAFFSRFETS1ATF3MAXELF1FOSL1MAX EGR1EGR1 MAFFATF3SRFFOSL1ETS1ELF1EGR1MAXMAX EGR1MAXMAXFOSL1ATF3MAFFSRFELF1ETS1 MAXMAFFMAXATF3FOSL1SRFETS1EGR1EGR1 ELF1 ELF1 MAXMAX SRFETS1ATF3FOSL1MAFFEGR1EGR1 ETS1EGR1MAFFEGR1FOSL1ATF3SRFMAXMAX ELF1 ELF1ETS1MAXFOSL1MAFFSRFEGR1ATF3EGR1 ETS1MAXFOSL1MAFFSRFATF3EGR1EGR1ELF1 ELF1 EGR1EGR1ATF3FOSL1ETS1SRFMAFFMAXMAX EGR1EGR1ATF3ELF1FOSL1SRFMAFFMAXETS1 input MYCMYCMEF2ATEAD4TEAD4MEF2ASIN3ASIN3AMAXETS1ZBTB7AZBTB7AE2F6E2F6 TEAD4inputTEAD4MEF2AMEF2ASIN3ASIN3AZBTB7AMYCMYCETS1ZBTB7AMAX E2F6 E2F6ZBTB7AZBTB7AMAXMYCTEAD4MYCTEAD4MEF2ASIN3AMEF2ASIN3AinputETS1 MAXinputMYCMYCE2F6TEAD4TEAD4MEF2ASIN3AMEF2ASIN3AZBTB7AETS1ZBTB7A SIN3AMYCMYCSIN3AMAXETS1MEF2ATEAD4E2F6E2F6ZBTB7AZBTB7Ainput MEF2ATEAD4MEF2AMYCZBTB7AETS1SIN3ASIN3AinputMAX E2F6E2F6 ZBTB7AinputSIN3AE2F6MEF2ASIN3ATEAD4MEF2AETS1TEAD4MYCMAXMYC E2F6E2F6ETS1MAXSIN3ATEAD4MYCMEF2ASIN3AMEF2AZBTB7Ainput E2F6ZBTB7AZBTB7AinputTEAD4TEAD4MEF2AMEF2AETS1MAXMYCSIN3ASIN3A MEF2AMEF2AZBTB7ATEAD4ZBTB7ATEAD4SIN3AETS1inputMYCE2F6MAXMYC input BCLAF1BCLAF1ZBTB33TAL1ZBTB33PMLTAL1GATA2MYCMYCPML MAX PMLPMLZBTB33TAL1GATA2ZBTB33BCLAF1inputTAL1BCLAF1MYCMYC MAX MAXZBTB33GATA2MYCTAL1PMLTAL1PMLinputBCLAF1BCLAF1 MAXinputMYCTAL1GATA2ZBTB33TAL1PMLBCLAF1PMLBCLAF1 MYCMYCMAXPMLPMLZBTB33BCLAF1GATA2BCLAF1TAL1ZBTB33TAL1 input ZBTB33TAL1ZBTB33TAL1PMLBCLAF1PMLBCLAF1GATA2MYCinputMAX inputBCLAF1PMLTAL1TAL1GATA2MYCMYCZBTB33MAX PMLinputTAL1MAXMYCMYCTAL1BCLAF1ZBTB33GATA2BCLAF1ZBTB33 inputPMLPMLBCLAF1BCLAF1TAL1TAL1GATA2ZBTB33ZBTB33MAXMYC PMLZBTB33PMLGATA2BCLAF1BCLAF1ZBTB33TAL1TAL1MYCMYCMAXinput YY1 GATA2 YY1 GATA2 GATA2 YY1 GATA2 YY1 YY1 GATA2 GATA2YY1 GATA2 YY1 YY1 GATA2 GATA2 YY1 YY1GATA2 YY1 YY1 YY1 YY1 YY1 YY1 YY1 YY1 YY1 YY1 YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 YY1YY1 USF1USF1 E2F6E2F6 E2F6E2F6 USF1USF1 E2F6 USF1USF1 USF1USF1 E2F6 USF1USF1 E2F6E2F6 USF1 E2F6E2F6 E2F6USF1USF1 USF1USF1E2F6E2F6 E2F6 USF1 USF1USF1 E2F6 MAX MAX MAX MAX MAX MAX MAX MAX MAX MAX USF2 MAXATF3 MAXATF3USF2 MAXUSF2ATF3 USF2MAX ATF3 ATF3MAXUSF2 ATF3 USF2MAX USF2MAXATF3 USF2ATF3MAX ATF3USF2MAX USF2ATF3 MAX USF2 BHLHE40BHLHE40MAXMAX MAXBHLHE40MAXBHLHE40USF2 BHLHE40MAXMAXUSF2 USF2BHLHE40BHLHE40MAXMAX USF2MAXMAXBHLHE40 BHLHE40BHLHE40MAXMAXUSF2 USF2MAXMAXBHLHE40 USF2 BHLHE40MAX BHLHE40USF2BHLHE40MAXMAX BHLHE40BHLHE40USF2 MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX MAXMAX NFE2 EGR1EGR1ZBTB7A ZBTB7AEGR1EGR1NFE2 EGR1ZBTB7ANFE2 NFE2 ZBTB7AEGR1EGR1 NFE2 ZBTB7AEGR1EGR1 EGR1EGR1ZBTB7ANFE2 ZBTB7ANFE2EGR1EGR1
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  • Cellular Responses to Erbb-2 Overexpression in Human Mammary Luminal Epithelial Cells: Comparison of Mrna and Protein Expression

    Cellular Responses to Erbb-2 Overexpression in Human Mammary Luminal Epithelial Cells: Comparison of Mrna and Protein Expression

    British Journal of Cancer (2004) 90, 173 – 181 & 2004 Cancer Research UK All rights reserved 0007 – 0920/04 $25.00 www.bjcancer.com Cellular responses to ErbB-2 overexpression in human mammary luminal epithelial cells: comparison of mRNA and protein expression SL White1, S Gharbi1, MF Bertani1, H-L Chan1, MD Waterfield1 and JF Timms*,1 1 Ludwig Institute for Cancer Research, Wing 1.1, Cruciform Building, Gower Street, London WCIE 6BT, UK Microarray analysis offers a powerful tool for studying the mechanisms of cellular transformation, although the correlation between mRNA and protein expression is largely unknown. In this study, a microarray analysis was performed to compare transcription in response to overexpression of the ErbB-2 receptor tyrosine kinase in a model mammary luminal epithelial cell system, and in response to the ErbB-specific growth factor heregulin b1. We sought to validate mRNA changes by monitoring changes at the protein level using a parallel proteomics strategy, and report a surprisingly high correlation between transcription and translation for the subset of genes studied. We further characterised the identified targets and relate differential expression to changes in the biological properties of ErbB-2-overexpressing cells. We found differential regulation of several key cell cycle modulators, including cyclin D2, and downregulation of a large number of interferon-inducible genes, consistent with increased proliferation of the ErbB-2- overexpressing cells. Furthermore, differential expression of genes involved in extracellular matrix modelling and cellular adhesion was linked to altered adhesion of these cells. Finally, we provide evidence for enhanced autocrine activation of MAPK signalling and the AP-1 transcription complex.
  • Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model

    Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model

    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 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/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.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 © 2016 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 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.
  • 2017.08.28 Anne Barry-Reidy Thesis Final.Pdf

    2017.08.28 Anne Barry-Reidy Thesis Final.Pdf

    REGULATION OF BOVINE β-DEFENSIN EXPRESSION THIS THESIS IS SUBMITTED TO THE UNIVERSITY OF DUBLIN FOR THE DEGREE OF DOCTOR OF PHILOSOPHY 2017 ANNE BARRY-REIDY SCHOOL OF BIOCHEMISTRY & IMMUNOLOGY TRINITY COLLEGE DUBLIN SUPERVISORS: PROF. CLIONA O’FARRELLY & DR. KIERAN MEADE TABLE OF CONTENTS DECLARATION ................................................................................................................................. vii ACKNOWLEDGEMENTS ................................................................................................................... viii ABBREVIATIONS ................................................................................................................................ix LIST OF FIGURES............................................................................................................................. xiii LIST OF TABLES .............................................................................................................................. xvii ABSTRACT ........................................................................................................................................xix Chapter 1 Introduction ........................................................................................................ 1 1.1 Antimicrobial/Host-defence peptides ..................................................................... 1 1.2 Defensins................................................................................................................. 1 1.3 β-defensins .............................................................................................................
  • Chicken CCDC152 Shares an NFYB-Regulated Bidirectional Promoter with a Growth Hormone Receptor Antisense Transcript and Inhibits Cells Proliferation and Migration

    Chicken CCDC152 Shares an NFYB-Regulated Bidirectional Promoter with a Growth Hormone Receptor Antisense Transcript and Inhibits Cells Proliferation and Migration

    www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 48), pp: 84039-84053 Research Paper Chicken CCDC152 shares an NFYB-regulated bidirectional promoter with a growth hormone receptor antisense transcript and inhibits cells proliferation and migration Shudai Lin1, Wei Luo1, Mingya Jiang1, Wen Luo1, Bahareldin Ali Abdalla1, Qinghua Nie1, Li Zhang2 and Xiquan Zhang1 1Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, College of Animal Science of South China Agricultural University, Guangzhou 510642, P.R. China 2Agricultural College, Guangdong Ocean University, Zhanjiang 524088, P.R. China Correspondence to: Xiquan Zhang, email: [email protected] Li Zhang, email: [email protected] Keywords: bidirectional promoter, GHR antisense transcript, coiled-coil domain containing 152, NFYB, cell cycle Received: December 15, 2016 Accepted: September 04, 2017 Published: September 20, 2017 Copyright: Lin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The chicken coiled-coil domain-containing protein 152 (CCDC152) recently has been identified as a novel one implicated in cell cycle regulation, cellular proliferation and migration by us. Here we demonstrate that CCDC152 is oriented in a head-to- head configuration with the antisense transcript of growth hormone receptor (GHR) gene. Through serial luciferase reporter assays, we firstly identified a minimal 102 bp intergenic region as a core bidirectional promoter to drive basal transcription in divergent orientations.
  • A Candidate Molecular Signature Associated with Tamoxifen Failure in Primary Breast Cancer

    A Candidate Molecular Signature Associated with Tamoxifen Failure in Primary Breast Cancer

    Available online http://breast-cancer-research.com/content/10/5/R88 ResearchVol 10 No 5 article Open Access A candidate molecular signature associated with tamoxifen failure in primary breast cancer Julie A Vendrell1,2,3,4,5,6, Katherine E Robertson7*, Patrice Ravel8*, Susan E Bray5, Agathe Bajard9, Colin A Purdie5, Catherine Nguyen10, Sirwan M Hadad5, Ivan Bieche11, Sylvie Chabaud9, Thomas Bachelot12, Alastair M Thompson5 and Pascale A Cohen1,2,3,4,6 1Université de Lyon, 69008 Lyon, France 2Université de Lyon, Lyon 1, ISPB, Faculté de Pharmacie de Lyon, 69008 Lyon, France 3INSERM, U590, 69008 Lyon, France 4Centre Léon Bérard, FNCLCC, 69373 Lyon, France 5Department of Surgery and Molecular Oncology, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK 6CNRS UMR 5160, Centre de Pharmacologie et Biotechnologie pour la Santé, Faculté de Pharmacie, 34090 Montpellier, France 7Division of Pathology and Neuroscience, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, UK 8Centre de Biochimie Structurale, CNRS, INSERM, Université Montpellier I, 34090 Montpellier, France 9Centre Léon Bérard, FNCLCC, Unité de Biostatistique et d'Evaluation des Thérapeutiques, 69373 Lyon, France 10INSERM ERM206, Laboratoire TAGC, Université d'Aix-Marseille II, 13288 Marseille Cedex 9, France 11INSERM U735, Centre René Huguenin, FNCLCC, 92210 St-Cloud, France 12Centre Léon Bérard, FNCLCC, Département de Médecine, 69373 Lyon, France * Contributed equally Corresponding author: Pascale A Cohen, [email protected] Received: 28 Feb 2008 Revisions requested: 7 Apr 2008 Revisions received: 13 Oct 2008 Accepted: 17 Oct 2008 Published: 17 Oct 2008 Breast Cancer Research 2008, 10:R88 (doi:10.1186/bcr2158) This article is online at: http://breast-cancer-research.com/content/10/5/R88 © 2008 Vendrell et al.; licensee BioMed Central Ltd.
  • Genome-Wide Inference of Natural Selection on Human Transcription Factor Binding Sites

    Genome-Wide Inference of Natural Selection on Human Transcription Factor Binding Sites

    ANALYSIS Genome-wide inference of natural selection on human transcription factor binding sites Leonardo Arbiza1, Ilan Gronau1, Bulent A Aksoy2, Melissa J Hubisz1, Brad Gulko3, Alon Keinan1–3 & Adam Siepel1–3 For decades, it has been hypothesized that gene regulation persistence in humans7,8. In addition, some genome-wide analyses has had a central role in human evolution, yet much remains have found bulk statistical evidence of natural selection in noncoding unknown about the genome-wide impact of regulatory regions near genes, presumably due to cis-regulatory elements9–12. mutations. Here we use whole-genome sequences and genome- Nevertheless, evidence in support of the overall prominence of wide chromatin immunoprecipitation and sequencing data to cis-regulatory mutations in evolutionary adaptation remains largely demonstrate that natural selection has profoundly influenced anecdotal and indirect, and there is continuing controversy about the human transcription factor binding sites since the divergence relative roles of regulatory and protein-coding sequences in evolu- of humans from chimpanzees 4–6 million years ago. Our tion8. Large-scale genomic studies of the evolution of transcription analysis uses a new probabilistic method, called INSIGHT, for factor binding sites have the potential to advance this debate, but a measuring the influence of selection on collections of short, major limitation of such studies so far has been a lack of precisely interspersed noncoding elements. We find that, on average, annotated binding sites across the genome. The analysis of con- transcription factor binding sites have experienced somewhat served noncoding sequences and/or promoter regions rather than weaker selection than protein-coding genes.
  • The Unique Transcriptional Response Produced by Concurrent Estrogen

    The Unique Transcriptional Response Produced by Concurrent Estrogen

    Need et al. BMC Cancer (2015) 15:791 DOI 10.1186/s12885-015-1819-3 RESEARCH ARTICLE Open Access The unique transcriptional response produced by concurrent estrogen and progesterone treatment in breast cancer cells results in upregulation of growth factor pathways and switching from a Luminal A to a Basal-like subtype Eleanor F. Need1*,LukeA.Selth2,3,AndrewP.Trotta1,4,DamienA.Leach1,LaurenGiorgio1, Melissa A. O’Loughlin1, Eric Smith5, Peter G. Gill6,WendyV.Ingman7,8, J. Dinny Graham9 and Grant Buchanan1,3 Abstract Background: In breast cancer, progesterone receptor (PR) positivity or abundance is positively associated with survival and treatment response. It was initially believed that PR was a useful diagnostic marker of estrogen receptor activity, but increasingly PR has been recognised to play an important biological role in breast homeostasis, carcinogenesis and metastasis. Although PR expression is almost exclusively observed in estrogen receptor positive tumors, few studies have investigated the cellular mechanisms of PR action in the context of ongoing estrogen signalling. Methods: In this study, we contrast PR function in estrogen pretreated ZR-75-1 breast cancer cells with vehicle treated ZR-75-1 and T-47D breast cancer cells using expression microarrays and chromatin immunoprecipitation-sequencing. Results: Estrogen cotreatment caused a dramatic increase in the number of genes regulated by progesterone in ZR-75-1 cells. In T-47D cells that have naturally high levels of PR, estrogen and progesterone cotreatment resulted in a reduction in the number of regulated genes in comparison to treatment with either hormone alone. At a genome level, estrogen pretreatment of ZR-75-1 cells led to a 10-fold increase in the number of PR DNA binding sites detected using ChIP-sequencing.