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  1. Article: Multiple mechanisms contribute to the activation of RNA polymerase III transcription in cells transformed by papovaviruses.

    Felton-Edkins, Zoë A / White, Robert J

    The Journal of biological chemistry

    2002  Volume 277, Issue 50, Page(s) 48182–48191

    Abstract: RNA polymerase (pol) III transcription is abnormally active in fibroblasts transformed by polyomavirus (Py) or simian virus 40 (SV40). Several distinct mechanisms contribute to this effect. In untransformed fibroblasts, the basal pol III transcription ... ...

    Abstract RNA polymerase (pol) III transcription is abnormally active in fibroblasts transformed by polyomavirus (Py) or simian virus 40 (SV40). Several distinct mechanisms contribute to this effect. In untransformed fibroblasts, the basal pol III transcription factor (TF) IIIB is repressed through association with the retinoblastoma protein RB; this restraint is overcome by large T antigens of Py and SV40. Furthermore, cells transformed by these papovaviruses overexpress the BDP1 subunit of TFIIIB, at both the protein and mRNA levels. Despite the overexpression of BDP1, the abundance of the other TFIIIB components is unperturbed following papovavirus transformation. In contrast, mRNAs encoding all five subunits of the basal factor TFIIIC2 are found at elevated levels in fibroblasts transformed by Py or SV40. Thus, both papovaviruses stimulate pol III transcription by boosting production of selected components of the basal machinery. Py differs from SV40 in encoding a highly oncogenic middle T antigen that localizes outside the nucleus and activates several signal transduction pathways. Middle T can serve as a potent activator of a pol III reporter in transfected cells. Several distinct mechanisms therefore contribute to the high levels of pol III transcription that accompany transformation by Py and SV40.
    MeSH term(s) 3T3 Cells ; Amino Acid Sequence ; Animals ; Antigens, Polyomavirus Transforming/physiology ; Base Sequence ; Cell Division ; Cell Transformation, Viral ; DNA Primers ; Mice ; Molecular Sequence Data ; RNA Polymerase III/genetics ; RNA Polymerase III/metabolism ; RNA, Messenger/genetics ; Simian virus 40/physiology ; Transcription, Genetic
    Chemical Substances Antigens, Polyomavirus Transforming ; DNA Primers ; RNA, Messenger ; RNA Polymerase III (EC 2.7.7.6)
    Language English
    Publishing date 2002-10-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M201333200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Epstein-Barr virus induces cellular transcription factors to allow active expression of EBER genes by RNA polymerase III.

    Felton-Edkins, Zoë A / Kondrashov, Alexander / Karali, Dimitra / Fairley, Jennifer A / Dawson, Christopher W / Arrand, John R / Young, Lawrence S / White, Robert J

    The Journal of biological chemistry

    2006  Volume 281, Issue 45, Page(s) 33871–33880

    Abstract: The EBER genes of Epstein-Barr virus (EBV) are transcribed by RNA polymerase (pol) III to produce untranslated RNAs that are implicated in oncogenesis. These EBER transcripts are the most highly expressed viral gene products in EBV-transformed cells. We ... ...

    Abstract The EBER genes of Epstein-Barr virus (EBV) are transcribed by RNA polymerase (pol) III to produce untranslated RNAs that are implicated in oncogenesis. These EBER transcripts are the most highly expressed viral gene products in EBV-transformed cells. We have identified changes to the cellular transcription machinery that may contribute to the high levels of EBER RNA. These include phosphorylation of ATF2, which interacts with EBER promoters. A second is induction of TFIIIC, a pol III-specific factor that activates EBER genes; all five subunits of TFIIIC are overexpressed in EBV-positive cells. In addition, EBV induces BDP1, a subunit of the pol III-specific factor TFIIIB. Although BDP1 is the only TFIIIB subunit induced by EBV, its induction is sufficient to stimulate EBER expression in vivo, implying a limiting function. The elevated levels of BDP1 and TFIIIC in EBV-positive cells stimulate production of tRNA, 7SL, and 5S rRNA. Abnormally high expression of these cellular pol III products may contribute to the ability of EBV to enhance growth potential.
    MeSH term(s) Blotting, Western ; Chromatin Immunoprecipitation ; DNA-Binding Proteins ; Electrophoretic Mobility Shift Assay ; Gene Expression Regulation, Viral/physiology ; Herpesvirus 4, Human/physiology ; Humans ; Mutagenesis, Site-Directed ; Nuclear Matrix-Associated Proteins ; Octamer Transcription Factors ; Promoter Regions, Genetic/genetics ; RNA Polymerase III/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Viral/genetics ; RNA-Binding Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factor TFIIIB/genetics ; Transcription Factor TFIIIB/metabolism ; Transcription Factors, TFIII/metabolism ; Transcription, Genetic ; Transfection
    Chemical Substances BDP1 protein, human ; DNA-Binding Proteins ; Epstein-Barr virus encoded RNA 1 ; Epstein-Barr virus encoded RNA 2 ; NONO protein, human ; Nuclear Matrix-Associated Proteins ; Octamer Transcription Factors ; RNA, Messenger ; RNA, Viral ; RNA-Binding Proteins ; Transcription Factor TFIIIB ; Transcription Factors, TFIII ; transcription factor TFIIIC ; RNA Polymerase III (EC 2.7.7.6)
    Language English
    Publishing date 2006-09-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M600468200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Epstein-Barr Virus Induces Cellular Transcription Factors to Allow Active Expression of EBER Genes by RNA Polymerase III

    Felton-Edkins, Zoë A / Kondrashov, Alexander / Karali, Dimitra / Fairley, Jennifer A / Dawson, Christopher W / Arrand, John R / Young, Lawrence S / White, Robert J

    Journal of biological chemistry. 2006 Nov. 10, v. 281, no. 45

    2006  

    Abstract: The EBER genes of Epstein-Barr virus (EBV) are transcribed by RNA polymerase (pol) III to produce untranslated RNAs that are implicated in oncogenesis. These EBER transcripts are the most highly expressed viral gene products in EBV-transformed cells. We ... ...

    Abstract The EBER genes of Epstein-Barr virus (EBV) are transcribed by RNA polymerase (pol) III to produce untranslated RNAs that are implicated in oncogenesis. These EBER transcripts are the most highly expressed viral gene products in EBV-transformed cells. We have identified changes to the cellular transcription machinery that may contribute to the high levels of EBER RNA. These include phosphorylation of ATF2, which interacts with EBER promoters. A second is induction of TFIIIC, a pol III-specific factor that activates EBER genes; all five subunits of TFIIIC are overexpressed in EBV-positive cells. In addition, EBV induces BDP1, a subunit of the pol III-specific factor TFIIIB. Although BDP1 is the only TFIIIB subunit induced by EBV, its induction is sufficient to stimulate EBER expression in vivo, implying a limiting function. The elevated levels of BDP1 and TFIIIC in EBV-positive cells stimulate production of tRNA, 7SL, and 5S rRNA. Abnormally high expression of these cellular pol III products may contribute to the ability of EBV to enhance growth potential.
    Language English
    Dates of publication 2006-1110
    Size p. 33871-33880.
    Publishing place American Society for Biochemistry and Molecular Biology
    Document type Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    Database NAL-Catalogue (AGRICOLA)

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  4. Article: c-Myc binds to human ribosomal DNA and stimulates transcription of rRNA genes by RNA polymerase I.

    Grandori, Carla / Gomez-Roman, Natividad / Felton-Edkins, Zoe A / Ngouenet, Celine / Galloway, Denise A / Eisenman, Robert N / White, Robert J

    Nature cell biology

    2005  Volume 7, Issue 3, Page(s) 311–318

    Abstract: c-Myc coordinates cell growth and division through a transcriptional programme that involves both RNA polymerase (Pol) II- and Pol III-transcribed genes. Here, we demonstrate that human c-Myc also directly enhances Pol I transcription of ribosomal RNA ( ... ...

    Abstract c-Myc coordinates cell growth and division through a transcriptional programme that involves both RNA polymerase (Pol) II- and Pol III-transcribed genes. Here, we demonstrate that human c-Myc also directly enhances Pol I transcription of ribosomal RNA (rRNA) genes. rRNA synthesis and accumulation occurs rapidly following activation of a conditional MYC-ER allele (coding for a Myc-oestrogen-receptor fusion protein), is resistant to inhibition of Pol II transcription and is markedly reduced by c-MYC RNA interference. Furthermore, by using combined immunofluorescence and rRNA-FISH, we have detected endogenous c-Myc in nucleoli at sites of active ribosomal DNA (rDNA) transcription. Our data also show that c-Myc binds to specific consensus elements located in human rDNA and associates with the Pol I-specific factor SL1. The presence of c-Myc at specific sites on rDNA coincides with the recruitment of SL1 to the rDNA promoter and with increased histone acetylation. We propose that stimulation of rRNA synthesis by c-Myc is a key pathway driving cell growth and tumorigenesis.
    MeSH term(s) Binding Sites ; Cell Nucleolus/metabolism ; Cell Nucleus/metabolism ; Cell Proliferation ; Chromatin Immunoprecipitation ; DNA/chemistry ; DNA Primers/chemistry ; DNA, Ribosomal/chemistry ; DNA, Ribosomal/metabolism ; Fibroblasts/metabolism ; G1 Phase ; HeLa Cells ; Histones/chemistry ; Humans ; Immunoprecipitation ; In Situ Hybridization, Fluorescence ; Microscopy, Fluorescence ; Models, Genetic ; Neoplasms/metabolism ; Promoter Regions, Genetic ; Protein Binding ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Interference ; RNA Polymerase I/metabolism ; RNA, Ribosomal/metabolism ; Resting Phase, Cell Cycle ; Retroviridae/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Transcription, Genetic
    Chemical Substances DNA Primers ; DNA, Ribosomal ; Histones ; Proto-Oncogene Proteins c-myc ; RNA, Ribosomal ; DNA (9007-49-2) ; RNA Polymerase I (EC 2.7.7.6)
    Language English
    Publishing date 2005-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/ncb1224
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5169: Show issues Location:
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  5. Article: The mitogen-activated protein (MAP) kinase ERK induces tRNA synthesis by phosphorylating TFIIIB.

    Felton-Edkins, Zoe A / Fairley, Jennifer A / Graham, Emma L / Johnston, Imogen M / White, Robert J / Scott, Pamela H

    The EMBO journal

    2003  Volume 22, Issue 10, Page(s) 2422–2432

    Abstract: RNA polymerase (pol) III transcription increases within minutes of serum addition to growth-arrested fibroblasts. We show that ERK mitogen-activated protein kinases regulate pol III output by directly binding and phosphorylating the BRF1 subunit of ... ...

    Abstract RNA polymerase (pol) III transcription increases within minutes of serum addition to growth-arrested fibroblasts. We show that ERK mitogen-activated protein kinases regulate pol III output by directly binding and phosphorylating the BRF1 subunit of transcription factor TFIIIB. Blocking the ERK signalling cascade inhibits TFIIIB binding to pol III and to transcription factor TFIIIC2. Chromatin immunoprecipitation shows that the association of BRF1 and pol III with tRNA(Leu) genes in cells decreases when ERK is inactivated. Furthermore, mutation of an ERK docking domain or phosphoacceptor site in BRF1 prevents serum induction of pol III transcription. These data identify a novel target for ERK, and suggest that its ability to stimulate biosynthetic capacity and growth involves direct transcriptional activation of tRNA and 5S rRNA genes.
    MeSH term(s) 3T3 Cells ; Animals ; Binding Sites ; CHO Cells ; Cricetinae ; Enzyme Activation ; Enzyme Inhibitors/metabolism ; Fibroblasts/metabolism ; MAP Kinase Signaling System/physiology ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Models, Molecular ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Subunits/metabolism ; RNA, Transfer/metabolism ; Transcription Factor TFIIIB/chemistry ; Transcription Factor TFIIIB/metabolism ; Transcription, Genetic ; ras Proteins/metabolism
    Chemical Substances Enzyme Inhibitors ; Protein Subunits ; Transcription Factor TFIIIB ; RNA, Transfer (9014-25-9) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2003-05-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 586044-1
    ISSN 1460-2075 ; 0261-4189
    ISSN (online) 1460-2075
    ISSN 0261-4189
    DOI 10.1093/emboj/cdg240
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1808: Show issues Location:
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  6. Article: Activation by c-Myc of transcription by RNA polymerases I, II and III.

    Gomez-Roman, Natividad / Felton-Edkins, Zoë A / Kenneth, Niall S / Goodfellow, Sarah J / Athineos, Dimitris / Zhang, Jingxin / Ramsbottom, Ben A / Innes, Fiona / Kantidakis, Theodoros / Kerr, Elaine R / Brodie, Jacqueline / Grandori, Carla / White, Robert J

    Biochemical Society symposium

    2006  , Issue 73, Page(s) 141–154

    Abstract: The proto-oncogene product c-Myc can induce cell growth and proliferation. It regulates a large number of RNA polymerase II-transcribed genes, many of which encode ribosomal proteins, translation factors and other components of the biosynthetic apparatus. ...

    Abstract The proto-oncogene product c-Myc can induce cell growth and proliferation. It regulates a large number of RNA polymerase II-transcribed genes, many of which encode ribosomal proteins, translation factors and other components of the biosynthetic apparatus. We have found that c-Myc can also activate transcription by RNA polymerases I and III, thereby stimulating production of rRNA and tRNA. As such, c-Myc may possess the unprecedented capacity to induce expression of all ribosomal components. This may explain its potent ability to drive cell growth, which depends on the accumulation of ribosomes. The activation of RNA polymerase II transcription by c-Myc is often inefficient, but its induction of rRNA and tRNA genes can be very strong in comparison. We will describe what is known about the mechanisms used by c-Myc to activate transcription by RNA polymerases I and II.
    MeSH term(s) Animals ; DNA-Directed RNA Polymerases/genetics ; DNA-Directed RNA Polymerases/metabolism ; Humans ; Mice ; Models, Biological ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Polymerase I/genetics ; RNA Polymerase I/metabolism ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; RNA Polymerase III/genetics ; RNA Polymerase III/metabolism ; RNA, Ribosomal/genetics ; RNA, Transfer/genetics ; Transcriptional Activation
    Chemical Substances Proto-Oncogene Proteins c-myc ; RNA, Ribosomal ; RNA, Transfer (9014-25-9) ; RNA Polymerase II (EC 2.7.7.-) ; DNA-Directed RNA Polymerases (EC 2.7.7.6) ; RNA Polymerase I (EC 2.7.7.6) ; RNA Polymerase III (EC 2.7.7.6)
    Language English
    Publishing date 2006-04-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 0067-8694
    ISSN 0067-8694
    DOI 10.1042/bss0730141
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Direct regulation of RNA polymerase III transcription by RB, p53 and c-Myc.

    Felton-Edkins, Zoë A / Kenneth, Niall S / Brown, Timothy R P / Daly, Nicole L / Gomez-Roman, Natividad / Grandori, Carla / Eisenman, Robert N / White, Robert J

    Cell cycle (Georgetown, Tex.)

    2003  Volume 2, Issue 3, Page(s) 181–184

    Abstract: The synthesis of tRNA and 5S rRNA by RNA polymerase (pol) III is cell cycle regulated in higher organisms. Overexpression of pol III products is a general feature of transformed cells. These observations may be explained by the fact that a pol III- ... ...

    Abstract The synthesis of tRNA and 5S rRNA by RNA polymerase (pol) III is cell cycle regulated in higher organisms. Overexpression of pol III products is a general feature of transformed cells. These observations may be explained by the fact that a pol III-specific transcription factor, TFIIIB, is strongly regulated by the tumor suppressors RB and p53, as well as the proto-oncogene product c-Myc. RB and p53 repress TFIIIB, but this restraint can be lost in tumors through a variety of mechanisms. In contrast, c-Myc binds and activates TFIIIB, causing potent induction of pol III transcription. Using chromatin immunoprecipitation and RNA interference, we show that c-Myc interacts with tRNA and 5S rRNA genes in transformed cervical cells, stimulating their expression. Availability of pol III products may be an important determinant of a cell's capacity to grow. The ability to regulate pol III output may therefore be integral to the growth control functions of RB, p53 and c-Myc.
    MeSH term(s) Animals ; Cell Division/genetics ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; DNA Polymerase III/genetics ; DNA Polymerase III/metabolism ; Eukaryotic Cells/enzymology ; Humans ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA/genetics ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism ; Transcription, Genetic/genetics ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Proto-Oncogene Proteins c-myc ; Retinoblastoma Protein ; Tumor Suppressor Protein p53 ; RNA (63231-63-0) ; DNA Polymerase III (EC 2.7.7.-)
    Language English
    Publishing date 2003-01-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5881: Show issues Location:
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