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  1. Book ; Conference proceedings: Papers given at the Workshop Molecular Radiation Biology

    Eckardt-Schupp, Friederike

    [plenary lectures at a meeting of the German Section of the DNA Repair Network ... in München-Neuherberg, March 21 - 23, 1990]

    1990  

    Institution Workshop Molecular Radiation Biology
    DNA Repair Information Network / German Section
    Author's details [Friederike Eckardt-Schupp ... eds.]
    Keywords DNA Repair / congresses ; Free Radicals / congresses
    Publishing country United States
    Document type Book ; Conference proceedings
    Note In: Radiation and environmental biophysics. - ISSN 0301-634X. - 29 (1990), S. 247 - 322
    HBZ-ID HT003728131
    Database Catalogue ZB MED Medicine, Health

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  2. Book ; Online: Aufbau eines Systems isogener stabil diploider Zelllinien mit gezielt durch RNA-Interferenz ausgeschalteten Genen zur Analyse des Zusammenhangs von DNA-Reparaturdefizienz, genomischer und chromosomaler Instabilität

    Eckardt-Schupp, Friederike / Moertl, Simone

    Schlussbericht zum Forschungsvorhaben ... ; (1.10.2005 - 31.12.2008)

    2009  

    Title variant Construction of a set of isogenic stable diploide cell lines with RNAi-mediated knockdown of genes for the analysis of the relationship between DNA repair deficiency, genomic instability and chromosomal instability ; Schlussbericht zum Forschungsvorhaben 02S8345
    Author's details vorgelegt von: Friederike Eckardt-Schupp und Simone Moertl
    Language German
    Size Online-Ressource (29 S., 0,98 MB), Ill., graph. Darst.
    Publisher Technische Informationsbibliothek u. Universitätsbibliothek ; Ludwig-Maximilians-Univ
    Publishing place Hannover ; Planegg-Martinsried
    Document type Book ; Online
    Note Auch als gedr. Ausg. vorhanden ; Förderkennzeichen BMBF 02S8345. - [Engl. Titel: Construction of a set of isogenic stable diploide cell lines with RNAi-mediated knockdown of genes for the analysis of the relationship between DNA repair deficiency, genomic instability and chromosomal instability] ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  3. Book ; Conference proceedings: GBS 2000

    Eckardt-Schupp, Friederike

    proceedings der 4. Jahrestagung der Gesellschaft für Biologische Strahlenforschung, Bad Kissingen, 4. - 6. Oktober 2000

    2000  

    Institution Gesellschaft für Biologische Strahlenforschung
    Event/congress Jahrestagung der Gesellschaft für Biologische Strahlenforschung (GBS) (4, 2000.10.04-06, BadKissingen)
    Author's details Friederike Eckardt-Schupp ... (Hrsg.)
    Language German
    Size 52 S
    Publishing place Bad Kissingen
    Document type Book ; Conference proceedings
    ISBN 3000068007 ; 9783000068003
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  4. Article ; Online: A novel function of Ubc13 in TNFR1 receptor activation.

    Angermeier, Marita / Eckardt-Schupp, Friederike / Moertl, Simone

    Cellular signalling

    2010  Volume 22, Issue 9, Page(s) 1388–1396

    Abstract: The tumour necrosis factor receptor 1 (TNFR1) activates prosurvival pathways by induction of the NFkappaB pathway and induces cell death via apoptosis. The ubiquitin-conjugating enzyme, Ubc13, mediates the ubiquitylation-dependent formation of protein ... ...

    Abstract The tumour necrosis factor receptor 1 (TNFR1) activates prosurvival pathways by induction of the NFkappaB pathway and induces cell death via apoptosis. The ubiquitin-conjugating enzyme, Ubc13, mediates the ubiquitylation-dependent formation of protein complexes crucial for the activation and regulation of both pathways. We describe a new role for Ubc13 in the regulation of TNFR1 activity after UV stimulation. Depletion of Ubc13 by RNAi produced a decreased NFkappaB activity and increased apoptosis after stimulation by TNFalpha and UV-C light. These results are consistent with the function of Ubc13 in the ubiquitylation of RIP1, which controls the proapoptotic or prosurvival response after TNFR1 activation. Moreover, we demonstrated that UV-C light induces a close interaction between the Ubc13 protein and the TNFR1 receptor. In the absence of Ubc13 TNFR1 clustering was increased. We conclude that Ubc13 has a regulatory role for the activation of TNFR1 and hence, apoptotic cell death. Thus, our results elucidated a new role for Ubc13 in the regulation of prosurvival or proapoptotic processes, which is upstream of so far investigated functions.
    MeSH term(s) Apoptosis ; Caspase 8/metabolism ; Humans ; NF-kappa B/metabolism ; RNA Interference ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Ubiquitin-Conjugating Enzymes/antagonists & inhibitors ; Ubiquitin-Conjugating Enzymes/metabolism ; Ubiquitin-Conjugating Enzymes/physiology ; Ultraviolet Rays
    Chemical Substances NF-kappa B ; Receptors, Tumor Necrosis Factor, Type I ; UBE2N protein, human (EC 2.3.2.23) ; Ubiquitin-Conjugating Enzymes (EC 2.3.2.23) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2010-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1002702-6
    ISSN 1873-3913 ; 0898-6568
    ISSN (online) 1873-3913
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2010.05.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book: Aufbau eines Systems isogener stabil diploider Zelllinien mit gezielt durch RNA-Interferenz ausgeschalteten Genen zur Analyse des Zusammenhangs von DNA-Reparaturdefizienz, genomischer und chromosomaler Instabilität

    Eckardt-Schupp, Friederike / Moertl, Simone

    Schlussbericht zum Forschungsvorhaben ... ; (1.10.2005 - 31.12.2008)

    2009  

    Title variant Construction of a set of isogenic stable diploide cell lines with RNAi-mediated knockdown of genes for the analysis of the relationship between DNA repair deficiency, genomic instability and chromosomal instability ; Schlussbericht zum Forschungsvorhaben 02S8345
    Author's details vorgelegt von: Friederike Eckardt-Schupp und Simone Moertl
    Language German
    Size 29 Bl., Ill., graph. Darst.
    Publisher Ludwig-Maximilians-Univ
    Publishing place Planegg-Martinsried
    Document type Book
    Note Auch als elektronische Ressource vorh. ; Förderkennzeichen BMBF 02S8345. - Engl. Zsfassung u.d.T.: Construction of a set of isogenic stable diploide cell lines with RNAi-mediated knockdown of genes for the analysis of the relationship between DNA repair deficiency, genomic instability and chromosomal instability ; Unterschiede zwischen dem gedruckten Dokument und der elektronischen Ressource können nicht ausgeschlossen werden
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  6. Book: Aufbau eines Systems isogener stabil diploider humaner Zelllinien mit gezielt durch RNA-Interferenz ausgeschalteten Genen zur Analyse des Zusammenhanges von DNA-Reparaturdefizienz, genomischer und chromosomaler Instabilitaet

    Eckardt-Schupp, Friederike
    Institution Universitaet Muenchen, Department Biologie I, Didaktik der Biologie, Winzererstr. 45/II, 80797, Muenchen, DE
    Keywords RNA ; Gen ; DNA ; Strahlendosis ; Wirkungsanalyse ; Mensch ; Chromosomen ; Zelle ; Wirkungsforschung ; Strahlenwirkung
    Document type Book
    Remark project start: 10/01/2005 project end: 09/30/2008 grant ID: 02S8345
    Database Environmental research database (UFORDAT) of the German Federal Environment Agency (UBA)

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  7. Article: Quantitative Phosphoproteomic Analysis of Early Alterations in Protein Phosphorylation by 2,3,7,8-Tetrachlorodibenzo-p-dioxin

    Schulz, Melanie / Andrae Ulrich / Brandner Stefanie / Eberhagen Carola / Eckardt-Schupp Friederike / Larsen Martin R

    Journal of Proteome Research. 2013 Feb. 01, v. 12, no. 2

    2013  

    Abstract: A comprehensive quantitative analysis of changes in protein phosphorylation preceding or accompanying transcriptional activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in 5L rat hepatoma cells was performed using the SILAC approach. Following ... ...

    Abstract A comprehensive quantitative analysis of changes in protein phosphorylation preceding or accompanying transcriptional activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in 5L rat hepatoma cells was performed using the SILAC approach. Following exposure of the cells to DMSO or 1 nM TCDD for 0.5 to 2 h, 5648 phosphorylated peptides corresponding to 2156 phosphoproteins were identified. Eight peptides exhibited a statistically significantly altered phosphorylation because of TCDD exposure and 22 showed a regulation factor of ≥1.5 in one of the experiments per time point. The vast majority of the TCCD-induced phosphorylation changes had not been reported before. The transcription factor ARNT, the obligate partner for gene activation by the TCDD-bound Ah receptor, exhibited an up-regulation of its Ser77 phosphorylation, a modification known to control the differential binding of ARNT homodimers and heterodimers to different enhancers suggesting that this phosphorylation represents a novel mechanism contributing to the alteration of gene expression by TCDD. Other proteins with altered phosphorylation included, among others, various transcriptional coregulators previously unknown to participate in TCDD-induced gene activation, regulators of small GTPases of the Ras superfamily, UBX domain-containing proteins and the oncogenic protein LYRIC. The results open up new directions for research on the molecular mechanisms of dioxin action and toxicity.
    Keywords dimethyl sulfoxide ; gene activation ; guanosinetriphosphatase ; hepatoma ; peptides ; phosphoproteins ; protein phosphorylation ; proteome ; proteomics ; quantitative analysis ; rats ; tetrachlorodibenzo-p-dioxin ; toxicity ; transcription (genetics) ; transcription factors ; transcriptional activation
    Language English
    Dates of publication 2013-0201
    Size p. 866-882.
    Publishing place American Chemical Society
    Document type Article
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021%2Fpr3009429
    Database NAL-Catalogue (AGRICOLA)

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  8. Book ; Online ; Thesis: Identifikation und funktionelle Analyse strahlenregulierter microRNAs in Endothelzellen

    Krämer, Anne [Verfasser] / Eckardt-Schupp, Friederike [Akademischer Betreuer]

    2012  

    Author's details Anne Krämer. Betreuer: Friederike Eckardt-Schupp
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language German
    Publisher Universitätsbibliothek der Ludwig-Maximilians-Universität
    Publishing place München
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  9. Article ; Online: Reduced expression of SRC family kinases decreases PI3K activity in NBS1-/- lymphoblasts.

    Sagan, Daniel / Eckardt-Schupp, Friederike / Eichholtz-Wirth, Hedda

    Biochemical and biophysical research communications

    2008  Volume 377, Issue 1, Page(s) 181–186

    Abstract: SRC family kinases (SFKs) are involved in the activation of phosphatidylinositol-3-kinase (PI3K). In addition, the activity of this lipid kinase can be regulated by the DNA repair protein NBS1. Here, we describe a disturbed expression of some members of ... ...

    Abstract SRC family kinases (SFKs) are involved in the activation of phosphatidylinositol-3-kinase (PI3K). In addition, the activity of this lipid kinase can be regulated by the DNA repair protein NBS1. Here, we describe a disturbed expression of some members of the non-receptor tyrosine kinase family in lymphoblastoid cell lines generated from cells of Nijmegen breakage syndrome (NBS) patients. Especially, only minor amounts of the kinases LCK and HCK are expressed in the NBS1(-/-) cell lines as compared to the consanguineous NBS1(+/-) cells. We demonstrate that SFK activity is important for a proper activation of PI3K in these cells and that it is reduced in NBS1(-/-) cells. We provide evidence that the observed reduced PI3K activity in NBS lymphoblasts is caused by an impaired expression of the SFKs LCK and/or HCK. Thus, our data establish a new function for the NBS1 protein as a regulator of PI3K activity via SFK members.
    MeSH term(s) Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Humans ; Nijmegen Breakage Syndrome/enzymology ; Nijmegen Breakage Syndrome/genetics ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Pyrimidines/pharmacology ; Tyrosine/metabolism ; src-Family Kinases/antagonists & inhibitors ; src-Family Kinases/genetics ; src-Family Kinases/metabolism
    Chemical Substances AG 1879 ; Cell Cycle Proteins ; NBN protein, human ; Nuclear Proteins ; Protein Kinase Inhibitors ; Pyrimidines ; Tyrosine (42HK56048U) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; src-Family Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2008-12-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2008.09.098
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Quantitative phosphoproteomic analysis of early alterations in protein phosphorylation by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

    Schulz, Melanie / Brandner, Stefanie / Eberhagen, Carola / Eckardt-Schupp, Friederike / Larsen, Martin R / Andrae, Ulrich

    Journal of proteome research

    2013  Volume 12, Issue 2, Page(s) 866–882

    Abstract: A comprehensive quantitative analysis of changes in protein phosphorylation preceding or accompanying transcriptional activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in 5L rat hepatoma cells was performed using the SILAC approach. Following ... ...

    Abstract A comprehensive quantitative analysis of changes in protein phosphorylation preceding or accompanying transcriptional activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in 5L rat hepatoma cells was performed using the SILAC approach. Following exposure of the cells to DMSO or 1 nM TCDD for 0.5 to 2 h, 5648 phosphorylated peptides corresponding to 2156 phosphoproteins were identified. Eight peptides exhibited a statistically significantly altered phosphorylation because of TCDD exposure and 22 showed a regulation factor of ≥ 1.5 in one of the experiments per time point. The vast majority of the TCCD-induced phosphorylation changes had not been reported before. The transcription factor ARNT, the obligate partner for gene activation by the TCDD-bound Ah receptor, exhibited an up-regulation of its Ser77 phosphorylation, a modification known to control the differential binding of ARNT homodimers and heterodimers to different enhancers suggesting that this phosphorylation represents a novel mechanism contributing to the alteration of gene expression by TCDD. Other proteins with altered phosphorylation included, among others, various transcriptional coregulators previously unknown to participate in TCDD-induced gene activation, regulators of small GTPases of the Ras superfamily, UBX domain-containing proteins and the oncogenic protein LYRIC. The results open up new directions for research on the molecular mechanisms of dioxin action and toxicity.
    MeSH term(s) Amino Acid Sequence ; Animals ; Aryl Hydrocarbon Receptor Nuclear Translocator/genetics ; Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cell Line, Tumor ; Chromatography, Liquid ; Cytochrome P-450 CYP1A1/genetics ; Cytochrome P-450 CYP1A1/metabolism ; Environmental Pollutants/toxicity ; Gene Expression Regulation/drug effects ; Isotope Labeling ; Mass Spectrometry ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Phosphoproteins/analysis ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Polychlorinated Dibenzodioxins/toxicity ; Proteome/analysis ; Proteome/genetics ; Proteome/metabolism ; RNA-Binding Proteins ; Rats ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; ras Proteins/genetics ; ras Proteins/metabolism
    Chemical Substances ARNT protein, rat ; Carrier Proteins ; Environmental Pollutants ; Membrane Proteins ; Mtdh protein, rat ; Phosphoproteins ; Polychlorinated Dibenzodioxins ; Proteome ; RNA-Binding Proteins ; Receptors, Aryl Hydrocarbon ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9) ; Cytochrome P-450 CYP1A1 (EC 1.14.14.1) ; ras Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2013-01-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2078618-9
    ISSN 1535-3907 ; 1535-3893
    ISSN (online) 1535-3907
    ISSN 1535-3893
    DOI 10.1021/pr3009429
    Database MEDical Literature Analysis and Retrieval System OnLINE

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