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  1. Article ; Online: Absence of Stat1 in donor CD4+ T cells promotes the expansion of Tregs and reduces graft-versus-host disease in mice.

    Ma, Huihui / Lu, Caisheng / Ziegler, Judith / Liu, Ailing / Sepulveda, Antonia / Okada, Hideho / Lentzsch, Suzanne / Mapara, Markus Y

    The Journal of clinical investigation

    2024  Volume 134, Issue 5

    MeSH term(s) Mice ; Animals ; CD4-Positive T-Lymphocytes ; T-Lymphocytes, Regulatory ; Graft vs Host Disease ; Mice, Inbred C57BL ; Mice, Inbred BALB C ; STAT1 Transcription Factor/genetics
    Chemical Substances Stat1 protein, mouse ; STAT1 Transcription Factor
    Language English
    Publishing date 2024-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI180350
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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  2. Book ; Thesis: Zwischen Karriere und Familie

    Ziegler, Judith

    eine Untersuchung über österreichische Führungskräfte

    (Dissertationen der Universität Wien ; [N.F.], 90)

    2002  

    Title variant "Weil die Familie ein enormer Prellbock ist ..."
    Author's details Judith Ziegler
    Series title Dissertationen der Universität Wien ; [N.F.], 90
    Keywords Führungskraft ; Familie ; Umfrage ; Geschlechtliche Arbeitsteilung ; Berufserfolg ; Führungskräfte ; Weibliche Führungskräfte ; Weibliche Arbeitskräfte ; Erwerbsverlauf ; Kinderbetreuung ; Österreich
    Language German
    Size 227 S., graph. Darst., 21 cm
    Publisher WUV-Univ.-Verl
    Publishing place Wien
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Univ., Diss. u.d.T.: Ziegler, Judith: "Weil die Familie ein enormer Prellbock ist.̤"--Wien, 1998
    ISBN 3851147421 ; 9783851147421
    Database Former special subject collection: coastal and deep sea fishing

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  3. Book ; Thesis: Zwischen Karriere und Familie

    Ziegler, Judith

    eine Untersuchung über österreichische Führungskräfte

    (Dissertationen der Universität Wien ; [N.F.], 90)

    2002  

    Title variant "Weil die Familie ein enormer Prellbock ist ..."
    Author's details Judith Ziegler
    Series title Dissertationen der Universität Wien ; [N.F.], 90
    Keywords Führungskraft ; Familie ; Umfrage ; Geschlechtliche Arbeitsteilung ; Berufserfolg ; Führungskräfte ; Weibliche Führungskräfte ; Weibliche Arbeitskräfte ; Erwerbsverlauf ; Kinderbetreuung ; Österreich
    Language German
    Size 227 S., graph. Darst., 21 cm
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Zugl.: Wien, Univ., Diss., 1998 u.d.T.: Ziegler, Judith: "Weil die Familie ein enormer Prellbock ist.̤"
    ISBN 3851147421 ; 9783851147421
    Database ECONomics Information System

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  4. Article ; Online: Apaf-1 deficiency confers resistance to ultraviolet-induced apoptosis in mouse embryonic fibroblasts by disrupting reactive oxygen species amplification production and mitochondrial pathway.

    Feng, Rentian / Han, Jie / Ziegler, Judith / Yang, Minying / Castranova, Vincent

    Free radical biology & medicine

    2012  Volume 52, Issue 5, Page(s) 889–897

    Abstract: Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to ... ...

    Abstract Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to demonstrate the decisive part of the mitochondrial pathway in UVC-induced apoptosis in mouse embryo fibroblasts (MEFs). UVC-induced apoptosis proceeded independent of the activation of death receptor components. In contrast, soon after UV radiation, MAPK activation and generation of reactive oxygen species (ROS) increased, followed by a decline in mitochondrial membrane potential (MMP) and cytochrome c release, as well as activation of caspase-9 and -3 and the upregulation of p47-phox. Deficiency of apaf-1, a critical member of the apoptosome, dramatically abolished all the UV-induced signal deterioration and cell death. In parallel, UVC-induced apoptosis was largely attenuated by either DN-caspase-9 or Bcl-X(L) overexpression. Pretreatment of cells with N-acetylcysteine or catalase but not Tempol decreased UVC-induced MAPK activation and apoptosis. Inhibition of JNK and caspase attenuated p47-phox upregulation. Altogether, we have for the first time demonstrated the critical role of Apaf-1 in the regulation of MAPK, ROS, and MMP in UVC-radiated MEFs and propose that the amplification feedback loop among mitochondrial signal molecules culminates in the demise of the cell.
    MeSH term(s) Animals ; Apoptosis/radiation effects ; Apoptotic Protease-Activating Factor 1/deficiency ; Caspase 8/metabolism ; Cell Cycle Proteins/metabolism ; Cell Division/radiation effects ; Cell Nucleus Shape/radiation effects ; Cells, Cultured ; Enzyme Activation ; Fas-Associated Death Domain Protein/genetics ; Fas-Associated Death Domain Protein/metabolism ; Fibroblasts/physiology ; Fibroblasts/radiation effects ; MAP Kinase Signaling System ; Membrane Potential, Mitochondrial ; Mice ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism ; Ultraviolet Rays
    Chemical Substances Apaf1 protein, mouse ; Apoptotic Protease-Activating Factor 1 ; Cell Cycle Proteins ; Fadd protein, mouse ; Fas-Associated Death Domain Protein ; Reactive Oxygen Species ; Casp8 protein, mouse (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
    Language English
    Publishing date 2012-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2011.11.028
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2109: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Apaf-1 deficiency confers resistance to ultraviolet-induced apoptosis in mouse embryonic fibroblasts by disrupting reactive oxygen species amplification production and mitochondrial pathway

    Feng, Rentian / Han, Jie / Ziegler, Judith / Yang, Minying / Castranova, Vincent

    Free Radical Biology and Medicine. 2012 Mar. 1, v. 52, no. 5

    2012  

    Abstract: Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to ... ...

    Abstract Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to demonstrate the decisive part of the mitochondrial pathway in UVC-induced apoptosis in mouse embryo fibroblasts (MEFs). UVC-induced apoptosis proceeded independent of the activation of death receptor components. In contrast, soon after UV radiation, MAPK activation and generation of reactive oxygen species (ROS) increased, followed by a decline in mitochondrial membrane potential (MMP) and cytochrome c release, as well as activation of caspase-9 and -3 and the upregulation of p47-phox. Deficiency of apaf-1, a critical member of the apoptosome, dramatically abolished all the UV-induced signal deterioration and cell death. In parallel, UVC-induced apoptosis was largely attenuated by either DN-caspase-9 or Bcl-XL overexpression. Pretreatment of cells with N-acetylcysteine or catalase but not Tempol decreased UVC-induced MAPK activation and apoptosis. Inhibition of JNK and caspase attenuated p47-phox upregulation. Altogether, we have for the first time demonstrated the critical role of Apaf-1 in the regulation of MAPK, ROS, and MMP in UVC-radiated MEFs and propose that the amplification feedback loop among mitochondrial signal molecules culminates in the demise of the cell.
    Keywords acetylcysteine ; apoptosis ; caspase-9 ; catalase ; cytochrome c ; death ; fibroblasts ; membrane potential ; mice ; mitochondrial membrane ; mitogen-activated protein kinase ; reactive oxygen species ; signal transduction ; ultraviolet radiation
    Language English
    Dates of publication 2012-0301
    Size p. 889-897.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2011.11.028
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2109: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Absence of Stat1 in donor CD4⁺ T cells promotes the expansion of Tregs and reduces graft-versus-host disease in mice.

    Ma, Huihui / Lu, Caisheng / Ziegler, Judith / Liu, Ailing / Sepulveda, Antonia / Okada, Hideho / Lentzsch, Suzanne / Mapara, Markus Y

    The Journal of clinical investigation

    2011  Volume 121, Issue 7, Page(s) 2554–2569

    Abstract: STAT1 is the main signal transducer for type I and II IFNs and plays a central role in the regulation of innate and adaptive immune responses. We used Stat1-deficient mice to test the role of donor Stat1 in MHC-matched minor histocompatibility antigen- ... ...

    Abstract STAT1 is the main signal transducer for type I and II IFNs and plays a central role in the regulation of innate and adaptive immune responses. We used Stat1-deficient mice to test the role of donor Stat1 in MHC-matched minor histocompatibility antigen-mismatched (mHA-mismatched) and fully MHC-mismatched models of bone marrow transplantation. Lack of Stat1 in donor splenocytes reduced graft-versus-host disease (GVHD) in both immunogenetic disparities, leading to substantially attenuated morbidity and mortality. Donor Stat1 deficiency resulted in reduced alloantigen-induced activation and expansion of donor T cells and correlated with the expansion of CD4+CD25+Foxp3+ Tregs in vivo. This expansion of Tregs was further confirmed by studies showing that Stat1 deficiency promoted the proliferation, while inhibiting the apoptosis, of natural Tregs, and that absence of Stat1 enhanced the induction of inducible Tregs both in vitro and in vivo. Ex vivo expanded Stat1-/- Tregs were superior to wild-type Tregs in suppressing alloantigen-driven expansion of T cells in vitro and in inhibiting the development of GVHD. These observations demonstrate that Stat1 is a regulator of Tregs and that targeting Stat1 in CD4+ T cells may facilitate in vitro and in vivo expansion of Tregs for therapeutic use.
    MeSH term(s) Animals ; Antigens, CD/immunology ; Bone Marrow Transplantation/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/transplantation ; Cell Death ; Cell Proliferation ; Female ; Forkhead Transcription Factors/immunology ; Graft vs Host Disease/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/immunology ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Antigens, CD ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; STAT1 Transcription Factor
    Language English
    Publishing date 2011-06-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI43706
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: Apaf-1 deficiency confers resistance to ultraviolet-induced apoptosis in mouse embryonic fibroblasts by disrupting reactive oxygen species amplification production and mitochondrial pathway

    Feng, Rentian / Han, Jie / Ziegler, Judith / Yang, Minying / Castranova, Vincent

    Free Radical Biology and Medicine

    Volume v. 52,, Issue no. 5

    Abstract: Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to ... ...

    Abstract Apoptosis requires tightly regulated cell death pathways. The signaling pathways that trigger a cell to undergo apoptosis after UV radiation are cell type specific and are currently being defined. Here, we have used pharmacological and genetic tools to demonstrate the decisive part of the mitochondrial pathway in UVC-induced apoptosis in mouse embryo fibroblasts (MEFs). UVC-induced apoptosis proceeded independent of the activation of death receptor components. In contrast, soon after UV radiation, MAPK activation and generation of reactive oxygen species (ROS) increased, followed by a decline in mitochondrial membrane potential (MMP) and cytochrome c release, as well as activation of caspase-9 and -3 and the upregulation of p47-phox. Deficiency of apaf-1, a critical member of the apoptosome, dramatically abolished all the UV-induced signal deterioration and cell death. In parallel, UVC-induced apoptosis was largely attenuated by either DN-caspase-9 or Bcl-XL overexpression. Pretreatment of cells with N-acetylcysteine or catalase but not Tempol decreased UVC-induced MAPK activation and apoptosis. Inhibition of JNK and caspase attenuated p47-phox upregulation. Altogether, we have for the first time demonstrated the critical role of Apaf-1 in the regulation of MAPK, ROS, and MMP in UVC-radiated MEFs and propose that the amplification feedback loop among mitochondrial signal molecules culminates in the demise of the cell.
    Keywords apoptosis ; death ; reactive oxygen species ; caspase-9 ; membrane potential ; catalase ; mitogen-activated protein kinase ; signal transduction ; ultraviolet radiation ; mice ; acetylcysteine ; fibroblasts ; mitochondrial membrane ; cytochrome c
    Language English
    Document type Article
    ISSN 0891-5849
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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