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  1. AU=Grassmann Ralph AU=Grassmann Ralph
  2. AU="Kofi Adu-Boahen"
  3. AU="Christoph Kicker"
  4. AU="Daniella, J."
  5. AU="Wimperis, J"
  6. AU="Usán, Pablo"
  7. AU="Khan, Wasif A"
  8. AU="Kamei, Kaeko"
  9. AU="Sakamoto, Kyouichi"
  10. AU="Zhao, Bingqing"
  11. AU="Edwards, Margaret Sanchez" AU="Edwards, Margaret Sanchez"
  12. AU=Cozar J M
  13. AU="Hang-Lo Lee"
  14. AU="Pitner, Mary Kathryn"
  15. AU="Riemenschneider, Christina"
  16. AU="Diana Farah"
  17. AU="Laniyati Hamijoyo"
  18. AU=Fiedler S
  19. AU="Grzegorz Zaguła"
  20. AU="Ong, Pio"
  21. AU="Fefelova, Elena A"
  22. AU=Hamid Husnain
  23. AU=Joske David J L

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  1. Buch ; Dissertation / Habilitation: Der transformierende Genomabschnitt des menschlichen T-Zelleukämie-Virus Typ 1

    Grassmann, Ralph

    1992  

    Verfasserangabe von Ralph Grassmann
    Sprache Englisch
    Umfang Getr. Zählung : Ill., graph. Darst.
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation Erlangen-Nürnberg, Univ., Habil.-Schr., 1993
    Anmerkung Text engl.
    HBZ-ID HT006796429
    Datenquelle Katalog ZB MED Medizin, Gesundheit

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    Verfügbar in ZB MED Köln/Königswinter

    SignaturLeihstatusStandort
    95 E 2160 bestellbar zur Ausleihe Magazin

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  2. Konferenzbeitrag: The Human T-Lymphotropic Virus and Adult T-Cell Leukemia/Lymphoma

    Grassmann, Ralph

    2006  , Seite(n) IS042

    Veranstaltung/Kongress 27. Deutscher Krebskongress; Berlin; Deutsche Krebsgesellschaft e.V.; 2006
    Schlagwörter Medizin, Gesundheit
    Erscheinungsdatum 2006-03-20
    Verlag German Medical Science; Düsseldorf, Köln
    Dokumenttyp Konferenzbeitrag
    Datenquelle German Medical Science

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  3. Artikel: The roles of microRNAs in mammalian virus infection.

    Grassmann, Ralph / Jeang, Kuan-Teh

    Biochimica et biophysica acta

    2008  Band 1779, Heft 11, Seite(n) 706–711

    Abstract: MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression that are important for the control of a multitude of critical processes in mammalian cells. Increasing evidence supports that miRNAs also have important functions in viral ... ...

    Abstract MicroRNAs (miRNAs) are post-transcriptional regulators of gene expression that are important for the control of a multitude of critical processes in mammalian cells. Increasing evidence supports that miRNAs also have important functions in viral replication and may be used by host cells to control viral infection. Expression of miRNAs has been reported for various groups of viruses including herpesviruses, small DNA viruses and retroviruses. The recent identification of target genes regulated by some of these viral miRNAs suggests that they may function in the control of lytic and latent viral replication, in the limitation of antiviral responses, in the inhibition of apoptosis, and in the stimulation of cellular growth. In this review, we summarize in brief recent findings on the antiviral activities of cellular miRNAs and the viral counter-responses to the cell's RNAi restriction.
    Mesh-Begriff(e) Animals ; Humans ; Mammals/virology ; MicroRNAs/metabolism ; RNA, Viral/metabolism ; Virus Diseases/metabolism
    Chemische Substanzen MicroRNAs ; RNA, Viral
    Sprache Englisch
    Erscheinungsdatum 2008-05-15
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbagrm.2008.05.005
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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  4. Artikel ; Online: Cell surface markers in HTLV-1 pathogenesis.

    Kress, Andrea K / Grassmann, Ralph / Fleckenstein, Bernhard

    Viruses

    2011  Band 3, Heft 8, Seite(n) 1439–1459

    Abstract: The phenotype of HTLV-1-transformed CD4(+) T lymphocytes largely depends on defined viral effector molecules such as the viral oncoprotein Tax. In this review, we exemplify the expression pattern of characteristic lineage markers, costimulatory receptors ...

    Abstract The phenotype of HTLV-1-transformed CD4(+) T lymphocytes largely depends on defined viral effector molecules such as the viral oncoprotein Tax. In this review, we exemplify the expression pattern of characteristic lineage markers, costimulatory receptors and ligands of the tumor necrosis factor superfamily, cytokine receptors, and adhesion molecules on HTLV-1-transformed cells. These molecules may provide survival signals for the transformed cells. Expression of characteristic surface markers might therefore contribute to persistence of HTLV-1-transformed lymphocytes and to the development of HTLV-1-associated disease.
    Mesh-Begriff(e) Biomarkers/metabolism ; CD4-Positive T-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/virology ; Cell Adhesion Molecules/metabolism ; Cell Differentiation ; Cell Line, Transformed ; Cell Proliferation ; Cell Transformation, Viral ; Costimulatory and Inhibitory T-Cell Receptors/metabolism ; Gene Products, tax/genetics ; Gene Products, tax/metabolism ; Human T-lymphotropic virus 1/genetics ; Human T-lymphotropic virus 1/metabolism ; Human T-lymphotropic virus 1/pathogenicity ; Humans ; Leukemia-Lymphoma, Adult T-Cell/metabolism ; Leukemia-Lymphoma, Adult T-Cell/virology ; Paraparesis, Tropical Spastic/virology ; Phenotype ; Receptors, Cytokine/metabolism ; Signal Transduction
    Chemische Substanzen Biomarkers ; Cell Adhesion Molecules ; Costimulatory and Inhibitory T-Cell Receptors ; Gene Products, tax ; Receptors, Cytokine ; tax protein, Human T-lymphotrophic virus 1
    Sprache Englisch
    Erscheinungsdatum 2011-08-16
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v3081439
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Cell Surface Markers in HTLV-1 Pathogenesis

    Andrea K. Kress / Bernhard Fleckenstein / Ralph Grassmann

    Viruses, Vol 3, Iss 8, Pp 1439-

    2011  Band 1459

    Abstract: The phenotype of HTLV-1-transformed CD4+ T lymphocytes largely depends on defined viral effector molecules such as the viral oncoprotein Tax. In this review, we exemplify the expression pattern of characteristic lineage markers, costimulatory receptors ... ...

    Abstract The phenotype of HTLV-1-transformed CD4+ T lymphocytes largely depends on defined viral effector molecules such as the viral oncoprotein Tax. In this review, we exemplify the expression pattern of characteristic lineage markers, costimulatory receptors and ligands of the tumor necrosis factor superfamily, cytokine receptors, and adhesion molecules on HTLV-1-transformed cells. These molecules may provide survival signals for the transformed cells. Expression of characteristic surface markers might therefore contribute to persistence of HTLV-1-transformed lymphocytes and to the development of HTLV-1-associated disease.
    Schlagwörter HTLV-1 ; Tax ; oncoprotein ; phenotype ; differentiation ; ATLL ; HAM/TSP ; TNFR ; cytokine receptor ; interleukin ; Microbiology ; QR1-502 ; Science ; Q ; DOAJ:Microbiology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
    Sprache Englisch
    Erscheinungsdatum 2011-08-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: MicroRNA miR-146a and further oncogenesis-related cellular microRNAs are dysregulated in HTLV-1-transformed T lymphocytes.

    Pichler, Klemens / Schneider, Grit / Grassmann, Ralph

    Retrovirology

    2008  Band 5, Seite(n) 100

    Abstract: Background: Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of a severe and fatal lymphoproliferative disease of mainly CD4+ T cell origin, adult T cell leukemia, which develops after prolonged viral persistence. Transformation of ... ...

    Abstract Background: Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of a severe and fatal lymphoproliferative disease of mainly CD4+ T cell origin, adult T cell leukemia, which develops after prolonged viral persistence. Transformation of infected cells involves HTLV-1's oncoprotein Tax, which perturbs cell cycle regulation and modulates cellular gene expression. The latter function is also a hallmark of microRNAs, a rather new layer in the regulation of gene expression. Affecting e.g. proliferation, microRNAs constitute a potential target for viral interference on the way to persistence and transformation. Hence, we explored the interconnections between HTLV-1 and cellular microRNAs.
    Results: We report that several microRNAs--miRs 21, 24, 146a, 155 and 223--are deregulated in HTLV-1-transformed cells. They are all upregulated except for miR-223, which is downregulated. Each of those microRNAs has ties to cancer. Their expression pattern forms a uniform phenotype among HTLV-transformed cells when compared to HTLV-negative control cells. In particular, miR-146a expression was found to be directly stimulated by Tax via NF-kappaB-mediated transactivation of its promoter; a single NF-kappaB site proximal to the transcription start point was necessary and sufficient for this to happen. An in silico analysis of potential target genes revealed candidates that might be coregulated by two or more of the aforementioned overexpressed microRNAs.
    Conclusion: These data demonstrate that cellular microRNAs are deregulated in HTLV-1-transformed T cells. In the case of miR-146a, this could be directly attributed to HTLV's oncoprotein Tax. Interference with cellular microRNAs may be crucial to maintaining persistence or may facilitate transformation of host cells.
    Mesh-Begriff(e) Binding Sites ; Cell Line ; Cell Transformation, Viral ; Gene Expression Regulation ; Gene Products, tax/metabolism ; Human T-lymphotropic virus 1/physiology ; Humans ; MicroRNAs/biosynthesis ; NF-kappa B/metabolism ; Protein Binding ; T-Lymphocytes/virology
    Chemische Substanzen Gene Products, tax ; MicroRNAs ; NF-kappa B ; tax protein, Human T-lymphotrophic virus 1
    Sprache Englisch
    Erscheinungsdatum 2008-11-12
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1742-4690
    ISSN (online) 1742-4690
    DOI 10.1186/1742-4690-5-100
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Stimulation of interleukin-13 expression by human T-cell leukemia virus type 1 oncoprotein Tax via a dually active promoter element responsive to NF-kappaB and NFAT.

    Silbermann, Katrin / Schneider, Grit / Grassmann, Ralph

    The Journal of general virology

    2008  Band 89, Heft Pt 11, Seite(n) 2788–2798

    Abstract: The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein transforms human lymphocytes and is critical for the pathogenesis of HTLV-1-induced adult T-cell leukaemia. In HTLV-transformed cells, Tax upregulates interleukin (IL)-13, a cytokine with ... ...

    Abstract The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein transforms human lymphocytes and is critical for the pathogenesis of HTLV-1-induced adult T-cell leukaemia. In HTLV-transformed cells, Tax upregulates interleukin (IL)-13, a cytokine with proliferative and anti-apoptotic functions that is linked to leukaemogenesis. Tax-stimulated IL-13 is thought to result in autocrine stimulation of HTLV-infected cells and thus may be relevant to their growth. The causal transactivation of the IL-13 promoter by Tax is predominantly dependent on a nuclear factor of activated T cells (NFAT)-binding P element. Here, it was shown that the isolated IL-13 Tax-responsive element (IL13TaxRE) was sufficient to mediate IL-13 transactivation by Tax and NFAT1. However, cyclosporin A, a specific NFAT inhibitor, revealed that Tax transactivation of IL13TaxRE or wild-type IL-13 promoter was independent of NFAT and that NFAT did not contribute to IL-13 upregulation in HTLV-transformed cells. By contrast, Tax stimulation was repressible by an efficient nuclear factor (NF)-kappaB inhibitor (IkBaDN), indicating the requirement for NF-kappaB. The capacity of NF-kappaB to stimulate IL13TaxRE was demonstrated by a strong response to NF-kappaB in reporter assays and by direct binding of NF-kappaB to IL13TaxRE. Thus, IL13TaxRE in the IL-13 promoter represents a dually active promoter element responsive to NF-kappaB and NFAT. Together, these results indicate that Tax causes IL-13 upregulation in HTLV-1-infected cells via NF-kappaB.
    Mesh-Begriff(e) DNA Primers ; Gene Expression Regulation ; Gene Products, tax/immunology ; HTLV-I Infections/immunology ; Human T-lymphotropic virus 1/immunology ; Humans ; Interleukin-13/genetics ; NF-kappa B/physiology ; NFATC Transcription Factors/physiology ; Promoter Regions, Genetic ; RNA, Messenger/genetics ; T-Lymphocytes/immunology ; T-Lymphocytes/virology ; TATA Box ; Transcriptional Activation
    Chemische Substanzen DNA Primers ; Gene Products, tax ; Interleukin-13 ; NF-kappa B ; NFATC Transcription Factors ; RNA, Messenger ; tax protein, Human T-lymphotrophic virus 1
    Sprache Englisch
    Erscheinungsdatum 2008-10-08
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219316-4
    ISSN 1465-2099 ; 0022-1317
    ISSN (online) 1465-2099
    ISSN 0022-1317
    DOI 10.1099/vir.0.2008/003699-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Buch ; Dissertation / Habilitation: Herpesvirus saimiri als selektionierbarer Expressionsvektor für T-Lymphozyten

    Grassmann, Ralph

    1989  

    Sprache Nicht zu entscheiden
    Umfang 138 S, Ill., graph. Darst, 21 cm
    Dokumenttyp Buch ; Dissertation / Habilitation
    Dissertation / Habilitation @Erlangen, Nürnberg, Univ., Diss. : 1989
    Datenquelle Ehemaliges Sondersammelgebiet Küsten- und Hochseefischerei

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  9. Artikel ; Online: MicroRNA miR-146a and further oncogenesis-related cellular microRNAs are dysregulated in HTLV-1-transformed T lymphocytes

    Schneider Grit / Pichler Klemens / Grassmann Ralph

    Retrovirology, Vol 5, Iss 1, p

    2008  Band 100

    Abstract: Abstract Background Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of a severe and fatal lymphoproliferative disease of mainly CD4 + T cell origin, adult T cell leukemia, which develops after prolonged viral persistence. Transformation ...

    Abstract Abstract Background Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of a severe and fatal lymphoproliferative disease of mainly CD4 + T cell origin, adult T cell leukemia, which develops after prolonged viral persistence. Transformation of infected cells involves HTLV-1's oncoprotein Tax, which perturbs cell cycle regulation and modulates cellular gene expression. The latter function is also a hallmark of microRNAs, a rather new layer in the regulation of gene expression. Affecting e.g. proliferation, microRNAs constitute a potential target for viral interference on the way to persistence and transformation. Hence, we explored the interconnections between HTLV-1 and cellular microRNAs. Results We report that several microRNAs – miRs 21, 24, 146a, 155 and 223 – are deregulated in HTLV-1-transformed cells. They are all upregulated except for miR-223, which is downregulated. Each of those microRNAs has ties to cancer. Their expression pattern forms a uniform phenotype among HTLV-transformed cells when compared to HTLV-negative control cells. In particular, miR-146a expression was found to be directly stimulated by Tax via NF- κ B-mediated transactivation of its promoter; a single NF- κ B site proximal to the transcription start point was necessary and sufficient for this to happen. An in silico analysis of potential target genes revealed candidates that might be coregulated by two or more of the aforementioned overexpressed microRNAs. Conclusion These data demonstrate that cellular microRNAs are deregulated in HTLV-1-transformed T cells. In the case of miR-146a, this could be directly attributed to HTLV's oncoprotein Tax. Interference with cellular microRNAs may be crucial to maintaining persistence or may facilitate transformation of host cells.
    Schlagwörter Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Immunologic diseases. Allergy ; RC581-607
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2008-11-01T00:00:00Z
    Verlag BioMed Central
    Dokumenttyp Artikel ; Online
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  10. Artikel ; Online: The tumour marker Fascin is strongly induced by Tax of HTLV-1 through NF-κB signals in T lymphocytes

    Fleckenstein Bernhard / Grassmann Ralph / Rowan Aileen G / Kalmer Martina / Kress Andrea K

    Retrovirology, Vol 8, Iss Suppl 1, p A

    2011  Band 186

    Schlagwörter Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Immunologic diseases. Allergy ; RC581-607
    Sprache Englisch
    Erscheinungsdatum 2011-06-01T00:00:00Z
    Verlag BioMed Central
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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