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Book ; Thesis: Der transformierende Genomabschnitt des menschlichen T-Zelleukämie-Virus Typ 1

Grassmann, Ralph

1992

Author's details	von Ralph Grassmann
Language	English
Size	Getr. Zählung : Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Erlangen-Nürnberg, Univ., Habil.-Schr., 1993
Note	Text engl.
HBZ-ID	HT006796429
Database	Catalogue ZB MED Medicine, Health

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Conference proceedings: The Human T-Lymphotropic Virus and Adult T-Cell Leukemia/Lymphoma

Grassmann, Ralph

2006 , Page(s) IS042

Event/congress	27. Deutscher Krebskongress; Berlin; Deutsche Krebsgesellschaft e.V.; 2006
Keywords	Medizin, Gesundheit
Publishing date	2006-03-20
Publisher	German Medical Science; Düsseldorf, Köln
Document type	Conference proceedings
Database	German Medical Science

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Article: The roles of microRNAs in mammalian virus infection.

Grassmann, Ralph / Jeang, Kuan-Teh

Biochimica et biophysica acta

2008 Volume 1779, Issue 11, Page(s) 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 term(s)	Animals ; Humans ; Mammals/virology ; MicroRNAs/metabolism ; RNA, Viral/metabolism ; Virus Diseases/metabolism
Chemical Substances	MicroRNAs ; RNA, Viral
Language	English
Publishing date	2008-05-15
Publishing country	Netherlands
Document type	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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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

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

Viruses

2011 Volume 3, Issue 8, Page(s) 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 term(s)	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
Chemical Substances	Biomarkers ; Cell Adhesion Molecules ; Costimulatory and Inhibitory T-Cell Receptors ; Gene Products, tax ; Receptors, Cytokine ; tax protein, Human T-lymphotrophic virus 1
Language	English
Publishing date	2011-08-16
Publishing country	Switzerland
Document type	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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cell Surface Markers in HTLV-1 Pathogenesis

Andrea K. Kress / Bernhard Fleckenstein / Ralph Grassmann

Viruses, Vol 3, Iss 8, Pp 1439-

2011 Volume 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.
Keywords	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
Language	English
Publishing date	2011-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; 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 Volume 5, Page(s) 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 term(s)	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
Chemical Substances	Gene Products, tax ; MicroRNAs ; NF-kappa B ; tax protein, Human T-lymphotrophic virus 1
Language	English
Publishing date	2008-11-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1742-4690
ISSN (online)	1742-4690
DOI	10.1186/1742-4690-5-100
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: 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 Volume 89, Issue Pt 11, Page(s) 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 term(s)	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
Chemical Substances	DNA Primers ; Gene Products, tax ; Interleukin-13 ; NF-kappa B ; NFATC Transcription Factors ; RNA, Messenger ; tax protein, Human T-lymphotrophic virus 1
Language	English
Publishing date	2008-10-08
Publishing country	England
Document type	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
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Thesis: Herpesvirus saimiri als selektionierbarer Expressionsvektor für T-Lymphozyten

Grassmann, Ralph

1989

Language	Undetermined
Size	138 S, Ill., graph. Darst, 21 cm
Document type	Book ; Thesis
Thesis / German Habilitation thesis	@Erlangen, Nürnberg, Univ., Diss. : 1989
Database	Former special subject collection: coastal and deep sea fishing

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Article ; 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 Volume 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.
Keywords	Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Immunologic diseases. Allergy ; RC581-607
Subject code	570
Language	English
Publishing date	2008-11-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The tumor marker Fascin is strongly induced by the Tax oncoprotein of HTLV-1 through NF-kappaB signals.

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

Blood

2011 Volume 117, Issue 13, Page(s) 3609–3612

Abstract: Oncogenic transformation of CD4(+) T cells by human T-cell lymphotropic virus type 1 (HTLV-1) is understood as the initial step to adult T-cell leukemia/lymphoma, a process that is mainly initiated by perturbation of cellular signaling by the viral Tax ... ...

Abstract	Oncogenic transformation of CD4(+) T cells by human T-cell lymphotropic virus type 1 (HTLV-1) is understood as the initial step to adult T-cell leukemia/lymphoma, a process that is mainly initiated by perturbation of cellular signaling by the viral Tax oncoprotein, a potent transcriptional regulator. In search of novel biomarkers with relevance to oncogenesis, we identified the tumor marker and actin-bundling protein Fascin (FSCN1) to be specifically and strongly up-regulated in both HTLV-1-transformed and adult T-cell leukemia/lymphoma patient-derived CD4(+) T cells. Fascin is important for migration and metastasis in various types of cancer. Here we report that a direct link can exist between a single viral oncoprotein and Fascin expression, as the viral oncoprotein Tax was sufficient to induce high levels of Fascin. Nuclear factor-κB signals were important for Tax-mediated transcriptional regulation of Fascin in T cells. This suggests that Fascin up-regulation by Tax contributes to the development of HTLV-1-associated pathogenesis.
MeSH term(s)	Adult ; Biomarkers, Tumor/physiology ; Carrier Proteins/antagonists & inhibitors ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Carrier Proteins/physiology ; Cells, Cultured ; Gene Expression Profiling ; Gene Expression Regulation, Leukemic/drug effects ; Gene Knockdown Techniques ; Gene Products, tax/metabolism ; Gene Products, tax/physiology ; Humans ; Leukemia-Lymphoma, Adult T-Cell/genetics ; Leukemia-Lymphoma, Adult T-Cell/metabolism ; Leukemia-Lymphoma, Adult T-Cell/pathology ; Leukemia-Lymphoma, Adult T-Cell/virology ; Microarray Analysis ; Microfilament Proteins/antagonists & inhibitors ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Microfilament Proteins/physiology ; NF-kappa B/metabolism ; NF-kappa B/physiology ; RNA, Small Interfering/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/physiology ; Up-Regulation/drug effects ; Up-Regulation/genetics
Chemical Substances	Biomarkers, Tumor ; Carrier Proteins ; Gene Products, tax ; Microfilament Proteins ; NF-kappa B ; RNA, Small Interfering ; tax protein, Human T-lymphotrophic virus 1 ; fascin (146808-54-0)
Language	English
Publishing date	2011-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2010-09-305805
Database	MEDical Literature Analysis and Retrieval System OnLINE

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