LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 5 of total 5

Search options

  1. Article: Tracking death dealing by Fas and TRAIL in lymphatic neoplastic disorders: pathways, targets, and therapeutic tools.

    Greil, Richard / Anether, Gabriele / Johrer, Karin / Tinhofer, Inge

    Journal of leukocyte biology

    2003  Volume 74, Issue 3, Page(s) 311–330

    Abstract: In the past decade, it was concluded from a number of investigations that death domain-containing members of the tumor necrosis factor-receptor (TNF-R) family and their ligands such as Fas/FasL and TNF-related apoptosis-inducing ligand (TRAIL)-R/TRAIL ... ...

    Abstract In the past decade, it was concluded from a number of investigations that death domain-containing members of the tumor necrosis factor-receptor (TNF-R) family and their ligands such as Fas/FasL and TNF-related apoptosis-inducing ligand (TRAIL)-R/TRAIL are essential for maintaining an intact immune system for surveillance against infection and cancer development and that nondeath domain-containing members such as CD30 or CD40 are involved in the fine tuning of this system during the selection process of the lymphatic system. In line with this conclusion are the observations that alterations in structure, function, and regulation of these molecules contribute to autoimmunity and cancer development of the lymphoid system. Besides controlling size and function of the lymphoid cell pool, Fas/FasL and TRAIL-R/TRAIL regulate myelopoiesis and the dendritic cell functions, and severe alterations of these lineages during the outgrowth and expansion of the lymphoid tumors have been reported. It is the aim of this review to summarize what is currently known about the complex role of these two death receptor/ligand systems in normal, disturbed, and neoplastic hemato-/lymphopoiesis and to point out how such knowledge can be used in developing novel, therapeutic options and the problems that will have to be faced along the way.
    MeSH term(s) Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; Humans ; Lymphoma/metabolism ; Lymphoma/therapy ; Membrane Glycoproteins/physiology ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha/physiology ; fas Receptor/physiology
    Chemical Substances Apoptosis Regulatory Proteins ; Membrane Glycoproteins ; TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Tumor Necrosis Factor-alpha ; fas Receptor
    Language English
    Publishing date 2003-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.0802416
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article: Tuning the rheostat of the myelopoietic system via Fas and TRAIL.

    Greil, Richard / Anether, Gabriele / Johrer, Karin / Tinhofer, Inge

    Critical reviews in immunology

    2003  Volume 23, Issue 4, Page(s) 301–322

    Abstract: During the last decade, the concerted effort of numerous scientific groups has expanded our understanding of the finely tuned network present within bone marrow for the regulation of the hematopoietic system. This network, comprising humoral and cellular ...

    Abstract During the last decade, the concerted effort of numerous scientific groups has expanded our understanding of the finely tuned network present within bone marrow for the regulation of the hematopoietic system. This network, comprising humoral and cellular cross talk, is responsible for the adaptation of hematopoietic populations to demands as they arise. Major components of this control system are death receptors and their specific ligands, which eliminate superfluous cells once they have fulfilled their respective functions. The important role of Fas (CD95/Apo-1), one member of this death receptor family, in the regulation of T- and B-cell functions has been established. Alteration of Fas expression and/or function in lymphoid cells may contribute to the development of autoimmunity and/or neoplastic diseases. In addition to controlling lymphoid compartments, Fas is also involved in the regulation of myeloid cell functions. More recently, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its specific receptors (TRAIL-R) have been identified as further members of this death receptor/ligand family. The TRAIL-R/TRAIL system is of vital importance for the maturation and functioning of immune effector cells of lymphoid, as well as myeloid, origin. In the present review, we have summarized current knowledge about both death receptor/ligand systems in the expansion and functioning of cells from the myeloid compartments, highlighted their role in normal hematopoiesis, and assessed their alterations in pathologic or neoplastic conditions.
    MeSH term(s) Animals ; Apoptosis Regulatory Proteins ; Fas Ligand Protein ; GPI-Linked Proteins ; Hematopoietic Stem Cells/immunology ; Hematopoietic Stem Cells/metabolism ; Humans ; Leukemia, Myeloid/immunology ; Leukemia, Myeloid/metabolism ; Membrane Glycoproteins/metabolism ; Membrane Glycoproteins/physiology ; Membrane Glycoproteins/therapeutic use ; Mice ; Models, Biological ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Member 10c ; Signal Transduction ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/physiology ; Tumor Necrosis Factor-alpha/therapeutic use ; fas Receptor/metabolism ; fas Receptor/physiology ; fas Receptor/therapeutic use
    Chemical Substances Apoptosis Regulatory Proteins ; FASLG protein, human ; Fas Ligand Protein ; Fasl protein, mouse ; GPI-Linked Proteins ; Membrane Glycoproteins ; Receptors, Tumor Necrosis Factor ; Receptors, Tumor Necrosis Factor, Member 10c ; TNF-Related Apoptosis-Inducing Ligand ; TNFRSF10C protein, human ; TNFSF10 protein, human ; Tnfsf10 protein, mouse ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha ; fas Receptor
    Language English
    Publishing date 2003-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1353116-5
    ISSN 1040-8401
    ISSN 1040-8401
    DOI 10.1615/critrevimmunol.v23.i4.30
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1699: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article: Tetrocarcin-A--induced ER stress mediates apoptosis in B-CLL cells via a Bcl-2--independent pathway.

    Anether, Gabriele / Tinhofer, Inge / Senfter, Monika / Greil, Richard

    Blood

    2003  Volume 101, Issue 11, Page(s) 4561–4568

    Abstract: Tetrocarcin-A (TC-A), an antibiotic agent isolated from actinomycetes, has recently been described to antagonize Bcl-2 functions, thereby sensitizing tumor cells to cell death signals under control of Bcl-2. In this study, we analyzed the direct ... ...

    Abstract Tetrocarcin-A (TC-A), an antibiotic agent isolated from actinomycetes, has recently been described to antagonize Bcl-2 functions, thereby sensitizing tumor cells to cell death signals under control of Bcl-2. In this study, we analyzed the direct proapoptotic effect of TC-A in the B-chronic lymphocytic leukemia (B-CLL) model. We focused on the signal cascade triggered by TC-A in B-CLL cells and identified activated mitochondrial as well as endoplasmatic reticulum (ER) stress signals. The expression levels of known effector molecules mediating mitochondrial signaling, such as Bax and Bid, and the antagonistic molecule Bcl-2 did not influence sensitivity of B-CLL cells to TC-A. Furthermore, the molecular chaperone and sensor of ER stress, HSP70, though significantly up-regulated in B-CLL cells undergoing TC-A-triggered apoptosis, was ineffective to exert its anti-apoptotic function described in multiple cell death pathways. Autologous T cells of B-CLL patients were significantly less sensitive to TC-A as were also T cells from healthy donors when compared with their normal B-cell fraction. Furthermore, sensitivity of B-CLL cells to TC-A treatment in vitro was dependent neither on the expression levels of CD38-a prognostic factor for survival of B-CLL patients as well as for their response to therapy-nor on the clinical stage or pretreatment status of patients. From our data showing that TC-A induced a cell death pathway via ER stress preferentially in B cells and that it acted independently of important markers of drug sensitivity and of clinical markers, we conclude that TC-A might represent an attractive candidate drug for further evaluation in preclinical trials.
    MeSH term(s) Aged ; Aminoglycosides ; Anti-Bacterial Agents/pharmacology ; Apoptosis/drug effects ; Case-Control Studies ; Caspase 8 ; Caspase 9 ; Caspases ; Female ; HSP70 Heat-Shock Proteins/biosynthesis ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Male ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53
    Chemical Substances Aminoglycosides ; Anti-Bacterial Agents ; HSP70 Heat-Shock Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Tumor Suppressor Protein p53 ; tetrocarcin A (73666-84-9) ; CASP8 protein, human (EC 3.4.22.-) ; CASP9 protein, human (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2003-01-30
    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-2002-08-2501
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.140: 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)
    Zs.MO 364: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article: Interleukin-15 as a potential costimulatory cytokine in CD154 gene therapy of chronic lymphocytic leukemia.

    Anether, Gabriele / Marschitz, Ingrid / Tinhofer, Inge / Greil, Richard

    Blood

    2002  Volume 99, Issue 2, Page(s) 722–723

    MeSH term(s) Apoptosis ; CD40 Antigens/immunology ; CD40 Ligand/genetics ; CD40 Ligand/physiology ; Fas Ligand Protein ; Genetic Therapy ; Humans ; Interleukin-15/genetics ; Interleukin-15/physiology ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/therapy ; Lymphocyte Activation ; Membrane Glycoproteins/physiology ; Neoplastic Stem Cells/transplantation ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; Th1 Cells/immunology ; fas Receptor/physiology
    Chemical Substances CD40 Antigens ; FASLG protein, human ; Fas Ligand Protein ; Interleukin-15 ; Membrane Glycoproteins ; fas Receptor ; CD40 Ligand (147205-72-9)
    Language English
    Publishing date 2002-01-15
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.v99.2.722
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.140: 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)
    Zs.MO 364: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Stressful death of T-ALL tumor cells after treatment with the anti-tumor agent Tetrocarcin-A.

    Tinhofer, Inge / Anether, Gabriele / Senfter, Monika / Pfaller, Kristian / Bernhard, David / Hara, Mitsunobu / Greil, Richard

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2002  Volume 16, Issue 10, Page(s) 1295–1297

    Abstract: The T-ALL cell lines CCRF-CEM and Jurkat were studied for their sensitivity toward apoptosis induced by tetrocarcin-A (TC-A), an antibacterial and antitumor agent isolated from the actinomycete Micromonospora. This substance promoted cell death via a ... ...

    Abstract The T-ALL cell lines CCRF-CEM and Jurkat were studied for their sensitivity toward apoptosis induced by tetrocarcin-A (TC-A), an antibacterial and antitumor agent isolated from the actinomycete Micromonospora. This substance promoted cell death via a mitochondrial signaling pathway, that is, by activation of Bid and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, and activation of effector caspases, even under conditions of Bcl-2 overexpression. Furthermore, sensitivity to TC-A was not dependent on expression of wild-type caspase-8. In contrast, this apoptotic pathway was inhibited markedly by pretreatment of cells with cycloheximide, an inhibitor of de novo protein synthesis. cDNA microarray chip analysis revealed that TC-A induced a significant up-regulation of members of the heat shock protein family known to be involved in the endoplasmic reticulum (ER)-stress-induced apoptotic program. The activation of caspase-12, the central inducer caspase involved in ER-stress by TC-A treatment, is in concordance with this result. These results show that, in T-ALL cells, TC-A induces an apoptotic machinery via mitochondrial and ER signaling, which is not inhibited by aberrant expression/function of important regulators of death receptor- and drug-induced apoptosis.
    MeSH term(s) Aminoglycosides ; Anti-Bacterial Agents/pharmacology ; Antineoplastic Agents/pharmacology ; Apoptosis ; Caspases/metabolism ; Endoplasmic Reticulum/metabolism ; Heat-Shock Proteins/biosynthesis ; Heat-Shock Proteins/genetics ; Humans ; Jurkat Cells ; Leukemia-Lymphoma, Adult T-Cell/drug therapy ; Leukemia-Lymphoma, Adult T-Cell/metabolism ; Leukemia-Lymphoma, Adult T-Cell/pathology ; Mitochondria/drug effects ; Mitochondria/metabolism ; Models, Biological ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; Transcription Factors/biosynthesis ; Transcription Factors/genetics ; Tumor Cells, Cultured ; Up-Regulation
    Chemical Substances Aminoglycosides ; Anti-Bacterial Agents ; Antineoplastic Agents ; Heat-Shock Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Transcription Factors ; tetrocarcin A (73666-84-9) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2002-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.02-0020fje
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: 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)
    Zs.MO 296: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top