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  • 1
    Online Resource
    Online Resource
    Differential Gene Expression Underlying the Functional Distinctions of Primary Human CD34 + Hematopoietic Stem and Progenitor Cells from Peripheral Blood and Bone Marrow
    Wiley ; 2003
    In:  Annals of the New York Academy of Sciences Vol. 996, No. 1 ( 2003-05), p. 89-100
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 996, No. 1 ( 2003-05), p. 89-100
    Abstract: A bstract : The restorative capacity of human CD34 + hematopoietic cells is clinically used in the autologous and allogeneic transplant setting to support cytotoxic therapy. We examined gene expression patterns of highly enriched bone marrow CD34 + (BM‐CD34 + ) or G‐CSF‐mobilized peripheral blood CD34 + (PB‐CD34 + ) cells by cDNA array technology, quantitative real‐time RT‐PCR, and flow cytometry, to identify molecular causes underlying the functional differences between circulating and sedentary hematopoietic stem and progenitor cells. The greater cell cycle and DNA synthesis activity of BM‐CD34 + compared to PB‐CD34 + cells was reflected by the 2‐ to 5‐fold higher expression of 9 genes involved in cell cycle, 11 genes regulating DNA synthesis, and the cell cycle‐initiating transcription factor E2F‐1. The 2‐ to 3‐fold greater expression of 5 pro‐apoptotic genes in PB‐CD34 + cells indicated a higher apoptotic activity, which could functionally be corroborated by apoptosis assays. Thrombin receptor (PAR1), known to play a role in trafficking of malignant cells, was 3.6‐fold higher expressed in circulating CD34 + cells than in BM‐CD34 + cells. Guidance via thrombin receptor might molecularly mediate stem cell migration. In summary, our study provides gene expression profiles of primary human CD34 + hematopoietic cells of blood and marrow. Our data molecularly confirm and explain the finding that CD34 + cells residing in the bone marrow are cycling more rapidly, whereas circulating CD34 + cells consist of a higher number of quiescent stem and progenitor cells. Moreover, our data give novel molecular insights into stem cell migration and differentiation.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2003.996.issue-1
    DOI: 10.1111/j.1749-6632.2003.tb03237.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2003
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  • 2
    Online Resource
    Online Resource
    The human formin-binding protein 17 (FBP17) interacts with sorting nexin, SNX2, and is an MLL -fusion partner in acute myelogeneous leukemia
    Proceedings of the National Academy of Sciences ; 2001
    In:  Proceedings of the National Academy of Sciences Vol. 98, No. 15 ( 2001-07-17), p. 8756-8761
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 15 ( 2001-07-17), p. 8756-8761
    Abstract: We have cloned a fusion partner of the MLL gene at 11q23 and identified it as the gene encoding the human formin-binding protein 17, FBP17. It maps to chromosome 9q34 centromeric to ABL . The gene fusion results from a complex chromosome rearrangement that was resolved by fluorescence in situ hybridization with various probes on chromosomes 9 and 11 as an ins(11;9)(q23;q34)inv(11)(q13q23). The rearrangement resulted in a 5′- MLL / FBP17 -3′ fusion mRNA. We retrovirally transduced murine-myeloid progenitor cells with MLL / FBP17 to test its transforming ability. In contrast to MLL / ENL , MLL / ELL and other MLL -fusion genes, MLL / FBP17 did not give a positive readout in a serial replating assay. Therefore, we assume that additional cooperating genetic abnormalities might be needed to establish a full malignant phenotype. FBP17 consists of a C-terminal Src homology 3 domain and an N-terminal region that is homologous to the cell division cycle protein, cdc15, a regulator of the actin cytoskeleton in Schizosaccharomyces pombe . Both domains are separated by a consensus Rho-binding motif that has been identified in different Rho-interaction partners such as Rhotekin and Rhophilin. We evaluated whether FBP17 and members of the Rho family interact in vivo with a yeast two-hybrid assay. None of the various Rho proteins tested, however, interacted with FBP17. We screened a human kidney library and identified a sorting nexin, SNX2, as a protein interaction partner of FBP17. These data provide a link between the epidermal growth factor receptor pathway and an MLL fusion protein.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.121433898
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2001
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  • 3
    Online Resource
    Online Resource
    Translocation of Helicobacter pylori CagA into Gastric Epithelial Cells by Type IV Secretion
    American Association for the Advancement of Science (AAAS) ; 2000
    In:  Science Vol. 287, No. 5457 ( 2000-02-25), p. 1497-1500
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 287, No. 5457 ( 2000-02-25), p. 1497-1500
    Abstract: The Gram-negative bacterium Helicobacter pylori is a causative agent of gastritis and peptic ulcer disease in humans. Strains producing the CagA antigen ( cagA + ) induce strong gastric inflammation and are strongly associated with gastric adenocarcinoma and MALT lymphoma. We show here that such strains translocate the bacterial protein CagA into gastric epithelial cells by a type IV secretion system, encoded by the cag pathogenicity island. CagA is tyrosine-phosphorylated and induces changes in the tyrosine phosphorylation state of distinct cellular proteins. Modulation of host cells by bacterial protein translocation adds a new dimension to the chronic Helicobacter infection with yet unknown consequences.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.287.5457.1497
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2000
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  • 4
    Online Resource
    Online Resource
    The human GRAF gene is fused to MLL in a unique t(5;11)(q31;q23) and both alleles are disrupted in three cases of myelodysplastic syndrome/acute myeloid leukemia with a deletion 5q
    Proceedings of the National Academy of Sciences ; 2000
    In:  Proceedings of the National Academy of Sciences Vol. 97, No. 16 ( 2000-08), p. 9168-9173
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 97, No. 16 ( 2000-08), p. 9168-9173
    Abstract: We have isolated the human GRAF gene (for GTPase regulator associated with the focal adhesion kinase pp125 FAK ). This gene was fused with MLL in a unique t(5;11)(q31;q23) that occurred in an infant with juvenile myelomonocytic leukemia. GRAF encodes a member of the Rho family of the GTPase-activating protein (GAP) family. On the protein level, it is 90% homologous to the recently described chicken GRAF gene that functions as a GAP of RhoA in vivo and is thus a critical component of the integrin signaling transduction pathway. The particular position of the human GRAF gene at 5q31 and the proposed antiproliferative and tumor suppressor properties of its avian homologue suggest that it also might be pathogenetically relevant for hematologic malignancies with deletions of 5q. To investigate this possibility, we sequenced 4–5 individual cDNA clones from 13 cases in which one allele of GRAF was deleted. We found point mutations within the GAP domain of the second GRAF allele in one patient. In two additional patients we found an insertion of 52 or 74 bp within the GRAF cDNA that generates a reading frame shift followed by a premature stop codon. GRAF maps outside the previously defined commonly deleted 5q31 region. Nevertheless, inactivation of both alleles in at least some cases suggests that deletions and mutations of the GRAF gene may be instrumental in the development and progression of hematopoeitic disorders with a del(5q).
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.150079597
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2000
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    SSG: 11
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Helicobacter pylori Vacuolating Cytotoxin Inhibits T Lymphocyte Activation
    American Association for the Advancement of Science (AAAS) ; 2003
    In:  Science Vol. 301, No. 5636 ( 2003-08-22), p. 1099-1102
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 301, No. 5636 ( 2003-08-22), p. 1099-1102
    Abstract: Helicobacter pylori ( Hp ) vacuolating cytotoxin VacA induces cellular vacuolation in epithelial cells. We found that VacA could efficiently block proliferation of T cells by inducing a G 1 /S cell cycle arrest. It interfered with the T cell receptor/interleukin-2 (IL-2) signaling pathway at the level of the Ca 2 + -calmodulin–dependent phosphatase calcineurin. Nuclear translocation of nuclear factor of activated T cells (NFAT), a transcription factor acting as a global regulator of immune response genes, was abrogated, resulting in down-regulation of IL-2 transcription. VacA partially mimicked the activity of the immunosuppressive drug FK506 by possibly inducing a local immune suppression, explaining the extraordinary chronicity of Hp infections.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1086871
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2003
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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
    Location Call Number Limitation Availability
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