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  • 1
    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
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    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2000
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  • 2
    Online Resource
    Online Resource
    Reassortment of pilin genes in Neisseria gonorrhoeae occurs by two distinct mechanisms
    Springer Science and Business Media LLC ; 1989
    In:  Nature Vol. 338, No. 6217 ( 1989-4), p. 651-652
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 338, No. 6217 ( 1989-4), p. 651-652
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/338651a0
    RVK:
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1989
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  • 3
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    Distinct Gene Expression Pattern of Malignant Hematopoietic Stem and Progenitor Cells in Polycythemia Vera
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1044, No. 1 ( 2005-06), p. 94-108
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1044, No. 1 ( 2005-06), p. 94-108
    Abstract: A bstract : Polycythemia vera (PV) is a chronic myeloproliferative disorder with an expansion of multipotent hematopoietic progenitor cells. Although it is known that hematopoietic progenitors in PV are erythropoietin independent and hypersensitive to several cytokines, the molecular oncogenic mechanisms in PV are largely unknown. In this study, we examined gene expression profiles of CD34 + cells from bone marrow of patients with de novo PV and from healthy volunteers to identify molecular changes associated with the malignant growth of hematopoietic stem and progenitor cells in this myeloproliferative disorder. Using cDNA arrays, we found significant differences ( P 〈 .01 ) in the expression of 107 genes. Proapoptotic genes (CASP2, CASP3, DAPK1, ALG2) were expressed at lower levels in PV‐CD34 + cells, reflecting a lower apoptotic activity. Fibrosis‐stimulating growth factors (transforming growth factor β1, transforming growth factor β2, bone morphogenetic protein 2, and endothelial growth factor) were expressed at significantly higher levels in PV‐CD34 + cells. Furthermore, PV‐CD34 + cells overexpressed several receptors, protein kinases, and proteasome subunits, which might be targets for directed therapeutic approaches. It is interesting that three retinoid receptors were overexpressed in PV‐CD34 + cells—retinoic acid receptor β (RARβ), retinoid X receptor β (RXRβ), and cellular retinoic acid binding protein 2 (CRABP2). Using methylcellulose colony‐forming assays, we found that the formation of erythroid colonies derived from PV hematopoietic progenitors was inhibited by all‐trans‐retinoic acid (ATRA), a natural ligand of those receptors, in a dose‐dependent manner, showing a maximum inhibition of 89% at 10 μM; the growth of myelomonocytic colonies was not significantly affected. These data suggest that the use of ATRA could be of therapeutic benefit for patients with PV.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1349.013
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    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
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  • 4
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    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:
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2000
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  • 5
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    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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  • 6
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    Structural insights into Helicobacter pylori oncoprotein CagA interaction with β1 integrin
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 36 ( 2012-09-04), p. 14640-14645
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 36 ( 2012-09-04), p. 14640-14645
    Abstract: Infection with the gastric pathogen Helicobacter pylori is a risk factor for the development of gastric cancer. Pathogenic strains of H. pylori carry a type IV secretion system (T4SS) responsible for the injection of the oncoprotein CagA into host cells. H. pylori and its cag -T4SS exploit α5β1 integrin as a receptor for CagA translocation. Injected CagA localizes to the inner leaflet of the host cell membrane, where it hijacks host cell signaling and induces cytoskeleton reorganization. Here we describe the crystal structure of the N-terminal ∼100-kDa subdomain of CagA at 3.6 Å that unveils a unique combination of folds. The core domain of the protein consists of an extended single-layer β-sheet stabilized by two independent helical subdomains. The core is followed by a long helix that forms a four-helix helical bundle with the C-terminal domain. Mapping of conserved regions in a set of CagA sequences identified four conserved surface-exposed patches (CSP1–4), which represent putative hot-spots for protein–protein interactions. The proximal part of the single-layer β-sheet, covering CSP4, is involved in specific binding of CagA to the β1 integrin, as determined by yeast two-hybrid and in vivo competition assays in H. pylori cell-culture infection studies. These data provide a structural basis for the first step of CagA internalization into host cells and suggest that CagA uses a previously undescribed mechanism to bind β1 integrin to mediate its own translocation.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1206098109
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    TA 1000
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    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2012
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  • 7
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    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
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    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2001
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  • 8
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    Tumor immune escape by the loss of homeostatic chemokine expression
    Proceedings of the National Academy of Sciences ; 2007
    In:  Proceedings of the National Academy of Sciences Vol. 104, No. 48 ( 2007-11-27), p. 19055-19060
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 104, No. 48 ( 2007-11-27), p. 19055-19060
    Abstract: The novel keratinocyte-specific chemokine CCL27 plays a critical role in the organization of skin-associated immune responses by regulating T cell homing under homeostatic and inflammatory conditions. Here we demonstrate that human keratinocyte-derived skin tumors may evade T cell-mediated antitumor immune responses by down-regulating the expression of CCL27 through the activation of epidermal growth factor receptor (EGFR)–Ras–MAPK-signaling pathways. Compared with healthy skin, CCL27 mRNA and protein expression was progressively lost in transformed keratinocytes of actinic keratoses and basal and squamous cell carcinomas. In vivo , precancerous skin lesions as well as cutaneous carcinomas showed significantly elevated levels of phosphorylated ERK compared with normal skin, suggesting the activation of EGFR–Ras signaling pathways in keratinocyte-derived malignancies. In vitro , exogenous stimulation of the EGFR–Ras signaling pathway through EGF or transfection of the dominant-active form of the Ras oncogene (H-RasV12) suppressed whereas an EGFR tyrosine kinase inhibitor increased CCL27 mRNA and protein production in keratinocytes. In mice, neutralization of CCL27 led to decreased leukocyte recruitment to cutaneous tumor sites and significantly enhanced primary tumor growth. Collectively, our data identify a mechanism of skin tumors to evade host antitumor immune responses.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0705673104
    RVK:
    TA 1000
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2007
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  • 9
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    Serum proteome profiling detects myelodysplastic syndromes and identifies CXC chemokine ligands 4 and 7 as markers for advanced disease
    Proceedings of the National Academy of Sciences ; 2007
    In:  Proceedings of the National Academy of Sciences Vol. 104, No. 4 ( 2007-01-23), p. 1307-1312
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 104, No. 4 ( 2007-01-23), p. 1307-1312
    Abstract: Myelodysplastic syndromes (MDS) are among the most frequent hematologic malignancies. Patients have a short survival and often progress to acute myeloid leukemia. The diagnosis of MDS can be difficult; there is a paucity of molecular markers, and the pathophysiology is largely unknown. Therefore, we conducted a multicenter study investigating whether serum proteome profiling may serve as a noninvasive platform to discover novel molecular markers for MDS. We generated serum proteome profiles from 218 individuals by MS and identified a profile that distinguishes MDS from non-MDS cytopenias in a learning sample set. This profile was validated by testing its ability to predict MDS in a first independent validation set and a second, prospectively collected, independent validation set run 5 months apart. Accuracy was 80.5% in the first and 79.0% in the second validation set. Peptide mass fingerprinting and quadrupole TOF MS identified two differential proteins: CXC chemokine ligands 4 (CXCL4) and 7 (CXCL7), both of which had significantly decreased serum levels in MDS, as confirmed with independent antibody assays. Western blot analyses of platelet lysates for these two platelet-derived molecules revealed a lack of CXCL4 and CXCL7 in MDS. Subtype analyses revealed that these two proteins have decreased serum levels in advanced MDS, suggesting the possibility of a concerted disturbance of transcription or translation of these chemokines in advanced MDS.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0610330104
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2007
    detail.hit.zdb_id: 209104-5
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  • 10
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    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:
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2003
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