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  • 1
    Online Resource
    Online Resource
    The Hepatitis B Virus X Protein Transactivates Viral Core Gene Expression In Vivo
    American Society for Microbiology ; 1999
    In:  Journal of Virology Vol. 73, No. 12 ( 1999-12), p. 10399-10405
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 73, No. 12 ( 1999-12), p. 10399-10405
    Abstract: The function of the X protein in the life cycle of mammalian hepadnaviruses is unclear. Based on tissue culture experiments it has been suggested that this protein represents a transcriptional transactivator which might be essential for the expression of the viral core gene. Here we have examined whether the activity of the human hepatitis B virus (HBV) core gene in vivo depends on X coexpression. To this end we compared core gene expression between four lineages of transgenic mice carrying the HBV core gene in cis arrangement with the X gene (cex lineage) and six lineages containing a modified construct in which the start codon of the X gene had been deleted (ce lineage). Whereas all cex lineages consistently exhibited a high-level hepatic core gene expression, the liver-specific core gene expression pattern of the ce lineages was heterogenous with four lineages virtually not expressing the core gene. This defect was due to a strongly reduced transcription since no core mRNA could be detected by Northern blotting. To test whether core gene expression could be restored by providing an intact X gene in trans , we crossbred mice of two lines which expressed no core mRNA or core protein with transgenic mice expressing the X-gene product under the transcriptional regulation of the liver-specific major-urinary-protein promoter/enhancer (MUP-X mice). The introduction of the MUP-X transgene induced core mRNA expression and core protein biosynthesis in the livers of the double-transgenic mice. This demonstrates that the X-gene product has the capacity to transactivate HBV core gene expression in vivo.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.73.12.10399-10405.1999
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
    detail.hit.zdb_id: 1495529-5
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  • 2
    Online Resource
    Online Resource
    Mus cervicolor Murine Leukemia Virus Isolate M813 Belongs to a Unique Receptor Interference Group
    American Society for Microbiology ; 2001
    In:  Journal of Virology Vol. 75, No. 10 ( 2001-05-15), p. 4490-4498
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 75, No. 10 ( 2001-05-15), p. 4490-4498
    Abstract: Murine leukemia virus (MuLV) M813 was originally isolated from the Southeast Asian rodent Mus cervicolor . As with the ecotropic MuLVs derived from Mus musculus , its host range is limited to rodent cells. Earlier studies have mapped its receptor to chromosome 2, but it has not been established whether M813 shares a common receptor with any other MuLVs. In this study, we have performed interference assays with M813 and viruses from four interference groups of MuLV. The infection efficiency of M813 was not compromised in cells expressing any one of the other MuLVs, demonstrating that M813 must use a distinct receptor for cell entry. The entire M813 env coding region was molecularly cloned. Sequence analysis revealed high similarity with other MuLVs but with a unique receptor-binding domain. Substitution of M813 env sequences in Moloney MuLV resulted in a replication-competent virus with a host range and interference profile similar to those of the biological clone M813. M813 thus defines a novel receptor interference group of type C MuLVs.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.75.10.4490-4498.2001
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
    detail.hit.zdb_id: 1495529-5
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  • 3
    Online Resource
    Online Resource
    RUNX1 DNA-Binding Mutants, Associated with Minimally Differentiated Acute Myelogenous Leukemia, Disrupt Myeloid Differentiation
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 2 ( 2007-01-15), p. 537-545
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 2 ( 2007-01-15), p. 537-545
    Abstract: Mutations in the RUNX1 gene are found at high frequencies in minimally differentiated acute myelogenous leukemia. In addition to null mutations, many of the mutations generate Runx1 DNA-binding (RDB) mutants. To determine if these mutants antagonize wild-type protein activity, cDNAs were transduced into murine bone marrow or human cord blood cells using retroviral vectors. Significantly, the RDB mutants did not act in a transdominant fashion in vivo to disrupt Runx1 activity in either T-cell or platelet development, which are highly sensitive to Runx1 dosage. However, RDB mutant expression impaired expansion and differentiation of the erythroid compartment in which Runx1 expression is normally down-regulated, showing that a RDB-independent function is incompatible with erythroid differentiation. Significantly, both bone marrow progenitors expressing RDB mutants or deficient for Runx1 showed increased replating efficiencies in vitro, accompanied by the accumulation of myeloblasts and dysplastic progenitors, but the effect was more pronounced in RDB cultures. Disruption of the interface that binds CBFβ, an important cofactor of Runx1, did not impair RDB mutant replating activity, arguing against inactivation of Runx1 function by CBFβ sequestration. We propose that RDB mutants antagonize Runx1 function in early progenitors by disrupting a critical balance between DNA-binding–independent and DNA-binding–dependent signaling. [Cancer Res 2007;67(2):537–45]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-1903
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Altered Development and Cytokine Responses of Myeloid Progenitors in the Absence of Transcription Factor, Interferon Consensus Sequence Binding Protein
    American Society of Hematology ; 1999
    In:  Blood Vol. 94, No. 11 ( 1999-12-01), p. 3764-3771
    Details
    In: Blood, American Society of Hematology, Vol. 94, No. 11 ( 1999-12-01), p. 3764-3771
    Abstract: Mice deficient for the transcription factor, interferon consensus sequence binding protein (ICSBP), are immunodeficient and develop disease symptoms similar to human chronic myeloid leukemia (CML). To elucidate the hematopoietic disorder of ICSBP−/− mice, we investigated the growth, differentiation, and leukemogenic potential of ICSBP−/−myeloid progenitor cells in vitro, as well as by cell-transfers in vivo. We report that adult bone marrow, as well as fetal liver of ICSBP-deficient mice harbor increased numbers of progenitor cells, which are hyperresponsive to both granulocyte macrophage colony-stimulating factor (GM-CSF) and G-CSF in vitro. In contrast, their response to M-CSF is strongly reduced and, surprisingly, ICSBP−/− colonies formed in the presence of M-CSF are mostly of granulocytic morphology. This disproportional differentiation toward cells of the granulocytic lineage in vitro parallels the expansion of granulocytes in ICSBP−/− mice and correlates with a 4-fold reduction of M-CSF receptor expressing cells in bone marrow. Cell transfer studies showed an intrinsic leukemogenic potential and long-term reconstitution capability of ICSBP−/− progenitors. Further experiments demonstrated strongly reduced adhesion of colony-forming cells from ICSBP−/− bone marrow to fibronectin. In summary, ICSBP−/− myeloid progenitor cells share several abnormal features with CML progenitors, suggesting that the distal parts of signaling pathways of these two disorders are overlapping.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V94.11.3764
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1999
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 5
    Online Resource
    Online Resource
    TIRC7 Inhibits T Cell Proliferation by Modulation of CTLA-4 Expression
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 177, No. 10 ( 2006-11-15), p. 6833-6841
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 177, No. 10 ( 2006-11-15), p. 6833-6841
    Abstract: Ab targeting of TIRC7 has been shown previously to inhibit T cell proliferation and Th1 lymphocyte-associated cytokine production. In this study, we demonstrate that Ab targeting of TIRC7 induces early cell surface expression of CTLA-4. The majority of stimulated CD4+ and CD8+ human T cells coexpress CTLA-4 and TIRC7. Similar to CTLA-4, TIRC7 rapidly accumulates at the site of Ag adhesion upon T cell activation. TIRC7 seems to colocalize with CTLA-4 in human T cells, and both molecules are associated with clathrin-coated vesicles, indicating they share intracellular transport systems. Moreover, Ab targeting of TIRC7 results in an early activation of CTLA-4 transcription. The inhibition of cell proliferation mediated by TIRC7 is dependent on CTLA-4 expression because the TIRC7-mediated inhibitory effects on cell proliferation and cytokine expression are abolished by Ab blockade of CTLA-4. Splenocytes obtained from CTLA-4-deficient mice are not responsive to TIRC7 Ab targeting. Thus, TIRC7 acts as an upstream regulatory molecule of CTLA-4 expression.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.177.10.6833
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Severe Impairment in Early Host Defense Against Listeria monocytogenes in Mice Deficient in Acid Sphingomyelinase
    The American Association of Immunologists ; 2003
    In:  The Journal of Immunology Vol. 170, No. 5 ( 2003-03-01), p. 2621-2628
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 170, No. 5 ( 2003-03-01), p. 2621-2628
    Abstract: The phagolysosomal compartment is crucial for the defense against infection with intracellular pathogens. Within this compartment, the TNF- and IFN-γ-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D. To investigate the possible role of ASMase as a mediator of the antibacterial effects of TNF and IFN-γ, ASMase−/− mice were infected with Listeria monocytogenes. ASMase−/− mice showed a dramatically increased susceptibility to L. monocytogenes (LD50 ∼100 CFU) when compared with syngeneic wild-type mice (LD50 ∼10,000 CFU). In L. monocytogenes-challenged ASMase−/− mice, IFN-γ serum levels as well as IL-1β and IL-6 secretion by macrophages were similar to those observed in wild-type C57BL/6 mice. Although macrophages and granulocytes from ASMase−/− mice showed intact production of reactive nitrogen intermediates and oxidative burst, ASMase−/− macrophages proved completely incapable of restricting the growth of L. monocytogenes in vitro. The results of this study suggest that ASMase is crucially required for the intracellular control of L. monocytogenes in macrophages and granulocytes by nonoxidative mechanisms.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.170.5.2621
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2003
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    AML1-ETO Inhibits Maturation of Multiple Lymphohematopoietic Lineages and Induces Myeloblast Transformation in Synergy with ICSBP Deficiency
    Rockefeller University Press ; 2002
    In:  The Journal of Experimental Medicine Vol. 196, No. 9 ( 2002-11-04), p. 1227-1240
    Details
    In: The Journal of Experimental Medicine, Rockefeller University Press, Vol. 196, No. 9 ( 2002-11-04), p. 1227-1240
    Abstract: The translocation (8;21), generating the AML1-ETO fusion protein, is one of the most frequent chromosomal abnormalities associated with acute myelogenous leukemia (AML). To elucidate its role in oncogenesis, bone marrow (BM) cells were infected with a retroviral vector carrying AML1-ETO and transplanted into mice. In contrast to previous transgenic mouse models, we show that AML1-ETO directly stimulates granulopoiesis, suppresses erythropoiesis, and impairs the maturation of myeloid, B, and T lymphoid cells in vivo. To determine the significance of earlier findings that expression of the tumor suppressor ICSBP is often downregulated in AML myeloblasts, AML1-ETO was introduced into BM cells derived from mice lacking the interferon regulatory factor ICSBP. Our findings demonstrate that AML1-ETO synergizes with an ICSBP deficiency to induce myeloblastic transformation in the BM, reminiscent of AML.
    Type of Medium: Online Resource
    ISSN: 1540-9538 , 0022-1007
    URL: Article
    DOI: 10.1084/jem.20020824
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2002
    detail.hit.zdb_id: 1477240-1
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  • 8
    Online Resource
    Online Resource
    Interleukin-2 Deficient Mice: A New Model to Study Autoimmunity and Self-Tolerance
    Wiley ; 1995
    In:  Immunological Reviews Vol. 148, No. 1 ( 1995-12), p. 35-44
    Details
    In: Immunological Reviews, Wiley, Vol. 148, No. 1 ( 1995-12), p. 35-44
    Type of Medium: Online Resource
    ISSN: 0105-2896 , 1600-065X
    URL: Issue
    URL: Article
    DOI: 10.1111/imr.1995.148.issue-1
    DOI: 10.1111/j.1600-065X.1995.tb00092.x
    Language: English
    Publisher: Wiley
    Publication Date: 1995
    detail.hit.zdb_id: 2038276-5
    SSG: 12
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  • 9
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    Online Resource
    Importance of Receptor Usage, Fli1 Activation, and Mouse Strain for the Stem Cell Specificity of 10A1 Murine Leukemia Virus Leukemogenicity
    American Society for Microbiology ; 2007
    In:  Journal of Virology Vol. 81, No. 2 ( 2007-01-15), p. 732-742
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 81, No. 2 ( 2007-01-15), p. 732-742
    Abstract: Murine leukemia viruses (MuLV) induce leukemia through a multistage process, a critical step being the activation of oncogenes through provirus integration. Transcription elements within the long terminal repeats (LTR) are prime determinants of cell lineage specificity; however, the influence of other factors, including the Env protein that modulates cell tropism through receptor recognition, has not been rigorously addressed. The ability of 10A1-MuLV to use both PiT1 and PiT2 receptors has been implicated in its induction of blast cell leukemia. Here we show that restricting receptor usage of 10A1-MuLV to PiT2 results in loss of blast cell transformation capacity. However, the pathogenicity was unaltered when the env gene is exchanged with Moloney MuLV, which uses the Cat1 receptor. Significantly, the leukemic blasts express erythroid markers and consistently contain proviral integrations in the Fli1 locus, a target of Friend MuLV (F-MuLV) during erythroleukemia induction. Furthermore, an NB-tropic variant of 10A1 was unable to induce blast cell leukemia in C57BL/6 mice, which are also resistant to F-MuLV transformation. We propose that 10A1- and F-MuLV actually induce identical (erythro)blastic leukemia by a mechanism involving Fli1 activation and cooperation with inherent genetic mutations in susceptible mouse strains. Furthermore, we demonstrate that deletion of the Icsbp tumor suppressor gene in C57BL/6 mice is sufficient to confer susceptibility to 10A1-MuLV leukemia induction but with altered specificity. In summary, we validate the significance of the env gene in leukemia specificity and underline the importance of a complex interplay of cooperating oncogenes and/or tumor suppressors in determining the pathogenicity of MuLV variants.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01430-06
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
    detail.hit.zdb_id: 1495529-5
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  • 10
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    Online Resource
    Simian Virus 40 Large-T-Antigen-Specific Rejection of mKSA Tumor Cells in BALB/c Mice Is Critically Dependent on both Strictly Tumor-Associated, Tumor-Specific CD8 + Cytotoxic T Lymphocytes and CD4 + T Helper Cells
    American Society for Microbiology ; 2001
    In:  Journal of Virology Vol. 75, No. 22 ( 2001-11-15), p. 10593-10602
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 75, No. 22 ( 2001-11-15), p. 10593-10602
    Abstract: Protective immunity of BALB/c mice immunized with simian virus 40 (SV40) large T antigen (TAg) against SV40-transformed, TAg-expressing mKSA tumor cells is critically dependent on both CD8 + and CD4 + T lymphocytes. By depleting mice of T-cell subsets at different times before and after tumor challenge, we found that at all times, CD4 + and CD8 + cells both were equally important in establishing and maintaining a protective immune response. CD4 + cells do not contribute to tumor eradication by directly lysing mKSA cells. However, CD4 + lymphocytes provide help to CD8 + cells to proliferate and to mature into fully active cytotoxic T lymphocytes (CTL). Depletion of CD4 + cells by a single injection of CD4-specific monoclonal antibody at any time from directly before injection of the vaccinating antigen to up to 7 days after tumor challenge inhibited the generation of cytolytic CD8 + lymphocytes. T helper cells in this system secrete the typical Th-1 cytokines interleukin 2 (IL-2) and gamma interferon. Because in this system TAg-specific CD8 + cells secrete only minute amounts of IL-2, it appears that T helper cells provide these cytokines for CD8 + T cells. Moreover, this helper effect of CD4 + T cells in mKSA tumor rejection in BALB/c mice does not simply improve the activity of TAg-specific CD8 + CTL but actually enables them to mature into cytolytic effector cells. Beyond this activity, the presence of T helper cells is necessary even in the late phase of tumor cell rejection in order to maintain protective immunity. However, despite the support of CD4 + T helper cells, the tumor-specific CTL response is so weak that only at the site of tumor cell inoculation and not in the spleen or in the regional lymph nodes can TAg-specific CTL be detected.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.75.22.10593-10602.2001
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
    detail.hit.zdb_id: 1495529-5
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