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  • Life and Medical Sciences  (2)
  • VCAM-1  (1)
  • interleukin-6-dependent B cells  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Significance of VLA-4–VCAM-1 interaction and CD44 for transendothelial invasion in a bone marrow metastatic myeloma model (1999)
    Springer
    Clinical & experimental metastasis 17 (1999), S. 623-629 
    Details
    ISSN: 1573-7276
    Keywords: bone marrow ; transendothelial invasion ; CD44 ; VCAM-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In previous work, we established the B9/BM1 syngeneic murine bone marrow metastasis model. Interleukin (IL)-6-dependent, IL-1-producing B9/BM1 cells, which colonize the vertebral and femoral marrow after i.v. injection, show great similarity in cell surface phenotype to human myeloma cells, especially the expression of 3 adhesion molecules, CD44, VLA-4 and ICAM-1. Here we investigated the function of these adhesion molecules by binding and transendothelial invasion assays using a newly established bone marrow-derived endothelial cell line (BMEC). A combination of monoclonal antibodies against CD44 and VLA-4 significantly inhibited the adherence of B9/BM1 cells to BMEC and anti-CD44 mAb especially blocked B9/BM1 transendothelial invasion of unstimulated BMEC cells. Results of additional experiments, in which the cells were treated with anti-CD44 and hyaluronidase, demonstrated that the interaction of CD44 molecules on B9/BM1 cells with hyaluronan on BMEC cells was a critical factor in both adhesion and transendothelial invasion in this model. However, stimulation of BMEC with TNFα resulted in increased invasion by B9/BM1 cells, which was completely suppressed by anti-VCAM-1 mAb, implicating a significant role of this adhesion molecule in this process during inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006715504719
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Association between ICAM-1 expression and metastatic capacity of murine B-cell hybridomas (1993)
    Springer
    Clinical & experimental metastasis 11 (1993), S. 213-226 
    Details
    ISSN: 1573-7276
    Keywords: bone marrow metastasis ; ICAM-1 ; interleukin-1a ; interleukin-6-dependent B cells ; natural killer cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: We previously reported that a derivative of the interleukin-6 (IL-6)-dependent B9 B-cell hybridoma (B9/LPNUIL) constitutively expressing an interleukin-1a (IL-1a) gene introduced by retrovirus-mediated gene transfer preferentially metastasized to bone marrow following intravenous injection into unirradiated syngeneic BALB/c mice. B9/LPNUIL cells recovered from the femoral marrow of a recipient with hind limb paralysis (denoted B9/BMl) retained their IL-6-dependency yet displayed enhanced metastatic capacity during serial transplantation in vivo. In contrast, autonomously-growing B9 variants spontaneously arising in vitro or IL-6-independent B9 derivatives created by infection with recombinant IL-6 retroviruses rarely gave rise to experimental metastases in syngeneic BALB/c or nude mice. Examination of cell adhesion molecule profiles by immunofluorescence flow cytometry has revealed high levels of CD44, moderate levels of VLA-4 and low levels of LFA-1 on all B9-series cells. By comparison, ICAM-1 expression was significantly elevated on B9/BMl cells, with independent isolates stably expressing about 4-fold higher levels which were paralleled by corresponding increases in the steady-state levels of ICAM-1 mRNA. l-Selectin was not expressed by any of the cell lines. Despite higher ICAM-1 levels, cell aggregation assays revealed that LFA-1-ICAM-1 adhesive interactions were not involved in the homotypic adhesion of B9/BM1 cells but rather that binding of CD44 to endogenously-synthesized hyaluronan was responsible. Furthermore, B9/BM1 cells expressing high levels of ICAM-1 were found to be less susceptible to cytolysis by natural killer (NK) cells than their weakly metastatic or nonmetastatic counterparts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00114979
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  • 3
    Electronic Resource
    Electronic Resource
    Transposition of intracisternal A-particle genes in mouse hybridomas (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 121 (1984), S. 29-38 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A nonfunctional immunoglobulin k-chain gene previously shown to contain intracisternal A-particle (IAP) sequences within one of its introns was further characterized by DNA and RNA blot analysis. The results of these experiments indicate that the joining of the IAP sequences to the k-chain gene was a consequence of an insertion event which presumably involved a complete IAP gene. It is postulated that the insertion of the IAP gene has altered the secondary or tertiary structure of the k-chain pre-mRNA, resulting in the utilization of a “cryptic” 5′ splice site. The detection of numerous IAPs in isogenous wild-type hybridoma cells by electron microscopy suggests that transposition of IAP genes might proceed via the reverse transcription of IAP-associated RNA. These findings raise the possibility that transposition of IAP genes might also occur in other IAP-positive mouse cells. In particular, insertional mutagenesis by IAP genes in IAP-producing tumor cells could play a role in tumor cell heterogeneity or tumor progression. We have also investigated the possibility that IAP-related sequences might be present in the human genome. Using nonstringent hybridization conditions, multiple discrete restriction fragments could be detected in human DNA with several mouse IAP-specific probes.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041210406
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Suppression of programmed death and G1 arrest in B-cell hybridomas by interleukin-6 is not accompanied by altered expression of immediate early response genes (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 145 (1990), S. 564-574 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The murine B-cell hybridoma B9 requires interleukin-6 (IL-6) for its survival and proliferation in vitro. We show here that withdrawal of IL-6 from B9 cultures results in programmed death, concomitant with arrest of the cells in the G1 phase of the cell cycle. Unlike several other systems that undergo programmed cell death, no induction of transcripts corresponding to the testosterone-repressed message-2 or transglutaminase genes is observed during this process. Upon readdition of IL-6 to G1-arrested B9 cells, viability is maintained and entry into S phase occurs after a lag period of 10 to 12 hr. Northern blot analysis showed that the immediate-early mRNAs normally induced shortly after growth factor stimulation in quiescent fibroblasts (c-fos, c-jun, Egr-1, c-myc, JE, and KC), and other growth-related genes (2F1, c-Ha-ras, and p53), are either not induced or remain unchanged during G1 to S phase progression. A correlation was found, however, between the temporal pattern of expression of several G1/S phase genes (dihy-drofolate reductase, thymidine kinase, transferrin receptor, and histone H3) and DNA synthesis. These results demonstrate that IL-6-induced viability and growth of hybridoma (and, presumably, plasmacytoma) cells is mediated via novel signal transduction pathways.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041450325
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    Paper (German National Licenses)
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