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  • Differentiation  (1)
  • Jun-B  (1)
  • 1
    ISSN: 1432-1335
    Keywords: Differentiation ; Leukemia cell ; Stromal cell ; Colony-stimulating factor ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Differentiation of the rat myelomonocytic leukemia cell line (c-WRT-7) was investigated, by co-culture with a rat embryonic bone marrow preadipose cell line (REC A16). Co-cultivation with REC A16, or with conditioned medium from REC A16 cultures (REC-CM), induced differentiation of c-WRT-7 cells to macrophages. A soluble factor(s) produced by REC A16 appeared to be responsible for the differentiation of c-WRT-7. Because REC-CM was associated with colony-stimulating activity on murine marrow progenitors, c-WRT-7 cells were cultured with various colony-stimulating factors (CSF) and it was found that macrophage CSF (M-CSF) significantly induced differentiation of c-WRT-7. We further demonstrated that both the colonystimulating and differentiation-inducing activities of REC-CM were significantly blocked by anti-M-CSF antiserum. These results suggest that the differentiation of c-WRT-7 is due to M-CSF produced by REC A16. Co-culture of these two cell lines should provide a useful model to study the mechanisms of interaction between leukemia cells and marrow stroma.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1572-994X
    Keywords: HPV16 ; enhancer ; cell type- specificity ; Jun-B ; c-Fos
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The epithelial cell type- specific enhancer of the human papillomavirus (HPV) type 16 termed the long control region (LCR) carries three AP-1 binding sites. We investigated the roles of the AP-1 sites for transactivation of the LCR byJun-B that may be a cell type specific- transactivator for the HPVs in human fibroblasts in which expression of the endogenousjun-B gene is low. Transient expression ofJun-B alone poorly activated transcriptional activity of the LCR. However, when combined with c-Fos,Jun-B activated the LCR. The promoter-proximal AP-1 site was required for transactivation of the LCR byJun-B:c-Fos, but the site itself was not sufficient for the maximal response. The proposed cell type specific- regulatory element that harbors binding sites for NF1 as well as TEF-1 and PEA3 motifs, but neither other AP-1 sites nor the proximal enhancer region, could augment the transcriptional response of the promoter-proximal AP-1 site toJun-B:c-Fos.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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