By Frank J. Dixon
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Extra info for Advances in Immunology, Vol. 55
Several lines of evidence now indicate that SCF can influence the development of T cells, B cells, and NK cells, but that SCF-independent mechanisms can compensate for the lack of SCF in early stages of lymphoid cell development and that mature lymphocytes exhibit little responsiveness to SCF. T cells are derived from bone marrow stem cells that migrate to the thymus; after maturation within the thymus, mature T cells enter the peripheral circulation (Palacios and Pelkonen, 1988). , 1992b). SCF transcripts have been observed in a number of thymic stromal cell lines (D.
1991). Duronio et al. In accord with the results of Rottapel et al. , 1992). Lev et al. (1991)investigated the signal transduction mediated by a chimeric receptor kinase composed of the extracellular ligand-binding domain of the epidermal growth factor (EGF) receptor and the transmembrane and cytoplasmic domains of the SCFR. They demonstrated that on binding EGF, the ligand-receptor complex underwent endocytosis and degradation, and showed that the activated SCFR kinase strongly associated with PI3'K and an 85-kDa phosphoprotein and coupled to PLC-yl and the Raf-1 protein kinase, but did not significantly change levels of inositol phosphate.
1 or HEL). In over 5 kb of upstream genomic DNA, we found no evidence for additional elements that significantly influenced luciferase activities. These data showed that the mouse c-kit promoter also functions in human c-kit-positive HEL cells, suggesting that important cis elements and trans-acting factors involved in the regulation of c-kit expression are likely to be conserved. , 1992). The mouse c-kit promoter lacks well-defined promoter elements such as TATA or CCAAT boxes. , 1991),even though c-kit is expressed in the erythroid and mast cell lineages.