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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Relationship of levels and kinetics of H-ras expression to transformed phenotype and loss of TGF-beta 1-mediated growth regulation in intestinal epithelial cells.

Immortalized, nontumorigenic rat intestinal epithelial cells (IEC-18) can be transformed to tumorigenicity by expression of an activated human H-ras gene. Here we describe the characteristics of an IEC-18 cell line in which the activated human H-ras gene has been introduced under the control of the steroid-sensitive promoter of the mouse mammary tumor virus long-terminal repeat. The clonal cell line (IEC-18 C125) is phenotypically normal in the absence of the transcription inducer, dexamethasone, and transformed when treated with high levels of inducer. Transformed morphology and growth characteristics are dependent on levels of H-ras expression. IEC-18 C125 cells have been used to demonstrate a general relationship (dose and kinetic) between H-ras expression and loss of TGF-beta 1-mediated growth regulation. This effect occurs concomitantly with a ras-dependent change in the profile of TGF-beta 1 binding proteins.[1]

References

  1. Relationship of levels and kinetics of H-ras expression to transformed phenotype and loss of TGF-beta 1-mediated growth regulation in intestinal epithelial cells. Zhao, J., Buick, R.N. Exp. Cell Res. (1993) [Pubmed]
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